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Vol. 17 Num. 67 April-June 2015
Vol. 17 Num. 67 April-June 2015 ISSN 1665-5796
Association between bullying
and major depressive disorder
in a psychiatric consultation
Internet addiction in university
medical students
Social networks in medical
practice
Is it an epileptic seizure?
MEDICINA UNIVERSITARIA
Migraine management
JOURNAL OF SCIENCE AND RESEARCH
SCHOOL OF MEDICINE AND “DR. JOSÉ ELEUTERIO GONZÁLEZ” UNIVERSITY HOSPITAL
UNIVERSIDAD AUTÓNOMA DE NUEVO LEÓN
EDITORIAL COMMITTEE
General Director
Editor in Chief
Santos Guzmán López
Ariel Ernesto Arias Ramírez
Ottawa, Canadá
Félix Ramón Cedillo Salazar
Alejandro Arroliga
Temple, EEUU
Editor
David Gómez Almaguer
Norbert W. Brattig
Hamburgo, Alemania
Editor
Francisco Javier Bosques Padilla
María de los Ángeles Castro Corona
Monterrey, México
Technical Editor
Carlos Alberto Acosta Olivo
Ricardo Cerda Flores
Monterrey, NL
Technical Editor
Beatriz Elizabeth De la Fuente Cortez
Salvador Cruz Flores
St. Louis, EEUU
Technical Editor
Alfredo Arias Cruz
Assistant Editor
José Carlos Jaime Pérez
José A. González González
Monterrey, México
Oscar González Llano
Monterrey, México
Patricia de Gortari
EDITORIAL BOARD
Hugo Alberto Barrera Saldaña
Monterrey, México
René Raúl Drucker Colín
DF, México
Rubén Lisker Y.
DF, México
Ruy Pérez Tamayo
DF, México
Guillermo J. Ruiz Argüelles
Ralph Weissleder
Oliverio Welsh Lozano
Puebla, México
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Monterrey, México
Madrid, España
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Mérida, México
Elvira Garza González
Pali Hungin
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Cuernavaca, México
Susana Kofman Alfaro
DF, México
David Kershenobich Stalnikowitz
DF, México
Francisco López Jiménez
Rochester, EEUU
Xavier López Karpovitch
DF, México
Monterrey, México
DF, México
Claudia Elizalde Molina
Monterrey, México
Guillermo I. Pérez Pérez
Nueva York, EEUU
Mario Henry Rodríguez
Cuernavaca, México
Isaías Rodríguez Balderrama
Monterrey, México
Alejandro Ruiz Argüelles
Puebla, México
Guillermo J. Ruiz Delgado
Puebla, México
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Madrid, España
Josep María Segur Vilalta
Gregorio A. Sicard
Eloy Cárdenas Estrada
Monterrey, México
Rolando Tijerina Menchaca
Antonio Costilla Esquivel
Monterrey, México
Lyuba Varticovski
Joseph Varon
Emma Bertha García Quintanilla
Stockton-on-Tees, Reino Unido
Patricia Ileana Joseph Bravo
Nahum Méndez Sánchez
English translation and style:
Monterrey, México
José Luis Iglesias Benavides
Laura E. Martínez de Villarreal
Biostatistics advisor:
DF, México
Francisco Forriol Campos
Carlos E. Baena-Cagnani
Jordi Sierra Gil
Barcelona, España
St. Louis, EEUU
Monterrey, México
Maryland, EEUU
Houston, EEUU
Córdoba, Argentina
Barcelona, España
Juan Pablo Figueroa Delgado
Medicina Universitaria, Volumen 17, número 67, abril-junio 2015, es una publicación trimestral de la Revista de Investigación y Ciencia de la Facultad de Medicina
y Hospital Universitario Dr. José E. González de la U.A.N.L. ISSN 1665-5796.
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JOURNAL OF SCIENCE AND RESEARCH
SCHOOL OF MEDICINE AND “DR. JOSÉ ELEUTERIO GONZÁLEZ” UNIVERSITY HOSPITAL
UNIVERSIDAD AUTÓNOMA DE NUEVO LEÓN
Contents
EDITORIAL
Volume 17
Issue 67
April-June 2015
69
Human communication, the internet, medicine and its addictions
D. Gómez-Almaguer, C.A. Acosta-Olivo, E.B. García-Quintanilla, J.C. Jaime-Pérez
ORIGINAL ARTICLES
71
Somatotype of patients with type 2 diabetes in a university hospital in Mexico
K. Urrutia-García, T.J. Martínez-Cervantes, O. Salas-Fraire, N.P. Guevara-Neri
75
Association between bullying and major depressive disorder in a psychiatric
consultation
L. Perales-Blum, M. Juárez-Treviño, N. Capetillo-Ventura, G. Rodríguez-Gutiérrez,
M. Valdés-Adamchik, J. Treviño-Treviño, M. Cáceres-Vargas
80
Levels of insulin and HOMA-IR in adolescents in Saltillo, Coahuila, Mexico
M.A. González-Zavala, A. Velasco-Morales, J.J. Terrazas-Flores, M.G. de la Cruz-Galicia,
A.C. Cepeda-Nieto, A. Hernández-del Río
88
Internet addiction in university medical students
N. Capetillo-Ventura, M. Juárez-Treviño
CLINICAL CASE
94
Decision-making in the management of an incomplete urethral duplication in a
young male
R.d.J. Treviño-Rangel, B.A. Bodden-Mendoza, N. Cantú-Salinas, M.A. García-Rodríguez
SCIENTIFIC LETTERS
97
Thrombosed great saphenous vein aneurysm accompanied by venous thrombosis
F.G. Rendón-Elías, R. Albores-Figueroa, L.S. Arrazolo-Ortega, F. Torres-Alcalá,
M. Hernández-Sánchez, L.H. Gómez-Danés
102
Case report: Diagnostic reconceptualization in the DSM-V on somatoform disorders
D. Ibarra-Patrón, G. Medina-Vidales, C. Garza-Guerrero
REVIEW ARTICLES
108
Social networks in medical practice
B.E. Ibarra-Yruegas, C.R. Camara-Lemarroy, L.E. Loredo-Díaz, O. Kawas-Valle
114
Complex regional pain syndrome (CRPS), a review
S. Castillo-Guzmán, T.A. Nava-Obregón, D. Palacios-Ríos, J.Á. Estrada-Cortinas,
M.C. González-García, J.F. Mendez-Guerra, O. González-Santiago
EXPERT’S CORNER: A PERSONAL APPROACH
122
Is it an epileptic seizure?
C.E. Muñiz-Landeros
126
Migraine management
A. Marfil
Medicina Universitaria. 2015;17(67):69---70
www.elsevier.es/rmuanl
EDITORIAL
Human communication, the internet, medicine and its
addictions
Communication amongst human beings is vital for the development and support of the human race. It is impressive how
we have gone from smoke signals, carrier pigeons, ‘‘foot’’
or ‘‘horse’’ messengers, to land and air mail, fax, and telephones. However, nothing is as interesting and as incredible
as communication through the internet and its derivations,
like ‘‘social networks’’ and the use of the smartphone. This
device allows the user to be connected with practically
everybody, it even allows audio and video recording and to
make commercial transactions. The question is, how does
this impact health, science and medicine? The answer is
not that simple, and we approach this topic in this issue
of Medicina Universitaria.
Nowadays the number of places where the internet is
considered necessary is growing. There are more and more
cities implementing public internet access in zones like
parks or squares. This reflects that the need for information
and to ‘‘be connected’’ is now a cultural imperative. Nevertheless, up to what point can we consider internet access
and social networking a part of the normal development of
the individual, and when this can be considered to be an
addiction?
It is worth noting that in the year 2011 the United Nations
(UN) declared access to the internet to be a human right.
However, there are some countries with restrictions for
internet use, such as China, North Korea, Iran and Egypt.
Moreover, there is the risk of being spied upon and having
private information stolen and used for criminal purposes,
like identity thief. The UN confirmed that access to the web
should be maintained, being especially valuable during ‘‘key
political moments’’ like elections, times of social unrest and
historic political anniversaries.
Social networks have become more and more sought
after by adolescents and young adults, who find a way of
‘‘socializing’’ and keeping in touch with others in order to
update their personal situation in social and professional
situations.
Up to what point is the relationship between doctor and
patient, established through social networks, considered to
be prudent? Patients can experience the vulnerability of
their personal information, due to the fact that a doctor
may publish the patient’s medical or personal information,
even when this occurs without giving out any personal information. We must find and maintain that line which divides
professional activities from personal relationships. We must
understand that patients trust in their right to privacy
implied in the doctor-patient relationship.
Internet addiction disorder (IAD) is recognized as a disease. First described in 1996 by Young,1 it has, however,
become a bigger issue in recent years, given the large
amount of people presenting said pathology. In a German report in 2013,2 where 71 patients with this disorder
were studied, a high incidence of depression, obsessivecompulsive symptoms and interpersonal sensitivity was
documented (Wölfing et al., 2013).
Scales have been developed in order to assess internet
addiction, like the one described by Young, which, in 20
items, allows us to assess the severity of addiction. The
highest score is between 80 and 100 points, an indication
that the use of the internet is causing serious problems in
the life of the patient, making these subjects, including
doctors, into patients who suffer from a type of addiction
whose consequences are still unknown in detail. Therefore,
in this issue of ‘‘Medicina Universitaria’’, we present two
interesting studies on the topic.
Social networks
The most famous social network is, without a doubt,
‘‘Facebook’’, with over 1.35 billion users worldwide. Among
the countries with the most accounts created are Brazil,
India, Indonesia, Mexico and the US. This social network is
on the rise to capture more users, and in 2012 it acquired
Instagram, which is a social network for photo and video
sharing. Moreover, the user is able to edit the pictures within
the same platform. It is estimated to have over 300 million
users worldwide.
http://dx.doi.org/10.1016/j.rmu.2015.03.004
1665-5796/© 2015 Published by Masson Doyma México S.A. on behalf of Universidad Autónoma de Nuevo León. This is an open access article
under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
70
EDITORIAL
Twitter is considered to be an internet messenger,
with over 500 million users worldwide, created as a
‘‘microblogging’’ site, where you have to express your idea
in 140 characters or less. It is currently one of the fastestgrowing social networks.
The other side of the coin
In contrast, social networks have become a very important
and useful medium for medical education. Generations of
medical students, who are our students for the time being,
are ‘‘cybernetic entities’’. They were born when the internet was just beginning, along with social networks, and it
is almost imprinted in their DNA. While in other professional careers not related to healthcare they have been
teaching through the internet, and everything related to it,
for some time, doctors and future doctors have now fully
entered this type of education. We have at our disposition,
as professors and students, e-books, the internet, tablets,
smartphones, Facebook, Twitter, ‘‘whatsapp’’, etc. where
through closed groups we are able to communicate instantly.
As a matter of fact, ‘‘Medicina Universitaria’’ uses several
of these means of communication to improve and expedite
reception, revision, editing, publication and access to our
scientific articles.
There are internet sites created by medical schools of the
major North American universities (www.medpedia.com)
(McKenna et al., 2011)3 where students can go to have
their questions answered. They are able to participate in
discussions right from their smartphones, send homework,
communicate with their counterparts in other countries,
etc.
Regarding the internet and our patients, we are able
to communicate with them through social networks and
educate them regarding the use of the internet to obtain
medical information, since there are some sites which are
fraudulent and offer erroneous, misleading or fake information. We are able to recommend sites we know, since
many of our patients and their families will ‘‘check’’ the
information given to them. The personal information of
our patients is something we have to take care of, since
this is confidential and we run the risk of being ‘‘hacked’’
and putting our patients’ information at risk.
One recommendation is to keep our public information
separate from our private information, having two accounts
and monitoring who may have access to our private Facebook or Twitter accounts.
We can’t look back. Social networks are, for better
(education, information, socializing) or for worse (Internet
addiction disorder), here to stay in our everyday life.
The Homo videns dilemma, to be or not to be
Up to what point is it possible to establish the limit between
what is ‘‘good’’, ‘‘healthy’’ or ‘‘right’’ in relationship to the
way human beings interact with each other and the content
to which we are exposed to when using the internet? Who
can establish the difference between use and abuse? On
a professional basis, which are the effects of the use of
or addiction to the internet in the behavior, diagnoses and
therapeutic decision-making of current and future doctors?
Perhaps our behavior adheres to the aspects exposed
and criticized by Vargas-Llosa in his crude analysis of contemporary society and its irrational expectation of being
relentlessly ‘‘entertained’’, exposed in his essay ‘‘The
Nightmare of the Entertainment Society’’ (La Civilización
del Espectáculo).
If, at the end of the day, Man is the measure of all things,
as proposed by the Greek sophist Protagoras 400 years before
Christ, then the questions and dilemmas proposed in this
paper should be answered according to the nature, education and the degree of consciousness and responsibility of
each individual. And that is the crux of the matter when it
comes to the use of the internet, and the influence of its
educational processes on the doctor. That is to say, in providing the mechanisms and intellectual processes that gives
each person the ability to utilize the available information
on the web in an optimal manner and use it for their own
personal benefit, and, principally and above all, as a doctor
with his patients.
References
1. O’Reilly M. Internet addiction: a new disorder enters the medical
lexicón. CMAJ. 1996;154:1882---3.
2. Wölfling K, Beutel ME, Koch A, Dickenhorst U, Müller KW. Comorbid internet addiction in male clients of inpatient addiction
rehabilitation centers: psychiatric symptoms and mental comorbidity. J Nerv Ment Dis. 2013;201:934---40.
3. McKenna MP, D’Alessandro D. Social networks and the practice
of medicine: harnessing powerful opportunities. J Pediatr.
2011;158:1---2, http://dx.doi.org/10.1016/j.jpeds.2010.09.037.
David Gómez-Almaguer ∗ , Carlos Alberto Acosta-Olivo,
Emma Bertha García-Quintanilla, José Carlos Jaime-Pérez
Editor de Revista Medicina Universitaria
∗
Corresponding author at: Av. Madero y Dr. Eduardo A.
Pequeño Col. Mitras Centro, Monterrey, N.L., Mexico.
E-mail address: [email protected]
(D. Gómez-Almaguer).
Medicina Universitaria. 2015;17(67):71---74
www.elsevier.es/rmuanl
ORIGINAL ARTICLE
Somatotype of patients with type 2 diabetes in a
university hospital in Mexico
K. Urrutia-García ∗ , T.J. Martínez-Cervantes, O. Salas-Fraire, N.P. Guevara-Neri
Department of Sports Medicine and Rehabilitation of the ‘‘Dr. José Eleuterio González’’ Univertisty Hospital of the Universidad
Autónoma de Nuevo León, Mexico
Received 12 September 2014; accepted 21 January 2015
Available online 13 May 2015
KEYWORDS
Somatotype;
Endomorph;
Mesomorph;
Ectomorph;
Diabetes
Abstract
Objective: The aim of the study was to determine the somatotype of Mexican type 2 diabetes
patients, using the Heath and Carter somatotype method.
Methods: The study was conducted on 180 subjects, who underwent an anthropometry following the restricted format established by the International Society for the Advancement of
Kinanthropometry (ISAK). A database was elaborated and we obtained descriptive measures
such as age, weight, height and the 3 somatotype components.
Results: The average age was 58 years (±11 SD); 58.6 years (±10.9 SD) for males and 56.8 years
(±11 SD) for females. The average weight was 77.5 kg (±16.7); 80.7 kg (±14.6 SD) for males and
75 kg (±17.8 SD) for females. The results indicate that the mean somatotype for Mexican type
2 diabetes patients was 6.3, 6.4, 0.6. Diabetic females have higher mean values for endomorphy (7.3) and mesomorphy (6.7) and lower mean values for ectomorphy (0.4) than their male
counterparts (5.0, 6.0 and 0.8, respectively). It is evident that endomorphy is predominantly
in females, in contrast to males, since there are known differences in fat and muscular mass
between both genders.
Conclusions: The results are similar to previous studies presented for other diabetic populations. Sex differences are significant and especially higher for the endomorphic component,
with generally higher values in females. It is important to continue this research direction with
bigger samples and the study of other risk factors that directly affect the somatotype of type
2 diabetes.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an
open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/bync-nd/4.0/).
∗ Corresponding author at: Departamento de Medicina del Deporte y Rehabilitación del Hospital Universitario ‘‘José Eleuterio González’’
de la Universidad Autónoma de Nuevo León, Ave. Gonzalitos Col. Mitras Centro, C.P. 64460 Monterrey, Nuevo León, Mexico.
Tel.: +52 81 83294207.
E-mail address: k [email protected] (K. Urrutia-García).
http://dx.doi.org/10.1016/j.rmu.2015.01.006
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
72
Introduction
Diabetes mellitus is a global health problem, as well as
the most well-known disorder for centuries. However, the
knowledge of its etiology, natural history and epidemiology
remain incomplete.1---2 The worldwide prevalence of diabetes mellitus has increased exponentially. In the last three
decades, the number of people with type 2 diabetes has
doubled.3 Despite being an elderly related disease, in the
last few years the number of young people diagnosed with
the disease is on the rise. Within its pathophysiology, the
genetic component is of great importance in diabetes mellitus; nevertheless, it has been linked to obesity and scarce
physical activity or a sedentary lifestyle.4
Mexico has suffered the fastest changes ever recorded
in the history of food and diet patterns and physical activities resulting in obesity. Diabetes plays a major role, being
responsible for almost 14% of all deaths. The increasing
prevalence of obesity in children and adults, in addition to
the metabolic syndrome, suggests that the situation could
have a greater impact in the next few years.5 The National
Health and Nutrition Survey of 2012 estimated that 9.2% of
Mexican adults had already been diagnosed with diabetes
mellitus. This reflects an important increase in comparison
to the observed results in 2000, where the rate was 5.8%,
and 2006, with 7%.6
The somatotype is a method used to evaluate, study and
comprehend body shape and composition in terms of bone,
muscle and fatty tissue dimensions.7 First described by Sheldon et al. in 1940, later modified by Heath and Carter in
1967, it was defined as the expression of the current typology of the individual.8,9 The first component, endomorphy,
refers to the relative fat and thinness. The second component, mesomorphy, refers to the relative musculoskeletal
development by size unit. And the third component, ectomorphy, refers to the relative linear aspect, based mostly
on the size/weight ratio. Ectomorphy assesses the form and
degree of longitudinal distribution of the first and second
component.7,8
An important and visually useful tool, individually and
for averages, is the somatochart. This should be used
on a more routine basis. It is the graphic representation of a two-dimensional format which uses X and Y
coordinates from the obtained measurements. The way a
somatochart is distributed for a sample provides useful
information and should be accompanied by a statistical
analysis. The relationship between the somatotype and different diseases was first described by Sheldon et al. in
1940. In 2002, Koleva et al. evaluated the relationship
between the somatotype and its main components with
the prevalence of several chronic diseases. In five groups
of patients, the prevalence was significantly linked to the
somatotype.10
Type 2 diabetes mellitus is a metabolic disorder, and as
such it affects the patients’ body composition elements. The
changes that the disease induces in patients complement
its anthropological characteristics. In fact, it is well-known
that obesity has a strong positive connection with the
development of diabetes mellitus.2,11 Tafeit et al. utilized
optical equipment (lipometer) to perform subcutaneous
fatty tissue measurements in different parts of the body on
patients with type 2 diabetes as well as in a control group.
K. Urrutia-García et al.
They documented a higher fat percentage in the upper
limbs than in the lower limbs, in both male and female.12
Several studies have made determinations of the somatotype in patients with type 2 diabetes. In 2013, Baltadijev
determined the average somatotype in diabetic Bulgarian women between 40 and 60 years old; observing a
mesomorph---endomorph somatotype, differing from the
mesomorphic somatotype of the control group. Endomorphy and mesomorphy significantly predominated, while
ectomorphy was significantly lower.13,14 He also observed
and determined the somatotype of the male counterpart
within the same age interval and those who presented
an endomorph---mesomorph somatotype. Mesomorphy was
greater, followed by endomorphy. Ectomorphy was also substantially lower.11
Currently, there are no papers where the somatotype of
patients with type 2 diabetes has been established, specifically in the Mexican population. Therefore, the objective of
this study was to establish the somatotype of patients with
type 2 diabetes of the ‘‘Dr. José Eleuterio González’’ University Hospital in Monterrey, Nuevo León, Mexico, in order
to have a phenotype for this type of population and begin a
new line of research.
Methods
This study was conducted at the ‘‘Dr. José Eleuterio
González’’ University Hospital in Monterrey, Nuevo León,
Mexico. The subjects were Mexican patients with a previous diagnosis of type 2 diabetes mellitus selected from the
Out Patients Clinics of Internal Medicine, General Medicine,
Endocrinology, and Sport Medicine and Rehabilitation wards
during the months of December 2013 through April 2014.
The patients needed to be willing to have the necessary
measurements taken to establish their somatotype. The
exclusion criteria were conditions or complications which
could alter body composition such as: lower limb edema,
amputations or pregnancy. Additionally, other exclusion criteria were situations or conditions which limited their ability
to stand up, such as fractures or recent surgeries.
The study included 180 subjects with type 2 diabetes,
previously diagnosed. All subjects underwent an anthropometry, under the restrained profile established by the
International Society for the Advancement of Kinanthropometry (ISAK).
The ISAK restrained anthropometry profile consists of
the taking of base measurements (weight and size), skin
folds (triceps, biceps, subscapular, iliac crest, supraspinal,
abdominal, anterior thigh, and medial calf), circumferences (relaxed arm, flexed arm, waist, hips and calves)
and diameters (biepicondylar humerus and femur breadth).
Regarding skinfolds, circumferences and diameters, these
were obtained from the subject’s right hemibody as
established by ISAK as a standardization method. All measurements were taken by the same measurer in order to
avoid variability. Furthermore, in order to reduce variability,
the measurer was Level I ISAK certified.
Different equipment was necessary to obtain anthropometric measurements: Fat analyzer TANITA (model
TBF-305), to determine weight, and a SECA wall-mounted
measuring tape (model 206) to determine size. A body
Somatotype of patients with type 2 diabetes
73
Table 1 Descriptive analysis of anthropometric measurements of patients with type 2 diabetes at the ‘‘Dr. Josè Eleuterio
Gonzàlez’’ University Hospital, 2014.
Descriptive analysis
Males
Age
Weight
Height
ENDO
MESO
ECTO
a
b
Value pa
Females
Mean
Median
Standard
deviation
Mean
Median
Standard
deviation
58.5
80.7
168.3
5.0
6.0
0.8
58.7
81.7
168.4
4.9
5.8
0.5
10.9
14.6
7.3
1.4
1.6
0.9
56.8
75.0
154.7
7.3
6.7
0.4
56.4
72.0
154.5
7.5
6.3
0.1
11.0
17.8
6.1
1.4
2.2
0.6
0.257
0.016
0.000
0.000
0.015
0.000
Value pb
0.115
0.006
0.000
0.000
0.473
0.000
Total
Mean
Median
Standard
deviation
57.6
77.5
160.6
6.3
6.4
0.6
57.5
76.1
160.0
6.3
6.1
0.1
11.0
16.7
9.5
1.8
2.0
0.7
Comparison of means test.
Comparison of medians test.
marker to establish reference points, and a Lufkin metallic
tape (model W696PM) for circumferences. A CESCORF sliding
anthropometer (INNOVARE 16 cm) and a Slim Guide plicometer (constant pressure 10 gr/mm2 ) were used to obtain bone
diameters and skin folds, respectively.
Once the anthropometry measurements were collected,
the following mathematical equations were made to obtain
the three components of the somatotype:
ENDOMORPHY:
−0.7182 + 0.1451(x) − 0.00068(x2 )
+ 0.0000014(x3 ), where x is the sum of the folds (triceps,
subscapular and supraspinal) multiplied by (70.18/size in
cm).
MESOMORPHY:
(0.858 × H) + (0.601 × F) + (0.188 × B)
+ (0.161 × P) − (0.131 × E) + 4.5, where H is the biepicondylar humerus breadth, F is the biepicondylar femur breadth,
B is the perimeter of the contracted arm, P is the medial
calf perimeter and E is height.
ECTOMORPHY: in order to obtain this parameter there are
3 formulas based on the weight index, which is the result of
Size
the following formula WI = √
a
Weight
If WI is ≥40.75 then the formula will be: 0.732 × WI − 28.58
If WI is <40.75 but >38.25 then the formula will be:
0.463 × WI − 17.63
If WI is ≤38.25 the value the given value will be 0.1.
With the obtained results we created a database using
Microsoft Excel 2013. This database was imported to SPSS
21.0. Before conducting the statistical analysis, we analyzed the data in order to obtain implausible values or
errors; abnormality and normality indexes were evaluated.
A descriptive statistical analysis was conducted where frequencies and proportions were reported according to age,
size, weight and the three somatotype components.
Mean values with t-distribution comparison tests were
performed where normality could be assumed, with a statistical significance of 95%. When normality could not be
assumed, medians comparison tests were performed.
Results
Out of the 180 subjects who underwent an anthropometry, 2
subjects were eliminated, being detected as atypical cases.
This way, we could obtain a normalized sample and avoid
skewed results. Out of the 178 remaining, 77 were males
and 101 were females. The mean age was: 57.6 years old
(±11 SD); 58.6 for males and 56.8 for females. The mean
weight was 77.5 kg (±16.7 SD) where males weighted 80.7 kg
(±14.6 SD) and females 75 kg (±17.8 SD).
From the collected data, we were able to observe an
average somatotype for patients with type 2 diabetes of 6.36.4-0.6, which corresponds to an endomorph---mesomorph
somatotype. The somatotype for females was 7.3-6.7-0.4,
corresponding to a mesomorph---endomorph somatotype;
while for males, it was 5.0-6.0-0.8, corresponding to
an endomorphic---mesomorph somatotype (see Table 1).
According to these results, we are able to say that in this
population of patients with type 2 diabetes, the endomorphic and mesomorphic components were dominant while the
ectomorphic component was significantly lower. Relative fat
was predominant in females, while the muscular component was predominant in males. In both groups the relative
linearity was lower.
In the somatogram we are able to see where the somatotypes are represented and offer an overview of the
dominance of each component explained earlier (See Fig. 1).
Discussion
Body composition and its evaluation can be performed
through the somatotype. There is scarce literature on the
characteristics of the somatotype of patients with type 2
diabetes and almost none offering data on the Mexican
population.13
Buffa et al., conducted an analysis on an Italian population of patients with type 2 diabetes using the same
Heath-Carter method.15,16 Fredman et al., also evaluated
the somatotype of Tamil Indians with type 2 diabetes, who
presented a somatotype with a predominant mesomorphic
component compared to healthy individuals.17
There was a great development of the mesomorphic
component in both groups for diabetic patients, male and
female, as observed in previously mentioned literature.13,14
In this study, patients with type 2 diabetes were characterized by certain peculiarities regarding somatotype. Patients
with type 2 diabetes presented a similar predominance to
74
K. Urrutia-García et al.
16
Conflict of interest
14
Meso
12
10
8
B
F
6
M
4
2
0
–2
–4
Endo
Ecto
–6
–8
–10
–8 –7 –6 –5 –4 –3 –2 –1 0 1 2
3 4 5 6 7
8
Figure 1 Somatochart: the colored circles indicate the average somatotype of patients with type 2 diabetes in a Mexican
population. B: both, F: female, M: male.
the endomorphic and mesomorphic components, while the
ectomorphic component was significantly lower. The differences between genders are significant, and are especially
high for the endomorphic component, which has higher values in females, as proven in previous researches.15,17
The somatotype can be considered a useful tool to evaluate the physical and health status of sick subjects, patients
with diabetes being one of these study groups. Additionally,
it can be used to develop intervention programs in these
populations.
Contrary to other anthropometric measurements, like
the body mass index (BMI) and waist---hip ratio (WHR), the
somatotype can help us evaluate the patient’s body composition in a more precise way and be able to link it to its
health risks, in addition to working as a follow-up and control
tool.
It is important to continue with this line of research and
with the study of other risk factors that may directly affect
type 2 diabetes physiopathology and which directly affect
these patients’ somatotype.
Funding
No financial support was provided.
The authors have no conflicts of interest to declare.
References
1. Moreno AL. Epidemiología y diabetes. Rev Fac Med UNAM.
2001;44:35---7.
2. Yadav VS, Koley S, Sandhu JS, Nigam S, Arota P. A study on somatotyping of patients with type 2 diabetes mellitus in Amristar.
Anthropologist. 2007;9:247---9.
3. Chen L, Magliano DJ, Zimmet PZ. The worldwide epidemiology
of type 2 diabetes mellitus --- present and future perspectives.
Nat Rev Endocrinol. 2012;8:228---36.
4. Inzucchi SE, Sherwin RS. Type 2 diabetes mellitus. In: Goldman
L, Schafer AI, editors. Goldman’s Cecil medicine. United States:
Academic; 2012. p. 1489---91.
5. Barquera S, Campos I, Aguilar C, Lopez R, Arredondo A, Rivera
J. Diabetes in Mexico: cost and management of diabetes and
its complications and challenges for health policy. Glob Health.
2013;2, 9:3.
6. Gutiérrez JP, Rivera J, Shamah T, et al. Encuesta Nacional
de Salud y Nutrición 2012. ResultadosNacionales. Cuernavaca,
México: Instituto Nacional de Salud Pública; 2012.
7. Singh SP. Somatotype and disease --- a review. Anthropologist.
2007;3:251---61.
8. Carter JEL. The Heath-Carter anthropometric somatotype:
instruction manual. USA: San Diego State University; 2002.
9. Anthropometry Procedures Manual. National Health and Nutrition Examination Survey (NHANES); 2009. p. 10---5.
10. Koleva M, Nacheva A, Boev M. Somatotype and disease prevalence in adults. Rev Environ Health. 2002;17:65---84.
11. Baltadjiev AG, Baltadjiev GA. Assessment of body composition of male patients with type 2 diabetes by bioelectrical
impedance analysis. Folia Med (Plovdiv). 2011;53:52---7.
12. Tafeit E, Möller R, Pieber TR, Sudi K, Reibnegger G. Differences
of subcutaneous adipose tissue topography in type-2 diabetic
(NIDDM) females and healthy controls. Am J Phys Anthropol.
2000;113:381---8.
13. Baltadjiev AG. Somatotype characteristics of female
patients with type 2 diabetes mellitus. Folia Med (Plovdiv).
2013;55:64---9.
14. Baltadjiev AG. Somatotype characteristics of male patients with
type 2 diabetes mellitus. Folia Med (Plovdiv). 2012;54:40---5.
15. Buffa R, Floris G, Putzu PF, Carboni L, Marini E. Somatotype in
elderly type 2 diabetes patients. Coll Antropol. 2007;31:733---7.
16. Buffa R, Succa V, Garau D, Marini E, Floris G. Variations of somatotype in elderly Sardinians. Am J Hum Biol. 2005;17:403---11.
17. Fredman M. Somatotypes in a group of Tamil diabetics. S Afr
Med J. 1972;46:1836---7.
Medicina Universitaria. 2015;17(67):75---79
www.elsevier.es/rmuanl
ORIGINAL ARTICLE
Association between bullying and major depressive
disorder in a psychiatric consultation
L. Perales-Blum ∗ , M. Juárez-Treviño, N. Capetillo-Ventura, G. Rodríguez-Gutiérrez,
M. Valdés-Adamchik, J. Treviño-Treviño, M. Cáceres-Vargas
Department of Psychiatry of the‘‘Dr. José Eleuterio González’’ University Hospital of the Universidad Autónoma de Nuevo León,
Mexico
Received 8 December 2014; accepted 27 January 2015
Available online 14 May 2015
KEYWORDS
Bullying;
Depression;
Adolescent
Abstract
Objective: Assess if there is a significant association between being bullied and presenting
depressive symptoms.
Materials and methods: In the March---October period of the present year, 8---16-year-old children and adolescents that attended psychiatric consultation for the first time in Dr. Eleuterio
González Hospital were included in this study. Test Bull-S was used to determine the presence
of bullying (Victim subtype); to evaluate depression 2 instruments were used according to age:
Children’s Depression Rating Scale-Revised (CDRS-R) for 8---12-year olds and the Birleson Depression Self-Rating Scale (DSRS) for 13---16-year olds. A total of 147 clinical patients were studied
(73 women and 74 men). Data were captured in excel and the Statistical Package for the Social
Sciences (SPSS) program was used for statistical analysis.
Results: A very significant association was found between being bullied and presenting depression (X2 = .289, p = .0004).
Conclusions: These data are in agreement with national and international studies, therefore,
reinforcing the evidence of such association. This is why we suggest inquiring about bullying in
children and adolescents whose chief complaint is depressive symptomatology.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/
licenses/by-nc-nd/4.0/).
∗ Corresponding author at: Departamento de Psiquiatría del Hospital Universitario ‘‘Dr. José Eleuterio González’’, de la Universidad
Autónoma de Nuevo León, Ave. Francisco I. Madero y Gonzalitos S/N, Col. Mitras Centro, C.P. 64460 Monterrey, Nuevo León, Mexico.
Tel.: +52 8113304708.
E-mail addresses: laurencia [email protected], [email protected] (L. Perales-Blum).
http://dx.doi.org/10.1016/j.rmu.2015.01.005
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
76
Introduction
The objective of this study is to determine whether or not
there is a significant correlation between being a victim of
bullying and presenting depression in the clinical population
of Nuevo León, Mexico. Bullying is a term used to describe
intimidations between equals. It is a form of intentional and
harmful abuse (intimidation, oppression, isolation, threats,
insults, beatings) from one student to another who is usually
weaker, thus making him a frequent and persistent victim.1,2
School harassment in Mexico has a reported frequency of
23.9% and has been linked with psychiatric disorders in
everyone implicated, with males in the majority.3 However,
it is the victim who may suffer the worse consequences:
anxiety, depressive symptoms and in the worst cases, suicide attempts. Reports show that victims of bullying have
a greater predisposition to present depressive symptoms
and psychological stress than non-victims.4 Different studies have confirmed that there is a link between bullying
and depression,5---7 reaching the conclusion that people who
suffer from bullying in their infancy-juvenile stage have
a greater risk of presenting depression in later stages in
life. 8---11
There are few studies conducted about bullying in schools
and its possible associations in our country, even when this
phenomenon seems to be on the rise, according to data from
the National Human Rights Commission (CNDH by its Spanish
acronym)12 and the Organization for Economic Co-operation
(OCDE by its Spanish acronym), who reported our country
as the number one in bullying.13 The present study seeks to
contribute with more data on these aspects of the Mexican
population, since, in order to study this phenomenon, we
must take into account cultural aspects of the community.
Materials and Methods
During the period of March---October 2014 an invitation to
participate in our study was made for all children and adolescents between 8 and 16 years old who attended our
consultation for the first time at the Department of Psychiatry of the University Hospital. The patients, as well as their
parents, had to agree to collaborate and a signed consent
was requested, all in accordance with the rules established
by the Committee of Ethics of our institution. Other requirements were that they were attending school, knew how to
read and write, did not have any intellectual disability symptoms or diagnosis and had to complete their evaluation.
A sample of 139 patients was calculated, considering a
confidence interval of 95%, with an estimation of error of
5%. The general census was considered as the ideal sampling method in order to increase the statistical potency.
To determine the presence of bullying, victim subtype, the
Bull-S Test1 was applied: to assess depression in children
between 8 and 12 years old we used the CDRS-R scale14 and
in the group between 13 and 16 years old the DSRS,15 these
were considered the optimal according to their age group.
The Bull-S Test is an elaborated instrument to measure
acceptance-rejection, bullying dynamics (characteristics of
the subjects involved) and situational aspects. It has a Cronbach’s alpha of 0.83 for victimization conducts.16 CDRS-R is a
semi-structured clinical interview, designed to measure the
L. Perales-Blum et al.
presence and severity of depression in children between 6
and 12 years of age. It has good internal consistency and
test---retest reliability. The cutoff point of 40 was utilized,
because it was considered that it best differentiates children
with depressive symptomatology and the control group, with
a sensitivity of 79.9% and a specificity of 99.7%.17
The DSRS scale is a useful tool for clinical and epidemiologic researches for populations between 13 and 17 years
of age. It is a self-administered scale. A cutoff point of 14
was determined, giving it a balance between sensitivity and
specificity, with a Cronbach’s alpha of 0.85. The information obtained was processed using Microsoft Excel; for the
inferential and descriptive statistics, we used the statistical
software SPSS 14.
Results
Within the period of March---September 2014, the gathering
of the sample was performed, identifying 162 patients who
attended their appointment for the first time at the Child
and Adolescent psychiatry consultation. From these, 5 were
under 8 years of age; 4 were not attending school; 3 had an
intellectual disability diagnosis; 2 did not accept to participate and 1 was eliminated due to an incomplete evaluation.
Finally, 147 subjects were included in the study. The group
was formed by 73 females (49.7%) and 74 males (50.3%),
with a mean age of 12.16 years (SD = 2.41), and a statistical
mode of 14 years old. Most of the participants had an educational level of elementary school (n = 66) and junior high
school (n = 65), only a few students had a high school level
education (n = 16). (Ver Table 1).
Bullying was present in 32% (n = 47) in the studied population, been implicated in 26 (35.6%) of the
total of females (n = 73) and 21 (28.4%) of the total of
males (n = 74); a significant difference in bullying status
(present/absent) was found according to their educational
level (x2 = 05.515, p = 0.023), but not according to gender (x2 = 1.565, p = 0.347). Regarding the type of bullying,
according to the total of the studied population (n = 147)
where they were able to select one or more subtypes;
54.4% (n = 80) reported the presence of insults and threats
being recognized as the most frequent. A significant difference in the type of bullying, according to gender was
not found (x2 = 4.878, p = 0.300). As far as the place, where
the subjects were able to select one or more places,
58.5% (n = 86) reported the classroom as the most common
place.
The reported frequencies of bullying were: ‘‘1---2 times
per week’’ in 23.8% (n = 35) and ‘‘everyday’’ in 8.2% (n = 12).
A significant difference in the frequency according to gender was not found. Out of the 147 subjects 63 (42.9%) were
reported with depressive symptoms. Of these, 65.1% (n = 41)
were females and 34.9% (n = 22) were males, finding a significant difference in the depressive status (present/absent)
according to gender (X2 = 10---486, p = .001).
Out of the depressed subjects, 50.8% (n = 32) reported
the presence of bullying. The group of patients with depression and bullying consisted of 19 females (19.37%) and 13
males (40.62%). A variable independence Pearson test was
performed, finding that there was a significantly greater
prevalence of bullying in depressed patients (X2 = 17.955,
Association between bullying and major depressive disorder
Table 1
significant association between presenting depressive symptomatology and being a victim of bullying (r = .289, p < .01).
Synthesis of the general sample.
Parameter
Sample (patients)
Gender
Males
Females
n
147
%
100
Discussion
74
73
50.3
49.7
16
10
15
13
20
23
26
11
13
x− ± s = 12.16 ± 241
10.9
6.8
10.2
8.8
13.6
15.6
17.7
7.5
8.8
Education level
Elementary
Junior high
High school
66
65
16
44.9
44.2
10.9
Bullying status
Positive
Negative
47
100
32.0
68.0
Types of bullying
None
Insults/threats
Physical mistreatment
Rejection
Other
12
80
48
31
2
8.2
54.4
32.7
21.1
1.4
Site of bullying
Nowhere
Classroom
Patio
Hallways
Other
11
97
33
12
11
7.5
66.0
22.4
8.2
7.5
Frequency of bullying
Never
Rarely
1---2 times a week
Daily
49
51
35
12
33.3
34.7
23.8
8.2
Role in bullying
Victim
Aggressor
Mixed
41
0
6
87.2
0
12.8
Age (years)
8
9
10
11
12
13
14
15
16
77
p <.001). A significant difference, according to gender was
not found (X2 = 1.125, p = .289).
In order to evaluate the association between presenting
depressive symptomatology and being involved in the bullying phenomenon (subtype victim), Pearson’s correlation
coefficient analysis was used. We were able to find a very
We are able to observe a prevalence of bullying of 32%
(n = 47) in the studied population. This number is higher
than the 25% reported in a survey conducted nationwide in
2008,18 but lower than that reported in a study conducted
in 2010 in a clinical population with an ADHD diagnosis of
our hospital,19 where a prevalence of 56.4% was found. In
general, the obtained prevalence is consistent with that
reported in other studies, situating the frequency of school
harassment ranging from 4.8 to 45.3%.20---23 A significant difference in the prevalence of bullying, according to gender
was not found, not in the totality of the sample, nor in
the subgroup with depressive symptomatology. These results
contrast with those observed in a study conducted in the
community population of the United States, where 3530 public school students were included for the period 2001---2002.
The results showed that boys are more implicated than girls
in school harassment, in the role of the offender as well
as the victim, and in the frequency and intensity of the
phenomenon.24 A possible explanation for this scenario is the
fact that they used a clinical population for this survey, with
a high prevalence of depression. As stated earlier, females
who are victims of bullying present an elevated prevalence
of depressive symptomatology.4,25
In the entire population, in the sub-samples of bullying
victims and in the depressed patients one, the same hierarchy remains in respect to the type of bullying presented, the
most frequent being insults/threats, followed by physical
abuse and rejection.
This information matches the results from a study conducted in Guadalajara, Mexico in 2007,26 as well as matching
data from international literature.27,28
Regarding the place where the abuse of bullied victims
occurs, the order remained the same: classrooms, backyards and halls. This concurs with the information reported
in the clinical population study of 2010 conducted within
our institution.19 At an international level, it adheres to the
same sequence of most frequent places of occurrence.29 The
fact that the classroom is the most frequent place where
bullying occurs, makes evident the need to provide psychoeducation to parents as well as in schools, because it occurs
in front of students who are considered ‘‘neutral’’, but they
are a part of the problem too. Even if one does not actively
participate in the harassment, they could be reinforcing
it under a synergic and passive effect: watching, laughing
and allowing intimidation.30 It has been demonstrated that
when no actions are taken, the ‘‘bullying culture’’ tends to
perpetuate for long periods of time.31
Regarding depression, a predominance in females was
observed, matching different researches where it has been
proven that females show a greater tendency of depressive
problems and internalized conducts in general.32---35
In patients with depressive symptomatology, a greater
prevalence of bullying was detected, 50.8% (n = 32), even
reaching to a significant relationship between the victim
subtype of bullying and depression. This association had previously been described in international articles3,16,36---39 and
78
it has been established that it involves difficulties in the
short and long term, like anxiety, irritability, low scholastic
performance and suicide risk.40 A possible explanation for
this outcome may be that being a victim of school harassment creates a negative cognitive style, where there are
feelings of humiliation, defeat and despair, similar to other
experiences of abuse,11 which negatively affects the clinical course of depression;41,42 besides this, it is possible for
bullying victims to generate a victimization cycle throughout their lives.43 Finally, the biological aspect should not
be left out: As a result of prolonged stress, there is usually an alteration in response to cortisol44 and a higher
methylation level in the genes which transport serotonin.
These effects have been associated with brain structural
changes in the hippocampus, for example, and altogether
can constitute paths, which explains the persistency of psychopathology throughout the subjects’ life after being a
victim of bullying.45
Due to the important link found between bullying and
depression, which also concurs with information reported
nationally and internationally,32,33,35,46 further research is
suggested on school harassment in all clinical populations of
children and adolescents who manifest depressive symptomatology. Furthermore, now that there are multiple studies
which have been able to stress the connection between psychopathology and bullying, further research must be done
on the causality of the problem. A theory suggests that psychiatric symptomatology precedes school harassment, while
others suggest that the harassment facilitates its onset.28 A
limitation of the present study is that, despite being able
to establish a correlation between suffering from bullying
and depression, the way one problem affects the other is
unknown.
Having a better understanding of school harassment
allows us to develop and implement the proper measures. In
general, authors who have studied this phenomenon in depth
recommend an integral management, going from psychoeducation of everyone involved and the evaluation of the
students, up to specific treatment for the associated psychopathology and the creation of programs and anti-bullying
laws.47,48
L. Perales-Blum et al.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
Conflict of interest
The authors have no conflicts of interest to declare.
Funding
18.
19.
No financial support was provided.
20.
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Medicina Universitaria. 2015;17(67):80---87
www.elsevier.es/rmuanl
ORIGINAL ARTICLE
Levels of insulin and HOMA-IR in adolescents in Saltillo,
Coahuila, Mexico
M.A. González-Zavala a,e,∗ , A. Velasco-Morales b , J.J. Terrazas-Flores a,e ,
M.G. de la Cruz-Galicia a,e , A.C. Cepeda-Nieto c,e , A. Hernández-del Río d
a
Autonomous University of Coahuila, School of Chemical Sciences, Clinical Analysis Laboratory, Mexico
Children’s Hospital ‘‘Federico Gómez Santos’’, Endocrinology Service, Mexico
c
School of Medicine, Saltillo Unit, Mexico
d
Autonomous Northeast University, Degree in Nutrition, Mexico
e
Health Sciences Network, Autonomous University of Coahuila, Mexico
b
Received 14 October 2014; accepted 11 February 2015
Available online 13 June 2015
KEYWORDS
Insulin;
Insulin resistance;
Obesity;
Adolescents
Abstract
Introduction: An alarming rise of obesity in adolescents has been observed, placing them at risk
of developing resistance to insulin (IR) and its adverse metabolic consequences such as diabetes
mellitus type 2 (DM2), metabolic syndrome and cardiovascular disease.
Objective: To know the prevalence of obesity, and the levels of glucose, insulin and HOMA-IR
and its association with the BMIz, waist circumference and the pubertal stage in a random
sample of adolescents.
Materials and methods: 292 adolescents between 12 and 15 years (152 female and 140 male),
whose anthropometric measurements (weight, height and waist circumference) were taken,
body mass index calculated and Z-score determined. Blood glucose and insulin levels were
evaluated from a sample of blood and their HOMA-IR was determined.
Results: The results showed that 32.5% were obese, 22.3% were overweight and 23.6%
showed adolescent central obesity. Glucose levels (p = 0.016), insulin (p = 0.0001) and HOMA-IR
(p = 0.0001) showed significant differences in the group with obesity. Values of the three parameters were increased with the stage of puberty. We found significant differences in the levels
of glucose (p = 0.0388), insulin (p = 0.0005) and HOMA-IR (p = 0.0001) between the prepubertal
and postpubertal stages.
∗ Corresponding author at: Universidad Autónoma de Coahuila, Facultad de Ciencias Químicas, Laboratorio de Análisis Clínicos. Blvd.
Venustiano Carranza s/n, colonia República, Saltillo, Coahuila C.P. 25280, Mexico. Tel.: +52 8444169213; fax: +52 8444159534.
E-mail address: [email protected] (M.A. González-Zavala).
http://dx.doi.org/10.1016/j.rmu.2015.02.004
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Levels of insulin and HOMA-IR in adolescents in Saltillo, Coahuila, Mexico
81
Conclusion: The results showed that the presence of central obesity, overweightness and obesity are closely associated with the prevalence of IR, and may be significant predictors of
DM2.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma
México S.A. This is an open access article under the CC BY-NC-ND license
(http://creativecommons.org/licenses/by-nc-nd/4.0/).
Introduction
Obesity in children and adolescents is an international
health problem. The relationship between it and the development of metabolic alterations like insulin resistance (IR),
Diabetes Mellitus type 2 (DM2), dyslipidemias and cardiovascular diseases (CVD) is well known. In the IR stage,
a compensating increase of insulin is produced, with the
objective of maintaining the homeostasis of glucose (GL).
This stage of chronic hyperinsulinemia, in the long term,
leads to the development of DM2, metabolic syndrome (MS)
and CVD.1---6 Obesity with an excess of adipose tissue, mainly
visceral, creates a determining factor in the establishment
of IR, since this tissue, in addition to fulfilling its duties
of energetic storage, exercises other activities involved
in homeostatic maintenance. The visceral adipose tissue
presents a greater amount of adrenergic beta receptors than
the subcutaneous tissue, significantly favoring the lipolytic
activity in this zone of the adipose tissue, generating a larger
output of free fatty acids toward the portal circulation and
liver, contributing to the establishment of insulin resistance
in hepatic, muscular and pancreatic tissue. Additionally, the
adipose tissue produces pro-inflammatory cytokines such as
adipokines, among which are interleukin-6 (IL-6) and tumor
necrosis factor alpha (TNF-␣) which blocks the cascade of
insulin signaling (INS). IL-6 and TNF-␣ promote lipolysis in
adipose tissue, favoring portal circulation which floods the
liver and other tissues with more free fatty acids, which
contributes to RI.7---10 INS sensitivity varies in the different stages from childhood to adolescence. In children and
adolescents, RI is the key element in MS associated with
obesity, and it is usually present for many years before the
onset of abnormalities like GL intolerance, dyslipidemia,
hypertension, DM2 and CVD.11---13 In Mexico, according to
the National Survey of Health and Nutrition 2012 (ENSANUT
by its Spanish acronym), the combined prevalence of overweightness and obesity in adolescents between 12 and 19
years of age is 35%, 35.8% (3 175 711) for females and
34.1% (3 148 146) for males.14 The HOMA index (Homeostatic
Model Assessment), built by Matthews (HOMA-IR), is the
most utilized method to determine IR.15---19 Nationally and
internationally, there is no consensus related to the average
values of INS and HOMA-IR in children and healthy adolescents, thus causing researchers to establish non-uniform
criteria and take previously conducted studies in different
populations as a reference. INS levels in eutrophic children and adolescents have been reported by Viso et al.
(2004) to be 5.47 ± 2.46 ␮UI/mL.20 Morales et al. (2007)
reported 6.15 ± 1.97 ␮UI/mL,21 Souki-Rincón et al. reported
13.0 ± 0.5 ␮UI/mL22 and Marcos-Daccarett et al. reported
7.0 ± 3.9 ␮UI/mL.23 Goran and Gower, after insulinemia
measurement studies in the pubertal stage, established
some cut points. They determined for the prepubertal stage
(Tanner 1 stage) insulinemia values ≥15 ␮UI/mL, for middle
prepubertal (Tanner 2---4 stage) values ≥30 ␮UI/m, and postpubertal (Tanner 4---5 stage) values of ≥ a 20 ␮UI/mL.24 Other
researchers determined their own cut levels for their respective areas of study, estimating tables with percentiles.
However, the lack of these tables in an important group of
countries for pediatric ages prevents uniform criteria from
being established.11,25 The same situation occurs for the cut
point in IR diagnosis. In 2005 Kinski et al. reported HOMA-IR
>3.16 and Hirschler et al. reported it as >3.29.26,27 Anthropometry is used in order to evaluate the degree of obesity,
like the body mass index (BMI) calculating its Z score (BMIz)
and the measurement of the circumference of the waist
(CW).3,28---30 Therefore, the objective of the present investigation was to know the prevalence of OW, OB and COB, GL
and INS levels, HOMA-IR and its connection to BMIz, CW and
the pubertal stage in adolescents between 12 and 15 years
of age in Saltillo, Coahuila, Mexico.
Materials and methods
The present investigation is descriptive/transversal. A total
of 292 adolescents were randomly analyzed between 2012
and 2013 from 5 public junior high schools of Saltillo,
Coahuila, Mexico, with ages ranging between 12 and 15,
who participated voluntarily with an informed consent
signed by their parents or tutors. Adolescents who suffered
from any sort of systemic or endocrinological chronic disease were excluded because they could alter the analytic
results. Physical and anthropometric exams were performed
in order to determine their nutritional stage and pubertal stage, according to Marshall and Tanner.31,32 Regarding
anthropometric measurements, size was measured using the
stadimeter (206 SECA BODYMETER, SECA AYN. Germany) in
a standing position, with their backs toward the front, barefoot, and the measurement was registered in centimeters.
The measurement of weight was performed using a digital scale with a capacity of 150 kg (Tanita TFB 300, Tanita
Corporation, Arlington Heights, IL, 60005, USA) with the
minimum amount of clothing on, without shoes, registered
in kilograms and grams. The circumference of the waist
was performed with an anthropometric flexible, inextensible tape (Lufkin W606PM Lufkin, USA), with the adolescent
in a standing position, arms relaxed on the side of the body,
measurement in the middle point between the costal edge
82
Table 1
M.A. González-Zavala et al.
Adolescents classified by BMIz in general and by gender Saltillo, Coahuila, Mexico (2012---2013).
Gender
General
Female
Male
Total
Low weight
Normal weight
Overweight
Obese
Morbidly obese
n
%
n
%
n
%
n
%
n
%
n
%
292
152
140
100
52
48
22
14
8
7.5
9.2
5.7
110
59
51
37.7
38.8
36.4
65
32
33
22.3
21.1
23.6
78
40
38
26.7
26.3
27.2
17
7
10
5.8
4.6
7.1
and the iliac crest, breathing out, and considering the cutoff
point >90 percentile for central obesity.33 Moreover, BMI was
calculated using the formula weight/height2 and the Z score
was evaluated (BMIz) in order to classify their nutritional
state using the charts of the WHO. The Z score is expressed
in units of standard deviation (SD); a Z score between −2
and −3 SD corresponds to severe low weight, between −1
and −2 SD corresponds to low weight, between +1 and −1
SD corresponds to normal weight, between +1 and +1 SD
corresponds to overweight, between +2 and +3 SD corresponds to obesity and greater than +3 SD corresponds to
morbid obesity.34 Blood was obtained via venous puncture
with a previous fasting of at least 12 h. The samples were
centrifuged at 35 000 rpm for 15 min in refrigerated centrifuge at 6 ◦ C (Thermo Scientific SL, 16R, USA); the serum
was conserved at 4 ◦ C up to the moment of processing of
the GL on the same day as extraction. An aliquot was preserved at −21 ◦ C for two days to perform the INS analysis.
The determination of the GL was conducted in automatized
‘‘Diconex’’ equipment InCCA (Intelligent Clinical Chemistry
Analyzer) (Diconex, USA) through the enzymatic method
(conversion to gluconate-6-phosphate by hexokinase and
glucose-6-phosphate-dehydrogenase in presence of ATP and
NAD) with Human reactives.
INS analysis was made with the automated equipment
TOSOH AIA-600 (Tokyo, Japan) by an IFALS (Immunofluorescence assay with labeled substrate) immunoassay with
TOSOH reactives. We used high- and low-level commercialgrade controls (Human brand) in both tests. The index of the
homeostatic model was calculated with the Matthews formula: HOMA = [Glucose (mmol/L) × Insulin (␮U/mL)/22.5].
We used the FID criteria for the fasting GL cutoff point
value ≥100 mg/dL,35 and for the fasting INS for the prepubertal state insulinemia values of ≥15 ␮UI/mL, for the
middle pubertal ≥30 mU/mL and for the postpubertal
≥20 mU/mL.24 We considered that the level of RI that predicts a greater rick of DM-2 was HOMA-IR ≥3.16.26 The results
were expressed as an average, standard deviation (SD) and
the analysis of the variables with the number of cases and a
percentage. We compared the average between the groups
with the Student’s t test; for more than 2 groups and the
comparison of multiples groups, we employed the variation
analysis (ANOVA, test by Tukey). The results were considered
statistically significant with a value of p ≤ 0.05. The predictability of the AUS to evaluate the efficacy of the HOMA-IR
index as an indicator of IR was determined by the analysis
of the ROCC (Receiver Operating Characteristic Curve) for
cutoff values of 3.16. The Minitab 16, GrapPad Prism 5 and
SPSS 21 programs were used to make the statistical analysis
of the results.
Results
Out of the 292 analyzed adolescents, 52% were women (152)
and 48% were men (140), with a mean age of 13.02 ± 0.94
years, a mean weight of 60.02 ± 15.69 kg (27.2---120.3) and a
mean size of 158.34 ± 8.03 cm (125---179). The prevalence of
central obesity (percentile >90) was at 23.6% corresponding
to 49.3% for females and 50.7% for males. According to their
BMIz, over half of the adolescents presented overweightness and obesity, this abnormality being more predominant
in males (Table 1).
The mean values obtained by the biochemical parameters in our general sample were the following: GL
85.8 ± 11.8 mg/dL, the percentage above ≥100 was 11.5%,
INS level was 13.2 ± 10.5 ␮UI/mL and the HOMA-IR value
was 2.9 ± 2.5 with a 46% over ≥3.16. When analyzing
the results by gender, we found that for females, GL
was 83.4 ± 11.2 mg/dL, INS 13.4 ± 10.2 ␮UI/mL and HOMAIR 2.9 ± 2.5, while for males, GL was 88.5 ± 11.8 mg/dL,
INS 12.9 ± 10.8 ␮UI/mL and HOMA-IR 2.9 ± 2.5. We found
statistically significant differences between genders for
GL (p = 0.0002) but not for INS (p = 0.6582) and HOMA-IR
(p = 0.9965). After studying the results of the biochemical
parameters concerning BMIz, we noticed that the values
increased as BMIz did, presenting the highest values in OB
(Table 2). After evaluating HOMA-IR results, we found it
notoriously high in OB (p ≤ 0.0001). There were statistically
significant differences in GL (p = 0.0161), INS (p ≤ 0.0001)
and HOMA-IR levels (p ≤ 0.0001) between the different BMIz
groups.
After examining the results of three biochemical parameters by gender and BMIz, it was noted that the percentage
of the highest values was observed in the OW and OB of
both genders. We noticed statistically significant differences
between genders with OW regarding GL levels (p = 0.0046)
and none in INS levels (p = 0.3006) or the HOMA-IR value
(p = 0.1015). Regarding OB, no statistically significant differences between genders were observed for GL (p = 0.0551),
INS (p = 0.3150) and HOMA-IR levels (p = 0.6537).
After analyzing the results of the three parameters in
relationship with pubertal development, it was observed
that the values increased when pubertal development was
raised (Table 3). There was a statistically significant difference between the prepubertal and the postpubertal in
relationship with GL levels (p = 0.0247), but not in INS
(p = 0.4398) or HOMA-IR (p = 0.2255). HOMA-IR values showed
that approximately half the studied adolescents (pubertal
and postpubertal) presented IR.
The study of the results of the biochemical parameters
regarding pubertal development by gender revealed that
Levels of insulin and HOMA-IR in adolescents in Saltillo, Coahuila, Mexico
Table 2
83
Glucose, insulin and HOMA-IR by BMIz Saltillo, Coahuila, Mexico (2012---2013).
BMIz
Glucose (mg/dL)
Low weight
Normal weight
Overweight
Obese
n
Average
(42---121)
22
110
65
95
82.5
85.2
83.7
88.8
±
±
±
±
9.50
11.8
10.6
12.4
HOMA-IR (␮UI/mL × mmol/L)
Insulin (␮UI/mL)
%a
p
Averge
(2,3---91.6)
3.4
10.6
6.4
18.5
0.0271
0.0367
0.0081
0.0161*
6.4
8.0
11.5
21.9
±
±
±
±
3.0
4.0
5.7
13.2
p
Average
(0,3---20,3)
<0.0001
<0.0001
<0.0001
<0.0001*
1.3
1.8
2.4
4.9
±
±
±
±
0.6
1.3
1.3
3.1
%a
p
0.04
10.7
21.4
66.9
<0.0001
<0.0001
<0.0001
<0.0001*
a % of values above the cutoff point. Cutoff points: Glucose ≥100 mg/dL; insulin: was not evaluated, there are no cutoff points for this
biochemical parameter in relation to BMI; HOMA-IR ≥3.16. For the value of p we collated all the IMCz against that of Obesity (t-Student).
* ANOVA.
Table 3
Glucose, insulin and HOMA-IR by pubertal stage Saltillo, Coahuila, Mexico (2012---2013).
Pubertal stage
(Tanner)
Prepubertal
Middle pubertal
Postpubertal
n
16
216
60
Glucose (mg/dL)
HOMA-IR (␮UI/mL × mmol/L)
Insulin (␮UI/mL)
Average
%a
p
Average
%a
p
Average
%a
p
83.5 ± 11.3
85.0 ± 12.1
89.5 ± 9.7
7.6
10.9
14
0.0388
0.0097
0.0247*
10.6 ± 4.4
13.1 ± 10.3
14.3 ± 12.0
16.2
5.1
31.8
0.235
0.4502
0.4398*
2.3 ± 1.3
2.8 ± 2.4
3.3 ± 3.0
21.3
44.7
52.3
0.1665
0.182
0.2255*
a % of values above the cutoff point. Cutoff points: glucose ≥100 mg/dL; insulin: prepubertal ≥15 mU/mL, middle pubertal ≥30 mU/mL,
postpubertal ≥20 mU/mL; HOMA-IR ≥3.16. For the value of p we collated the pubertal with the postpubertal states (t-Student).
* ANOVA.
INS (p ≤ 0.0001)and HOMA-IR (p ≤ 0.0001). There were no
significant differences in GL (p = 0.7171), INS (p ≤ 0.0001)
or HOMA-IR (p ≤ 0.0001) in the postpubertal stage. When
comparing the results of adolescents with COB and the
pubertal and postpubertal stages there were no significant
differences in GL (p = 0.3061), INS (p = 0.8707) or HOMA-IR
(p = 0.9734) values.
The result of the sensitivity and specificity analysis
revealed the fact that HOMA-IR proved to be a good predictor of IR presence (Fig. 1), which reflects a higher
discriminating power in the evaluation of this syndrome.
Discussion
This study showed an elevated prevalence of overweightness (22.3%), obesity (32.5%), central obesity (23.6%) and
1
0.75
Sensibility
the highest values in females occurred in the postpubertal
stage, while in males the highest values for INS and HOMA-IR
occurred in the pubertal stage and the highest values for GL
occurred in the postpubertal stage (Table 4).
The results of each of the parameters were compared
with each pubertal stage by gender; we found that there
were no statistically significant differences in the prepubertal stage, while in the pubertal stage there were differences
in GL (p ≤ 0.0001) and HOMA-IR (p = 0.0408) and differences
in INS (p = 0.0085) and HOMA-IR (p = 0.0101) in the postpubertal stage were also observed.
Mean values obtained from the three biochemical parameters concerning adolescents without COB (76.4%) were GL
84.2 ± 11.4 mg/dL, HOMA-IR 2.1 ± 1.5 with 8.5 and 24.2%
of values over the cutoff points, respectively, and INS
9.9 ± 6.1 ␮UI/mL. For adolescents with COB (23.6%), GL
was 91.1 ± 11.2 mg/dL, HOMA-IR 5.4 ± 3.4 with 21.3 and
74.4% of values over the cutoff points, respectively, and INS
23.7 ± 14.2 ␮UI/mL. When the results of the three biochemical parameters of adolescents with and without COB were
compared, there were statistically significant differences in
all three parameters (p ≤ 0.0001).
Concerning COB prevalence and pubertal stage, it was
reported that 6.7% occurred in the prepubertal stage, 22.2%
in the pubertal stage and 33.3% in the postpubertal stage.
When the results of the biochemical parameters were associated with pubertal stage and waist circumference, it was
noted that in all pubertal stages, the adolescents who displayed COB presented higher values, observing a high IR
incidence in pubertal and postpubertal stages (Table 5).
When performing a comparative study of the results of
the biochemical parameters in adolescents with and without
COB in each of the pubertal stages, statistically significant
differences were found in pubertal stage in GL (p ≤ 0.0001),
0.5
0.25
0
0
0.25
0.5
0.75
1
Specificity
Figure 1 The area below the ROC curve of the HOMA-IR as a
predictor of insulin resistance.
84
Table 4
Glucose, insulin and HOMA-IR by pubertal stage (Tanner) and gender. Saltillo, Coahuila, Mexico (2012---2013).
Pubertal stage (Tanner)
n
Glucose (mg/dL)
%a
Average
HOMA-IR (␮UI/mL × mmol/L)
Insulin (␮UI/mL)
p
Average
Prepubertal
Middle pubertal
Postpubertal
4
104
44
84.3 ± 10.4
81.0 ± 10.6
89.0 ± 11.0
8.2
3.7
16
<0.0001
0.0003*
Female
12.1 ± 5.2
12.1 ± 8.6
16.7 ± 13.1
Prepubertal
Middle pubertal
Postpubertal
12
112
16
83.3 ± 12.0
88.7 ± 12.4
90.6 ± 4.9
8.7
18
3
0---0014
<0.0001
<0.0001*
Male
10.1 ± 4.2
14.0 ± 11.6
7.6 ± 3.9
**
%a
p
Average
%a
p
30.3
1.9
40.1
**
35.3
36.7
59.2
**
0.0133
0.0425
2.6 ± 1.4
2.5 ± 2.0
3.9 ± 3.3
12.8
8.5
0.1
0.1196
0.325
0.0547*
2.2 ± 1.0
3.2 ± 2.7
1.7 ± 0.9
17.3
50
5.5
0.2276
0.0379
0.0557*
1
0.9961*
a % of values above the cutoff point. Cutoff points: Glucose ≥100 mg/dL; insulin: prepubertal ≥15 mU/mL, middle pubertal ≥30 mU/mL, postpubertal ≥20 mU/mL; HOMA-IR ≥3.16. For
the value of p we collated the pubertal with the postpubertal states (t-Student).
* ANOVA.
** This statistic was not analyzed because of the low number of n.
Table 5
Glucosa, insulin and HOMA by pubertal stage (Tanner) and waist circumference. Saltillo, Coahuila, Mexico (2012---2013).
Pubertal stage (Tanner)
Prepubertal
Postpubertal
<90
>90
<90
>90
<90
>90
n
15
1
168
48
40
20
Glucose (mg/dL)
HOMA-IR (␮UI/mL × mmol/L)
Insulin (␮UI/mL)
Average
%a
p
Average
%a
p
Average
%a
p
82.5 ±
98
83.1 ±
91.9 ±
89.8 ±
88.8 ±
6
--7.7
22.5
10.7
18.7
----<0.0001
10 ±
19.6
10.1 ±
23.6 ±
9.3 ±
24.2 ±
9.8
--0.1
32.5
2.3
60.8
----<0.0001
2.1 ±
4.7
2.1 ±
5.4 ±
2.9 ±
5.4 ±
13.3
--23.2
75.3
30.5
71.8
----<0.0001
11.0
11.9
10.7
8.2
12.4
0.7171
3.8
6.4
13.9
5.3
15.3
<0.0001
0.9
1.4
3.3
1.7
3.9
<0.0001
PC: waist percentile.
a % of values above the cutoff point. Cutoff points: glucose ≥100 mg/dL; insulin: prepubertal ≥15 mU/mL, middle pubertal ≥30 mU/mL, postpubertal ≥20 mU/mL; HOMA-IR ≥3.16.
M.A. González-Zavala et al.
Middle pubertal
PC
Levels of insulin and HOMA-IR in adolescents in Saltillo, Coahuila, Mexico
HOMA-IR (46%). These results were higher than those
reported in adolescents in the same age range for overweightness (19%) and obesity (13%) in Chiapas, Mexico,5
and even lower than those reported in adolescents between
10 and 17 years with obesity (49.2%) in Lima, Peru.1 As
expected, adolescents with obesity and central obesity
showed significantly higher INS and HOMA-IR numbers compared to those adolescents with a normal BMIz.
In this manner, the adolescents without obesity manifested average values for INS (8 ␮UI/mL) and HOMA-IR (1.8),
and the adolescents with obesity had averages of INS as
21.9 ␮UI/mL and HOMA-IR 4.9. We would like to point out
the fact that adolescents with morbid obesity reached INS
levels of 91.6 ␮UI/mL and HOMA-IR values of 20.3, values
never before reported in the Mexican population. These findings in adolescents of both genders confirm those reported
by other authors in the sense that they observed a positive relationship between IR and the presence of obesity
and that it increases progressively in function of the excess
of weight.1,5---7,37
Regarding basal GL levels, this increased as BMIz
increased. We found that the average levels are greater
in males than in females, just as reported by Souki-Rincón
et al.22
Similar to other studies previously conducted, we found
in ours that INS concentrations are higher in female adolescents than in males.21 In this study, approximately 2 out of
every 10 adolescents with overweightness and 7 out of 10
with obesity displayed IR, the male gender being the most
affected. A significant correlation between INS concentrations and HOMA-IR was found, which was expected, because
HOMA-IR values are derived from INS and GL concentrations.
Antropometric measurements, BMIz, and WC are independently associated with GL, INS and HOMA-IR levels. We were
able to observe that WC predicted these variables more
accurately in comparison to BMIz.
Furthermore, given the fact that INS and HOMA-IR concentrations followed the same distribution, we were able to
consider the latter as a meter to be as good as basal INS to
establish IR. Keskin et al. showed that HOMA-IR had a high
specificity and sensitivity for IR measurement in children and
adolescents.36
The prevalence of IR found in the studied population
(46%) exceeds that reported by Acosta et al.7 These authors
also used HOMA-IR values higher than 3.1 for an IR diagnosis. On the other hand, it was found that approximately
half of the adolescents in the postpubertal state (IV and
V) displayed higher levels of INS and HOMA-IR. When analyzing pubertal stage by gender, the highest values of
chemical parameters were found in females in the postpubertal (IV and V) and males with pubertal stage (II and
III). Rojas-Gabulli et al.1 suggested that IR, which results
in hyperinsulinemia, according to Arslanian and Kalhan38
is observed between Tanner stages II and IV. These results
agree with our results. Also, IR found in the study’s adolescents was lower than that reported by Kurtoglu et al.39 in
adolescents in the prepubertal (male 37% and female 27.8%)
and pubertal stages (male 61.7% and female 66.7%). These
differences are based on the fact that these authors utilized
different reference values according to gender and sexual
maturation stage for their IR diagnosis, using the following HOMA-IR values: for the prepubertal stage the following
85
values were used: male 2.67 and female 2.22, and for the
pubertal stage: male 5.22 and female 3.82. Thus, we present
the need to continue conducting studies on adolescents,
allowing the establishment of normal levels for INS as well as
for HOMA-IR. The highest insulin and HOMA-IR values were
observed in adolescents with COB. Moreover, the incidence
of higher INS and HOMA-IR values were observed in adolescents with COB in the pubertal and postpubertal stages, like
other authors.7,39 The evaluation of HOMA-IR’s ability to predict an IR diagnosis through the analysis of the ROC curve,
indicates that it has a high sensitivity and specificity for this
purpose.
The main strengths of this study are the homogeneity of
the conditions at which samples were taken, conducting simple non-invasive studies like WC (waist circumference) BMIz,
INS, basal GL and HOMA-IR, and HOMA-IR being a high sensitivity and specificity indicator. The limitations of this study
are the following: since it is a relatively small demographic
sample, it was not necessarily a sample representative of
the population of the same age intervals (however, it may
serve for comparison of other Mexican adolescents); not
having cutoff points in HOMA-IR for Mexican adolescents of
different ages and pubertal stages, and not having a balanced representative number for each one of the pubertal
maturation stages.
Conclusion
This study shows a high OW, OB and COB incidence. It
revealed a positive correlation between the rise in GL, INS
and HOMA-IR levels and the rise of BMIz and COB, showing a
high IR incidence. Therefore, OW, OB, COB and HOMA-IR can
be used as a reference in clinical practice for IR diagnosis and
can be significant predictors of DM2. These data highlight the
importance of early IR detection in adolescents with OW, OB,
and COB, and stress the importance of managing early intervention strategies, which allow the identification of IR risk,
for its timely management and prevention of DM2, CVD and
MS development.
Funding
No financial support was provided.
Conflict of interest
The authors have no conflicts of interest to declare.
Acknowledgements
We thank public schools in Saltillo, Coahuila, (Mexico)
‘‘Nazario S. Ortiz Garza’’ Federal Secondary School No. 1,
‘‘Margarita Maza de Juárez’’ Secondary School, ‘‘Ismael
Rodríguez’’ Technical Secondary School No. 4, ‘‘Ejercito
Mexicano’’ Secondary School No. 16 and ‘‘Ricardo Flores
Magón’’ Secondary School No. 11, for their availability and
co-operation with this investigation. Special thanks to the
authorities, training staff, parents and students who participated in this investigation of public schools.
86
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www.elsevier.es/rmuanl
ORIGINAL ARTICLE
Internet addiction in university medical students
N. Capetillo-Ventura ∗ , M. Juárez-Treviño
Department of Child and Adolescent Psychiatry and Psychology, University Hospital ‘‘Dr. José Eleuterio González’’,
UANL, Nuevo León, Mexico
Received 11 January 2015; accepted 19 February 2015
Available online 14 May 2015
KEYWORDS
Internet addiction;
Psychiatric
symptoms;
Personality type
Abstract
Objective: To determine the prevalence of Internet addiction, psychiatric symptoms and personality type in university students, and to correlate these variables.
Methods: We enrolled 522 medical students, 281 men and 241 women, with a mean age of
21.2 years. We used a socio-demographic questionnaire, an Internet questionnaire (Young’s
Internet Addiction Test [IAT]), the General Health Questionnaire, and the Zuckerman-Kuhlman
Personality Questionnaire III (ZKPQ).
Results: The mean raw score of respondents in the IAT test was 19.72 points. IA had a highly significant correlation with impulsivity (rs = 0.244, p < 001), neuroticism-anxiety (rs = 0.304, p < 001)
and aggression-hostility (rs = 0.143, p = 0.001). It also negatively correlated with work effort
(rs = −0.136, p = 0.002). As for mental health, IA had a highly significant correlation with somatic
symptoms (rs = 0.174, p < 001), anxiety and insomnia (rs = 0.219, p < 001), social dysfunction
(rs = 0.118, p < 001) and severe depression (rs = 0.199, p < 001).
Conclusions: The Internet is a tool for various activities. When used with control it does
not cause any problems. However, when control is lost, addiction occurs together with its
comorbidities. Certain personality types are predisposed to this loss of control and Internet
abuse.
© 2015 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is
an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/
by-nc-nd/4.0/).
Introduction
∗ Corresponding author at: Gonzalitos Avenue and Francisco I.
Madero Avenue, Monterrey, Mitras Centro, Monterrey Nuevo León,
Mexico. Tel.: +52 18181787404.
E-mail address: [email protected] (N. Capetillo-Ventura).
The Internet is currently a critical component of telecommunications, business, education, and entertainment. It is
available worldwide and is used to search for information,
online communication, financial transactions, retail sales,
http://dx.doi.org/10.1016/j.rmu.2015.02.003
1665-5796/© 2015 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Internet addiction
sexual services and games, among many other uses. With its
growing popularity, overuse soon appeared and thus a new
disorder, Internet Addiction (IA).1
The first to propose the term IA was the American psychiatrist Ivan Goldberg in 1995, who described the pathological
compulsive use of the Internet, with this term being definitely defined by Kimberly S. Young.2 IA is a deterioration
in the control of its use, manifested as a set of cognitive,
behavioral and physiological symptoms. That is, the person
is ‘‘net dependent’’, making extensive use of the Internet,
which generates a distortion of her/his personal, family or
professional goals.3
Griffiths4 proposed assessing seven specific areas for
Internet addiction: (a) tolerance, (b) spending more time
than planned on the Internet, (c) spending most of their
time in activities that allow them to be online, (d) spending
more time online than in social or recreational activities, (e)
continuing use despite work, academic, economic or family
concerns, (f) failed attempts to stop or reduce use of the
Internet and (g) withdrawal. According to this author, the
diagnosis should be made in the presence of three or more
of the areas described.
Hong et al5 found a reduction in thickness of the right
orbitofrontal cortex in adolescents with Internet addiction.
This reflects a common neurobiological mechanism between
IA and other addictive disorders. Young6 classified it into
5 types: (1) cybersexual addiction to adult chat rooms or
pornography; (2) addiction to online friendships or situations that replace real-life relationships; (3) web compulsion
to gamble, auction, or obsessively trade; (4) the compulsive
search for information on the web, and (5) addiction to computer games and programming. Goldberg7 prefers to replace
the term IA with pathological computer use.
Some researchers suggest the existence of vulnerable or
high risk groups for Internet addiction, primarily focusing
on students. A review in Mexico8 concluded that although
it is not yet possible to make the diagnosis of ‘‘Internet
addiction’’ as such, it is clear that the behavior associated
with excessive Internet use has features that, because of its
impact on an individual’s functioning and interpersonal relationships, warrants an intervention aimed at this problem.
Investigators have attempted to define the clinical and
epidemiological profile of individuals with IA, such as that
in a study by Cruzado et al.2 who found that patients with
IA were characterized by their young age, high daily Internet user time, predominant use of web games, and a high
frequency of marked psychotic behaviors. Young9 assessed
depression and IA, and her findings suggest an increase
in levels of depression associated with Internet addiction.
Due to the susceptibility of young people to present addictions, in this study we determined the presence of Internet
addiction, psychiatric symptoms, and personality type in
university students and correlated these variables.
Methods and subjects
Questionnaires were administered during the period of
March-April 2013 to medical students who had Internet and
agreed to participate voluntarily in the study. It was decided
to perform this study in this population because of the ease
89
of processing it at the University. The project was reviewed
and approved by the Ethics Committee of our institution.
We determined the size of the sample population (p)
to be studied by means of a bilateral interval with a
95% confidence interval (˛ = 0.05), with an estimation of
error limits ± 5% (B = 0.05) and considering a conservative
approach (p = q = 0.5). The result meant that, for a population of 5192 students, a sample of 358 individuals was
required. The sampling design used was two-stage. In the
first stage we stratified by school year (6 strata) and in the
second, clusters were selected. The group formed a conglomerate of students and a census was conducted in each of
the eight clusters present in the sample. Sample allocation
was proportional to the size of the stratum, that is, proportional to the total number of students of that school year.
For the first and second school years, we randomly selected
2 groups each, while in the rest (third, fourth, fifth and sixth)
a group or cluster was randomly selected by school year.
Application of the instruments was performed in the
regular classroom, on the day and time agreed with the
course coordinator. The instruments were applied by groups.
A member of the research team explained the purpose of
the study, conditions and data confidentiality, and voluntary participation of the students who were present was
requested. The average time to complete the questionnaires
was approximately 30 to 40 min. Questionnaires were administered to a total of 543 students, of whom 21 did not answer
completely, therefore these were eliminated.
Instruments and variables
The instruments considered for the study were: a questionnaire of socio-demographic variables including age, sex,
marital status, level of study, persons with whom the
individual lives, academic performance, and recreational
activities; an Internet questionnaire that collects information on frequency of weekly use, time of use for each
connection, connection location, and purpose of the connection, and an IA test consisting of a 20-item questionnaire
with Likert type responses with a minimum score of 20 and
a maximum of 100 (the higher the score, the greater the
problem caused by the use of Internet). A score of 20---39
points is an average online user who has complete control
over its use, a score of 40---69 means frequent problems with
Internet use, and a score of 70---100 means that use of the
Internet is causing significant problems.10,11
Goldberg’s General Health Questionnaire in its 28-item
version (GHQ 28)12 was also included. This instrument
consists of four scales: somatic symptoms, anxiety and
insomnia, social dysfunction, and severe depression. Internal consistency (Cronbach’s alpha) of the total questionnaire
varies between 0.82 and 0.93. Test---retest reliability ranges
from 0.85 to 0.90.
The Zuckerman-Kuhlman Personality Questionnaire III,
translated and adapted with permission from the authors
by González et al.13 , consists of 99 items with an alternative true or false answer. This questionnaire isolates the five
major personality factors proposed by Zuckerman. Impulsive
Sensation Seeking (ISS) consists of 19 items that refer to a
willingness to take risks to experience arousal and seek new
experiences. They also relate to the lack of planning and the
90
N. Capetillo-Ventura, M. Juárez-Treviño
Table 1 Level of education, subject under study, and
groups of students.
Year
Subject
Group
N
1
Anatomy
Biochemistry
Microbiology
Pathology
General Surgery
Psychiatry
Obstetrics
2
11
5 and 11
3
1
1
1
45
46
75
82
67
142
65
2
3
4
5
6
Total
522
%
8.6
8.8
14.4
15.7
12.8
27.2
12.5
100
tendency to act impulsively without thinking. The Scale of
Neuroticism and Anxiety (NA) also has a total of 19 items that
describe emotional instability, stress, worry, phobias and/or
fears, obsessive indecision and susceptibility to criticism.
Aggression Hostility (AH) is a scale that consists of 17 items
related to verbal aggression, rudeness-impoliteness, antisocial behavior, and anger. The Activity (A) scale consists of 17
items referring to the need for activity and an inability to sit
around doing nothing. The Sociability (S) scale consists of 17
items, and refers to the number of friends you have and the
time devoted to them, the desire for partying, preference
for being with others as opposed to being alone and doing
activities alone. Finally, the Infrequency scale (I) consists of
10 items related to social desirability, which are not entirely
true for everyone.
Statistical analysis
Descriptive and inferential statistics were used. For the first
proportions, percentages and absolute frequencies for categorical variables were obtained. For continuous and/or
numeric variables, measures of central tendency, variability and positioning were calculated. Confidence intervals
of 95% for both ratios and means were obtained for inferential statistics. For numeric or continuous variables, the
Kolmogorov-Smirnov test was used to test the hypothesis of
normality. To examine correlations, parametric (Pearson’s)
or non-parametric (Spearman’s) correlation coefficients
were used.
Results
Data analysis was carried out in 522 students, comprising 281
men and 241 women. Of these, 509 were single, 11 married,
one common-law married and 1 separated with a mean age
of 21.24 years, median 21, SD 3.046 with an age range of
15---61 years (KS = 0.147, p = 0 001). The level of education,
the subject under study and the group of students are shown
in Table 1.
Regarding academic performance, 23 considered themselves excellent, 107 very good, 347 good, 42 poor and 3
very poor. Of the total, 327 students engaged in recreational
activities and 195 did not. Activities were mainly sports,
arts, reading, and video games. Most lived with their family
(84.5%).
By analyzing Internet use, it was found that 15 students
used the Internet 1 day a week, 5 students, 2 days, 14 students, 3 days, 33 students, 4 days, 25 students, 5 days, 33
students, 6 days and 397, 7 days a week. Connections per day
were 0 to 10 times, 86%, 11 to 20 times, 2.4%, 21 to 30 times,
0.4%, 50 times, 0.2%, 144 times, 0.6%, and always, 10.4%.
The approximate time of Internet use each time a user
logged in was 1 to 960 min and 10.4% referred to staying
connected always. Most would connect for 60 min (20.1%)
followed by 120 min (13.2%), and 30 min (12.6%). The place
chosen as the most frequently used was the home, in 442
(84.7%).
The main reason for being connected to the network most
of the time was social networks (Facebook, Twitter, Tumblr,
chats) in 43.86%, academic and research activities in 32.95%
and entertainment/leisure in 23.18%.
There are differences in IA due to the perception that
students have of their academic performance (2 = 10.25,
df = 3, p = 0.016). Those who perceive their academic performance as poor and very poor had the highest Internet
addiction test scores.
There was no significant difference in IA due to whether
or not a recreational activity was practiced (Z = −0.49,
p = 0.620). Also, there was no significant difference in IA due
to who the person was living with (2 = 2.47, df = 2, p = 0.29).
The mean raw score of respondents in the IA test was
19.72, with a standard deviation of 12.54 and a range of
0---72 with a possible maximum of 100 points.
The classification of scores according to the interpretation of the IA test showed that 91.8% of the sample had
complete control over its use, while 8% had frequent problems and in 0.2%, use caused significant problems.
Internet use caused a greater problem in men with a
mean of 21.25 (median 18.00, SD 13.38) unlike women with a
mean of 17.95 (median 16, SD 11.25 (U = 28,914.5, Z = −2.88,
p = 0.004). Second, fourth and fifth year students had a
greater problem in Internet use (2 = 15.62, df = 5, p = 0.008).
The students’ personality and mental health are shown
in Tables 2 and 3.
According to the results of the Kormogorov---Smirnov test
with Lilliefors correction, a normal distribution was not
found for any of the variables (p < 0.01).
IA has a highly significant correlation with impulsivity (rs = 0.244, p < .001), neuroticism-anxiety (rs = 0.304,
p < .001) and aggression-hostility (rs = 0.143, p=.001). This
was only significant with sensation seeking (rs = 0.95,
p = 0.030). It was also negatively correlated with work effort
(rs = −0.136, p = 0.002); the greater the addiction, the lower
the work effort.
Regarding mental health, IA had a highly significant
correlation with somatic symptoms (rs = 0.174, p < .001),
anxiety and insomnia (rs = 0.219, p < .001), social dysfunction (rs = 0.118, p < .001) and severe depression (rs = 0.199,
p < .001). Personality and mental health in the groups formed
according to IA test interpretation are shown in Table 4.
Discussion
We found, like Young3 and others, that men have a higher
prevalence of Internet addiction. Despite the low frequency
of IA reported by the students in our analysis, it appears
Internet addiction
Table 2
91
Results of the Zuckerman-Kuhlman III questionnaire subscales.
Subscale
Mean
Neuroticism-anxiety
0.3534
Activity
General Activity
0.4650
Work Effort
0.5943
Sociability
Parties and Friends
0.3795
Intolerance to being alone
0.5194
Impulsiveness and sensation seeking
Impulsiveness
0.3123
Sensation Seeking
0.5536
Aggressiveness-hostility
0.3826
Infrequent
0.2316
Median
Minimum
Maximum
0.3158
0.3326
0.3743
0.2421
0.123
0.4444
0.6250
0.4447
0.5757
0.4853
0.6129
0.2359
0.2160
0.104
0.150
0.3333
0.500
0.3606
0.4969
0.3984
0.5419
0.2195
0.2611
0.150
0.121
0.250
0.5455
0.3529
0.2
0.2921
0.5322
0.3656
0.2169
0.3324
0.5751
0.3995
0.2463
0.2339
0.2490
30.34
1.710
0.139
0.092
0.091
0.171
that most use the network seven days a week, mostly 10
times a day, spending an hour on each connection, which
seems generally an everyday behavior of young people. It is
notable that most responded that they frequently surf the
web for a longer period than intended, which shows a lack
of control in their use.
We noted a remarkably ludic nature of Internet use since
most of the time they connected to the network to participate in social networks and leisure.
Overall, we found a small percentage of students who
have problems with Internet use (8.2%); however, this agrees
with the literature and the comorbidities found in Internet
addiction.
It has been stated that problematic use of the Internet is
only the manifestation of an underlying problem, highlighting frequent comorbidities with mood disorders, anxiety,
and other addictions.14 Mustafa15 investigated the relationship between IA and psychiatric symptoms and he found a
significant relationship between daily use of the Internet
and the degree of psychiatric symptoms such as depression,
obsessive compulsion, interpersonal sensitivity, anxiety, hostility, phobic anxiety, paranoid ideation and psychoticism.
With longer use, more psychiatric symptoms occur. He also
found a significant association between the severity of IA
and the degree of psychiatric symptomatology.
Ebeling-Witte et al.16 found that scores of shyness were
associated with problematic Internet use. That is, the network is used to reduce the deficit perceived in social life
by establishing virtual friendships online and to alleviate
feelings of loneliness and depression and to avoid attending
stressful places. In contrast, Shapira and Goldsmith17 found
in a population of subjects with problems with Internet use
that 100% met DSM-IV criteria for impulse control disorders
not otherwise specified.
Table 3
SD
KS
In an exploratory study on behavioral problems related to
Internet use, a subgroup of netizens who expressed greater
anxiety and social dysfunction was identified through the
GHQ-28.18
Armstrong, Phillips and Saling19 concluded that selfesteem and the number of hours per week using the network
were the variables that best predicted problems related to
the Internet. However, impulsivity was not related, which
made the authors conclude that unlike other addictions, IA
is not characterized by this trait.
In 2012, a study of Egyptian adolescents found that subjects with problematic Internet use were more likely to have
anxiety disorders (social phobia, specific phobia, and generalized anxiety disorder).20
Articles that mention the coexistence of psychiatric disorders and Internet addiction were found in a review of data
from PubMed carried out up to November 3, 2009. Based
on this review, IA is associated with substance use disorder, attention deficit and hyperactivity disorder, depressive
disorder, social phobia, and hostility.21
Kubey et al.22 reported four times more academic deterioration in students with IA than was noted in the perception
of academic performance in our sample. As to the question
of whether or not performing any recreational (extracurricular) activities has an effect --- seeking a possible protective
factor --- no significant difference was found in terms of IA
and practicing (or not) these activities.
Garcia del Castillo23 found in his study of university students that the psychosocial profile of the group with the
highest frequency of Internet use showed a higher score in
the ‘‘cognitive social skills’’ dimension (F = 3.76, p = 0.01),
which indicates that there is a greater presence of ‘‘negative
thoughts’’ in the group with the greatest frequency of use,
interfering in different social situations. The presence of
Results of Mental Health subscales.
Subscale
Mean
Median
Minimum
Maximum
SD
KS
Somatic symptoms
Anxiety and insomnia
Social dysfunction
Severe depression
10.98
11.01
13.17
8.22
10.00
10.00
13.00
7.00
10.69
10.65
12.91
8.00
11.26
11.36
13.42
8.42
3.316
4.083
2.999
2.473
0.159
0.168
0.132
0.311
42.85
48.87
69
8.05
10.07
12
13.08
14.00
18
10.85
12.65
19
10.86
12.14
20
0.2300
0.2463
0.4000
Infrequent
0.5515
0.5809
0.4545
Use control
Frequent problems with use
Significant problems
0.2997
0.4543
0.5000
Agressiveness/
Hostility
Sensation
Seeking
Impulsivness
Impulsiveness and Sensation Seeking
Activity
0.3760
0.4577
0.4706
Total
Anxiety and
insomnia
Somatic
symptoms
Mental health
Social
dysfunction
Severe
depression
0.5276
0.4329
0.1250
0.3745
0.4390
0.3333
0.6026
0.5022
0.3750
0.4657
0.4566
0.4444
0.3369
0.5340
0.8947
21.21
21.66
19
Age
Frequency
92%
7.9%
0.2%
Use control
Frequent problems with use
Significant problems
Table 4
Internet addiction, personality and mental health.
Activity
NeuroticismAnxiety
General
Activity
Work Effort
Parties and
Friends
Intolerance
to being
alone
N. Capetillo-Ventura, M. Juárez-Treviño
Sociability
92
negative thoughts is associated with the use and abuse
of the Internet in searching for ‘‘relationships and friendship’’ (r = 0.14; p = 0.016) and improving ‘‘emotional state’’
(r = 0.16; p = 0.007). These results agree with those of other
authors who emphasize the tendency to escape, shyness
and introversion, social phobia, and also, in contrast to the
levels of neuroticism, self-confidence, self-reliance, or the
search for feelings as personal characteristics associated
with greater use and even abuse of the Internet, coinciding
with our study regarding the highly significant correlation of
IA with neuroticism-anxiety (rs = 0.304, p < 0.001), described
as emotional instability, stress, worry, phobias and/or fears,
obsessive indecision, and susceptibility to criticism. This
also coincides with what some researchers think about the
network; that it is a means of easy access for anonymous
social interaction, thus constituting a space where communication can be less hampered by deficits in the ability
of interpersonal relationships. It is important to remember that the network has become the medium for social
development. In this sense it often does not eliminate
social relations, only changes the means to develop or even
generate emotional wellbeing in those with difficulties in
face-to-face socialization. Therefore, we would have to
rethink those items of interference in social life for the
diagnosis of Internet abuse.
We agree with the conclusion of Salman et al.24 , that psychiatrists and psychologists involved in the field of mental
health must be well informed about mental problems due
to Internet addiction, such as anxiety, depression, aggression, and employment and educational dissatisfaction, and
consider that IA and its comorbid disorders should be properly evaluated and treated at the same time. Finally, it is
also important to pay attention to Internet addiction in the
treatment of people with these psychiatric disorders.
Because the participant sample is composed exclusively
of university students, we could say that generalization of
the results to the entire population is not possible because of
their high cultural level. However, the results can generate
some idea of what happens in the social group --- namely,
young individuals --- who are being influenced by use of the
Internet.
The means by which access to the Internet was achieved,
including home computers, laptops or smart phones, were
not taken into account in the study. This fact interferes
with network access and facilitates more frequent, even
problematic use. In addition, since the sample was medical
students, they could have similar characteristics in lifestyle
and personality. Therefore, research in other university
groups could give a less biased idea of these characteristics.
Conclusion
Although an association between IA and psychiatric symptoms exist, it may be beneficial for those with difficulty in
establishing face-to-face relationships. Due to the prevalence of impulsivity and neuroticism/anxiety in people
with Internet addiction, we think it would be prudent to
better define the diagnostic criteria of addiction since
impulsivity is related to other addictions and, in the case
of Internet use, could be harmful. It is important to note
that the Internet is a tool for various activities (research,
Internet addiction
education, socialization, and as a means of long-distance
communication), which, used with control, does not cause
any problems, but losing that control causes addiction
and its comorbidities. Also, certain personality types are
predisposed to this loss of control and abuse.
Conflicts of interest
The authors declare that they have no conflicts of interest
and they received no funds for this work.
Acknowledgements
We thank Sergio Lozano-Rodríguez, M.D. for his help in
translating the manuscript, Marco V. Gómez-Meza for his statistical advice and Ana E. Gutierrez Cortés for reviewing the
manuscript.
References
1. Navarro A, Rueda E. Adicción a Internet: revisión crítica de la
literatura. Rev Colomb Psiquiatr. 2007;36:691---700.
2. Cruzado Díaz L, Matos Retamozo L, Kendall Folmer R. Adicción
a Internet: perfil clínico y epidemiológico de pacientes hospitalizados en un instituto nacional de salud mental. Rev Med
Herediana. 2006;17:196---205.
3. Young KS. Caught in the net: how to recognise the signs of Internet addiction and a winning strategy for recovery. New York:
John Willey and Sons; 2000.
4. Griffiths M. Internet addiction: does it really exist. Psychology
and the Internet: Intrapersonal, interpersonal and transpersonal implications; 1998. p. 61---75.
5. Hong SB, Kim JW, Choi EJ, Kim HH, Suh JE, Kim CD, et al.
Reduced orbitofrontal cortical thickness in male adolescents
with Internet addiction. Behav Brain Funct. 2013;9:11.
6. Young KS. Internet addiction: the emergence of a new clinical
disorder. CyberPsychol Behav. 1998;1:237---44.
7. López AL. Adicción a Internet: conceptualización y propuesta de intervención. Rev Prof Española Ter Cognit-Conduct.
2004;2:22---52.
8. Martínez A, Ortiz S, Lara M. Uso excesivo o adicción a Internet?
Psiquiatría. 2011;28:1---9.
93
9. Young KS, Rogers RC. The relationship between depression and
Internet addiction. Cyberpsychol Behav. 1998;1:25---8.
10. Young KS, de Abreu CN, editors. Internet addiction: a handbook and guide to evaluation and treatment. John Wiley & Sons;
2010.
11. Widyanto L, McMurran M. The psychometric properties of the
internet addiction test. Cyberpsychol Behav. 2004;7:4.
12. Lobo A, Pérez-Echeverría MJ, Artal J. Validity of the scaled version of the General Health Questionnaire (GHQ-28) in a Spanish
population. Psychol Med. 1986;6:135---40, 1.
13. Herrero M, Viña C, Gonzalez M, Ibañez I. El cuestionario
de personalidad de Zuckerman-Kuhlman-III (ZKPQ-III): version
española. Rev Latinoam Psicol. 2001;003:269---87.
14. Huisman A, Van den Eijnden RJ, Garretsen H. Internet addiction --- a call for systematic research. J Subst Use. 2001;6:
7---10.
15. Mustafa KOÇ. Internet addiction and psychopatology. Turk
Online J Educ Technol. 2011;10:1.
16. Ebeling-Witte S, Frank M, Lester D. Shyness, Internet use and
personality. Cyberpsychol Behav. 2007;10:5.
17. Shapira NA, Goldsmith TD, Keck PE Jr, Khosla UM, McElroy SL.
Psychiatric features of individuals with problematic Internet
use. J Affect Disord. 2000;57:267---72.
18. Gracia M, Vigo M, Fernández M, Marcó M. Problemas conductuales relacionados con el uso de Internet: un estudio
exploratorio. Anales Psicol. 2002;18:2.
19. Amstrong L, Phillips JG, Saling LL. Potential determinats of heavier Internet usage. Int J Hum-Comput Stud.
2000;53:537---50.
20. Reda M, Rabie M, Mohsen N, Hassan A. Problematic Internet
users and psychiatric morbidity in a sample of Egyptian adolescents. Psychology. 2012;3:8.
21. Ko CH, Yen JY, Yen CF, Chen CS, Chen CC. The association
between Internet addiction and psychiatric disorder: a review
of the literature. Eur Psychiatry. 2012;27:1---8.
22. Kubey R, Lavin M, Barrows J. Internet use and collegiate academic performance decrements: early findings. J Commun.
2001;51:366---82.
23. García del Castillo JA, Terol MC, Nieto M, Lledó A, Sánchez S,
Martín-Aragón M, Sitges E. Uso y abuso de Internet en jóvenes
universitarios. Adicciones. 2008;20:131---42.
24. Salman S, Alaghemandan H, Reza M, Jannatifard F, Eslami M,
Ferdosi M. Impact of addiction to Internet on a number of
psychiatric symptoms in students of Isfahan Universities, Iran,
2010. Int J Prevent Med. 2012;3:122---7.
Medicina Universitaria. 2015;17(67):94---96
www.elsevier.es/rmuanl
CLINICAL CASE
Decision-making in the management of an incomplete
urethral duplication in a young male
R.d.J. Treviño-Rangel a,∗ , B.A. Bodden-Mendoza a , N. Cantú-Salinas b ,
M.A. García-Rodríguez c
a
School of Medicine of the Universidad Autónoma de Nuevo León, Monterrey, Nuevo León, Mexico
Urology Services, Sierra Madre Hospital, Monterrey, Nuevo León, Mexico
c
Surgery Institute, Centro Médico Zambrano Hellion, San Pedro Garza García, Nuevo León, Mexico
b
Received 3 June 2014; accepted 31 July 2014
KEYWORDS
Accessory urethra;
Effmann’s
classification;
Urethral duplication
Abstract
Objective: This is a case report of a 27-year-old Mexican man complaining of a double urethral
meatus located at the tip of the glans.
Material and methods: An exhaustive physical examination was performed together with an
intravenous excretory urography and retrograde urethrogram in order to evaluate the case
properly.
Results: The patient presented an incomplete urethral duplication type 1B according to
Effmann’s classification.
Conclusion: The lack of symptoms as well as the absence of significant clinical or functional
repercussion in the patient led us to recommend therapeutic abstention for the time being.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights
reserved.
Introduction
Urethral duplication is an extremely rare lower urinary
tract anomaly (more frequent in males) that was first
described by Aristotle, and includes a wide spectrum of
anatomical variants in which the urethra is partially or
completely duplicated.1 The most frequent anomaly occurs
in the sagittal plane, in which the duplicated urethra is
in either the dorsal or ventral position in relation to the
orthotopic urethra.2 The therapeutic management of these
conditions is complex and depends on the presence of symptoms as well as the type of anomaly.
∗
Corresponding author at: Facultad de Medicina, Universidad
Autónoma de Nuevo León, Ave. Madero & Dr. Eduardo A. Pequeño,
Col. Mitras Centro, Monterrey, Nuevo León, 64460, Mexico.
Tel.: +52 81 8329 4177; fax: +52 81 8676 8605.
E-mail address: [email protected] (R.d.J. Treviño-Rangel).
Case report
A 27-year-old Mexican man without personal or family
medical history of interest, attended the Urology Clinic
http://dx.doi.org/10.1016/j.rmu.2014.07.003
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights reserved.
An incomplete urethral duplication
Figure 1
95
Double urethral meatus in glans.
complaining of a double urethral meatus located at the tip
of the glans, one in the orthotopic position and another in
the ventral or hypospadic position, respectively (Fig. 1). The
patient informed us that micturition and ejaculation occur
just through the hypospadic meatus. He reported no voiding
problems or difficulties such as ejaculatory abnormalities,
urinary incontinence or urinary tract infections. An integral
physical examination of the patient confirmed the presence
of a ventral urethral duplication, a retractable foreskin, and
the testicles were normal to palpation without any evidence
of mass or tumors. The intravenous excretory urography of
the upper urinary tract and the bladder was unremarkable.
On the other hand, the retrograde urethrogram revealed
a unique origin urethra at the vesical level, which presented an incomplete proximal duplication in its anterior
section with a short stenotic segment in the penile urethra of
approximately 2.5 cm (Fig. 2). Because of the fact that other
anomalies were not present, and due to the absence of functional repercussions, therapeutic abstention was advised.
Discussion
Urethral duplication is an infrequent congenital malformation with an estimate of 150 reported cases worldwide.2,3
Embryogenesis of this phenomenon is uncertain and likely
multifactorial. In this sense, many hypotheses have been
proposed to explain this unusual condition, including
ischemia, abnormal Műllerian duct termination and growth
failure of the urogenital sinus.1 However, a universal etiology or embryological explanation cannot be applied to all
subtypes of urethral duplication.
Clinical relevance of urethral duplication is diverse.
Patients may have a double stream, urinary incontinence, outflow obstruction, recurrent urinary infection or
be completely asymptomatic. In the case presented, the
patient did not suffer any associated problem, remaining
asymptomatic to date. A proper clinical examination,
Figure 2 Retrograde urethrogram that shows the proximal
duplication of the penile urethra.
voiding cystourethrography, retrograde urography, urethrocystoscopy and intravenous excretory urography orientate
in the diagnosis of these anomalies.1 The retrograde urography, as well as the intravenous excretory urography, were
particularly useful to diagnose the condition of the patient.
Several classifications distinguish between complete and
incomplete urethral duplication. However, the most exhaustive and widely used classification, based on radiological
findings, has been offered by Effmann et al.4 as it is functional and represents all clinical aspects involved (Fig. 3).
Effmann’s classification divides urethral duplications into
incomplete (type 1), complete (type 2) and coronal (type 3),
the last one being the one usually associated with bladder
duplication.5 Type 1 is the most common variant of urethral
duplication and is usually asymptomatic. Based on the clinical findings obtained in this case and according to Effmann’s
classification, the patient presented a urethral duplication
type 1b due to the proximal localization of the accessory
urethra, which originated from the principal urethra and had
a blind end in the periurethral tissue.
The treatment of these conditions must be personalized, taking into consideration the anatomic variant and
functional outcome, as well as the coexistence of other malformations. The treatment criteria ranges from therapeutic
abstention, to the excision of the accessory urethra.6 The
surgical approach is not always required, as patients are at
risk of developing a variety of postoperative complications,
such as urethrocutaneous fistula, recurrent meatal stenosis and urethral diverticulum with calculi.7 According to the
Salle et al. recommendations for the management of each
urethral duplication subtype,6 in this particular case, the
lack of symptoms as well as the absence of significant clinical or functional repercussion in the patient led us to advised
therapeutic abstention for the time being.
96
R.d.J. Treviño-Rangel et al.
IA
IB
IIA 2 “Y type”
Figure 3
IIA 2
IIA 1
IIB
III
Effmann’s classification for urethral duplication.4
Conflict of interest
The authors declare that they have no financial or nonfinancial conflicts of interest related to the subject matter
or materials discussed in the manuscript.
Funding
No financial support was provided.
References
1. Arena S, Arena C, Scuderi MG, et al. Urethral duplication in
males: our experience in ten cases. Pediatr Surg Int. 2007;23:
789---94.
2. Onofre LS, Gomes AL, Leão JQ, et al. Urethral duplication
--- a wide spectrum of anomalies. J Pediatr Urol. 2013;9:
1064---71.
3. Slavov C, Donkov I, Popov E. Case of duplication of the urethra
in an adult male, presenting with symptoms of bladder outlet
obstruction. Eur Urol. 2007;52:1521---2.
4. Effmann EL, Lebowitz RL, Colodny AH. Duplication of the urethra.
Radiology. 1976;119:179---85.
5. Woodhouse CR, Williams DI. Duplications of the lower urinary
tract in children. Br J Urol. 1979;51:481---7.
6. Salle JL, Sibai H, Rosenstein D, et al. Urethral duplication in the
male: review of 16 cases. J Urol. 2000;163:1936---40.
7. Podesta ML, Medel R, Castera R, et al. Urethral duplication in children: surgical treatment and results. J Urol.
1998;160:1830---3.
Medicina Universitaria. 2015;17(67):97---101
www.elsevier.es/rmuanl
SCIENTIFIC LETTER
Thrombosed great saphenous vein aneurysm
accompanied by venous thrombosis
F.G. Rendón-Elías a,∗ , R. Albores-Figueroa a , L.S. Arrazolo-Ortega a , F. Torres-Alcalá a ,
M. Hernández-Sánchez b , L.H. Gómez-Danés a
a
b
Service of Thoracic and Cardiovascular Surgery of the ‘‘Dr. José Eleuterio González’’, University Hospital of the UANL, Mexico
Service of Pediatrics, UMAE ·21, IMSS Monterrey, Nuevo León, Mexico
Received 14 May 2014; accepted 22 July 2014
Available online 23 June 2015
KEYWORDS
Great saphenous vein;
Venous aneurysms;
Vascular
malformations;
Venous thrombosis
Abstract Superficial venous aneurysms of the lower extremities are considered rare and their
clinical significance is poorly defined. The purpose of this article is to report a case of a 72year-old woman with a thrombosed great saphenous vein aneurysm along with deep venous
thrombosis and review its clinical presentation, diagnosis and treatment.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights
reserved.
Introduction
Venous aneurysms (VA) are a rare vascular pathology. First
described by Sir William Osler in 1913,1 VAs can be located
anywhere throughout the venous system and do not have a
preference regarding sex or age.2
VAs are usually located in the lower extremities, and
can be deep or superficial, depending on whether the
affected vein is over or under the muscle fascia. Deep
VAs are the most frequent, because the popliteal vein is
the most commonly affected (between 60% and 70% of
∗ Corresponding author at: Servicio de Cirugía Torácica y Cardiovascular del Hospital Universitario ‘‘Dr. José Eleuterio González’’,
de la Universidad Autónoma de Nuevo León, Av. Madero y Gonzalitos
S/N, CP. 64460, Monterrey, Nuevo León, Mexico.
E-mail address: [email protected] (F.G. Rendón-Elías).
the cases), and the most studied because of their high
thromboembolism risk.3
Superficial VAs are rare, with under 60 reported cases in
medical literature4 and are taken less seriously than deep
VAs, due to the fact that superficial VAs are considered to
have a low risk of life-threatening complications.
The purpose of this article is to present a case of a patient
affected by a thrombosed great saphenous vein aneurysm
along with deep venous thrombosis. Additionally, the literature is reviewed with a discussion on clinical implications
and the diagnostic and therapeutic approach of this lesser
known vascular pathology.
Clinical case
The patient is a 72-year-old female, with no positive
background of chronic degenerative diseases or of any
other type, and a negative history of smoking. The patient
http://dx.doi.org/10.1016/j.rmu.2015.02.002
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights reserved.
98
F.G. Rendón-Elías et al.
Figure 1 Reconstructed ultrasound image which shows an internal saphenous vein venous aneurism of 9 × 5 cm, which compression
did not remove.
presented an increase in volume of the right pelvic limb 10
days after undergoing surgery to correct a direct inguinal
hernia using the Bassini---Shouldice technique. The subject
pointed out that for over 40 years she presented a soft
tumor of approximately 10 cm, located in the middle third
of the medial part of the right thigh 22 cm from the inguinal
fold. The tumor was soft, palpable and painless with a
variation in volume depending on the position and did not
cause any discomfort. Subsequent to the hernioplasty the
patient began noticing that the tumor hardened and caused
pain, along with redness and an increase in local temperature, consequently the physician diagnosed a cellulitis and
prescribed antibiotic therapy. The symptomatology did not
improve with the prescribed treatment and now presented
an increase in volume of the entire pelvic member. She was
therefore referred to our service. During the examination a
difference of 5 cm in volume between both pelvic members
was observed, noticing a hard, non-mobile, painful lump of
9 × 6 cm. The rest of the examination was normal. A vascular ultrasound was performed, showing a non-palpable,
anechoic growth, connected to the great saphenous vein,
of 9 × 5 cm (Fig. 1) without the presence of venous reflex
neither in the great saphenous nor in the saphenofemoral
junction. Moreover, a posterior tibial vein thrombosis was
detected. With a great saphenous vein aneurysm diagnosis,
the patient was transferred to surgery where an aneurysmectomy and SFJ ligation were performed (Figs. 2 and 3).
There were no complications during the procedure, the
evolution was good and the patient was discharged on the
second postoperative day with a compressive and anticoagulant DVT treatment for a period of 3 months.
Figure 2 Surgical excision of the internal saphenous vein
venous aneurisms.
the vein’s diameter is twice as large as the normal diameter, then it is considered to be an aneurysm (the saphenous
vein’s normal size at the saphenofemoral joint is 3---5 mm,
2---4 mm at the thigh and 1---3 mm at the ankle).8 . Nevertheless, in order to consider it a primary venous aneurysm size
is not the only factor considered. It must also be a localized dilation, conformed by three histological layers which
constitute the normal venous wall. This could be saccular or
Discussion
The terminology used to describe venous dilatations can
cause confusion. The terms phlebectasia, varicose vein
and/or venous aneurysm are considered synonyms in the
medical community; however, they mean different things.
Phlebectasiais defined as a fusiform and diffusely dilated
vein. The association of dilated and tortuous veins is known
as varicose veins.5 There is no precise criteria regarding
size and when a venous dilation is considered an aneurysm;
however, Mateo6 and McDevitt7 established that whenever
Figure 3
aneurysm.
Thrombosed internal saphenous vein venous
Thrombosed great saphenous vein
fusiform (an important distinction because of its hemodynamic implications that influence the course of treatment)
and should only communicate to the corresponding vein in a
proximal and distal manner and neither be secondary to an
arteriovenous fistula,9 nor be related to a varicose vein.10
Hilscher coined the term primary venous aneurysm, making a comparison to arterial aneurysms. Abbott was the one
who integrated the criteria to define VAs.11 Our patient met
the required criteria to classify her venous pathology as a
primary venous aneurysm.
Primary VAs occur in the head and neck, thoracic and visceral veins as well as veins of the extremities. Aneurysms
of the deep venous system are characteristic on the
extremities, where a greater incidence of thromboembolic
complications is reported.
The incidence of superficial venous aneurysms is approximately 0.1%,12 with a prevalence of 1.5%,13 equally in both
sexes and it may occur at any age.
The pathogenesis of venous aneurysms is unknown; several mechanisms have been implicated in its formation, such
as hemodynamic changes, arteriovenous fistulae, inflammatory processes, infections, trauma, congenital weakness of
the venous wall and degenerative changes.5,14 The most
accepted theory states that it is a result of the loss of
connective tissue components of the venous wall, which
can be caused by a congenital defect or secondary to a
degenerative process due to aging.15,16 In a recent study,
tissue from the wall of venous aneurysms was examined
and it was reported that structural changes of the aneurysmatic wall can be related to the increased expression of
metalloproteinase,17 which can be translated to a reduction
of the muscle layer, fragmented elastic tissue, an increase
in the fibrous tissue and infiltration of inflammatory cells.
Schatz and Fine,18 believed that edophlebohypertophy was
a major factor in the formation of VA, which begins with
an increase in venous flow leading to a hypertrophy of the
venous wall, then dilation and sclerosis. Pascarella et al.4
informed that superficial VAs on lower limbs were generally
located distal to an incompetent venous valve, which causes
venous reflex, hitting the venous wall and producing a turbulent flow, causing structural changes on the wall of the
spleen, while those in deep veins are secondary to intrinsic
changes of the venous wall.
The difference among findings in the reports suggests
that the etiology of VAs is diverse and depends on their location and natural history.16,19---22 In our case, the etiology may
come as a result of a congenital defect in the connective
tissue structure, which generated a weak venous wall susceptible to dilation, hence contributing to the onset of the
inguinal hernia.
According to the etiopathogeny, VAs can be divided into
primary (congenital) or acquired. Based on the Hamburg
classification for congenital vascular malformations,23 VAs
correspond to a venous malformation of the troncular type,
which can be presented as aplasia, hyperplasia, stenosis
(i.e. the left iliac vein in May-Turner syndrome), dilations
or aneurysms (the most common being the popliteal vein).24
Congenital VAs are less common but can occur in any vein
of the body. In a study, Guillespie et al.,2 reported that 77%
of VAs were located in the lower extremities (57% in the
deep venous system), 10% in the upper extremities and 13%
in the neck.
99
The clinical presentation of superficial VAs in lower
extremities is that of a palpablesoft lump. It can change
its size and location with the body’s position or the Valsalva
maneuver; they can be completely asymptomatic or painful
with edema, and have signs and symptoms similar to those
described in our case.
The diagnosis can be made by the clinical history and
physical examination in most cases, but it is usually confirmed by image studies. Within image studies, vascular
ultrasound is the method of choice for the study of VAs.25
In the ultrasound, VAs are presented as an anechoic cystic
structure, with well-defined walls, which can be secular or
fusiform and with a low flow volume; also, they provide us
with information on vascular connections, the existence of
thrombosis, or if there is an associated arteriovenous fistula or any other pathologies,26 in addition to guiding the
therapeutic approach. The CAT scan, the MRI and the phlebography are studies which can be performed in case of
diagnostic doubt or when more exact information is required
(size, extension, associated lesions and vascular origin).27
Clinical history and examination are the basis for reaching
any diagnosis, but in the case of venous problems, vascular ultrasound evaluation is fundamental to reaching a
correct diagnosis, and thus choosing the proper treatment.
It is only in case of doubt, where further imaging studies
are required. In the differential diagnosis, we must consider
varicose veins, soft tissue tumors, hygromas, hemangiomas
and, depending on location, inguinal hernias. Vascular
aneurysm complications are: thrombophlebitis, deep venous
thrombosis, pulmonary embolism and bleeding caused by
rupture.
Coagulation disorders associated with VAs are characterized by blood stasis in the dilated vessels and with a low
blood flow, which activates the coagulation cascade with the
subsequent production of thrombin and the conversion of
fibrinogen into fibrin.28,29 Then the fibrinolysis process begins
which is reflected in the rise in fibrinogen derived products, including D-dimer. This is the simplified description
of located intravascular coagulopathy which characterizes
coagulopathy associated with venous malformations.30,31
Newly formed microthrombus attach to calcium and phleboliths are formed.32,33 These can be detected during
physical examination and verified by imaging studies. The
presence of phleboliths in VAs can indicate treatment with
anticoagulants, especially in large and extensive VAs.34
Localized intravascular coagulopathy is of utmost importance because it is linked to the presence of local pain,
thrombophlebitis, deep venous thrombosis and pulmonary
embolism.
Even though deep venous aneurysms are more susceptible to presenting pulmonary embolism and their frequency is
more common in this type of VA, superficial VAs are not free
from presenting this complication. Due to this, they must be
treated with anticoagulant therapy, just as the deep ones.
Recapitulating Virchow’s triad for venous thrombosis, which
consists of venous stasis, hypercoagulability and endothelial lesion, in our case it presented venous stasis because
of the hemodynamic changes brought on by the dimensions
of the venous aneurysm, the existing coagulation disorders
of this pathology associated with bed rest subsequent to
hernioplasty, and the existing risk of thrombosis in any type
of surgery, and constitute risk factors which contributed
100
to the presence of superficial and deep venous thrombosis
described in our report.
Regarding the risk of VA rupture, it represents something
theoretical since there are no reported cases of this complication.
Superficial VA treatment can be conservative, endovascular or surgical. If the VA is not too large and does not
cause symptoms it may be treated conservatively through
compressive therapy and prophylaxis in order to avoid
thrombophlebitis or deep venous thrombosis. The indications for surgical treatment in superficial VAs are: the
presence of symptoms, the risk of thrombosis, compression of nearby structures and, more commonly, esthetic
problems.35 Surgical treatment36 consists of ligation and
total excision of the aneurysm. However, in some cases,
endovascular methods can be used, like foam, laser or
radiofrequency sclerotherapy.37 In the case of patients who
present superficial venous thrombosis above the knee (as
in our case) or deep venous thrombosis at any location, it
is important to treat with anticoagulants for 3---6 months
in patients with normal thrombophilic profiles, otherwise
the anticoagulant is prescribed indefinitely. In the presented
case, there is no doubt that the chosen surgical treatment is
adequate and the treatment with anticoagulants due to the
presence of deep thrombosis for a period of three months is
acceptable.
The results of the treatment of these types of pathologies are excellent as long as they are not associated with
other vascular malformations or pathologies; there are no
reports of mortality in superficial VA surgical intervention in
the lower extremities and the morbidity is the same as any
venous surgical procedure.36
In our case, the primary care physician diagnosed the
increase in volume as a soft tissue tumor (first differential
diagnosis which should be made) and since it was asymptomatic, they did not give it much importance despite the
fact that the patient reported that the tumor was growing progressively. As a result of the inguinal hernioplasty
the patient was on bed rest for two weeks. Surgical trauma
and prolonged bed rest are risk factors for thrombosis. The
patient did not receive prophylaxis for thrombosis.
At first, and because the tumor looked red and was
causing severe pain, it was treated as if it was cellulitis
(thrombophlebitis, which is commonly confused with soft
tissue infections). It was not until the size of the patient’s
leg began to increase that there was a suspicion of venous
thrombosis and the case was referred to our service.
Thus we conclude that it is important to: (1) perform
the clinical history and a thorough physical examination in
all of our patients, (2) we must keep in mind all possible
differential diagnoses before giving a definite one, (3) one
must never forget prophylaxis for deep vein thrombosis in
surgical patients, (4) not all skin redness equals infection,
(5) venous thrombosis must be ruled out in every patient
who presents a sudden increase in leg volume, (6) vascular
ultrasound is an essential tool for diagnosis and (7) venous
aneurysms do exist and they are not just varicose veins.
Conflict of interest
The authors have no conflicts of interest to declare.
F.G. Rendón-Elías et al.
Funding
No financial support was provided.
References
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31. Mazoyer E, Enjolras O, Bisdorff A, et al. Coagulation disorders in
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Medicina Universitaria. 2015;17(67):102---107
www.elsevier.es/rmuanl
SCIENTIFIC LETTER
Case report: Diagnostic reconceptualization in the
DSM-V on somatoform disorders
D. Ibarra-Patrón ∗ , G. Medina-Vidales, C. Garza-Guerrero
Department of Psychiatry, ‘‘Dr. José Eleuterio González’’ University Hospital, UANL, Monterrey, Nuevo León, Mexico
Received 26 August 2014; accepted 11 November 2014
KEYWORDS
Somatic symptoms
disorder;
DSM-5;
Classification;
Evaluation;
Diagnosis;
Treatment
Abstract Psychosomatic disorders are among the most common psychiatric disorders in general practice, with a prevalence of 16%. These patients often turn to different general
practitioners and/or non-psychiatric specialists for long periods of time and represent a diagnostic and therapeutic challenge, as the possible organic component makes it complex and
difficult to manage.
The reported case is a 24-year-old male patient with a diagnosis of Somatic Symptoms Disorder
and multiple psychiatric comorbidities. The purpose of this study is to review the reconceptualization of Somatoform Disorders’ DSM-5 diagnosis, which can be useful for psychiatrists and
non-psychiatric physicians for the approach and management of these patients.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights
reserved.
Introduction
Psychosomatic disorders are among the most common psychiatric disorders in general practice, with a prevalence
of 16%.1---3,5 Before going to a psychiatrist, these patients
usually see general physicians and/or non-psychiatric specialists for long periods of time2,4,6 which is enabled by these
patients’ resistance to acknowledging that their physical
∗ Corresponding author at: Departamento de Psiquiatría, Hospital
Universitario ‘‘Dr. José Eleuterio González’’, UANL, Av. Francisco I
Madero y Gonzalitos s/n, Colonia Mitras Centro, C.P. 64460 Monterrey, Nuevo León, Mexico. Tel.: +52 81 8348 0585.
E-mail address: diana [email protected] (D. Ibarra-Patrón).
problem can be linked to or exacerbated by an emotional
and not only an organic origin, resulting in multiple therapeutic managements and chronic use of health services.2,4,5,8
Moreover, the important association of psychiatric
comorbidity (depression, anxiety and psychopathology of
character), as well as medical illnesses,1,2,4,6,7 makes them a
diagnostic and treatment challenge not only for the psychiatrist, but also for general practitioners and other specialties,
since the possible organic component makes them complex
and difficult to manage.4,7
Regarding its evolution, chronicity, social and interpersonal dysfunction, difficulties at work and the frequent
use of medical services are the common characteristics
of these disorders, which lead to an elevated level of
dissatisfaction in both the doctor and the patient.5,7,8
http://dx.doi.org/10.1016/j.rmu.2015.02.001
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. All rights reserved.
Diagnostic reconceptualization in DSM-V on somatoform disorders
The present article presents the case of a patient who exemplifies this pathology.
Case presentation and discussion
The patient is a 24-year-old male, from Monterrey, Mexico.
He is single, works at a flea market, with an upper secondary
level of completed education and a low socioeconomic status. He had a background of excellent school performance
with academic scholarship through secondary school and
high school. Prior to the onset of the psychopathology, there
was adequate and constant work activity, as well as more
social, recreational and interpersonal involvement. During
his childhood, he refers to being sexually abused (improper
touching) on two occasions and describes a stressing family
environment with constant verbal and psychological abuse
toward him and other family members. This prolongs until
adolescence. Subsequent to his parents’ separation, he
maintains a scarce, almost null, relationship with his father,
which stands as an event which impacts his childhood and
personal development in a negative way.
He has attended the Psychiatric Outpatient Clinic voluntarily on July 2012 after presenting depressive symptoms
for more than 6 months, secondary to pollakiuria with
an evolution of 4 years, which began after his father’s
Table 1
103
death, presenting 20---25 urinations a day, with intervals
of 10---20 min in-between and without disrupting sleeping
hours. He denies pain while urinating, pushing, tenesmus,
fever or any other added symptoms. Over 4 years the
patient saw multiple doctors and different urologists, who
requested para-clinical studies, with different non-certain
diagnoses and diverse pharmacological treatments without
improvements in the urinary symptom. (Table 1)
At first, in view of the diagnostic doubt and lack of
response to treatments, the patient thought that the origin of the symptom was caused by a physical illness; then,
he associated it with the unresolved mourning of his father’s
death which concurs with the onset of the symptoms.
Secondary to the onset of the urinary symptom, the
patient interrupts his personal and professional growth:
quits his job, stops frequenting his friends and remains isolated at home for over 2 years, focusing his life on attending
specialists and trying to solve his symptoms. Two years later,
the patient reduces the frequency of urination, accomplishing a urination rate of once every 2 h, and begins working
part-time. However, the sense of urgency to urinate as well
as the constant preoccupation of not being able to reach a
place to urinate, lead to a poor working growth and avoidance of interpersonal relationships with limited social and
recreational activities.
Medical history in relation to the urinary symptom.
Date
Diagnostic studies
Diagnosis
Treatment
March 2009
Not specified
Not specified
Urinary tract infection
Lincomycin IM Erythromycin
VO
Prostatitis
Prostatitis
Erythromycin
TMP/SMZ
Prostatitis
Alfuzosin
Prostatitis
Prostatitis
February 2010
EGO --- normal
Pelvis and kidney Eco --- normal
Prostatic Ag. --- normal
EGO --- normal
Urine culture --- Enterococcus Sp.
Spermculture: Klebsiella Sp.
Spermculture --- S. aureus
Klebsiella
Retrograde urethrography: narrowness of the
prostatic urethra. Checked with US finding the
prostate to have normal dimensions and
caliber. Complete emptying of urine.
Spermculture --- S. aureus
Spermculture --- S. aureus + Proteus vulgaris
Urine culture --- negative
EGO --- normal
No studies prescribed (review of previous).
June 2010
No studies prescribed.
November 2010
December 2010
Excretory urography: normal
Urodynamic study prescribed: not performed
due to lack of economic resources.
Refer nondiagnostic ureterocele
Urine smear --- negative
Urine culture --- Enterobacter cloacae
EGO - normal
Prostatic US --- normal
Overactive bladder
syndrome
Likely left ureterocele
Not specified
TMP/SMZ
TMP/SMZ
Meloxicam
Terazosin
Alfuzosin
Espectinomicina
Azithromycin Finasteride
Pregabalin
Solifenacin
Fluoxetine
Recommends surgery
Diazepam
Prostatitis
Not specified
Solifenacin
Levofloxacin
March 2009
May 2009
June 2009
July 2009
December 2009
January 2010
January 2011
May 2012
Not specified
104
Six months prior to attending psychiatric consultation
he begins to feel sadness every day for almost the entire
day; this sadness is linked to his urinary problem and his
difficulties in accomplishing things in his personal life and
at work. He refers to feeling ‘‘handicapped’’, saying he
felt ‘‘like trash’’, occasional crying, anhedonia and melancholy. A month ago he began to present terminal insomnia,
reduction of appetite, weakness and occasional feelings of
hopelessness, causing significant discomfort which interferes with his performance in his everyday activities. He
denies having thoughts of death, or suicidal thinking and/or
planning.
Previous to the pollakiuria, a pattern of preoccupation
about trivial situations with a tendency for the catastrophic
is noticed, which causes a persistent and general anxiety
not limited to a specific situation and is manifested by constant hand sweating, palpitations, mild tremors, occasional
irritability, fatigue and difficulty focusing. The anxiety symptoms fluctuate, but have a long evolution, which has been
exacerbated over the last 6 months.
Structural exam
The patient manifests evasive and dependent behavior,
which has had him working for the last 2 years at a place
which does not represent a significant challenge nor does it
demand formal obligations, hiding behind his urinary problem to avoid looking for a stable job, with a dependent
and victimized line. The evasive behavior is also manifested
by his disproportional fear when facing everyday situations,
generating anguish and resulting in deterioration of work
and interpersonal relations.
He presents a predominately devaluated self-concept,
describing himself as scared, insecure and feeling that he
has little value; this interferes with his interpersonal relationships with others. He displayed defense mechanisms,
mainly repressive, like rationalization, constantly using his
urinary symptom as an excuse to justify his evasive and
dependent traits; affective isolation when describing his
father’s death as an event that caused little pain and displacing, redirecting that pain toward his urinary symptom.
Despite his difficulty to relate to others, he manifests
an ability to empathize with others and an ability to be
grateful, expressing gratitude for the time dedicated to his
evaluation. Regarding his aggressive impulses’ control, he
does not present frequent situations which put him in conflict, thus making his ability to contain and repress emotions
evident. However, on a few occasions we were able to see
the infiltration of primary process thinking, causing him to
make impulsive decisions, later realizing this through his
ability for self-reflexive thinking.
In respect to the quality of his interpersonal relationships, he is unable to establish long lasting friendships
or romantic relationships and maintains a superficial and
not very affective relationship with his family members.
Regarding his tolerance of anxiety, we can observe a perennially apprehensive tendency and a tendency to exaggerate
catastrophes, which is expressed through his urinary frequency and in everyday situations, like sweaty palms when
interacting with people, and in his sex life, presenting anticipatory anxiety of not reaching a full erection.
D. Ibarra-Patrón et al.
Despite observing in the patient the cognitive ability and
desire to develop the personal and professional aspects of
his life, he does not perform any type of activities where he
experiences pleasure and satisfaction.
The patient has self-reflexive ability to suggest that pollakiuria is the superficial symptom covering deeper problems
related to self-esteem and his character.
DSM-V diagnosis
300.82. Somatic Symptom Disorder.
300.02. Generalized Anxiety Disorder.
296.21 Major Depressive Disorder.
3001.9 Unspecified Personality Disorder.
Diagnostic analysis
The DSM-V modifies the Somatomorphic Disorders and creates a new diagnostic entity in its place; Somatic Symptoms
Disorder (SSD) and related disorders. Evidence of multiple
lab and imaging studies without significant pathological findings, which explain the severity of the symptoms, along with
the lack of response to several medical treatments given
by different urologists, ruled out the presence of a known
medical condition that could explain the patient’s urinary
symptom, thus concluding, according to the DSM-V, the presence of a SDD (Table 2).8
The urinary symptom generated discomfort and major
anxiety which impacted the different areas of the patient’s
life in a negative way, since the constant feeling of inability
hindered his development in his work, social and personal
life (Criterion A). The symptom became the center of his
life, and he devoted excessive time and energy worrying
about his health and searching for an effective treatment
for over 4 years (Criteria B and C). The sudden onset, with a
persistent course and long evolution of a single very severe
somatic symptom, producing marked anxiety and disability
in his everyday life, specifies the diagnosis as Severe Persistent Somatic Symptoms Disorder.
The new components of somatic symptoms disorders are
incorporated in this new edition of the DSM-V: affection,
cognition and behavior within SSD criteria, providing a more
accurate and more comprehensive vision of the patients’
real signs and symptoms, in comparison to the DSM-IV, which
evaluates only somatic symptoms (1 or more). This diagnostic reconceptualization provides a useful tool for primary
care doctors or any other non-psychiatrist specialist. This
could be very beneficial in order to reach a proper diagnosis
and treatment in an earlier manner, improving the prognosis
and avoiding economic expenses in healthcare.6,7,9,10
Additionally, the criteria for a major depressive disorder,
with a moderate single episode, are met, clinically evident
and verbally expressed by the patient.
Regarding anxiety symptoms, these were reported before
the onset of the urinary symptom, with exacerbation in
the last 6 months, causing significant discomfort. The nonspecified personality disorder is justified by presenting
evasive traits manifested in social inhibition, feelings
of inability, hypersensitivity to negative evaluation and
avoidance of activities which require significant interpersonal contact, causing clinically significant dysfunction and
Diagnostic reconceptualization in DSM-V on somatoform disorders
Table 2
105
Diagnostic criteria for Somatic Symptoms Disorder DSM-V.
Somatic Symptoms Disorder
A. One or more somatic symptoms that cause discomfort or lead to significant problems in everyday life.
B. Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated with preoccupation over
health as is manifested by one or more of the following characteristics:
1. Disproportionate and persistent thoughts about the severity of the patient’s own symptoms.
2. Persistently elevated degree of anxiety about the patient’s health or symptoms.
3. Excessive time and energy dedicated to these symptoms or to worrying about health.
Although a somatic symptom may not be continually present, the symptomatic disorder is persistent (generally more than
six months).
Specify if:
Predominance of pain (before painful condition): this specifier applies to individuals whose somatic symptoms imply
pain over all.
Specify if:
Persistent: A persistent course is characterized by the presence of intense symptoms, important alteration and
prolonged duration (more than six months).
Specify the actual severity:
Light: Only matches one of the symptoms specified in criterion B.
Moderate: Matches 2 or more of the symptoms specified in criterion B.
Severe: Matches 2 or more of the symptoms specified n criterion B and additionally multiple somatic complaints exist
(or one very intense somatic symptom).
discomfort in social, work and interpersonal areas. We can
also observe dependent personality traits with the patient’s
difficulty to make decisions and not assuming responsibility
according to his age and stage in life.
Therapeutic plan
When SSDs coexist with a mood or anxiety disorder, the
administration of psychiatric medications is indicated, along
with a psychotherapeutic treatment. Therefore, we decided
to follow a combined treatment.2,5,12---14
Pharmacological treatment
The pharmacological treatment approach to SSDs has been
complicated due to the lack of conceptual clarity and excessive emphasis on the psychosocial causation and efficacy
of psychological treatments.15 Every type of psychiatric
medication is used in clinical practice to treat SSDs, and
there are systemic studies focused on five main medication
groups: tricyclic antidepressants (TCAs), inhibitors of serotonin reuptake (SRI), serotonin and noradrenaline reuptake
inhibitors (SNRIs), atypical antipsychotics, and herbal-based
medications.12,15 Evidence shows that these five groups are
effective for a wide variety of disorders and that all types
of antidepressants seem to have certain degree of effectiveness on SDDs and related disorders.12,13,15 TCAs and SRIs are
the most utilized pharmacological agents in SSDs. Nevertheless, there are little data supporting its effectiveness as a
stand-alone treatment.2,5,12,13
The research leaves many unanswered questions about
dosage, treatment duration, improvement sustainability in
the long run and variability in responses to different types
of medications.15 According to Carlat (2012) the evidence of
somatic treatment of depression in adults reports sertraline
to be a first-choice antidepressant that is hard to top, given
its combination of efficacy, tolerability and low cost.16
In the reported case, 50 mg of sertraline/day is prescribed, along with long-acting benzodiazepine (clonazepam
0.5 mg) at night due to the presence of comorbidity
with depression and anxiety. The depression symptoms are
resolved within 2 months; however, doctors decided to double the sertraline dosage (100 mg) at 6 weeks and triple it
(150 mg) at 3 months due to the persistence of the anxiety
symptom. The urinary symptom occurs with less frequency
until it is fully resolved after 6 months of combined treatment. Clonazepam is suspended after 4 months due to a good
response to the antidepressant and to avoid dependence on
the medication. Because of the significant improvement in
the urinary symptom as well as the depressive and anxiety
symptoms, SRI is gradually reduced to 50 mg/day until its
full suspension 2 years later. The patient tolerates the medication adequately without any report of significant adverse
side effects.
Psychotherapeutic treatment
From the non-pharmacologic treatment, cognitive behavioral therapy (CBT) proved to be the most effective;
however, these interventions have not been proven efficient
in the long run.5,12,13 According to Kaplan and Sadock, in
both the individual and group psychotherapy fields, the idea
is to help patients face their somatic symptoms, express
subjacent emotions and develop alternative strategies to
express their feelings. Additionally, some results indicate
that psychodynamic psychotherapy is beneficial to psychosomatic patients, where the therapeutic alliance plays an
important role and is solidified through empathy with the
patient’s suffering.17
Doctors are not recommended to face patients who
somatize with comments like ‘‘It’s all in your head’’.
106
Instead, they must recognize the reality of the physical ailments, even if they understand that their origin is basically
intrapsychic.2,4,5 An easy route of entry into the emotional
aspects of physical suffering is the examination of its interpersonal ramifications in the patient’s life.7,17
We decided to begin with individual, expressive psychodynamic psychotherapy, with a focus on object relations,
twice a week, in 45---50-min sessions. During the first
6 months they included behavioral techniques focused
on the urinary symptom. These techniques consisted of:
emptying the bladder every 2 h, going to the bathroom
only to wash his hands and/or face and performing jaw
exercises.
In parallel to the pharmacological treatment, the patient
commits to psychotherapeutic treatment, with results which
impacted his life in a positive way; he enrolls in university, takes responsibility for his school expenses and his
treatment and gradually becomes involved in social and
recreational activities. The patient continues with psychodynamic psychotherapy to keep working on his evasive and
dependent personality traits, which contributed to the onset
of the physical symptom and the subsequent personal and
professional deterioration.
D. Ibarra-Patrón et al.
that it obliges all non-psychiatric colleagues in the mental
health area to place stress, not on the description of the
symptom per se, but in exploring how the symptom affects
the patient: (a) emotionally (i.e. makes him depressed,
anguished, irritated, etc.); (b) cognitively (i.e. rumination
on the symptom, catastrophic ideas, etc.); and (c) behaviorally (i.e. constant medical consultations, stop working,
etc.).8
Even though the chief complaint was pollakiuria, by
understanding how it affected the patient, not only physically, but also in other aspects of his life and his
surroundings, it helped us situate the functioning of the
symptom in his life, to have a more realistic idea of the
patient’s ailment and to have a more empathic treatment
toward him. This more integral approach allowed the creation of a treatment plan which included not only the
symptom, but other aspects of the patient’s life which were
subjacent to the physical symptom.
The DSM-V modifications in SSD diagnostic criteria lead all
healthcare professionals toward a more integral evaluation
and approach, which may help doctors to have a more realistic comprehension of the patient, thus avoiding improper or
incomplete diagnosis and/or management, which only favors
chronicity and worsens prognosis.6,7,9---11,18
Therapeutic plan analysis
The combination of treatments (pharmacological/
psychotherapeutic) can be necessary in patients with
severe SSD of a long evolution as in the case presented,
even more when there is a comorbidity with depression
and/or anxiety. Consequently, despite the fact that there
is no compelling evidence for the effectiveness of antidepressants in SSDs, the choice was based on tolerability,
therapeutic efficiency in depression and anxiety and low
cost, given the patient’s economic problems.
Despite the psychotherapeutic treatment of choice of
SSDs being CBT, above the pharmacological treatment by
itself or any other type of psychotherapy, these types of
interventions have not been proven to be effective in the
long run, since most clinical trials only evaluate results in
the short-term. In this case, the patient attends the psychiatric outpatient clinic with the idea and hope that his
physical symptom may have a psychological cause; as well
as a great motivation to improve his personality aspects
which prevented him from relating to others. Therefore,
it is decided in conjunction with the patient to begin a
long-term psychodynamic psychotherapy process complemented with behavioral techniques. The success of the
treatment obtained thus far seems favored by a good therapeutic alliance, self-reflective ability and commitment to
the treatment.
Conclusions
The common characteristic evolution of chronicity, social
dysfunction, work difficulties and frequent use of medical
services lead to a level of dissatisfaction and frustration on
the patient as well as the doctor, as well as a high economic
cost in healthcare services.2,4,5,18
One of the most valuable contributions in the reconceptualization of the DSM-V for somatic disorders is
Conflict of interest
The authors have no conflicts of interest to declare.
Funding
No financial support was provided.
References
1. Fink P, Hansen MS, Oxhoj ML. The prevalence of somatoform
disorders among internal medical inpatients. J Psychosom Res.
2004;56:413---8.
2. Burton C. Beyond somatisation: a review of the understanding and treatment of medically unexplained physical symptoms
(MUPS). Br J Gen Pract. 2003;53:231---9.
3. Nimnuan C, Hotopf M, Wessely S. Medically unexplained
symptoms: an epidemiological study in sevenspecialities. J Psychosom Res. 2001;51:361---7.
4. Stephenson DT, Price JR. Medically unexplained physical
symptoms in emergency medicine. Emerg Med J. 2006;23:
595---600.
5. Oyama O, Paltoo C, Greengold J. Somatoform disorders. Am
Fam Physician. 2007;76:1333---8.
6. Mayou R, Kirmayer LJ, Simon G, et al. Somatoform disorders: time for a new approach in DSM-V. Am J Psychiatry.
2005;162:847---55.
7. Ghanizadeh A, Firoozabadi A. A review of somatoform disorders
in DSM-IV and somatic symptom disorders in proposed DSM-V.
Psychiatr Danub. 2012;24:353---8.
8. Diagnostic and statistical manual of mental disorders. 5th ed.
DSM-5. Somatic symptom and related disorders. American Psychiatric Association; 2013. p. 309---14.
9. Rief W, Mewes R, Martin A, et al. Evaluating new proposals for
the psychiatric classification of patients with multiple somatic
symptoms. Psychosom Med. 2011;73:760---8.
Diagnostic reconceptualization in DSM-V on somatoform disorders
10. Kroenke K, Sharpe M, Sykes R. Revising the classification of
somatoform disorders: key questions and preliminary recommendations. Psychosomatics. 2007;48:277---85.
11. Voigt K, Nagel A, Meyer B, et al. Towards positive diagnostic
criteria: a systematic review of somatoform disorder diagnoses and suggestions for future classification. J Psychosom Res.
2010;68:403---14.
12. Kroenke K. Efficacy of treatment for somatoform disorders:
a review of randomized controlled trials. Psychosom Med.
2007;69:881---8.
13. Sumathipala A. What is the evidence for the efficacy
of treatments for somatoform disorders? A critical review
of previous intervention studies. Psychosom Med. 2007;69:
889---900.
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14. Jackson JL, Kroenke K. Prevalence, impact, and prognosis of
multisomatoform disorder in primary care: a 5-year follow-up
study. Psychosom Med. 2008;70:430---4.
15. Somashekar B, Jainer A, Wuntakal B. Psychopharmacotherapy of somatic symptoms disorders. Int Rev Psychiatry.
2013;25:107---15.
16. Carlat D. Evidence-based somatic treatment of depression in
adults. Psychiatr Clin N Am. 2012;35:131---42.
17. Sadock BJ, Sadock VA. Kaplan & Sadock. Sinopsis de Psiquiatría
Clínica. Décima edición. Trastornos Somatomorfos. Lippincott
Williams and Wilkins; 2009, 634, 636, 647---649.
18. Rief W, Isaac M. Are somatoform disorders ‘mental disorders’?
A contribution to the current debate. Curr Opin Psychiatry.
2007;20:143---6.
Medicina Universitaria. 2015;17(67):108---113
www.elsevier.es/rmuanl
REVIEW ARTICLE
Social networks in medical practice
B.E. Ibarra-Yruegas a,∗ , C.R. Camara-Lemarroy b , L.E. Loredo-Díaz a , O. Kawas-Valle a
a
Department of Psychiatry at the ‘‘Dr. José Eleuterio González’’ University Hospital at the Autonomous University of Nuevo
León, Monterrey, Mexico
b
Neurology Service at the ‘‘Dr. José Eleuterio González’’ University Hospital at the Autonomous University of Nuevo León,
Monterrey, Mexico
Received 28 October 2014; accepted 27 January 2015
Available online 14 May 2015
KEYWORDS
Social networks;
Medical
professionalism;
Medical ethics
Abstract The number of social network users is rising meteorically, a trend that also includes
health-care workers. Even though social networking can serve educational functions and is an
effective means of communicating medical resources, it is associated with a variety of important challenges. Misuse of social networks by health-care workers can have dire consequences,
ranging from seemingly simple issues such as affecting the doctor’s reputation to serious legal
matters. Maintaining professionalism and preserving the concepts of confidentiality and privacy
is essential. In this review we will analyze some of the dilemmas that have been brought about
by the use of social networks in the healthcare environment, as well as existing guidelines on
the matter.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is
an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/
by-nc-nd/4.0/).
Introduction
The use of electronic information tools, including the use of
social networks (SNs), have led doctors to reconsider how
∗ Corresponding author at: Departamento de Psiquiatría, Hospital Universitario ‘‘Dr. José Eleuterio González’’ de la Universidad
Autónoma de Nuevo León, Monterrey, Madero y Gonzalitos S/N, Monterrey, NL 64460, Mexico. Tel.: +52 81 83480585;
fax: +52 81 83480585.
E-mail address: [email protected]
(B.E. Ibarra-Yruegas).
to apply the code of ethics that govern the doctor---patient
relationship and maintain their professional behavior. Even
though these mediums present interesting possibilities of
beneficial interactions, they also bring with them different ethical and professional dilemmas. Some of the main
challenges we face when using these technologies are the
preservation of confidentiality and privacy and maintaining
the boundaries of the doctor---patient relationship, as well as
reducing the possibility of making public information which
may be unprofessional, improper and even illegal.1,2
There are many SNs, among which the most popular
are Facebook, Twitter and LinkedIn (Table 1). Together this
group of technologies has been defined as ‘‘Web 2.0’’.1,2 In
http://dx.doi.org/10.1016/j.rmu.2015.01.008
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Social networks in medical practice
109
Table 1 Social networks and other electronic mediums
(non-exhaustive list).
Table 2 Some of the potential dangers of the use of SNs by
doctors.
•
•
•
•
•
•
•
• Loss of confidence in the doctor---patient relationship.
• Divulgence of the patients’ confidential information,
which may be punishable by law.
• Publication of improper material which brings into doubt
the professionalism and prestige of the doctor or
institution where one works.
• Association with false information or fraudulent
treatments.
• Disappearance of the distinction between professional
and social behavior, public and private, in the life of the
doctor.
Facebook
LinkedIn
Youtube
Twitter
Instagram
MySpace
Flickr
recent years, the rise in popularity and use of said SNs has
been exponential. Up to June 2014, Facebook reported 1.32
billion monthly users.3 In this review, a summary of the available information on the impact of SNs on modern medical
practice will be made, highlighting the ethical complexities
that these may involve.
Health 2.0
‘‘Health 2.0’’ is a new concept which comprises the use
of technology to promote and facilitate the interaction
between healthcare providers and patients.
It includes the search for information, medical advances,
updates and education in the field of healthcare.4 Even
though this definition is not universally accepted, the
concept appears in different scientific publications, and the
impact that this will have on the evolution of healthcare
services has not yet been fully established.5
The use of SNs can bring benefits to the institutions
in charge of healthcare as well as the patients and the
clinicians. The institutions may use them as publicity, customer service, and patient education; on the other hand, the
patients can use SNs to obtain information, evaluate their
progress and receive support. Finally, clinicians can obtain
updated information, providing facilities in the research
area a fast means of communication between colleagues in
order to comment on complicated cases.6
In a meta-analysis of the literature on the use of SNs by
patients, results showed that almost 30% of then use some
kind of SN or ‘‘blog’’ related to their disease.7 In the majority of cases, the intention of this conduct was to educate
themselves on topics related to self-care. In fact, it has been
determined that there are 757 pages of SNs dedicated to
groups of patients with specific diseases. Some of the most
prevalent, according to the International Classification of
Diseases 10, have over 300,000 users.8
Use of social networks: benefits and
challenges
professional behavior (in Table 2 there is a list of some areas
where SNs present dangers in the medical practice).
Even though there are some cases where online
‘‘surveillance’’ of the current state of the patient has
had beneficial results (notably in suicide watch cases,
or a monitoring of neurological symptoms after a cerebral concussion), these are anecdotal, and in everyday
practice electronic doctor---patient interactions bring more
complications than benefits most of the time.10,11
(a) Confidentiality
One of the basic principles in the doctor---patient relationship is confidentiality. However, it is difficult to maintain in
the context of electronic registries. The retention period of
these registries may be undetermined and access may not
always be restricted.
The most common examples where the use of SNs
comes to violate medical confidentiality include cases where
images, where there is the possibility of identifying the
patient because of specific characteristics, are made public,
either by showing his/her face, some part of his/her body
or objects marked with the logo of a specific institution.12,13
Some experts consider that even when all information which
may lead to the recognition of the patient is removed, there
is still the possibility that someone may recognize them
through context. Therefore, discussing clinical cases in an
open forum should be avoided.
The use of expressions or improper language in the context of the publication of said images has even led to the
termination of the doctors responsible. On this point, it
is important to clarify that in some countries the existing
medical---legal guidelines regarding medical confidentiality
also apply to information disclosed online, and the violations of this class are subject to disciplinary and/or legal
action.
(b) Privacy
Nowadays SNs are considered a useful tool for medical
teaching and practice.9 Although using it brings benefits
like facilitating information to patients, a quick communication channel between the doctor and the patient and
the establishment of national and international professional
networks, it also confronts us with different challenges like
preserving confidentiality, privacy, maintaining the boundaries in the doctor---patient relationship and maintaining
The use of social networks has provoked a diffusing of
the fine line between the private and professional life of
the healthcare worker. It is recommended to regularly check
the privacy configuration of our profiles. However, the use of
the highest standards of privacy does not guarantee that the
published content will continue to be private and confidential, or that any person will not be capable of accessing the
110
published information. Once the information is published
online, it may be difficult to eliminate.
There are many other instances where the use of SNs by
health professionals can lead to situations which violate the
privacy of the patients.
Beneficence is the concept that the doctor always tries to
do good for the patients. In psychiatry, there are cases where
a therapist has obtained information about the patient
through his/her SN pages with the purpose of making a better alliance and therapeutic plan (i.e. regarding a traumatic
background). Nevertheless, the patient found out about
this, felt an invasion of privacy and decided to end the therapeutic relationship.14 In this case the doctor may argue
having acted under the concept of beneficence, but with
consequences completely opposite than those expected. To
access SNs with the patient’s consent may offer the doctor
important information and it may be productive for his/her
treatment, but doing this without the patient’s consent may
lead to a loss of doctor---patient trust.11
The use of SNs has substantially impacted the work and
private life of health professionals. A good example of this is
the competence for admission to general medicine programs
at a higher education system, as well as in the working environment, with interview processes, personal or standardized
evaluations and panels of representatives that usually make
a decision, at the end of the process choosing the candidate with a certain group of characteristics desirable for
an institution. To make use of the information available on
SNs constitutes another area of controversy in the selection
processes mentioned above. Almost 70% of human resources
professionals from different institutions admitted to having
used SNs to obtain information about a candidate, significantly influencing their acceptance/rejection decision for a
professional position.15 In a survey conducted among directors of programs of medical residencies, 17% had used a SN
to assess a candidate, modifying the candidate’s place in a
priority list in 33% of these cases.16 In our study of candidates for an orthopedic surgery residency, it was found that
near half of them (200 candidates) had a SN profile. Our
of these, 85% did not have restricted access to them, and
unprofessional content was found in 16%.17
Candidates should make sure their online profiles reflect
standards of professionalism, as well as stress their academic strengths and personal accomplishments. This has
certainly raised ethical and legal considerations, concepts
like privacy, discrimination and professionalism.18
The use of portable smart devices like cellphones and
tablets complicates the panorama regarding the preservation of privacy. In surveys, close to 20% of residents
communicate with patients via email using their phones.
Out of these, 73% did not have their device passwordprotected.19 This information, provided by the patient,
would be at risk of being made public if the device were
lost. The use of apps like Whatsapp, an extremely popular
communication tool among medical colleagues, also leaves
an electronic trace of information for an undetermined
period of time: legal implications to making this information public have not yet been established. In a recent study,
around 95% of medical students admitted to having used text
messaging through their mobile phones to receive patients’
information, and out of these just 50% had security measures
to access their device.20 While text messaging between the
B.E. Ibarra-Yruegas et al.
doctor and the patients or other colleagues can facilitate
communication, most doctors fear these interactions may
transgress privacy.1,21
(c) Maintaining limits in the doctor---patient relationship
It has been proven that patients are the ones who send
‘‘friend requests’’ via Facebook to their doctors, yet they
respond to these requests on only a few occasions.22,23 In a
recent study, around 35% of external doctors had received
a friend request on Facebook, while the rate was closer to
8% for residents.23 In most cases, the doctors considered the
requests to be unethical, either for medical or personal reasons. Indeed, all available guidelines suggest the rejection
of these types of requests.
(d) Professionalism and e-professionalism
Health institutions have developed disciplinary guidelines with the purpose of ensuring an adequate public
image. Some authors have even developed the concept of eprofessionalism (e stands for electronic). Cain et al. define
this concept as those attitudes and behaviors (some of which
may occur in private) which reflect the paradigms of traditional professionalism, manifested through social media.24
This concept successfully translates the idea of professionalism, usually considered only in the ‘‘real world’’ and in
specific contexts (work, academic), to the ‘‘online’’ world.
It involves the way professionals present themselves in SNs
and how it should be subjected to the same exigencies as
the ones in their work environment.
Some factors which are believed to promote the lack of
professionalism in SNs are the apparent state of anonymity
and the perception of privacy by the user.25,26 Information
which may question the prestige of the doctor or institution
which he/she works for (for example, a video was uploaded
to Youtube where a group of medical students were dancing mockingly with skeletons and drinking from skulls used
as containers, making the logo of the implicated institution visible)27 or any content including explicit, sexual or
offensive images involving alcohol or drug consumption can
negatively affect the prestige of a doctor or student. A study
of graduates of a medical school reports that 37% of the
graduates who use any type of SN publish information like
sexual orientation, marital status, religion and pictures of
themselves intoxicated by different substances.28
Emphasis must be made on the fact that shared information through SNs is subject to the same standards of
professionalism as any other interpersonal interaction.
Almost 60% of North American medical schools report
incidents involving students and the publication of unprofessional content on their SNs.29
Surveys conducted show that most medical students
agree with the idea of professionalism in the work environment (either clinic or hospital), while only 43% believed
that this also applied to their ‘‘spare time’’.30 This
proves an important discrepancy between what the students understand of professionalism and what they believe
is appropriate or inappropriate in their online behavior
through SNs. At the same time, the defamatory or inappropriate content of this information can be utilized in
a judiciary context as evidence for which the author is
Social networks in medical practice
legally responsible.25,26 Nevertheless, the legal boundaries
regarding the concept of privacy are not entirely clear.18
(e) Regarding colleagues
Considering that the main function of SNs is to promote communication and interconnectivity among users,
not surprisingly many times the first to notice professional
transgressions are colleagues. This brings a whole new set
of ethical dilemmas into the medical practice. Should a doctor, resident or student report this activity to the authorities
of the institution? Guidelines suggest in the first instance to
approach the implicated colleague, and turn to the authorities only if, despite the intervention, there is no change in
the content or conduct of the implicated person.1,25,26
Another important point regarding medical ethics is that,
under certain circumstances within the professional medical environment, it is considered an obligation to report
any medical disability or incompetence, when there is evidence. Disability refers to a process which impedes proper
execution of the medical practice as a result of an illness
(i.e. dementia) or substance abuse (i.e. alcoholism), while
incompetence refers to a lack of knowledge or the necessary abilities. What would the implications be of obtaining
information about a colleague’s medical inability or incompetence from a SN? For example, a surgeon may reveal,
only to a few people through their SN, that he has early
Parkinson’s disease. Based on the principle previously mentioned, one would be obliged to report this situation to
the authorities of the institution, or in some cases the
police. These circumstances represent ethical, professional
and legal dilemmas, which are still in the process of being
solved.
Social networks in psychiatry
The incursion of SNs in medical practice has presented
particular challenges and benefits in psychiatry. 95% of psychiatry residents have SN pages, about 10% of them have
received friendship requests from their patients, and 18%
have entered some of their patients’ SN pages.23 We have
commented specific cases where privacy and trust have been
transgressed in the patient---therapist relationship.
Concepts like addiction to SNs, can become a new diagnosis and a great challenge in modern psychiatry.31 On the
other hand, the use of social media has opened new lines
of investigation and evaluation opportunities. For example,
a recent study proved that SN activity (number of pictures,
friendships, amount of information, usage hours, etc.) can
predict the type of personality disorder (schizotipy) in a
group of outpatient subjects.32
The impact of SNs on psychiatry is vast and will remain
in constant change and evolution for years to come.
Guidelines and recommendations
Despite the uncertainty surrounding the use of SNs in
a medical context, several professional associations have
accomplished major advances in the regulation of these
activities. Some have even published formal recommendations, as well as specific guidelines, like the American
111
Table 3
Guidelines to follow in the use of social networks.
Guidelines of the University of Vanderbilt (Taken from
Landman et al., 2010)
• Monitor their online reputation
• Understand the privacy measures of the social network
they utilize
• Keep their audience in mind
• Be conscious of the permanency of online content
Guidelines of the American College of Physicians (Taken
from Farnan et al., 2013)
• Apply ethical principles to preserve confidentiality,
privacy, respect and the doctor---patient relationship
• Keep the professional sphere and the online social sphere
separate
• E-mail and other electronic mediums should only be used
by doctors in established doctor---patient relationships,
and under informed consent
• Periodically review the information available online
regarding your person
Guidelines of the American Medical Association (Taken
from Shore et al., 2011)
• Do not make identifiable patient information available
online, keeping strict standards of privacy and
confidentiality
• Monitor their online presence and use the highest
methods of privacy when using a social network
• Be guided by the same ethic professional principles in
interactions with patients online as those that apply to
any other context
• Separate social and professional online content
• If a doctor finds inappropriate or unprofessional content
made available by a colleague, he has the responsibility
to bring it to his knowledge so that corrective action can
be taken. If it is not taken, or the content violates
professional norms, he has the obligation to report it to
the correct authorities
• Doctors must be conscious that their actions and content
online may affect their own reputations, as well as their
patients’, and may affect their careers as well as their
credibility as a medical professional
College of Physicians at the University of Vanderbilt and the
American Medical Association, among others.1,2,33 However,
the universalization of these guidelines has been slow and
incomplete.
In a study where web pages from 132 accredited medical schools (in the USA) were being evaluated, only 10% had
guidelines or policies which mentioned in a specific manner
the proper way of utilizing SNs for their students.34 Summaries of some of these guidelines can be found in Table 3.
These guidelines may be very effective, and some
positive tendencies can be discerned from a review of
medical literature. Even when the amount of doctors
who have admitted having a SN page is on the rise, from
numbers under 15%,29 up to studies where between 73 and
85% have them,22,23 the proportion that have public profiles
has decreased, from 50---67%29,33 to 12%.23 This indicates
the increasing popularity of SNs as well as a possible rise in
consciousness on behalf of healthcare professionals
112
B.E. Ibarra-Yruegas et al.
regarding the use of the highest and most strict privacy
measures.
How can ‘‘e-professionalism’’ be taught?
All of the above recommendations make clear the need to
include this topic in medical education programs. There
have been studies conducted which have made useful recommendations for the teaching of electronic professionalism
to doctors and medical students. A simple spreading of the
guidelines may be insufficient. The use of scenario simulation where professionalism is violated on SNs, as well as
suggestions of use, can be valuable interventions.35 Mentor
observation and the presentation of examples of the proper
use of SNs are an important part of the education of students of the medical field.26 In a study, it was demonstrated
that after going to a class where they presented specific
cases of violation of online professionalism, explaining the
consequences and the steps to follow in detail, a group of
radiology residents had acquired a better understanding of
the professionalism and importance of preserving the confidentiality and privacy of their patients and colleagues.36
These simple interventions seem to be effective, even after
a single academic session.
Conclusions
It is clear that the popularity of SNs does not seem to be
slowing down. It is more and more common for doctors,
residents, students and healthcare professionals to interact, one way or another, through electronic media and SNs,
whether among themselves or with their patients. This fact
has been associated with different ethical, legal and professional difficulties, some of which we have reviewed.
However, there are specific guidelines formulated to face
these challenges. Moreover, these mediums have opened
new ways to improve medical learning and healthcare management. Institutions should adopt or create guidelines
which ensure a professional and proper use of SNs, and its
training should be a regular part of the curriculum in faculties of medicine. This way, healthcare professionals will be
better prepared to face the challenge which we are facing
in modern technology era.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
Conflict of interest
20.
The authors have no conflicts of interest to declare.
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Medicina Universitaria. 2015;17(67):114---121
www.elsevier.es/rmuanl
REVIEW ARTICLE
Complex regional pain syndrome (CRPS), a review
S. Castillo-Guzmán a,∗ , T.A. Nava-Obregón a , D. Palacios-Ríos a , J.Á. Estrada-Cortinas a ,
M.C. González-García a , J.F. Mendez-Guerra a , O. González-Santiago b
a
b
Pain and Palliative Care Clinic, Anesthesiology Service, ‘‘Dr José Eleuterio González’’ University Hospital, Mexico
Postgraduate Division, School of Chemical Sciences, Universidad Autónoma de Nuevo León, Mexico
Received 4 December 2014; accepted 6 March 2015
Available online 30 April 2015
KEYWORDS
Complex regional
pain syndrome;
Reflex sympathetic
dystrophy;
Causalgia
Abstract Complex regional pain syndrome is a chronic and painful condition that affects the
quality of life of patients. It is usually triggered by a traumatic event of the soft tissues involving the nervous tissue. Although the factors that cause the syndrome are varied and not well
known, different etiopathologic concepts have been proposed to explain the presence of this
syndrome, such as autonomic dysfunction and changes in CNS plasticity, among others. The
patient characteristically presents pain, sensory abnormalities, vasomotor disturbances in the
skin, edema, changes in sweating, and motor alterations. The pain is associated with changes
in the autonomic nervous system and has a distal predominance. Since there is no definitive
diagnostic test, diagnosis is mainly based on a complete medical history and physical examination. Treatment is multidisciplinary and based on pain relief. Although in most cases evolution is
favorable, rapid diagnosis and treatment are recommended to avoid dystrophic stage as much
as possible.
© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/
licenses/by-nc-nd/4.0/).
Introduction
The first description of complex regional pain syndrome
(CRPS) dates from the seventeenth century and was reported
∗ Corresponding author at: Clínica del Dolor y Cuidados Paliativos,
Servicio de Anestesiología del Hospital Universitario ‘‘Dr. José Eleuterio González’’ de la Universidad Autónoma de Nuevo León, Ave.
Francisco I. Madero y Gonzalitos, Col. Mitras Centro, C.P. 64460,
Monterrey, N.L., Mexico. Tel.: +52 83 89 11 75.
E-mail address: [email protected]
(S. Castillo-Guzmán).
by the French surgeon Ambroise Paré to describe persistent pain and contractures of the arm suffered by King
Charles IX after the bloodletting to which he was subjected. During the American Civil War, Mitchell described
cases in which the soldiers suffered from burning pain
secondary to gunshot wounds. This was described as causalgia. In 1900 Sudeck described traumatic complications
in the extremities characterized by intractable pain,
edema, and limitations in motor function. Lerich in
1916, suggested that causalgia was caused by excessive activity of the sympathetic nervous system. It was
http://dx.doi.org/10.1016/j.rmu.2015.03.003
1665-5796/© 2014 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Complex regional pain syndrome (CRPS), a review
not until 1946 when Evans proposed reflex sympathetic
dystrophy.1
In 1979 the International Association for the Study of
Pain (IASP) defined causalgia as ‘‘a syndrome of sustained,
burning pain after a traumatic nerve injury, combined with
vasomotor and sudomotor and later trophic changes’’ and
reflex sympathetic dystrophy as ‘‘similar, but from other
causes.’’1
The term proposed by the IASP in 1994, which differentiates complex regional pain syndrome into type 1 and 2, is
currently used with the dissimilarity that type 1 is caused by
an injury or trauma to tissue and in type 2 there is prior and
obvious neurological damage.
Since the characteristics of these two types of disease are
essentially the same and treatment is not different, the rest
of this text will not distinguish between them with respect
to pathophysiology, diagnosis or treatment.
Epidemiology
Worldwide, the incidence and prevalence of CRPS is
unknown. Some studies have reported an incidence rate that
ranges from 5.46 to 26.2 per 100,000 persons year.2,3 In addition, the prevalence subsequent to trauma ranges from 0.03
to 37%, based on retrospective studies. In 40% of cases it is
associated with a fracture or surgery, with compression of
the median nerve being the most common, although it can
also appear after a sprain (10%), root lesions (9%), lesions
of the spinal cord (6%), and spontaneously (5---10%). It was
found that it more frequently affects women (2---3:1) with a
peak between 50 and 70 years of age, with a predominance
in the arms.4
It is noteworthy that the severity of the original injury is
not correlated with the severity of the symptoms of CRPS,
although psychological factors such as stress are risk factors
that worsen symptomatology.5
CRPS is also associated with other diseases and conditions
such as stroke, mastectomy, pregnancy, and the use of drugs
such as phenobarbital and isoniazid. There are predisposing
factors for the development of this syndrome in addition to
trauma and diabetes mellitus.6
The main feature of the history is a fracture, and immobilization has been proposed as a possible predisposing
factor for CRPS. Immobilization studies in animals have
found increased sensitivity to stimuli, and changes at the
spinal level. In humans it was found that plaster splint
immobilization results in an increase in cerebral blood
flow in areas related to sensory, motor, and emotional
processing.7
It is believed that psychogenic or hysterical factors,
mainly associated with depressive symptoms, may contribute to CRPS. Any psychological factor can interact with
catecholamine release and thus interfere with the pathophysiological mechanisms mentioned; however this is only a
hypothesis.8 The success of psychotherapy and occupational
and cognitive therapy in CRPS patients shows that the symptoms of dystonia and myoclonus are of a psychogenic origin
in some patients. It is not always easy to distinguish these
symptoms from simulation.9
CRPS often occurs in several family members and at
younger ages, which may indicate a genetic predisposition.
115
Accordingly, HLA has been proposed to have a role in CRPS.
Genetic studies have also identified polymorphisms in the
TNF-␣ gene and the angiotensin converting enzyme gene,
but no contrasting results have been found with the latter.10
Studies have shown that the use of ACE inhibitors at
the time when the causal trauma is suffered, as well as
a medical history of asthma or migraines, is associated
with an increased risk of developing CRPS. It is noteworthy that these factors imply underlying inflammation, since
ACE inhibitors increase the availability of substance P, and
both migraines and asthma share neurogenic inflammation
mechanisms.10
Pathophysiology
CRPS is a chronic pain condition that usually arises after
a traumatic event of the soft tissues. The ‘‘definitive’’
cause still remains unknown, although different pathogenetic concepts have been proposed; three of the most
studied are: autonomic dysfunction, neurogenic inflammation, and changes in CNS neuroplasticity, all of which are
still in dispute. However, current evidence shows that this
problem could have a multifactorial origin.
Autonomic dysfunction
Refers to an alteration of the sympathetic nervous system.
It has been suggested that its degree depends on the stage
in which the syndrome is found. This suggests the existence of inhibition of sympathetic vasoconstrictor neurons,
expressing lower levels of norepinephrine in the affected
limb compared to its counterpart. This triggers vasodilation,
and chronicity of this condition allows vasoconstriction.
This chronicity contributes to a redistribution of blood flow
through arterioles, causing inadequate capillary nutrition,
which results in hypoxemia and acidosis. These alterations
can produce free radicals, which cause histopathological
changes by oxidative stress.
There is evidence of an increase in the number of ␣adrenergic receptors in the skin of patients with CRPS.
Their activation would trigger an increase in noradrenaline
release, which in turn produces hyperstimulation of nociceptive fibers causing pain and hyperalgesia, even in
sympathectomized patients.
Cutaneous injection of norepinephrine induces pain via
these adrenoreceptors in patients who respond to sympathetic blockade, whereas there is no reaction in patients
who showed no response to the blockade. These data imply
that CRPS may involve abnormal adrenoreceptors expressed
in nociceptors which, when stimulated by circulating catecholamines, are activated and cause hyperalgesia and
possibly alodinia.11
Another group of researchers found that in CRPS II, nerve
damage causes an upward regulation of catecholamine
receptors (Fig. 1).
Catecholamine levels
Plasma norepinephrine levels were lower in the affected
limb compared to its healthy counterpart. However
adrenaline levels were similar in both extremities.6
116
S. Castillo-Guzmán et al.
Ipsilateral and
contralteral cortical
changes
Central sensitization
Sensitization
By a supposed mechanism
of
Inhibition
excitation
Treshold to pain
Cathecolamines flow
Vasodilatation (acute)
Endothelial injury
Sympathetic afferent
Pain
treatment with immunoglobulins, and of those, most
carry serum IgG autoantibodies directed against autonomic
receptors.12
NO
ET-1
Circulatory impairment
Peripheral sensitization
Inflammatory cytokines
Figure 1 Clinical manifestations of CRPS and pathophysiological mechanisms proposed to each.
Inflammation
Recent studies suggest the existence of two different
sources of inflammation: Acute, tissue damage mediated
by classical inflammation mechanisms (IL-1, IL-6, TNFalpha, CD4, macrophages, neutrophils) and neurogenic,
mediated by proinflammatory cytokines and neuropeptides
released directly by nociceptors in response to various
causal factors.8
The following are related substances:
Not sympathetic neurotransmitters
Substance P, one of the principal pain mediators and a
vasodilator, triggers mast cell degranulation and activates
osteoblasts.
The calcitonin gene-related peptide (CGRP) is a vasodilator that plays a role in glandular secretion, is involved
in sensory transmission, and stimulates endothelial cell
growth. Bradykinin has also been associated.
Sympathetic neurotransmitters
Vasoactive intestinal peptide is located in the bones and
promotes bone resorption, in addition to being a vasodilator and stimulating sweat gland secretion. Neuropeptide
Y is a potent vasoconstrictor that enhances the effects of
adrenaline. It is the most abundant peptide in the CNS and
its periphery.6,8
The nociceptive stimulus not only causes an inflammatory response, but also a low pain threshold. Recent
research has shown that some patients respond to
Peripheral: After tissue injury, local primary afferent fibers
release various substances, which sensitize nociceptive
nerve endings to other substances such as histamine and
bradykinin, contributing to the development of hyperalgesia
and allodynia.8 Sympathetic denervation causes an increase
in the sensitivity of blood vessels to catecholamines, produced by an increase in the number or sensitivity of
adrenoceptors. This increase may be responsible for the
decrease in blood flow to the skin in chronic conditions. It
is hypothesized that sympathectomy causes sensitization in
the long-term, which could explain why some patients have
transient benefits.
Central: It has been found that N-methyl d-aspartate
(NMDA) receptors play an important role in central sensitization; two controlled clinical trials showed that low doses of
ketamine (an NMDA antagonist) dramatically reduce pain in
patients with CRPS.13
Moreover, electrical stimulation of nociceptive
mechanical-insensitive fibers (CMi HI ), characterized by
a large electrical excitation threshold and innervation of
wide areas, can be the cause of secondary hyperalgesia.
In studies, low-frequency stimulation caused mechanical
hyperalgesia and hypoesthesia, whereas high frequency
stimulation generated hypoalgesia and hypoesthesia. It was
also found that pain itself can trigger inhibitory mechanisms
which develop hypoalgesia; this type of pain relief is known
as ‘‘counter irritation’’.14
Microvascular pathology of soft tissues
This hypothesis suggests an underlying cause in muscle,
bone and perineural microvasculature that cuases ischemia
and subsequent inflammation originating persistent abnormal pain, creating central sensitization. Coderre et al.,
in 2004, developed a mouse model that they called CPIP
(chronic post-ischemia pain), which involved a period of
ischemia-reperfusion produced by placing a tourniquet on
the hind leg of a rat, then withdrawing it and recording
their findings. They observed a reduction in the density
of sensory fibers and capillaries, spontaneous afferent discharge, decreased blood flow, elevated malondialdehyde
(free radical product of lipid peroxidation) then, when
attenuated by antioxidants, there was a dose-dependent
improvement in allodynia in the animal. They also observed
an increase in the production of proinflammatory cytokines,
an increase in lactate levels in the limb subjected
to ischemia-reperfusion and hypersensitivity to norepinephrine; symptoms similar to some patients with CRPS
type I.15
This steady state of inflammation due to partial or intermittent ischemia ended up causing endothelial dysfunction,
which could explain the increase in constriction, tissue
hypoxia, metabolic acidosis, and increased permeability to
macromolecules. Chronic ischemia can also lead to a state of
capillary ‘‘no-reflow’’ where the decrease in vessel lumen is
Complex regional pain syndrome (CRPS), a review
not only functional, but also physical; this could also explain
why some patients, after undergoing sympathetic blockade,
do not improve.7
Central changes
Neuroplasticity: Janin and Baron were the first to suggest a
central origin in the pathophysiology of CRPS. It is currently
known that chronic pain can create a change in the cortical
representation of the affected area, in particular, the representation of the affected area or limb in the somatosensory
cortex (S1) which is relatively small compared to the healthy
limb.8
Spinal neurons may increase their sensitivity in response
to nociceptive bombardment caused by autonomic changes.
A reorganization of the primary somatosensory area can
be generated in the supraspinal space, as in amputee
patients, demonstrated by MRI; due to this, it is said
that peripheral, spinal, and supraspinal nociceptive cortical processing scales are involved in the genesis of
CRPS.5
It is recognized that this neuronal plasticity, induced
by pain, causes hyperalgesia but it can also cause
hypoalgesia and hypoesthesia. Several studies show that
neuronal plasticity may be a decline effect in response to
pain.14
Altered functional connectivity in the resting state
In recent years, there have been several studies regarding an
alteration in the interconnections of different brain regions
in patients with CRPS. This is based on previous research
of chronic pain that has demonstrated a spatiotemporal disruption in functional connectivity at rest, also known as DMN
(default mode network), which shows an increase in diffuse
interconnections, unlike control groups. These areas show a
proportional correlation to the intensity of pain experienced
by patients.16
117
Autonomic alterations
Among these alteration we can find early onset distal
edema (in its soft and congestive form) in up to 80% of
cases, as well as changes in skin color and temperature,
which is reddish and hyperemic (≥1 ◦ C in comparison to
the other limb), usually in the early stages; however, in
40% of cases it can progress with decreased skin temperature and pallor. Sudomotor phenomena, such as hypohidrosis
or hyperhidrosis (the latter being the most common) are
also seen; trophic changes, which can present as excessive
hair growth, thin nails, and skin atrophy, evidenced by the
appearance of ‘‘glowing’’ skin, thinning of the epidermis
and muscle atrophy, as well as contractures, are also found.
Finally, another alteration that is present in some cases is
bone atrophy, which can be associated with osteoporosis
(Figs. 2 and 3).
The main and most common symptom (90%) is pain,
which is described as burning or stinging. It is usually felt
as deep (68%) rather than superficial (32%) pain. It can
be exacerbated after temperature changes, exercise or
episodes of stress and/or anxiety, and there have been
cases where it increases at night. Pain is often accompanied by other phenomena such as hyperalgesia and
allodynia. Of these the most important is muscle weakness; other manifestations in this category are essential
tremors in the affected limb, myoclonus and dystonia,
which is most frequently observed in patients with type II
CRPS.
It is important to remember that the manifestations may
change depending on the location of the condition. Proximal and deep joints undergo a reduction in function.19
This differs from other neuropathic syndromes due to the
presence of edema, vasomotor and sudomotor changes, in
addition to an orthostatic component which is reduced in
intensity when the limb is raised, and increased when it is
held down.5 It was thought that CRPS could have a temporal
progression of symptoms; however, this idea was rejected
by the International Association for the Study of Pain
(IASP).1
Dysfunction in the motor cortex
Because pain can interfere with the processing of afferent
signals that contribute to the sense of positioning, and the
mental image of the affected limb is distorted in patients
with CRPS, proprioception could be significantly affected.
There are observations that these patients need to carefully
look at their affected limb to control movements, making
it possible for them to compensate.17 However, more and
better studies are required to have consistent evidence,
since the only significant fact that has been found is an
area of spatial representation of S1 lower on the side of the
affected limb, unlike its healthy counterpart or in control
groups.18
Clinical manifestations
The onset of clinical manifestations may be hours or even
months after the noxious event, characteristically they
includes a triad of autonomic, sensory and motor abnormalities.
Diagnosis
There are no pathognomonic signs or symptoms and there
is no definitive diagnostic test. Diagnosis is based on a
complete medical history that includes the severity and
duration of symptoms and signs, fracture type and severity of the injury and physical examination of the affected
limb.20
The IASP published a review of the clinical diagnostic
criteria in 2007 called the ‘‘Budapest Criteria’’, which has
a sensitivity of 85% and a specificity of 69% (Table 1). There
must be regional pain that exceeds a dermatome or a single
nerve territory, continuous or evoked pain of an intensity
and/or duration disproportionate to the trauma or injury
that may have caused it, and which is associated with a
range of symptoms and signs of sensory, motor, vasomotor,
sudomotor and trophic disturbances. Symptoms and signs
can be variable depending on the time of evolution of the
syndrome.4 There are other approaches to the diagnosis,
118
Table 1
S. Castillo-Guzmán et al.
IASP Diagnostic criteria for complex regional pain Syndrome (2007 Budapest criteria).
1. Continuous pain disproportionate to the event that caused it
2. Symptoms (must meet at least one symptom in three of the four categories)
Sensory: hyperesthesia and/or allodynia
Vasomotor: asymmetry in skin temperature and/or asymmetry of skin color and/or changes in skin color
Sudomotor: edema and/or sweating changes and/or asymmetric sweating
Motor: decreased range of motion and/or motor dysfunction (tremor, dystonia, weakness) and/or trophic changes (skin,
hair, nails)
3. Signs (must meet at least one sign in two or more of the four categories)
Sensory: evidence of hyperalgesia (to puncture) and/or allodynia (touch/temperature/deep pressure/joint movement)
Vasomotor: asymmetry in skin temperature >1 ◦ C and/or asymmetry of skin color and/or changes in skin color
Sudomotor: evidence of edema and/or sweating changes and/or asymmetric sweating
Motor: evidence of decreased range of motion and/or motor dysfunction (tremor, dystonia, weakness) and/or trophic
changes (skin, hair, nails)
4. Rule out other conditions that may explain the previous symptoms and signs.
Figure 2 (a) Female patient with right upper limb CRPS affected before treatment. (b) Same patient with hyperemic, shiny bow
and decreased range of motion secondary to the presence of edema, during initiation of treatment with infusion pump (Ropivacaine
2%/20 days22 ).
such as the diagnostic criteria of Kozin (Table 2) and Veldman
(Table 3).
Complementary tests
Radiography
An ill-defined subchondral heterogeneous ‘‘mottled’’ demineralization of varying intensity is observed with a
sensitivity of 73% and a specificity of 57%, maintaining a
regional character in later stages of the disease.20
Gammagraphy
This study is recommended in stages I and II with a sensitivity
of 97% and a specificity of 86%. Its main use is for the early
diagnosis of CRPS. In the initial stages, intense and early
bone hyper-uptake that exceeds the limits of the affected
joint is seen.20
Figure 3 Female with upper member CRPS affected, posterior entitled to 20 days of completing treatment with infusion
pump to the infraclavicular brachial plexus (Ropivacaine 2%22 ).
Complex regional pain syndrome (CRPS), a review
Table 2
Kozin diagnostic criteria.
1. Pain and tenderness of a limb
2. Symptoms or signs of unsteadiness
Raynaud’s Phenomenon
Cold, pale skin
Hot or erythematous skin
Hyperhidrosis
3. Swelling of limb
Edema with or without fovea
4. Trophic skin changes
Atrophy
Desquamation
Hypertrichosis
Hair loss
Nail changes
Thickening of the palmar aponeurosis
Defined: meets 4 criteria; probable: meets criteria 1, 2, and 3;
possible: meets criteria 1 and 2.
Magnetic resonance imaging
This method provides a differential diagnosis with
osteonecrosis, especially of the hip. It also provides
information about bone marrow edema, alteration of soft
tissue, and the presence of joint effusion.6
Skin fluximetry by the laser doppler technique
This is one of the most precise techniques that are currently
available for the early diagnosis of CRPS I. It provides information of changes in flow, volume and velocity of cutaneous
microvascularity in CRPS I in stages I and II.
Thermography
An increase in local temperature, especially in the first
weeks of development, is found, although this is not a consistent finding (sensitivity 45%).21
Differential diagnosis
The differential diagnosis will depend on the stage of evolution. In the initial phase, infectious arthritis, rheumatic
arthritis, inflammatory joint disease, peripheral arterial
disease and deep vein thrombosis should be considered.
In the chronic phase, Dupuytren’s disease, scleroderma,
Table 3
Veldman diagnostic criteria.
1 The presence of 4---5 of the following:
Unexplained diffuse pain
A difference in skin color in relation to another extremity.
Diffuse edema
A difference in skin temperature relative to another
extremity.
Limited range of active motion.
2. Occurrence or increase in the above signs and symptoms
after use.
3. The above signs and symptoms are present in a larger
area than the primary area of injury or operation and
includes the area distal to the primary lesion.
119
Table 4
•
•
•
•
•
•
•
•
•
Differential diagnosis of CRPS.
Deep vein thrombosis
Thrombophlebitis
Cellulite
Lymphedema
Vascular insufficiency
Infectious arthritis
Rheumatoid arthritis
Inflammatory arthropathy
Dupuytren’s disease
and plantar fasciitis should be taken into account. In hip
conditions, osteonecrosis and coxitis should be ruled out. If
there is bone demineralization, it would be recommended
to rule out osteoporosis and bone tumors (Table 4).20
Treatment
Early treatment is necessary to achieve complete recovery
and prevent damage. Treatment of CRPS requires a multidisciplinary approach to pain management which is also aimed
at functional recovery of the affected limb.
Pharmacotherapy
Nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids, cyclooxygenase (COX) 2 inhibitors and free radical
scavengers are used with the intention of treating pain in
addition to the inflammatory process in CRPS. However,
inflammation in CRPS may be largely neurogenic (initiated
by inflammatory mediators of the terminals of afferent nociceptors) and no drug has been studied for this type of
inflammation.22
NSAIDs represent first-line treatment, especially in the
early stages and at non-specialized units, although their
efficacy specifically for CRPS is unproven, and they are
not prescribed in the treatment of neuropathic pain. In
initial phases they can be prescribed for treatment of
inflammation.23
Oral corticosteroids are the only anti-inflammatory drugs
for which there is direct evidence from CRPS clinical trials
(evidence level 1). Most trials included acute cases, when
inflammation is more common, and it is unknown if corticosteroids offer a similar benefit for chronic CRPS, where
levels of proinflammatory cytokines are lower, or in CRPS
cases with only mild inflammation. A short course of steroids
may be indicated early in CRPS with prominent inflammation, but in longer courses there are contraindications to
chronic use of steroids.22
Both minor (tramadol) and major (morphine, oxycodone,
fentanyl, hydromorphone, buprenorphine) opioids have
their place in moderate-severe pain that is difficult to control, and they have demonstrated efficacy in neuropathic
pain.4
Antiepileptics (gabapentin) and tricyclic antidepressants
(amitriptyline) and pregabalin have been used as adjuvants
in the treatment of CRPS. There are no controlled trials of
CRPS type I with these drugs, but their efficacy has been
demonstrated in the treatment of neuropathic pain. These
act by inhibiting pain pathways and neuronal plasticity, and
are prescribed in acute phases with nerve injury, nerve
ectopic activity or chronic phases.4
120
Free radical scavengers have shown some efficacy in
the prevention and treatment of CRPS, although in acute
phases and with moderate involvement. Vitamin C at doses
of 500 mg/day and N-acetyl cysteine at 600 mg/day have
shown efficacy in the prevention of CRPS in patients who
have suffered wrist fractures. Dimethyl sulfoxide 50% cream
seems to reduce pain and inflammation of the limb in the
acute phase.4
There is evidence that several bisphosphonates have an
acceptable safety profile and can significantly relieve spontaneous pain and improve the functional status of patients
with an early disease (duration of 6 months) and with
an abnormal uptake on the 3-phase bone scan. There are
indications that the doses necessary to achieve long-term
remission are very high, i.e., neridronate at 100 mg or
pamidronate at 90 mg, each given via IV four times over
a period of 10 days. Bisphosphonates have analgesic properties that go beyond their effect on bone metabolism,
and preclinical data suggest that they have antinociceptive
effects in animal models of neuropathic pain. Therefore,
their efficacy cannot be limited to patients with CRPSrelated bone pain, but relevant clinical data are not yet
available.9
The recent use of ketamine, a potent agonist of Nmethyl-d-aspartate (NMDA), in the management of CRPS-I, is
due to the phenomenon of central sensitization. This central
sensitization is expressed mainly in the first relay of nociceptive information integration, where the synapses formed by
the central ends of the A␦ and C fiber nociceptors to nociceptive neurons in the dorsal horn of the spinal cord are
very active. Several ketamine dosing schemes have been
tested, from transcutaneous application to coma induced by
ketamine. Although lower doses seem to provide the best
results, the lack of regulatory approval for this indication
and various side effects limit the use of ketamine in current
practice.8
Topical anesthetics such as lidocaine cream or transdermal absorption patches at 5%, can be suitable in cases of
allodynia and/or hyperalgesia.22
Interventional techniques
Sympathetic nerve block is a treatment option for patients
who are refractory to pharmacological treatments, especially when performed early in the course of the disease.24
Nerve blockage improves short-term pain and joint mobility
and its effectiveness is greater when performed in the early
stages of the disease, although there are few reliable studies
and a few controlled studies that have failed to demonstrate
long-term efficacy. Blockage provides a pain-free period that
improves limb mobility, allowing performance of intensive
physiotherapy, especially when using continuous techniques,
such as local anesthetic infusion via an auxiliary or lumbar
epidural catheter.4
Some uncontrolled studies have shown initial improvement in pain after percutaneous sympathectomy, but there
is a high risk of recurrence between 6 months and 2 years,
with neuralgia and post-sympathectomy pain (up to 10%.).9
Placement of a cervical or lumbar spinal epidural neurostimulator for posterior column spinal cord stimulation
may be an option in severe disabling pain in CRPS cases that
S. Castillo-Guzmán et al.
have not responded to other treatments. A study of 36 cases
showed efficacy in reducing pain and improving quality of
life in both the short and long term.4
A retrospective study found that intramuscular injection
of botulinum toxin A (BTXA) in waist muscles of the upper
limb was beneficial for short-term relief of pain caused by
CRPS. There was a 43% reduction in local pain scores 4 weeks
after intramuscular injections of BTXA. Studies that prove its
efficacy and support its use in the long-term treatment of
CRPS are still lacking.25
Rehabilitation
Early rehabilitation is essential to try to prevent muscle
atrophy and contractures, which in extreme cases can be
irreversible, although it requires the active participation of
the patient and this is not always possible due to severe pain
and associated psychological disorders.
Physical therapy can reduce pain and improve limb
mobility, although the intensity of treatment varies depending on the severity of the syndrome. Lymphatic drainage
can improve edema. Transcutaneous electrical stimulation
(TENS) may improve pain, although its use is not recommended in patients with severe allodynia or hyperalgesia.
Occupational therapy can also enhance limb function and
coordination.
Some studies suggest that mirror therapy may have a role
in the treatment of CRPS. The patient performs the exercises
in front of a mirror, perpendicular to the midline, which
only allows him/her to observe the unaffected limb during
treatment; this creates a sense of normality of the affected
limb, probably due to activation of the frontal cortex, and
pain relief, especially in acute phases of the disease.26
Conclusion
Although the exact causes of CRPS have not yet been discovered, the progress made in recent years in the understanding
of the pathophysiological mechanisms involved in the disease allow us to foresee new treatment options targeting the
etiology. Understanding the etiological factors will lead to an
early diagnosis and a better implementation of treatment.
Conflict of interest
The authors have no conflicts of interest to declare.
References
1. Dommerholt J. Complex regional pain syndrome----1: history, diagnostic criteria and etiology. J Bodyw Mov Ther.
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2. Sandroni P, Benrad-Larson LM, McClelland RL, Low PA.
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3. de Moss M, de Bruijin AG, Huygen FJ, et al. The incidence
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4. Márquez Martínez E, Ribera Canudas MV, Mesas Idáñez A, et al.
Revisión Síndrome de dolor regional complejo. Semin Fund Esp
Reumatol. 2012;13:31---6.
5. Rodríguez RF, Ángel Isaza AM. Síndrome doloroso regional complejo. Rev Colombia Anestesiol. 2011;39:71---83.
6. Seguel BM. Síndome de Dolor Regional Complejo Tipo 1. Rev Chil
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7. Groeneweg G, Huygen FJ, Coderre TJ, Zijlstra FJ. Regulation of
peripheral blood flow in Complex Regional Pain Syndrome: clinical implication for symptomatic relief and pain management.
BMC Musculoskelet Disord. 2009:116---29.
8. Gay A-M, Béréni N, Legré R. Recent advance Type I complex
regional pain syndrome. Chir Main. 2013:269---80.
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2014;13:242---65.
10. Marinus J, Moseley GL, Birklein F, et al. Clinical features and
pathophysiology of complex regional pain syndrome. Lancet
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of diagnostics, pathophysiologyc mechanisms, and treatment
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2013:682---6. Review.
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14. De Col R, Maihöfner C. Centrally mediated sensory decline
induced by differential C-fiber stimulation. Pain. 2008:556---64.
15. Coderre TJ, Bennett GJ. A hypothesis for the cause of complex
regional pain syndrome-type I (reflex sympathetic dystrophy):
pain due to deep-tissue microvascular pathology. Pain Med.
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16. Bolwerk A, Seifert F, Maihöfner C. Altered resting-state functional connectivity in complex regional pain syndrome. J Pain.
2013:1107---15.
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dysfunction of complex regional pain syndrome is related to
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Neurol. 2010;17:649---60.
20. Cuenca González C, Flores Torres M, Méndez Saavedra K, Barca
Fernándeza I, Alcina Navarro A, Villena Ferrer A. Síndrome
Doloroso Regional Complejo. Rev Clín Méd Fam. 2012:120---9.
21. Gaspar AT, Antunes F. Síndrome Doloroso Regional Complexo
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22. Harden N, Oaklander AL, W. Burton A, et al. Complex regional
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4th ed. American Academy of Pain Medicine.; 2013. p. 1---50.
23. Ghosh J, Hazra S, Haque M, Ghamsari P, Singha S. Review of
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Sci. 2012:160---4.
24. Dworkin RH, O’connor AB, Kent J, et al. Interventional management of neuropathic pain: NeuPSIG recommendations. Int Assoc
Study Pain. 2013;224:9---61.
25. Kharkar S, Ambady P, Venkatesh Y, Schwartzman RJ. Intramuscular botulinum toxin in complex regional pain syndrome: case
series and literature review. Pain Phys J. 2011:419---24.
26. Porro Novo J, Estévez Perera A, Prada Hernández DM, Garrido
Suárez B, Rodríguez García A. Enfoque rehabilitador del Síndrome de Dolor Regional Complejo Tipo I. Rev Cubana Reumatol.
2012;16(20):1---8.
Medicina Universitaria. 2015;17(67):122---125
www.elsevier.es/rmuanl
EXPERT’S CORNER: A PERSONAL APPROACH
Is it an epileptic seizure?
C.E. Muñiz-Landeros ∗
Neurology Service of the ‘‘Dr. José Eleuterio González’’ University Hospital at the UANL, Monterrey, N.L., Mexico
Received 20 January 2015; accepted 21 January 2015
Available online 7 May 2015
One of the most frequent situations which occur in medical
practice is the moment of categorically defining if the symptomatology to which a patient or another reliable source
refers corresponds to an epileptic seizure or any of the clinical events presented as differential diagnoses, ranging from
lypotimia, a syncope, hyperventilation syndrome, anxiety,
somatization, conversion or pseudo seizure.1,2
The main element physicians have is the information
provided by the patient or the person accompanying the
patient. It depends on the way the doctor obtains precise
data for the symptomatology study in question, that is, the
semiology. Thus, it is essential to keep in mind that clinical training is substantial to collect only useful, complete
information and discard data which can cause distraction or
confusion. Therefore, the semiology study must include very
specific characteristics like: type of symptom, form of onset,
mode of installation, duration, intensity and quality of the
symptoms, as well as temporal evolution, frequency of presentation, precipitating factors, or symptoms accompanying
or following initial onset, in addition to the symptomatology
which exacerbates or diminishes the symptom. This information will be best evaluated if obtained from the patient or a
trustworthy source who had witnessed the event. This will
make it possible to obtain the highest degree of data, which
will be useful for the study of the symptom.
In medical literature a series of useful questions for
the study of these types of clinical phenomena has been
reported:
• Is there a symptom premonitory to the seizure?
∗ Corresponding author at: Ave. Francisco I. Madero y Gonzalitos
Col. Mitras Centro, Monterrey, N.L. C.P. 64460, Mexico.
E-mail address: drmuniz [email protected]
•
•
•
•
•
•
•
•
What is that symptom?
Which is the pattern of presentation of the seizure?
How long does the seizure last?
Does the patient keep his state of consciousness during
the seizure?
What symptoms are there after the seizure?
How long does the patient take to recover?
How frequent are the seizures?
Are there any changes in the patient with treatment?
These 10 questions allow us to cover the minimum
required information to begin the study of a patient’s symptomatology.
A well-structured clinical history is key for diagnosis,
because there are several medical conditions which can
mimic convulsive and non-convulsive epileptic seizures,
either partial or generalized. Differential diagnosis will vary
according to the patient’s age, medical co-morbidity and
characteristics of presentation. For example, generalized
tonic---clonic seizures can be confused with a ‘‘convulsive
syncope’’ or non-epileptic psychogenic events; moreover,
temporal lobe epilepsy can be confused with panic attacks
or a cognitive disorder. Patients must be evaluated based
on their personal pathological background and establish the
possibility of presenting potential risk factors for developing
epileptic seizures, like: a head injury, encephalitis, meningitis, febrile seizures, or a family history of epilepsy.
The presence of past medical history of one or more of
these risk factors may help strengthen a clinical diagnosis
of epilepsy when a patient presents recurrent seizures. At
the same time, it can also be useful in locating the onset of
the seizures. For example, a history of complicated febrile
seizures is observed more commonly in patients with mesial
temporal lobe epileptic seizures. Simple febrile epileptic
seizures are really common and are not considered a risk
http://dx.doi.org/10.1016/j.rmu.2015.03.002
1665-5796/© 2015 Published by Masson Doyma México S.A. on behalf of Universidad Autónoma de Nuevo León. This is an open access article
under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Is it an epileptic seizure?
factor in the development of epilepsy.3 Reports show that
nearly 10% of the population may experience some epileptic
seizure throughout their lives.4
Seizure classification is more than a simple academic
exercise, because it can determine subsequent decisions
in its evaluation and treatment. Epileptic seizures can be
divided into provoked and non-provoked seizures. Provoked seizures are denominated, acute and symptomatic
and are attributed to an acute central nervous system
injury (CNS), or a metabolic alteration like hypoglycemia.
By definition, provoked seizures occur close in time to the
triggering event. These seizures represent about 40% of all
seizures (excluding pediatric febrile seizures) and have an
incidence of 29 to 39/100,000 habitants.5,6
They can occur at any other age, but are more frequent
during childhood and adulthood. In adults the most frequent
etiologies are cerebrovascular disease, drug or alcohol suppression, brain injury and cerebral neoplasias.4 These are
usually isolated, non-recurrent seizures, thus the treatment
is aimed at the primary etiology and antiepileptic medications are not required regularly.
Epilepsy is a condition with a tendency of non-provoked
recurrent seizures and is generally diagnosed by having
presented two or more episodes. Non-provoked seizure
incidence in the general population is 57 to 63/100,000
habitants and for epilepsy is 46 to 48/100,000 habitants.7---9
Epilepsy is not considered a single disease, but a group of
alterations which have the presence of seizures (convulsive
and non-convulsive epileptic) in common.
Non-provoked seizures are a result of chronic or functional structural alterations, which affect the neuronal
cortical function and are denominated symptomatic. In
adults, the most common causes are brain injury, cerebrovascular disease and cerebral neoplasias. 7---9 Among the
elderly, cerebrovascular disease is responsible for two-thirds
of symptomatic seizures, followed by neurodegenerative
alteration.7---9 In most cases the etiology can be unknown.
When a structural injury or functional alteration is suspected
but not proven, the epilepsy is classified as cryptogenic.
Idiopathic epilepsy is considered genetically mediated.
In some papers described in medical literature the reported
incidence ranges from 33 to 42% symptomatic, from 21
to 53% cryptogenic and 14 to 37% idiopathic. 9,10 . Nonprovoked seizures can occur at any age. However, its highest
incidence is in children and the elderly. Non-provoked
seizures are subdivided by their anatomic origin and by the
specific epileptic syndrome. The types of generalized primary seizures include: generalized tonic---clonic, myoclonic,
atonic, tonic, clonic and absences.7---9 Generalized seizures
are more frequent during childhood and adolescence. 9 .
Partial seizures start in a region of the brain and may be
subdivided into those that remain aware (simple partial) or
those where awareness is affected (complex partial). Some
may progress into generalized and are called secondarily
generalized. First-time epilepsy in adults and elderlies is
usually partial.9 Partial seizures start more frequently in the
frontal and temporal lobes.11
These types of seizures have distinctive characteristics
and can be identified by their clinical description. The
seizures originating at the parietal and occipital lobes are
characterized by sensitivity and visual phenomena, respectively. For the syndromic classification of epilepsy the
123
following information is needed: type of seizure, associated
neurological symptoms, age of onset, electroencephalographies and family or genetic history. This will allow a proper
prognosis and treatment.12
The physician must keep in mind that a convulsive or nonconvulsive epileptic seizure is subdivided into three stages:
pre-ictal, ictal and post-ictal:
Pre-ictal period --- characteristic precipitant factors are
rarely reported. These occur frequently during the sleeping period (frontal lobe seizures). Some patients report
non-specific neurological lateralization premonitory symptoms, like: dizziness, a strange feeling, focal paresthesias,
and complex abdominal, olfactory, hearing and visual sensations. Fainting, acral paresthesias and palpitations can
indicate hyperventilation. It is important to mention that
any real epileptic seizure cannot be ‘‘induced’’.12
Ictal period --- During this stage the mental state is
altered, with poor or no response. The stereotyped manifestation is considered characteristic in epileptic seizures, thus
considering certain characteristics to be ‘‘typical’’ in some
epileptic seizures, for example, in Jacksonian seizures, or
frontal lobe epilepsy. In these ones, they present a prone
position, atonic posture with abduction of upper extremities, a short duration, and occurrence during sleep. In
all seizure types, there is usually an abrupt onset (sudden) between 1 and 2 min long. The patient displays a poor
response to verbal stimuli. This may sometimes occur during complex partial seizures (CPS). In the motor phase of
the generalized clonic---tonic convulsive seizures (GCTCS)
there is a tonic posture or clonic response of the upper
and lower extremities, varying according to the onset and
whether it is partial motor with generalization or generalization from onset. The opisthotonic posture ‘‘arc de cercle’’
is never adopted; there may be intense body movements
during frontal lobe epilepsy, as well as lateral head movements, but the version of lateral rotation of the head is
more frequent in the GCTCS. In case of pelvic movement, it
will be toward the posterior region, and never toward the
front. In this tonic phase of the GCTCS the rigid posture is
characteristic, there is rarely a fluctuating pattern or motor
response pauses and it is usually continuous. There is no
motor response to any external stimuli. There is vocalization or ‘‘epileptic scream’’, characterized by a stertortous
sound of moderate intensity. Palpebral closure is extremely
rare, if it occurs there is no resistance to manual opening, it
generally tends to occur during ocular opening with an occasional deviated look. There are no visual fixations to head
rotation maneuvers (Henry and Woodruff sign), which consist of: ‘‘the eyes open and the head rotates to the sides,
then the gaze diverts to the ground, in the contralateral
rotation the eyes deviate again to the ground’’.
Extensor plantar response occurs (Babinski sign) bilaterally, usually in the 5 min subsequent to the seizure. The
presence of urinary incontinence is frequent in GCTCS.
Occasionally, there is a tongue injury, more often than not
in the lateral regions. The respiratory pattern is usually regular, interrupted by the tonic phase, ‘‘noisy’’, intense and
prolonged. Corneal reflex response is altered.
Post-ictal phase-In this stage the degree of recovery is
generally insidious and sometimes prolonged. There is rarely
a full sudden recovery. The patient presents a state of confusion, headache, lethargy, or he may refer to having fatigue or
124
diffuse myalgias. As a general rule, he/she does not remember the ictal event. It is important that a physician does not
assume that the ‘‘first seizure’’ is in fact the ‘‘first seizure’’.
Accumulated incidence of the presence of epileptic
seizures for age 74 in most reported studies in the literature
is close to 4---5%.13,14 The risk of relapse after an isolated
non-provoked seizure is close to 30%.15 A history of seizures
can modify the risk; therefore, proper interrogation must
be done. It is important to interrogate about the ‘‘spaced
out’’ episodes, independently from their length. This will
rule out the possibility of absence seizures or complex partial seizures. It is important to obtain information about
whether or not the patient woke up with oral injuries, like
tongue bites, or urinary incontinence. This will help detect
the possibility of epileptic seizures during the sleep phase.
Likewise, the presence of involuntary movements like muscular twitches right after waking up, which would rule out
the possibility of myoclonus or myoclonic seizures. Some
patients may report myoclonic movements of the physiological type at the beginning of the sleep phase or in a state
of somnolence, these are not considered pathological.
The presence of abnormal movements of the convulsive
type is not always an indicator that we are dealing with
epilepsy, we must rule out the possibility of convulsive syncope. Therefore, we will approach the patient if there is a
trigger factor (trauma, excessive heat, the sight of blood),
which could trigger a vasovagal syncope.16
Patients with convulsive syncope usually report premonitory symptoms, which could be explained by a cerebral
hypoperfusion, such as: loss of equilibrium, dizziness, flaccidness, reduced vision (darkened or blurry), tunnel vision,
palpitations, diffuse cold and hot sensations and muscle
tone loss. Diaphoresis and paleness are usually present. The
patient presents a sudden, complete recovery, and in this
phase myoclonic, short and generally transitory abnormal
movements are reported.17---19
The presence of stereotyped anxiety symptoms may be
confused with either a panic attack, or frontal lobe epilepsy.
In the latter, the anxiety symptoms are followed by confusion, alteration in response or loss of consciousness, in
addition to being associated with automatisms (repetitive
movements of the mouth or extremities). However, there
are reports of ictal events of fear and panic in frontal or
parietal lobe epileptic seizures.20,21
The presence of nonspecific or ‘‘strange’’ attacks is not
always psychogenic, as in frontal lobe seizures, since there
are reports of sudden ‘‘pedaling-type’’ stereotyped movements or ‘‘bed shakes’’ with a short duration. In these
cases, history and the use of simple or videoed electroencephalograms during sleep phases will help diagnosis.7,8 The
presence of forced or palpebral closure with resistance suggests a mainly psychogenic event.22,23 This is associated
with intense shaking movements, anterior pelvic movements, swinging head movements, emotional or behavioral
changes, ictal ‘‘stuttering’’ or the presence of ‘‘multiple
seizures’’ at the moment of clinical consultation.23,24
The electroencephalogram (EEG) is a tool used to confirm an epileptic seizure diagnosis, as well as to classify the
type of epilepsy and epileptic syndrome. We must keep in
mind that obtaining an EEG with ictal activity in a standard
ambulatory study in adult patients is not common; nevertheless, interictal epileptiform discharges (IEDs) are highly
C.E. Muñiz-Landeros
linked to a tendency to clinical seizures. A normal EEG does
not rule out a clinical diagnosis of epilepsy. Epileptiform
discharges are present in the initial EEG only in 25---50% of
patients with epilepsy, since the sensitivity of EEGs may vary
considerably depending on the frequency of the seizures,
epileptic syndrome and site location of the seizure. EEG’s
diagnostic performance is incremented with low stimulation studies like: sleep deprivation, hyperventilation and
photostimulation, in addition to using the prolonged videoelectroencephalogram technique. It is important to keep in
mind that there are abnormal variants of non-epileptic cerebral graphoelements, since this could lead to an incorrect
diagnosis, hence the diagnosis interpretation must be done
within the context of clinical history.25---28
Conclusion
Once again, like in most situations in medical attention,
performing a complete clinical history with all its semiologic elements of study is the diagnostic cornerstone in
‘‘seizure’’ cases. A proper integration of the characteristics
of presentation will allow us to make a probable diagnosis for epileptic events (convulsive or non-convulsive) more
precisely. Thus, being able to make an accurate differential diagnosis, among the main medical causes, in addition
to being able to create a proper diagnostic approach with
laboratory studies and paraclinical procedures like electroencephalogram, or neuroimaging if necessary, and being
able to begin an efficient medical treatment, avoiding the
possibility of sub-diagnostics, over-diagnostics or iatrogeny.
Conflict of interest
The authors have no conflicts of interest to declare.
Funding
No financial support was provided.
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Medicina Universitaria. 2015;17(67):126---130
www.elsevier.es/rmuanl
EXPERT’S CORNER: A PERSONAL APPROACH
Migraine management
A. Marfil ∗
Headache and Non Oncologic Pain Clinic, Neurology Service at the University Hospital, ‘‘Dr. José Eleuterio González’’ of
the Universidad Autónoma de Nuevo León, Mexico
Received 12 February 2015; accepted 24 February 2015
Available online 11 June 2015
Introduction
Migraines are common illnesses. Studies conducted in 12
Latin American cities, including two in Mexico, have found
that its prevalence in our country is 15%. The rate in gender
is 3:1 (Women/Men) worldwide.
The diagnostic criteria for migraines were published for
the first time in 1988, in the first edition of the International
Headache Classification, promoted by the International
Headache Society, with its second edition in 2003, and
a third beta version that will probably be published in
2015. Diagnostic criteria for the different forms of migraines
were first described in this document, which has simplified
communication among doctors and made possible comparisons between studies. The current migraine criteria (with
and without aura) are shown in Table 1.
As in all primary headaches, paraclinic and imaging studies are normal and rarely necessary, exception made for the
cases where there is clinical doubt or whenever the patient
is too anxious and wishes to be ‘‘as certain as you can be’’.
This may be a valid reason; however it may increase the cost
of medical attention and can be problematic in institutions
with a high volume of patients.
The management of migraines must contemplate two
aspects:
1. Acute management (abortive).
2. Preventive management.
∗
Corresponding author at: Servicio de Neurología del Hospital
Universitario ‘‘Dr. José Eleuterio González’’, de la Universidad
Autónoma de Nuevo León. Av. Madero y Gonzalitos s/n Col. Mitras
Centro, Monterrey C.P. 64460, N.L., Mexico. Tel.: +52 81 83471059.
E-mail address: amarfi[email protected]
In both cases, the following pharmacological and nonpharmacological measures must be contemplated.
Management generalities
Before beginning management of a migraine, as in any other
pathological entity, we must ask ourselves, several questions:
Are medications necessary?
If so, are there parameters to choose one as the best?
How will results be measured?
Which will the success and failure criteria be to decide
a change in management? In other words, how long to
maintain a medication before considering it did not work.
5. How long will a successful treatment last?
6. What is the a priori probability of recovery/recurrence?
1.
2.
3.
4.
Answering each and every one of these questions before
beginning management is fundamental. It gives the management sense and direction, for both the doctor as well
as the patient. Additionally, it brings the patient the feeling that he/she is able to do something, or cooperate in the
treatment, and thus the patient perceives he/she has some
control over his/her illness.
Abortive management
General guidelines:
1. To treat as early as possible. The instruction is: ‘‘Take the
medication, or do as indicated, as soon as the patient
recognizes if a crisis arises.’’ Patients learn to recognize when this happens, and we know that abortive
http://dx.doi.org/10.1016/j.rmu.2015.05.001
1665-5796/© 2015 Universidad Autónoma de Nuevo León. Published by Masson Doyma México S.A. This is an open access article under the
CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
Migraine management
Table 1
127
Diagnostic criteria of frequent migraines.
Migraine without aura
A. At least five attacksfulfilling criteria B---D
B. Headache attacks lasting 4---72 hours (untreated or unsuccessfully treated)
C. Headache has at least two of the following four characteristics:
1. unilateral location
2. pulsating quality
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs)
D. During headache at least one of the following:
1. nausea and/or vomiting
2. Photophobia and phonophobia
E. Not better accounted for by another ICHD-3 diagnosis.
Migraine with Aura
A. At least two attacks fulfilling criteria B and C
B. One or more of the following fully reversible aura symptoms:
1. visual
2. sensory
3. speech and/or language
4. motor
5. brainstem
6. retinal
C. At least two of the following four characteristics:
1. one aura symptom spreads gradually over 5 minutes, and/or two or more occur in succession
2. each individual aura symptom lasts 5---60 minutes
3. at least one aura symptom is unilateral
4. the aura is accompanied, or followed within 60 minutes, by headache
D. Not better accounted for by another ICHD-3 diagnosis, and transient ischaemic attack has been excluded.
treatment loses effect in a direct proportion to the delay
in treatment.
2. To have a record of the amount of analgesic used. Set
limits and have a ‘‘plan B’’ and ‘‘plan C’’ ready in case
of acute therapeutic failure.
3. If we are going to try a medication (i.e. a triptan), try
it in at least two crises before declaring therapeutic
failure.
4. Remember that the abortive treatment is exactly that:
abortive. Although there are exceptions; it must not be
used with a schedule. The principle is to NEVER give
abortive medication on a schedule. Exceptions would be
situations where we can anticipate the onset of the crisis,
like migraines associated with menstruation (with regular cycles) or episodic cluster headache. In general, the
evolution of the crisis in most migraines is predictable;
thus the patient is able to know when to take the
medication.
crisis. Its effectiveness is estimated to be between 30% and
40%.
Diet is reserved for those cases where there is a close
temporal relationship between the dietary element imputed
and the onset of the crisis. There is no point in giving a restrictive diet a priori. The idea of prohibiting
the consumption of specific food, like chocolate, cheese,
canned foods, sausages, Chinese food, wine (especially red)
or any form of alcohol, among others, is highly popular. The experience in our center is that food trigger are
rare.
A careful interrogatory is the best tool to indicate
a restrictive diet. Therefore, it is mandatory to keep
a headache diary where the patient must record the
number of attacks, intensity, time, response to medications, and relationship to external events or foods. This
diary will give us the parameters to make changes in
management.
Non-pharmacological measures
Medications
Some patients learn some techniques which can help attenuate the pain or make it disappear. The most utilized method
is sleep. The physician can try to compress both superficial
temporal arteries in front of the tragus (or on the side where
there is pain, if it is hemicranial) in order to try to abort the
The best results of abortive treatment are with medications. Individual sensitivity to a medication is unpredictable;
however, we have probabilities of effectiveness. The most
effective medications are triptans, and within this group,
rizatriptan and eletriptan have the most favorable evidence.
128
However, there is no way of predicting the result of a particular medication in a particular patient. Furthermore, failure
of one triptan does not predict the failure of another, thus
trying out two or three different triptans may be justified. Our protocol is to start with one of these two, to
try it for at least 2 crises, and decide whether or not
they worked. If they did not work, switch to a different
triptan. The instruction to the patient is: take (or place
the wafer of rizatriptan or zolmitriptan over/under the
tongue) the medication as soon as the patient recognizes
the onset of a crisis. Keep in mind that the effectiveness
of the medication decreases with the interval before taking it; once the first dosage of medication is taken we ask
them to wait for an hour; if at the end of the hour the
crisis is not over, take the second dose. If after the second hour (an hour after the second dose), the crisis has
not disappeared, begin with a second, different, medication. The concept of ‘‘crisis disappearance’’ is precisely
that: to completely stop not only the pain (which should
completely disappear), but also the autonomic and cognitive symptoms, etc. If residual symptoms persist, the
probability of recurrence is greater. Recurrence is defined
as the reappearance of a crisis in a period shorter than
24 h from treatment. It is important to remember that all
abortive medications, if used frequently, can cause rebound
headaches. Thus the need to keep track of any medication
that the patient may take, even if they are over-the-counter
medications.
Ergotamine is also effective and low-cost, making it
a good option for institutions with a high volume of
patients. It has an effectiveness of 40---60% in pain reduction/disappearance. The main problem is that it is highly
addictive and we must take all precautions when utilizing potentially addictive drugs: keep track of medication,
supervise prescriptions, and review results frequently. Indications to the patient are: initiate treatment as soon as a
crisis is recognized; start with 1 mg of the usual presentations (two tablets of 0.5 mg) and give an additional 0.5 mg
every half hour until one of these three things occur: the
crisis aborts, the patient starts vomiting, or 6 tablets (3 mg)
are taken. The consumption of more than 6 tablets in a 24 h
period, or 16 (8 mg) in a week is the threshold to develop
rebound headaches, in addition to increasing the risk of
addiction. If the episode ceases at, let us suppose, 2 mg
(four tablets), and the pain returns within the following 24 h,
medication will be given to the patient ‘‘as if it were the
next half an hour’’ If longer, it will be considered as a new
episode.
Over-the-counter medications are commonly utilized,
motu proprio, by patients. Many learn that certain medications or a combination of analgesics give them relief
or abort the crisis. The problem with self-medication is
that it is the single most important factor for chronification and the transformation of an episodic migraine to a
chronic one. There will always be the need to investigate
the use, dosage, frequency, etc. of such self-medication.
The same principle applies with ‘‘natural’’ medications or
herbal medicine. The physician should intentionally ask for
their use because there may be active pharmacological principles that can complicate the evolution or result of the
treatment.
A. Marfil
Table 2
Level of evidence for preventive medicines.
Level A: Medications with a well-established efficiency
(≥2 Class 1 clinical trials)
A. Antiepileptics: Divalproex sodium, topiramate
sodium valproate
B. Beta blockers: metoprolol, propranolol, timolol
C. Triptans: frovatriptan
Level B: Medications that are likely to be effective (1
class 1 study/2 class 2 studies)
A. Antidepressants/SISRs/SISNRs/ATT: Amitriptyline,
venlafaxine
B. Beta blockers: atenolol, nadolol
C. Triptans: naratriptan, zolmitriptan
Level C: Possibly effective medications (one class 2
study)
A. ACEIs: lisinopril
B. ARAs: candesartan
C. Alpha agonists: clonidine, guaifenesin
D. Antiepileptics: carbamazepina
E. Beta blockers: nebivolol, pindolol
F. Antihistamines: cirpoheptadina
Level U: Insufficient or inadequate data to make
recommendations
A. Carbonic anhydrase inhibitor: acetazolamide
B. Antithrombotics: acenocoumarol, coumadin,
picotamide
C. Antidepressants SISRs/SISNRs: fluvoxamine,
fluoxetine
D. Antiepileptics: gabapentin
E. Tricyclics: protriptyline
F. Beta blockers: bisoprolol
G. Ca channel blockers: nicardipine, nifedipine,
nimodipine, verapamil
H. Vascular smooth muscle relaxants: cyclandelate
Other: Medications established as possibly/probably
ineffective
A. Established as ineffective: lamotrigine
B. Probably ineffective: clomipramine
C. Possibly ineffective: acebutolol, clonazepam,
nabumetone, oxcarbazepine, telmisartan
ACEIs: angiotensin converting enzyme inhibitors; ARAs:
angiotensin receptor antagonists; SISRs: selective inhibitors of
serotonin recovery; SISNR: selective inhibitors of serotonin and
norepinephrine recovery.
It is important to keep in mind that the ideal objective of
treatment is not to use abortive medications, because there
are no more episodes.
It is important not to mix ergotamines and triptans in the
same session of treatment. It is a paramount contraindication that one must keep in mind.
Preventive treatment
There are publications of international guidelines for
preventive management of episodic migraines with medications. Table 2 shows the different groups of drugs with
Migraine management
their levels of evidence from the American Academy of Neurology guidelines, 1 that in general agree with the rest of
international organizations.
In our country there is no hard data on the effectiveness of medications in our population, however there
is some useful information. In 2005, the Headache Study
Group of the Mexican Academy of Neurology published
a consensus on the management of migraines. Combining experiences, we proposed that our population required
lower doses than those published. This data has been commented on international meetings and our colleagues in
Latin America and Spain concur with the impression that the
doses generally needed in our respective populations are
lower. Regarding the preferences of medications, in 2008
our group conducted a national survey on the behavior of
neurologists and neuropediatricians in the management of
migraines.2
Non pharmacological treatment
As mentioned above, one must identify the individual triggering factors, should there exist. Even though they are
not very frequent, they can be: dietary elements, lack
or excess of sleep, irregular meal times, and exposure to
intense light. The causal relationship between stress and
the production of a crisis is hard to prove, even if it is
an idea that ‘‘sounds good’’. Obesity has been proven
as a risk factor for migraine chronification and diminished response to medication. Thus it is recommended,
as in other situations, to comply with general rules of
hygiene.
Preventive medications
In Table 2 there is a list of medications with better evidence.
The recommendations for non-neurologists are:
1. Always keep a ‘‘headache diary’’ recording the number
of crises, intensity, duration, time, associated symptoms, triggers, effect of used medications, unwanted
or adverse effects, need of rescue medication and days
without pain. It is fundamental in order to assess the
result of the treatment. Aside from this, the MIDAS
scale can be used to assess the impact of the disease
on activities of daily living.
2. There are no specific guidelines or criteria to start a
preventive treatment. In general, we take into account
the number of crises and the impact on quality of life.
With two or more crises per month the risk/benefit ratio
of medications is considered satisfactory to justify the
beginning of treatment. In some people (i.e. women
with migraines associated with menstruation and regular cycles) we are able to begin ‘‘short preventive
treatments’’, three days before and after the expected
onset of the crisis, in each cycle. The same happens in
other types of headaches where we are able to predict
the onset of a crisis.
3. Learn to manage two or three medications well. Preferably from two different groups.
129
4. Consider comorbidities. Rule out if the patient is
hypertensive, suffers from asthma, anxiety, depression,
obesity or other conditions that may indicate or contraindicate a specific medication.
5. Encourage the patient to comply with nonpharmacological measures: enough sleep, regular
meal schedules, weight loss, regular exercise, avoiding
excesses of food, drinks and alcohol and other general
hygiene measures.
6. Establish, along with the patient, a treatment plan with
specific measurable goals and commit him to accomplishing them. The incidence of non compliance or
abandonment of treatments is high and should always
be investigated in each visit, since it may be a cause of
therapeutic failure.
7. There is not a guideline or specific evidence on the
duration of a successful treatment. The intervals vary.
In our national survey, most neurologists and pediatricians considered maintaining a successful treatment
for 6---8 months. However, there were responses from
3 to 12 months. In general, a treatment is planned
to last 8 months without a crisis. The first two
months are useful to assess the effectiveness of the
medication.
8. At the beginning of treatment we know there is a probability of effectiveness. We must maintain the use of
a medication for at least two months at proper doses
before deciding it is not working. A frequent cause of
‘‘treatment failure’’ is not giving it enough time to
work. This should be clearly explained to the patient
so that he/she cooperates during this period and exert
enough patience.
9. At the end of the planned period, stop the medication
and observe. The rate of recurrence is 30---40%.
10. While the goal is zero crises, sometimes a few may be
tolerated, either because of low tolerability of the medication or because the patient is reluctant to increase
the dose. In these cases there are no specific numbers about the cure/recurrence rate after completing
a treatment. We must explain to the patient that
migraines are diseases that tend to recur in different
epochs in life.
11. In case of recurrence after a successful treatment
(months or years later), the most reasonable thing to
do is to restart the treatment which was useful.
Migraines are a condition which can be controlled and,
sometimes ‘‘cured’’. We ought to understand that the
concept of curing is similar to that of other chronic
conditions of difficult prognosis (rheumatics, oncological,
etc.), which is the absence of recurrence in a determined period of time after treatment. The doctor should
pay attention to the details of the treatment in order
to communicate to the patient what he is trying to
be accomplish, and thus be able to gain his trust and
cooperation.
Conflict of interest
The author has no conflicts of interest to declare.
130
Funding
No financial support was provided.
References
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Ashman E. Evidence-based guideline update: pharmacologic
A. Marfil
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