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“Beyond” by April Mueller
Medical Dialogue
Review
FALL 2014 Volume
| VOLUME
15
MEDICAL15
DIALOGUE REVIEW
1
MEDICAL DIALOGUE REVIEW
Artwork by Chloe Chan
The content of the Journal of Medical Dialogue Review represents perspectives of students,
professionals, or patients on issues in healthcare. These ideas do not represent the opinions
of Medical Dialogue or New York University. Information that is presented is reviewed for
accuracy, but should not be used for medical diagnosis or as a substitute of medical advice.
MDR is a New York University student publication. NYU is not responsible for its content.
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MEDICAL DIALOGUE REVIEW
Fall 2014
EDITOR-IN-CHIEF
Grace Tartaglia
In This Issue
LAYOUT EDITOR
Neha Srivatsa
PRESIDENT
6
From Drug-High to SugarHigh: Recovering Drug Addicts
Turn to Sugar
By Kayana Jean-Philippe
9
Diptesh Tailor
SENIOR EDITORS
REVIEWERS
By Diptesh Tailor
The Threat of Misdiagnoses:
Are There Forms of Dementia That Could Be So Similar
That They Are Nearly
Indistinguishable?
By Julia Schneider
Although Normal pressure Hydrocephalus (NPH)
and Alzheimer’s Disease (AD) are two different
types of dementia, their overlapping symptoms
have led health care professionals to misdiagnose
AD patients with NPH, and vise versa. Author
Julia Schneider details the nature of both diseases
to the molecular level, ultimately allowing her audience to understand why these misdiagnoses are
so prevalent, and what health care professionals
can do to distinguish between the two illnesses.
17
VICE PRESIDENT
Manuela von Sneidern
Vasiliki Gliagias
Ardalan Khalafi
Oasis in the Desert
14
Sehrash Shabbir
Has the Medical Field Acknowledged Artists Make
Better Doctors?
By Nicole Marie D’Alessio
Amy Lei
Aqssa Mohammad
Ayesha Shah
Aiman Shaaban
Arisheniah Sothilingam
Bismah Akhter
Chelsea Leonard
Christina Octavia Martin
Deshana Barua
Gagarin Zhao
Harsh Patel
Harvinder Bassi
Joseph Aryankalayil
Jason Lin
Joyce Chen
Jessica Miller
Jaewoo Shin
Kartika Upadhyaya
Leana Emma King
Martinus Megalla
Mona Hassanein
Nihal Patel
Natahsa Pandit
Parth Patel
Swan Cho
Shawn Paustian
Sophie Rosenmoss
Tina Yu
Yu Guan
Yu Kong
CLUB ADVISOR
Nanci H Healy
Volume 15
MEDICAL DIALOGUE REVIEW
3
19
Stem Cell Therapy – A Novel Treatment for Duchenne’s
Muscular Dystrophy
By Syed Rahman
22
Coconut Oil Unmasked
25
Controlling the Control Center of the Body
By Chris Torres
By Sally Buttar
Sleep, once regarded as passive, has been assessed as an active phenomenon due to the discovery of a new neuron, the PZ GABA, which may
lead to new methods of sleep inducement. The complex nature of this
neuron stems from its need to activate after a ligand, clozapine-N-oxide
(CNO), binds to G-protein coupled receptors and induces PZ neuron
activity, releasing the GABA neurotransmitter and resulting in deep sleep
for the affected individual.
28
From Degenration to Regeneration
34
Orthognathic Surgery 101
By Mark Robles-Long
By William Pang
In “Orthognathic Surgery 101,” author Will Pang describes the various
ways that maxillofacial deformities can affect the health and physical appearance of the individual, and details how these irregularities can be
fixed through orthognathic surgery. Despite its complexity and length,
this procedure is often successful in increasing the quality of life in patients affected by skeletally related jaw discrepancies.
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MEDICAL DIALOGUE REVIEW
Fall 2014
42
NYU’s Police Stress and Health Program Gains
Insight Into Stressors Police Officers Face
By Rebecca Fabbro
For the past eight years, researchers at the NYU Langone Medical
Center have collaborated with Scientists from the University of California, San Francisco to gain insight into the unique psychological
and physiological stressors that affect police officers nationwide. In
“NYU’s Police Stress and Health Program Gains Insight Into Stressors Police Officers Face,” author Rebecca Fabbro details their findings and highlights the ways in which PTSD affects the minds, and
eventually the lives of American police officers.
47
The Ebola Epidemic and its Fallout in West Africa
By Alina Popkova
51
Political Conditions on Humanitarian Aid: How
Health and Political Relations Mix and Why It
Concerns You
By Andrea Martinez
55
The Ebola Time Bomb
By Mariya Reztsova
This article explores the Ebola virus from its ancestry and make-up to
its effects on the countries in western Africa where the virus is prevalent. Reztsova goes on to make the call of action for further intervention by the UN in partnership with nations around the globe, threatening that if such intervention does not occur, the epidemic can spread
and become a global problem.
Artwork by Alina Popkova
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Jean-Philippe
From Drug-High to SugarHigh: Recovering Drug
Addicts Turn to Sugar
By Kayana Jean-Philippe
“The idea of using sugar as a replacement drug is called a ‘transfer addiction.’ This is an issue for many recovering addicts, as they use sugar
consumption to mask their cravings for drugs.”
At 21 years old, Rodney Zimmers became heroin and cocaine-free and weighed 135
pounds. In the following three years, although
he had remained sober, he gained a whopping
115 pounds, now weighing in at 250 pounds.
Zimmers blamed his 115-pound weight
gain to another drug--sugar. The idea of using
sugar as a replacement drug is called a ‘transfer
addiction.’ This is an issue for many recovering
addicts, as they use sugar consumption to mask
their cravings for drugs.
Why sugar? Sugar releases opioids, a
chemical that produces euphoria; and dopamine,
a neurotransmitter that controls the brain’s reward and pleasure centers.
According to Brooke Alpert, M.S.,
R.D., CDN, author or The Sugar Detox and founder of B Nutritious, a private nutrition counseling
practice in New York City, sugar has been shown
to be as addicting as many hardcore drugs. “It
activates the rewards and pleasure center in your
brain to make you feel good each time you eat
it,” said Alpert.
“Unfortunately that feeling only lasts a
short time so as that feeling leaves, it causes a
person to want to reach for more sugar. This results in a continuous cycle with sugar highs and
lows.”
Sugar has been proven to yield the
same addictive effect as cocaine. A study conducted by Yale University researchers found
that the sight of a sugary chocolate milkshake
activated the same reward centers of the brain
as cocaine among people with addictive eating
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MEDICAL DIALOGUE REVIEW
habits. The addicting nature of sugar contributes to weight gain because instead of the sugar
being used as energy, when consumed in excess,
sugar is stored in the liver and is later converted
into fat. This causes an increased risk of obesity,
which can then lead to chronic health concerns
such as high blood pressure and cholesterol,
metabolic syndrome, diabetes, heart disease and
certain types of cancers.
The problem arises when individuals
are not educated on what food items contain
sugar.
This hard-to-avoid substance is found
in nearly every food item except meat, oil and
butter. Try looking through your pantry to find
a food item with 0 grams of sugar--it may not
be easy. The American Heart Association recommends that men limit their sugar intake to
nine teaspoons of added sugar per day and six
teaspoons for women. As a point of reference,
a standard 12-ounce can of Coca Cola contains
eight teaspoons of sugar. Excessive consumption of this sweet toxin can also be linked to
cataracts, Alzheimer’s disease and early wrinkling
of skin and weight gain, which may result in further decline of self-esteem.
But like many recovering drug addicts,
Zimmer was not taught the negative effects of
using sugar as a ‘transfer addiction’ drug and he
was unaware that he was doing so. In his testimonial on the Solutions Recovery Center website, he stated, “Once I got sober, I continued to
eat all this awful stuff. I learned how to be sober,
but I didn’t learn how to take care of all
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Jean-Philippe
of me. I didn’t know how to cook or grocery
shop because I’d never done it. I didn’t learn any
life skills or how to live like an adult.”
For Zimmer, who is now the founder
of Blueprints for Recovery, an all-male treatment facility in Arizona, the availability of sugary and fatty foods in the rehabilitation centers
including vending machines, unknowingly contributing to his weight gain. He was not given
the means to be able to choose nutritious foods
and beverages, cook, and gain necessary skills to
adopt a healthier lifestyle.
In addition, there is a high likelihood
that drug addicts were malnutritioned even before entering the facility. Those who have previously consumed excess beer, liquor or wine
have high caloric intakes, leaving addicts with
no appetite for eating nutritious meals. Oppositely, marijuana is shown to promote what is
commonly known as the “munchies” due to its
appetite-stimulating ingredient, tetrahydrocannanicol or THC. In a mice study conducted at
the University of Bordeaux, researchers found
that THC enhanced the smell and taste receptors and stimulated their appetite, which then
increased their food intake. Another study published on the Journal of Biological Chemistry
found that THC causes the release of ghrelin,
a hunger-stimulating hormone, which increases
cravings and food consumption.
Alpert recognized the likelihood of
malnourished people entering drug rehabilitation centers. She stated, “Many addicts have
been living an unhealthy lifestyle, where nutrition and exercise were not the focus of their pre-
vious life. A [Registered Dietitian] can help teach
new lifestyle behaviors to help promote a new
healthy life.”
While some private elite rehabilitation
facilities have dietitians on staff, many, especially
public facilities do not take nutrition into consideration in the healing process.
After suffering from a near-fatal drug
and alcohol addiction, Christopher Kennedy
Lawford, author of What Addicts Know: 10 Lessons
from Recovery to Benefit Everyone, has maintained a
life of sobriety for the past 24 years. In an interview with the New York Times, he stated, “You
can’t get an addict into recovery until you deal
with every aspect of their life. What you think,
how you think, how you relate to people, what
you put in your body, how you exercise – it’s all
related. And we need to get smarter about it.”
Nutrition education and awareness not
only alleviates issues concerning ‘transfer addiction’ and weight gain, but also self-efficacy.
The recovering drug addicts may have felt a lack
of control over their drug usage, but they can
have control over their food choices and how
they treat their bodies. Dr. Gabor Maté, author
of In The Realm of Hungry Ghosts: Close Encounters
with Addiction wrote, “Methods for gaining selfknowledge and self-mastery through conscious
awareness strengthen the mind’s capacity to act
as its own impartial observer.” By educating recovering drug addicts on proper nutrition, eating
habits and exercise, they will be empowered to
make healthful decisions, live a healthier lifestyle
and achieve self-sustainability.
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REFERENCES
"5 Stomach-Turning Side Effects of Sugar." Addiction Treatment Magazine. Addiction Treatment in Food Addiction, 28 Aug.
2013. Web. 12 Nov. 2014.
Callahan, Daniel. "Healthy Habits - Solutions Center." Solutions Center Healthy Habits Comments. N.p., n.d. Web. 12 Nov. 2014.
Ellin, Abby. "Off the Drugs, Onto the Cupcakes." Well Off the Drugs Onto the Cupcakes Comments. The New York Times, 15
Sept. 2014. Web. 12 Nov. 2014.
E, Stice, Burger KS, and Yokum S. "Relative Ability of Fat and Sugar Tastes to Activate Reward, Gustatory, and Somato
sensory Regions." National Center for Biotechnology Information. U.S. National Library of Medicine, 16 Oct. 2013. Web. 12 Nov. 2014.
Go, A. S., D. Mozaffarian, V. L. Roger, E. J. Benjamin, J. D. Berry, W. B. Borden, D. M. Bravata, S. Dai, E. S. Ford, C. S. Fox, S. Franco, H. J. Fullerton, C. Gillespie, S. M. Hailpern, J. A. Heit, V. J. Howard, M. D. Huffman, B. M. Kissela, S.
J. Kittner, D. T. Lackland, J. H. Lichtman, L. D. Lisabeth, D. Magid, G. M. Marcus, A. Marelli, D. B. Matchar, D.
K. Mcguire, E. R. Mohler, C. S. Moy, M. E. Mussolino, G. Nichol, N. P. Paynter, P. J. Schreiner, P. D. Sorlie, J.
Stein, T. N. Turan, S. S. Virani, N. D. Wong, D. Woo, and M. B. Turner. "Heart Disease and Stroke Statis
tics--2013 Update: A Report From the American Heart Association." Circulation127.1 (2013): E6-E245. 2013.
Web. 12 Nov. 2014.
Klein, Sarah. "Is Sugar The New Tobacco?" The Huffington Post. TheHuffingtonPost.com, 05 Aug. 2014. Web. 12 Nov. 2014.
Kola, Blerina, Erika Hubina, Sonia A. Tucci, Tim C. Kirkham, Edwin A. Garcia, Simon A. Hawley, D. Graham Hardie,
Ashley B. Grossman, and Marta Korbonits. "Redirecting." Redirecting. The Journal of Biological Chemistry, n.d.
Web. 12 Nov. 2014.
M, Peet. "Result Filters." National Center for Biotechnology Information. U.S. National Library of Medicine, May 2014. Web. 12
Nov. 2014.
Stromberg, Joseph. "A Scientific Explanation of How Marijuana Causes the Munchies." Smithsonian. Smithsonian.com, 9
Feb. 2014. Web. 12 Nov. 2014.
"Study Identifies Neural Activity Linked to Food Addiction." ScienceDaily. ScienceDaily, 5 Apr. 2011. Web. 12 Nov. 2014.
"The Importance of Nutrition in Addiction Recovery - Promises Addiction Treatment | Alcohol Drug Rehab Malibu."
Promises Addiction Treatment Alcohol Drug Rehab Malibu. N.p., 11 Dec. 2012. Web. 12 Nov. 2014.
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Tailor
Oasis in the Desert
By Diptesh Tailor
“The farm facilitates long-lasting change, fostering beneficial trends
which can sustainably mitigate and prevent disease disparity at its
roots for generations to come.”
The thought of deserts usually invokes images of
endless, evanescent dunes of
sand swirling to zephyrs swiveling amongst the scorching
backdrop of the Saharan sun
- not the dense urban foliage
that is the steel skyscrapers and
subways, bodegas and bustle,
and people of colors and culture which typifies the metropolitan landscape. However,
closer inspection reveals the
very real presence of ‘deserts’
in the concrete jungle familiar
as New York City.
Manifesting in both
rural and urban locales, food
deserts are neighborhoods lacking ready access to healthy,
fresh, and affordable foods.1,8
Although there are many variables that define a food desert, the Economic Research
Service division of the United
States Department of Agriculture reported in August 2012
that food deserts are associated with “smaller populations,
higher rates of abandoned or
vacant homes, and residents
who have lower levels of education, lower incomes, and
higher unemployment.”13 In
addition to these variables, urban food deserts, such as the
South Bronx in New York City,
are correlated with greater levels of minority groups.13,14 Epidemiologists at the University
of North Carolina reported
in a 2002 publication that four
times more supermarkets (as
a measure of relative food accessibility) were located in
predominantly white neighborhoods compared to predominantly black ones in a study
spanning four states.14
and obesity.15 Unfortunately,
this outcome is disproportionately
felt by minority, immigrant,
and other lower socioeconomic status (SES) inhabitants
as they are already limited in
their consumer awareness and
choice capacities (e.g. health
knowledge gaps, lack of automobile ownership, more limited purchasing power), aug-
Due to the
consistent lack of
access to affordable,
healthy food options, such as fresh
fruits,
vegetables,
whole grains, lowfat
milk, and wholesome
snacks, food desert
phenomenon
contributes to poor diet,
which can increase
one’s risk of noncommunicable diseasNYC Supermarket Need Choropes such as cardiovasleth Map.26
cular disease, diabetes,
obesity, and cancer.1,2,3,12
menting the burden of limited
Empirical evidence support- supermarket options and high
ing this intuitive trend was ob- food prices characteristic of
tained in a 2014 publication in food deserts on the long-term
the American Journal of Preventive health of our neighbors.
16,17
Medicine in which researchers
found a statistically significant Indeed, medicine has
positive correlation between discovered a number of addistance to stores / food prices vanced treatments to address
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Tailor
noncommunicable
diseases.
Among these include insulin
therapy, angioplasty, weightloss surgery, and the development of targeted chemotherapy, which have all maintained
revolutionary implications in
the short-term addressing of
chronic illnesses and their impending courses. However, a
sense of superficiality promulgates into the discussion as
these conventional approaches
mitigate symptoms but fail to
deracinate the vicious roots,
the fundamental causes, which
perpetuate chronic disease pervasiveness. This can be attributed to the fact that modern
medicine intervenes with proximal risk factors for disease,
such as abnormal blood glucose levels, hypertension, unbalanced cholesterol profiles,
and excess adiposity, instead of
addressing the distal risk factors
for chronic illness.
As contended by researchers Jo Link and Bruce
Phelan in their landmark publication “Social Conditions as
Fundamental Causes of Disease,” the fundamental, root
causes of disease disparity are
implicated with distal risk factors, such as low socioeconomic status and limited purchasing
power, lack of education and
awareness, poor community
development, and poor social
networks, all of which influence multiple disease outcomes.7
These distal, rather than proximal, risk factors are the subtle
yet systemic and persistent
causes of disease disparity.7
Treating proximal risk factors
does not ensure true long-term
10
solution nor prevention as distal risk factors would continue
to inhibit access to resources
which could allow for disease
intervention, retaining diseases
within the populations. More-
low SES populations who may
find such expenditures overwhelming.2,5,19 Moreover, the
CDC has reported that medical
costs linked to obesity, diagnosed diabetes, cardiovascular
La Finca del Sur.27
over, there are tremendous social costs associated with merely treating manifested cases
and their immediate, proximal
causes.
According to a 2010
report by the Johns Hopkins
Bloomberg School of Public
Health in conjunction with the
Robert Wood Johnson Foundation, healthcare spending for
an individual with one chronic
disease is three times greater
than a that of a healthy individual.18 With chronic diseases
accounting for 75% of health
expenditures, the cost per affected American totals nearly
$7,900.20,21 These rising healthcare costs can be significant
burdens, especially since chronic disease disproportionately
affects minorities and other
MEDICAL DIALOGUE REVIEW
Fall 2014
disease, and cancer amounted
to, respectively, $147 billion
(2008), $245 billion (2012),
$315.4 billion (2010), and $157
billion (2010).22-25 There are
also serious human costs associated with noncommunicable
diseases, which cause 70% of
deaths in the United States.
Chronic illnesses can be seriously disabling and can sharply
decrease one’s autonomy and
quality of life.20,21 Thus, this
underwrites the need for a
more fundamental approach
to preventing chronic diseases
and reducing their incidence
and prevalence.
Proximal risk factors
are analogous to the leaves of
a weed plant while the distal
factors are associated with the
roots. Intervening by removing
Tailor
the leaves (proximal factors)
would be a temporary intervention; only razing the roots
(distal factors) would provide
long-term solution. Increased
knowledge, enhanced community infrastructure, and
mutual social networks would
augment health through multiple modalities, such as by improving the populace’s dietary
options and consumption,
preventing noncommunicable
disease incidence within food
deserts.1,2,3,12 Although noncommunicable diseases can
be immediately addressed by
medicine, it would be a mirage to view such intervention
as all-encompassing. It is the
above strategies which would
provide long-term treatment
and prevention of multiple
disease outcomes. However,
distal risk factors cannot be addressed as simply as proximal
counterparts; more pervasive
roots require more pervasive
involvement. Therefore, they
require the active involvement
of the entities affected - individual & communal. It requires
the uplifting of vicious roots,
and ingraining of nurturing,
curative ones. What better way
to translate this metaphorical
conceptualization into a physical reality than through the art
of farming?
Indeed it was this
very thirst that led to the creation of an oasis in the stagnant food desert than is the
South Bronx.8 In 2009, under the leadership of a group
of women of color, a rotting
2.5 acre lot located between
a highway ramp and Metro-
North train tracks in the South
Bronx was transformed into
New York City’s first womenrun, non-profit community
farm named La Finca del Sur.9
Today, La Finca del Sur is a
beautiful urban farm “committed to building healthy neighborhoods through economic
empowerment, increased nutritional awareness, training
and education, and advocating
for social and political equality
and food justice in low-income
communities.”9 Indeed, this
farm is not merely an oasis
for its evident and significant
impact on the urban food desert phenomenon, but more
fully because of its impact in
addressing distal risk factors fundamental causes of disease
- which cause disease disparity
in minority and low SES communities.
Among the distal
risk factors addressed are the
lower purchasing power (directly proportional to SES)
and educational gaps amongst
the population, limiting their
access to resources such as
healthy foods, which could
curb more proximate risk factors (unhealthy body weight,
high blood pressure, high
blood sugar levels), and fullblown chronic disease.7 La Finca del Sur addresses this limited
access by allowing community
members and neighbors to
grow and harvest their own
foods and sell them at local
markets, further augmenting
the accessibility of affordable, fresh, healthy produce
for the neighbors and their
community.9,10 The farm also
Volume 15
educates school groups and
neighbors on proper diet and
nutrition to amplify its impact
on these food desert regions
and increase consumer awareness and discretion.11 Through
these strategies, La Finca del
Sur addresses the distal risk
factors for disease, preventing
the development of proximal
risk factors and, ultimately, illness, such as obesity, diabetes,
and cardiovascular diseases.
Other distal risk factors addressed include poorly
developed communities and
social networks. With its name
translating to “Farm of the
South” in Spanish, La Finca
del Sur serves as an epicenter
of cultural heritage for many
of the immigrant volunteers,
supporters, and growers, nostalgic of the crucial role of agriculture in Hispanic countries.
Through poetry, music, film
festival, open mic, storytelling and various other cultural
programmings, La Finca del
Sur serves as a commune for
South Bronx and neighboring
communities.11 The lack of
meaningful, positive, bidirectional relationships, especially
for immigrants posed with
cultural and linguistic barriers, can amplify unhealthy and
uninformed decision and behaviors such as sedentary lifestyle, poor dietary choices and
mental health issues.7 However, through the presence of a
community center like La Finca del Sur, members can form
positive, lasting relationships in
an open, friendly, and serene
environment. These social networks in turn allow
MEDICAL DIALOGUE REVIEW
11
Tailor
for disease prevention both
directly (e.g. promoting active,
outgoing lifestyle & developing supportive social relationships) and indirectly (e.g.
fostering advancement and
progress, such as via community initiatives and projects) to
enable communities to adapt,
grow, and thrive in a food desert oasis.
La Finca del Sur addresses distal risk factors for
disease such as low socioeco-
nomic status and limited purchasing power, lack of education and awareness, poor
community development, and
poor social networks through
robust farming and harvesting
opportunities, communal education and awareness programmings, and community-building cultural events. La Finca
del Sur exemplifies a self-sufficient neighborhood movement
which addresses fundamental
causes of disease disparity, as
experienced by populaces in
food deserts. The farm facilitates long-lasting change, fostering beneficial trends which
can sustainably mitigate and
prevent disease disparity at its
roots for generations to come.
Indeed, the sprouting of cultivation, culture and community
has allowed the people of the
South Bronx to transfigure a
desert into an oasis, planting
inspiration once thought only a
mirage.
REFERENCES
1. Agricultural Marketing Service (n.d.). Food Desserts. United States Department of Agriculture. Retrieved from https://apps.
ams.usda.gov/fooddeserts/foodDeserts.aspx
2. CDC (2014, May 9). Chronic Diseases and Health Promotion. Centers for Disease Control and Prevention. Retrieved from http://www.cdc.gov/chronicdisease/overview/index.htm
3. Singh, M. (2014). Mood, food, and obesity. Frontiers in Psychology, Vol. 5: 925, pp. 1 – 20
4. Drewnowski, A., & Specter, SE. (2004). Poverty and obesity: the role of energy density and energy costs. American Society for Clinical Nutrition, Vol. 79: 1, pp. 6-16. Retrieved from http://ajcn.nutrition.org/content/79/1/6.long
5. CDC (2013, Nov 22). CDC Health Disparities and Inequalities Report - United States, 2013. Centers for Disease Control and Prevention Morbidity and Mortality Weekly Report, Vol 62: 3. Retrieved from http://www.cdc.gov/mmwr/pdf/
other/su6203.pdf
6. WHO (2011, April). Global status report on noncommunicable diseases 2010. World Health Organization. Retrieved from http://www.who.int/nmh/publications/ncd_report2010/en/
7. Link, B.G., & Phelan, J. (1995). Social Conditions as Fundamental Causes of Disease. Journal of Health and Social Behavior, Vol. 35, pp. 80-94.
8. Mansour, I. (2013, Aug 15). How access to fresh food divides American. FortuneMagazine. Retrieved from http://fortune.
com/2013/08/15/how-access-to-fresh-food-divides-americans/
9. La Finca del Sur - South Bronx Farmers: About La Finca del Sur. (n.d.). Retrieved from http://bronxfarmers.blogspot.
com/p/about-la-finca-del-sur.html
10. News12 The Bronx. (2014, April 4). La Finca del Sur to bring new Bronx farmer’s market to Alexander Avenue. News12 The Bronx. Retrieved from http://bronx.news12.com/news/la-finca-del-sur-to-bring-new-bronx-farmer-s-mar
ket-to-alexander-avenue-1.7610105
11. Gonzalez, D. (2011, October 7). At Harvest Time, Bronx Farm Works Through a Tough Patch. New York Times: City Room. Retrieved from http://cityroom.blogs.nytimes.com/2011/10/07/at-harvest-time-bronx-farm-works-
through-a-tough-patch/
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12. Walsh, B. (2008, June 12). It’s Not Just Genetics. Time. Retrieved from http://www.time.com/time/magazine/ar
ticle/0,9171,1813984,00.html
13. Dutko, Paula, Michele Ver Ploeg, and Tracey Farrigan. Characteristics and Influential Factors of Food Deserts, ERR-
140, U.S. Department of Agriculture, Economic Research Service, August 2012. 14. Morland K, Wing S, Diez Roux A, Poole C. (2002). Neighborhood characteristics associated with the location of food stores and food service places. American Journal of Preventive Medicine, Vol 22, pp.23-9.
15. Ghosh-Dastidar B, Cohen D, Hunter G, Zenk SN, Huang C, Beckman R, Dubowitz. (2014). Distance to store, food prices, and obesity in urban food deserts. American Journal of Preventive Medicine, Vol47, pp.587-95
16. Ward BW, Schiller JS. Prevalence of Multiple Chronic Conditions Among US Adults: Estimates From the Nation
al Health Interview Survey, 2010. Prev Chronic Dis 2013;10:120203. DOI: http://dx.doi.org/10.5888/
pcd10.120203
17. Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA. 2012;307:491-7.
18. Robert Wood Johnson Foundation. Chronic Care: Making the Case for Ongoing Care. Princeton, NJ: Robert Wood Johnson Foundation; 2010:16. http://www.rwjf.org/content/dam/farm/reports/reports/2010/rwjf54583.Accessed November 11, 2014.
19. Crook ED, Peters M. Health disparities in chronic diseases: where the money is. Am J Med Sci. 2008;335(4):266-70
20. Centers for Disease Control and Prevention. Chronic Disease Overview: Costs of Chronic Disease. Centers for Disease Control and Prevention Web site. Available at http://www.cdc.gov/nccdphp/overview.htm. Accessed Novem
ber 11, 2014.
21. Triple Solution for a Healthier America (2014). The Impact of Chronic Diseases on Healthcare. GlaxoSmithKline. Re
trieved from http://www.forahealthieramerica.com/ds/impact-of-chronic-disease.html
22. Finkelstein EA, Trogdon JG, Cohen JW, Dietz W. Annual medical spending attributable to obesity: payer- and service-
specific estimates. Health Affairs. 2009;28(5):w822-w831. http://content.healthaffairs.org/content/28/5/w822.
full.html. Accessed November 11, 2014.
23. American Diabetes Association. The Cost of Diabetes Web site. http://www.diabetes.org/advocate/resources/cost-of-
diabetes.html. Accessed November 11, 2014.
24. American Heart Association. Heart Disease and Stroke Statistics—2014 Update. AHA Statistical Update Web site. http://circ.ahajournals.org/content/early/2013/12/18/01.cir.0000441139.02102.80.full.pdf . Accessed Novem
ber 11, 2014.
25. National Cancer Institute. Cancer Prevalence and Cost of Care Projections Web site. http://costprojections.cancer.
gov/. Accessed November 11, 2014.
26. New York City Department of Health & Mental Hygiene [Publisher]. (2008). Supermarket Need [Choropleth Map], Retrieved Nov 14, 2014, from: http://foodmapper.wordpress.com/2008/05/13/nyc-food-deserts-talk-and-
action/
27. Citizens Committee for New York City [Publisher]. (n.d.). [Volunteers tending to garden beds]. Retrieved Nov 14, 2014, from: http://www.citizensnyc.org/grantee/la-finca-del-sursouth-bronx-farmers
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Schneider
The Threat of Misdiagnoses: Are
There Forms of Dementia That
Could Be So Similar That They Are
Nearly Indistinguishable?
By Julia Schneider
“With the evolution of case studies showing ways to differentiate a reversible form of dementia from an irreversible type using radiographic
findings, neurologists are able to see the differences. Since AD is more
widely recognized all across the world compared to NPH, doctors jump
to the former to make a clinical diagnosis.”
There are many forms of dementia but
Normal Pressure Hydrocephalus (NPH) and Alzheimer’s disease (AD) are the two types that are
the most similar. Their overlapping symptoms
engenders a hindrance for physicians to make
a definitive diagnosis. Even though AD is more
prevalent and widely known, there has been a
plethora of misdiagnoses. It turns out that what
physicians thought to have been AD was, in fact,
NPH. Though they are very close on the pedigree chart of dementias -- practically siblings
-- NPH and AD have been differentiated in a
number of ways that have contributed to changing a patient’s life forever.
AD is the most widespread cause of
dementia with about 5.3 million Americans diagnosed per year.1 Despite how common AD is,
there are no treatments to reverse this disease.
Cholinesterase inhibitors are used to alleviate
symptoms such as memory loss and cognitive
deterioration, and despite attempts to halt the
progression of AD, a patient usually has 4 to 6
years, on average, to live.1 Although AD is an irreversible form of dementia, NPH is reversible.
It is characterized by a triad of symptoms: gait
disturbance, cognitive impairment, and urinary
incontinence.2 NPH’s prevalence is not as high
as AD’s -- being responsible only for a meager
5% of dementia cases. However, the correct
numbers are not known exactly since the range
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of NPH cases is anywhere between 2 to 20 million cases per year.2 Furthermore, NPH’s etiology is interesting because there are two types: idiopathic and secondary which can be caused by
a subarachnoid hemorrhage, aneurysms, or any
type of brain traumas.2 Despite the technical differences between AD and NPH, their relationship tends to be overlooked. It is common for
physicians to diagnose an elderly person—sixtyfive years or older—with AD, but NPH seems
to be forgotten about. In a way, it is a hidden
form of dementia. Unless NPH’s symptoms are
comprehensively analyzed, a patient may be misdiagnosed with AD for the rest of his life.
In order to examine the similarity and
overlap between AD and NPH, a case study
was conducted using 761 brains that were autopsied.3 Based on neuropathologic evidence,
563 of these cases were found to have had dementia and of those 563, almost half -- 56% -were diagnosed with AD. However, of the 563
cases, only nine patients had a clinical diagnosis
of NPH. Eight of these patients were found to
have met the National Institute on Aging and
the Reagan Institute criteria of AD.3 These results suggest that AD pathology is present in
NPH cases which shows how challenging it is to
distinguish the two forms of dementia.
Furthermore, AD and NPH are even
more difficult to differentiate on a molecular
Fall 2014
Schneider
level. In the brain, the choroid plexus is the main
tissue that secretes cerebrospinal fluid (CSF),
which continuously circulates in order to get rid
of noxious metabolites. If CSF circulation fails
to serve its role, then amyloid-beta peotide and
microtubuluar associated protein tao (MAP- tao)
accumulate, and this failure and associated accumulation seems to occurs in AD and NPH
patients.4 This in turn may result in the overproduction of CSF in the brain which causes the
excess fluid to enter the ventricles, or the spaces
in the brain. Once this occurs, ventricles become
enlarged. Using an MRI would show enlarged
ventricles for both AD and NPH patients; this
overlap shows another example of a similarity
between AD and NPH that makes diagnosing
and differentiating between the two difficult and
uncertain.
Neurologists have difficulty differentially diagnosing NPH and AD because NPH’s
triad of symptoms are common occurrences in
the elderly. Studies have shown that gait disturbance occurs in 20% of people over the age of
75; cognitive decline occurs in about 4.5 million
people over the age of 65; and urinary incontinence reportedly occurs in 38% of women and
in 17% of men over the age of 60.5 Also, ventricle size tends to increase with age.5 Thus, NPH
seems to have commonplace symptoms that do
not seem anomalous. However it is the combination of the symptoms acting together that becomes an eye-opener for neurologists since this
triad of “Wet, Wacky, Wobbly” is the hallmark
of NPH.
Despite the triad of symptoms standing out in a patient thought to have NPH, there
are detailed ways to differentiate NPH from AD
radiographically. Usually radiographic findings
show ventriculomegaly and normal CSF pressures in NPH patients.2 Since CSF fluid flows into
the ventricles of the brain, it would be expected
for CSF pressure to change as well as intracranial
pressure, but this covert type of dementia is so
sneaky that it doesn’t present with any significant
change in pressure. Typically, an MRI is used to
pinpoint NPH, but a case study has proven successful for the use of Positron Emission Tomography (PET) to differentiate NPH from AD
using [18 F]Fluorodeoxyglucose (FDG).6 This
study included 3 NPH patients, 17 AD patients,
and 7 elderly controls. NPH showed lower cortical rates of FDG use than AD. Between the AD
and NPH categories, the former indicated bilateral temporoparietal hypometabolism, yet the
latter showed an even distribution of cortical activity which showed a global lack of glucose utilization.6 The PET scan is much more useful in
ruling out a patient who may seem to have NPH
but in actuality has AD. Hypometabolism in the
temporoparietal junction is a notable marker for
identifying AD. On an MRI, AD would be noted
to have a sulcal enlargement, unlike the focally
dilated sulci over a convex or medial surface of
a hemisphere, which would indicate NPH. Also,
a higher Sylvian CSF volume would further corroborate NPH.5 Radiographic findings continue
to distinguish AD from NPH since they both
exhibit the enlargement of ventricles. Specifically, MRI’s have shown that AD patients usually
present with atrophy mostly in the CA1 region
of the hippocampus in conjunction with dilation of the perihippocampal fissures (PHFs).7
On the other hand, NPH patients do not present with enlarged PHFs, especially after being
surgically treated with a Ventriculoperotineal
shunt (VP), a catheter that changes the route of
CSF flow. In this case, excess CSF goes into the
peritoneal cavity. It is specifically important to
examine PHFs in post-VP shunt NPH patients
to see if the shunt does its job. If it doesn’t, then
it would be clear that the patient doesn’t have
NPH and PHFs may have been enlarged; this
suggests AD since these patients do not respond
to shunts and are not surgically treatable.7 In order to avoid surgically placing a shunt, two common methods are used: the first being a Lumbar
Tap test which consists of a lumbar puncture
removing 30-50 mL of CSF.2 The patient is observed about an hour afterwards to see if his gait
disturbance and cognitive function improves. A
similar procedure, called a Lumbar Drainage, encompasses the continuous drainage of CSF at 5
to 10 mL per hour with the drainage system attached to a patient.2 He is then observed for two
to three days to see if his symptoms improve.
If each procedure shows improvement, with
the Lumbar Drainage being more reliable due
to its lengthy and thorough examination, then
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Schneider
a shunt would most likely work as well. NPH
patients have had success with shunts. Although
it is mercurial to predict if a shunt will malfunction, a case study, that followed fifty-five patients
three years after the surgical placement of a VP
shunt; indicated that fifty-three percent of those
patients did need revision.2 Thus a shunt, as of
now, is the most ideal solution for patients with
NPH. Fortunately, a shunt works well, which is
why NPH is a reversible type of dementia; the
symptoms subside indefinitely, until the shunt
must be replaced.
AD and NPH are two similar forms of
dementia. They both show enlarged ventricles
and cognitive decline. However, there has been
much concern with regards to overlooking NPH
symptoms and nuances in the presence of AD
competitors. With the evolution of case studies
showing ways to differentiate a reversible form
of dementia from an irreversible type using ra-
diographic findings, neurologists are able to see
the differences. Since AD is more widely recognized all across the world compared to NPH,
doctors jump to the former to make a clinical
diagnosis. Consequently, not only is this misdiagnosis detrimentally covert, but this deleterious
mistake hinders a patient from improving his
health. Fortunately, more differences are being
discovered with an augmentation in case studies so that NPH will be more widely recognized.
Consider a rudimentary example: You go to a
restaurant and order a salad that has green vegetables, but unfortunately, you are allergic to avocados. You make sure that the salad is bereft of
any. In fact your allergic reaction is so extreme
that if you do eat an avocado, it will prove fatal.
If you were to have not seen that an avocado
inadvertently ended up in your salad you would
die. This is like not being able to recognize NPH
though it would makes things infinitely easier.
REFERENCES
1. Russell, T, and S Richards. "Alzheimer's Disease." (2013): CINAHL Plus with Full Text. Web. 17 Nov. 2013.
2. Siraj, S. "An Overview Of Normal Pressure Hydrocephalus And Its Importance: How Much Do We Really Know?."
Journal Of The American Medical Directors Association 12.1 (2011): 19-21. Scopus®. Web. 17 Nov. 2013.
3. Cabral, Danielle, et al. "Frequency Of Alzheimer's Disease Pathology At Autopsy In Patients With Clinical Normal Pres
sure Hydrocephalus." Alzheimer's & Dementia: The Journal Of The Alzheimer's Association 7.5 (2011): 509-513.
MEDLINE. Web. 17 Nov. 2013.
4. Silverberg, Gerald D, et al. "Alzheimer's Disease, Normal-Pressure Hydrocephalus, And Senescent Changes In CSF
Circulatory Physiology: A Hypothesis." Lancet Neurology 2.8 (2003): 506-511. MEDLINE. Web. 17 Nov. 2013.
5. Graff-Radford, Neill R. "Normal Pressure Hydrocephalus." Neurologic Clinics 25.3 (2007): 809. MEDLINE. Web. 17 Nov.
2013.
6. Jagust, W J, R P Friedland, and T F Budinger. "Positron Emission Tomography With [18F]Fluorodeoxyglucose Differ
entiates Normal Pressure Hydrocephalus From Alzheimer-Type Dementia." Journal Of Neurology, Neurosurgery &
Psychiatry 48.11 (1985): 1091. Publisher Provided Full Text Searching File. Web. 17 Nov. 2013.
7. Holodny, A.I. ( 1,3,5 ), et al. "MR Differential Diagnosis Of Normal-Pressure Hydrocephalus And Alzheimer Disease:
Significance Of Perihippocampal Fissures." American Journal Of Neuroradiology 19.5 (1998): 813-819. Scopus®.
Web. 17 Nov. 2013.
16
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Fall 2014
D’Alessio
Has the Medical Field
Acknowledged Artists Make
Better Doctors?
By Nicole Marie D’Alessio
“There has been a rise in the number of medical schools which acknowledge the edge artistic applicants might have over those who do
not have a background in the arts.”
The medical community is beginning
to believe artists make better doctors. There has
been a rise in the number of medical schools
which acknowledge the edge artistic applicants
might have over those who do not have a background in the arts. “Being accepted into medical school used to mean selecting time-honored
disciplines such as biology or chemistry, taking
a more traditional route as a “pre-med” to gain
entrance…to be the most prepared for the onslaught of biochemistry, pharmacology, anatomy
and science-related material that has traditionally permeated the first several years of medical
school…” says Robert Glatter, MD for Forbes
magazine. As the selection process has become
increasingly competitive, schools are looking for
students who not only have a high GPA. They
are looking for applicants who have an edge. For
many of schools, one of the best advantages is a
background in the arts and related creative experiences.
Prominent medical institutions such as
Columbia, Yale, and Brown have implemented
programs which teach students medicine while
explaining the importance of an artistic mindset. For example, Columbia’s program in Narrative Medicine, describes their mission to be that
it “…fortifies clinical practice with the narrative competence to recognize, absorb, metabolize, interpret, and be moved by the stories of
illness.” At The Irvine College of Medicine, a
program has been implemented with a mission
stating:
“The Program in Medical Humanities & Arts
at the University of California, Irvine, College
of Medicine has been in existence for five years.
The program was implemented to enhance aspects of professionalism including empathy, altruism, compassion, and caring toward patients,
as well as to hone clinical communication and
observational skills.”
--“Can Poetry Make Better
Doctors? Teaching the Humanities and Arts to
Medical Students and Residents at the University
of California, Irvine, College of Medicine.”
Brown University holds an annual lecture series entitled “Creative Medicine Lecture
Series.” Collaboration between the fields of
medicine and art emerged as the focal point of
the lecture by guest speaker, Alexa Miller, who
develops alliances between medical schools and
art museums through her company, Arts Practica. “Realizing the benefits of the arts in medical education emerged as a school of thought
around 15 years ago,” Miller said. Initial research
at Yale revealed that medical students enrolled
in a modest art education program demonstrated greatly increased sensitivity to visual information. Miller’s research at Harvard heralded
similar results – medical students who took
part in a 10-session museum observation workshop increased their amount of written clinical observation by 38 percent,” writes Phoebe
Draper, senior staff writer for The Brown Daily
Herald. Rutgers University has introduced an
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17
D’Alessio
interdisciplinary humanities course designed to
graduate better doctors last year. “We need to
address the educational foundation of health
care providers by making them rethink how they
view the human body,” says Bachmann, interim
chair of the Department of Obstetrics, Gynecology and Reproductive Sciences and the director of the Women’s Health Institute at Rutgers
Robert Wood Johnson Medical School. The
course, which combines art history, medical
courses, and narrative writing, will be offered for
the first time to Robert Wood Johnson medical
students the spring semester of 2015. They cite
their ultimate goal as to “Prepare better doctors
by making them more observant diagnosticians
and more effective communicators.”
Some of the cited reasons supporting
artistic applications in doctoral training include
the theory that artists may be more empathetic
or humane; and since the study of medicine
is largely a visual learning experience, when it
comes to understanding the human body and its
intricacies, artists may have an element that others do not. Or, as Pheobe Draper for The Brown
Daily Herald describes, the idea that the longer
you look, the more you see. The practice of
medicine benefits from physicians who observe,
think counter-intuitively, and think creatively.
At tradition-minded Harvard, faculty
members were fairly skeptical when proposed
with the idea of using art in the curriculum.
Doctor Joel Katz proposed his class of Harvard
Medical School students meet regularly at the
Museum of Fine Arts, “especially since the firstand second-year students who enroll are already
overwhelmed with work.” But Katz’s belief that
physicians can improve their diagnostic skills by
observing art was bolstered…when he and his
colleagues published a study in the Journal of
General Internal Medicine showing that after
completing the class, students’ ability to make
accurate observations increased 38 percent.”
Previous experience with critical thinking in the sciences has been a common theme
for success in curing others. Characteristics including strong talents for imagery, imagination,
thinking “outside the box” and compassion towards humanity may actually prove to be just as
valuable as a scientific mindset in the eyes of
some experts.
REFERENCES
"Columbia University Medical Center | Program in Narrative Medicine."Program in Narrative Medicine. N.p., n.d. Web. 15
Sept. 2014.
Department of Family Medicine, Program in Medical Humanities & Arts, Orange, CA 92868-3298, USA. [email protected].
"Can Poetry Make Better Doctors? Teaching the Humanities and Arts to Medical Students and Residents at
the University of California, Irvine, College of Medicine." National Center for Biotechnology Information. U.S.
National Library of Medicine, 10 Oct. 2003. Web. 19 Sept. 2014.
Draper, Pheobe. "Lecture Stresses Art's Impact on Medicine." Brown Daily Herald. Brown University, 21 Sept. 2013. Web.
17 Sept. 2014.
Gladdix, Robert, MD. "Can Studying Art Help Medical Students Become Better Doctors?" Forbes. Forbes Magazine, 20
Oct. 2013. Web. 16 Sept. 2014.
Kowalczyk, Liz. "Monet? Gauguin? Using Art to Make Better Doctors."Boston.com. The New York Times, 20 July 2008.
Web. 19 Sept. 2014.
Pugh, Rachel. "Art and Literature Could Make Doctors More Competent and Humane." The Guardian. The Guardian, 19
Nov. 2013. Web. 16 Sept. 2014.
Verbinas, Patti. "Training the Doctor's Eye Through the Study of Art." Rutgers, A World of Discovery. Rutgers University
of New Jersey, 27 Oct. 2013. Web. 19 Sept. 2014.
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Fall 2014
Rahman
Stem Cell Therapy – A Novel
Treatment for Duchenne’s
Muscular Dystrophy
By Syed Rahman
“The new discovery could lead to new therapies for degenerative diseases like muscular dystrophy, which is characterized by progressive
weakening of skeletal muscle tissue.”
Duchenne Muscular
Dystrophy (DMD) is a recessive disease that results from
a mutation in the dystrophin
gene. This gene, located on the
X chromosome, codes for the
protein dystrophin- an important component in muscle tissue. People with this mutation
suffer from muscle degeneration and death. DMD currently
affects 1 in 3600 males in the
United States, with most of the
affected individuals receiving
rigorous corticosteroid treatments (Goldring et al., 2002).
However, this treatment is not
curative; DMD ultimately leads
to death as a result of complications arising from lack of
muscular function, such as the
impairment of cardiovascular
function due to weakened cardiac tissue (Galli et al., 2000).
This concept that multipotent
stem cells can be derived from
bone marrow had led the notion of actually using them as
a potential treatment option
to replaced damaged muscle
tissue in individuals suffering
from DMD. One of the areas
of focus has been the usage
of these so-called muscle stem
cells to replace diseased tissue
with cells that are capable of
renewal and maintenance characteristic of normal muscle
cells. This has led to a great
deal of research looking into
the efficacy of using stem cell
therapies in order to regenerate functional muscle tissue,
much of which will
be explored in this
article. The idea of
using muscle stem
cells as a potential treatment for
patients suffering
from DMD could
lead to research for
other muscular degenerative diseases.
scription factors - or proteins
that bind to gene regulatory
elements in order to regulate
gene expression., researchers
can specify cell type, inducing
stem cells to enter particular
lineages. In its application as a
treatment for DMD, this technique would replace the muscle
For the
past decade, researchers have attempted to find apFigure 1. Skeletal Muscle Cells.
plications for stem
cells in regenerating certain cell types. As cells cells patients have lost by using
that have not yet entered the stem cells to create functional
differentiation process, stem muscle cells. New findings
cells have the potential to be- concerning muscular stem cells
come one of a multitude of dif- have increased the potential efferent cell types. By controlling ficacy of this technique (Goldthe expression of certain tran- ring et al., 2002).
Volume 15
MEDICAL DIALOGUE REVIEW
19
Rahman
A 1999 study by Jackson and Goodell found that
adult neural stem cells (ANSCs) derived from the central
nervous system can differentiate into myogenic cells in
the absence of certain inhibitory signals from the cellular
environment (Jackson and
Goodell, 1999). Jackson and
Goodell found that certain
signals from embryonic stem
cells, can induce the expression of myogenic markers in
ANSCs, ultimately resulting in
their differentiation into skeletal muscle cells. These new
cells can potentially be implanted into patients lacking
functional muscle cells (Figure
1).
The discovery that
ANSCs that are clustered together stay undifferentiated
has lead scientists to postulate
that signaling between ANSCs
may inhibit myogenic signaling
and myogenic differentiation.
Additionally, culturing ANSCs
with undifferentiated embryoid
bodies has the potential to produce a diverse array of skeletally derived myogenic cells in-vivo and in-vitro. The myogenic
cells produced from ANSCs
were shown to retain the ability
to differentiate into a wide variety of muscle cells, thus giving
these ANSC derived myogenic
cells the capacity to replace
a wide variety of muscle cells
in-vivo (Jackson and Goodell,
1999). Later studies have come
to similar conclusions (Galli et
al., 2002).
In February of 2014,
Natalia Sych conducted a study
20
with a large group of DMD
patients suffering from a wide
range of muscle pains such as
weakness in the wrists, lower
extremities, pelvic muscles, and
chest. Patients received a suspension containing preserved
fetal stem cells expressing
myogenic markers. The control
group patients underwent the
normal treatment for DMD,
which included a rigorous treatment of corticosteroids and
muscle supporting medications
such as L-carnitine, vitamins,
and amino acids. Based on an
arbitrary point scale, patients
who received fetal stem cells
therapy (FSCT) scored on average 5 points higher in terms
of physical functioning, mental
health, vitality, and emotional
health when compared to
the control group of patients
throughout the course of 6
months. The FSCT patients
also had increased levels in all
these categories in 12 months
as opposed to 6 months, demonstrating the long lasting effects of FSCT. It was previously known that a lack of
dystrophin (characteristic of
DMD) leads to increased CPK
(creatine phosphokinase) penetration from the damaged muscle cells into the bloodstream,
thus making CPK levels a good
indicator of DMD. However,
in this study, the FSCT patients
showed a much lower level of
CPK in the blood stream when
compared to the control group,
results that persisted as long as
12 months after the stem cell
treatment took place. This
demonstrates the potential
long-term benefits that FSCT
can offer to patients suffering
MEDICAL DIALOGUE REVIEW
Fall 2014
from DMD (Sych et al., 2014).
The next problem
is finding a way to culture the
large numbers of stem cells
necessary to give rise to muscle cells. A study by Rudnicki
found that mouse muscles contain two types of precursors to
skeletal muscle cells, or satellite cells (Swaminithan, 2007).
90% of the cells are preprogrammed to become muscle
tissue while another 10% are
undifferentiated (Swaminithan,
2007). The researchers in this
study found that the gene Myf5
codes for a protein that functions as the “first genetic entry
point into the muscle lineage”
(Swaminithan, 2007). When
stem cells had a functional and
positive Myf5 gene inserted,
they went on to become muscle cells. Thus, the activation of
Myf5 can increase the production of muscle cells from stem
cells (Swaminithan, 2007). Another study by Akizawa in 2013
showed that the up-regulation
of MYOD1 transcription factors in mesenchymal stem
cells leads to the activation of
Myf5, which in turn leads to
increased levels of dystrophin.
This shows that up-regulation
of MYOD1 can increase the
production of muscle cells
specifically capable of combating the decreased levels of dystrophin characteristic of DMD
(Akizawa et al, 2013).
Overall, stem cell
therapy can have long term
benefits for patients suffering
from DMD. However, simply
giving functional muscle cells
to DMD patients isn’t enough
Rahman
to ensure survival. Professor
Simone Spuler of the Experimental and Clinical Research
Center (ECRC) argues that a
genetic muscle disease such as
DMD requires treatment with
a healthy gene that repairs or
masks the defective gene. This
is essentially the basis for gene
therapy (Bactler, 2014). While
stem cell therapy shows potential as a treatment for DMD,
the complications of immune
rejection of the muscle cells
have prevented it from its
widespread uptake. Further re-
search must focus on combining the stem cells with a healthy
gene that can replace the defective DMD gene and create
muscle cells that can evade the
risks associated with immune
rejection.
REFERENCES
Akizawa, Y., et al. "Enhanced expression of myogenic differentiation factors and skeletal muscle proteins in human am
nion-derived cells via the forced expression of MYOD1." Brain Development 35.4 (2013): 349-55. Print.
Bachtler, Barbara. "New Research Method Opens Door to Therapy with Human Muscle Stem Cells Scientists and Physi
cians in Germany Collaborate to Develop Promising Method." MDC. N.p., 27 Aug. 2014. Web. 18 Oct. 2014.
<https://www.mdc-berlin.de/43612981/en/news/2014/ 20140827 new_research_method_opens_door_to_
therapy_>. Clarke DL, Johansson CB, Wilbertz J, et al. Generalised poten- tial of adult neural stem cells. Science
2000; 288: 1660–1663.
Galli R, Borello U, Gritti A, et al. Skeletal muscle potential of human and mouse neuronal stem cells. Nature Neurosci
2000; 3: 986–991.
Goldring, Kirstin, Terence Partridge, and Diana Watt. "Muscle stem cells." Journal of Pathology 197.1 (2002): 457-67. Print.
Jackson, K. A, Mi, T. & Goodell, M. A. Hematopoietic potential of stem cells isolated from murine skeletal muscle. Proc.
Natl. Acad. Sci. USA 96, 14482–14486 (1999)
Swaminithan, Nikhil. "Newfound Stem Cells May Lead to Regenerative Therapies for Damaged Muscles." Scientific Ameri
can. N.p., 31 May 2007. Web. 18 Oct. 2014.
Sych, N., et al. "Efficacy of fetal stem cells in Duchenne muscular dystrophy therapy." Journal of Neurorestoratology
2014.2 (2014): 37-46. Print.
Volume 15
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21
Torres
Coconut Oil Unmasked
By Chris Torres
“This confusion and skepticism in the scientific community has led neither the American Heart Association or the U.S. government’s Dietary
Guidelines to suggest that coconut oil is any better or preferable over
other saturated fats over other saturated fats.”
Coconut oil is not a recently discovered health source. Coconut oil is an edible oil
extracted from the kernels of extracted coconuts harvested from the coconut palm trees.
The uses for coconut oil existed for as long
as 4000 years ago in Sanskrit texts. Yet, even
One theory proposed by Ancel Keys states that
a major intake of saturated fats can lead to high
cholesterol and heart failure. However, these
findings may be flawed since, they hydrogenated coconut oil when they fed it to animal subjects. Hydrogenation of the unsaturated fatty
acids converts it to saturated fatty acids
which leads to more production than
the original 92% saturated fat makeup;
it also leads to less absorption of essential amino acids. With a more saturated
coconut oil testing, animals would intake
the transformed coconut oil and have
different results than those who would
intake normal amounts of saturated fats
in coconut oil.
To answer this question whether coconut oil is a healthy or an unhealthy fat,
one must investigate the pathway for absorption of cholesterol. When humans
consume fats, our body breaks it down
Figure 1: Mortality Rate from Heart Disease.
into cholesterol. However, cholesterol
cannot be readily absorbed in the bloodwith knowledge about this oil in history, the oil’s stream without the help of carrier proteins. Two
documented uses throughout history has been different types of carrier proteins exist, called
less known. There has been much modern de- low-density lipoprotein(LDL) and high-density
bate about its true health benefits. Coconut oil lipoprotein(HDL). LDL proteins are known as
contains a mixture of short and medium chain the “bad” kind because they cause the formation
fatty acids primarily lauric acid (44%) and my- of plaque inside the arteries and HDL proteins
ristic acid (16.8%) (Zelman). The oil’s high satu- are the “good” kind because they are known to
rated fat content (about 92%) has lead many to remove LDL cholesterol from the arteries. Yet,
fear that coconut oil can lead to atherosclero- a study showed that coconut oil had a “combisis (Schardt). Atherosclerosis occurs when fats nation of fatty acids [that]improved the ratio of total
build up on the walls of the arteries, forming cholesterol: HDL (good) cholesterol but they also raised
plaques that eventually clog the arteries and LDL (bad) cholesterol (Zelman).” Therefore, the chemicauses problem with blood flow. This excessive cal makeup of coconut oil proved to show that levels of
intake of lipids may in fact lead to heart disease. both good and bad cholesterol increased. However, epi22
MEDICAL DIALOGUE REVIEW
Fall 2014
Torres
demiologic studies were conducted in several itchy. Coconut oil’s affinity for hair protein and
Asian countries where coconut oil was used in its ability to enter deep into the hair shaft gives
their daily diets. The 1978 Demographic Year- the oil its beneficial effects.
book of the United Nations claimed that in Sri However, researched conducted by
Lanka 1 in 100,000
Florencio showed
people die of heart
that 40 obese womdisease. In a suben who consumed
sequent study, 16
coconut oil had rehealthy Sri Lanka
ductions in blood
males
replaced
lipid levels and abtheir consumption
dominal
obesity.
of coconut oil with
Yet, researchers are
corn oil. After 6
skeptical about the
weeks, researchers
benefits of the infound higher levtake of coconut oil.
els of LDL (bad
“There are a lot of
Figure 2. Coconut Oil.
cholesterol) in the
claims that coconut
blood of those who
oil may have health
had consumed corn oil as opposed to those con- benefits, but there is no concrete scientific data
suming coconut oil. Furthermore, Filipinos in yet to support this,” said Dr. Daniel Hwang, a
the Bocal region consume a large amount of research molecular biologist specializing in lauric
coconut oil, about 26 grams daily. But a nutri- acid at the at the University of California, Davis.
tional survey taken in different regions of the This confusion and skepticism in the scientific
Philippines showed that though the Filipinos community has led neither the American Heart
of the Bocal region eat more coconut oil, their Association or the U.S. government’s Dietary
diets contain fewer calories than the typical US Guidelines to suggest that coconut oil is any betdiet. By calculating their dietary intake, the sur- ter or preferable over other saturated fats over
vey revealed that out of all regions, the Bocal other saturated fats. According to both agenregion had less heart disease reported. This was cies, “Coconut oil, like all saturated fats, should
recorded by overseeing the amount of cases of be limited to 7 percent of daily calories because
heart disease reported. In accordance with this it can increase risk for heart disease.” Overall,
study, Figure 1 shows that the Philippines, as a the studies conducted are short-term studies and
whole, have lower rates of death due to heart need further investigation and long-term projdisease compared to the USA, Australia, and ects to be more validated.
New Zealand.
More research must be conducted to
Although there is much scrutiny of give a final validated answer to ensure the safety
studies showing the health benefits of consum- of consuming coconut oil regularly. However,
ing coconut oil, there are supporters of the ben- heart disease is caused by more than dietary inefits of the external uses of coconut oil. One take but it also has other influences that can lead
study showed that topical application of coco- one predisposed to it. Hence, there are many
nut oil improved skin and hair conditions. In factors that can lead to such diseases and more
a follow-up investigation, moisturization with research must be performed in order to see how
coconut oil was shown to relieve xerosis, a skin coconut oil can fit into the web of factors.
condition in which the skin is dry, rough, and
Volume 15
MEDICAL DIALOGUE REVIEW
23
Torres
REFERENCES
Assunção ML, Ferreira HS, dos Santos AF, Cabral CR Jr, Florêncio TM. Effects of dietary coconut oil on the biochemical
and anthropometric profiles of women presenting abdominal obesity. Lipids. 2009 Jul;44(7):593-601. Epub 2009
May 13.
Agero AL, Verallo-Rowell VM. A randomized double-blind controlled trial comparing extra virgin coconut oil with mineral
oil as a moisturizer for mild to moderate xerosis. Dermatitis. 2004 Sep;15(3):109-116.
Coconut Oil. Digital image. HealthJunk. N.p., n.d. Web.
Kaunitz H: Biological and therapeutic effects of “MCT” (Medium Chain Triglycerides) from Coconut Oil. Coconuts Today 1983: 27-30.
"Mesnick, R. American Journal of Clinical Nutrition, May 2003; vol 77: pp 1146-55..
"Good vs. Bad Cholesterol." Good vs. Bad Cholesterol. N.p., n.d. Web. 15 Oct. 2014.
Blackburn GL, Kater G, EA Mascioli, M Kowalchuk,. VK Babayan and BR Bistrian: “A reevaluation of coconut oil’s effect
on serum cholesterol and atherogenesis” February 1990, Philippine Medical Association, 24-31
Keys A: Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp 1953: 20; 118-139
David, Schardt, "Coconut Oil." Coconut Oil. N.p., n.d. Web. 14 Nov. 2014.
24
MEDICAL DIALOGUE REVIEW
Fall 2014
Buttar
Controlling the Control
Center of the Body
By Sally Buttar
“Even though the location of this SWS-promoting/EEG-synchronizing
circuitry is still a mystery, the activation of this sleep node could potentially allow scientists to discover a method where humans can trigger
their own SWS. ”
Sleep disorders, such as insomnia, affect the lives of 10-15% of the whole population. Associated symptoms include: inability to
fall asleep, inability to sleep soundly through the
night, and fatigue. Although sleep disorders are
not headlining the news, they are more prevalent in today’s society than before. We live in a
stress-filled environment, which contributes to
insomnia. This, in turn, induces more stress as
an individual with insomnia is continuously in a
sleep-deprived state; the cycle never ends. Physicians employ a variety of methods in an attempt
to inhibit this disorder. One of these methods includes paradoxical intention, which is a method
that encourages the patient to address their most
feared behavior, for example staying awake. The
goal of this method is to “alleviate performance
anxiety,” which attempts to reduce an individual’s stress level, and allow them to sleep (Saddichha 2010). Another method includes changing
the patient’s beliefs and attitudes about sleep.
Insomnia has different characteristics for each
person, thus individuals may respond to different approaches (Saddichha 2010). While these
methods seem to work for some patients, there
are still no certain cures for most sleep disorders, leaving patients to resort to taking various
pills. Scientists are now exploring new methods
that may allow us to operate the brain ourselves,
which will potentially be able to alter the lives of
many who endure sleep disorders.
Before Horace Magoun and Giuseppe
Moruzzi shared their research, sleep was described as passive. Passive sleep was the idea that
if we diminished all of the arousal activity from
the brainstem, it would lead to the stability of
the neural activity in the central nervous system.
Now, following Magoun and Moruzzi’s research,
we acknowledge sleep as an active phenomenon
due to the neurons that are found to promote
sleep. In the brain, the hypothalamus is responsible for managing the body’s sleep. While neuronal activity is increasing during wakefulness,
sleep regulatory substances add up to eventually trigger the ventro-lateral prepotic nucleus
(located in the anterior hypothalamus), which
allows sleep to occur. Thus, many support the
hypothesis that sleep is triggered due to many
sleep regulatory substances that helps regulate
slow-wave sleep (SWS) (Coulon et al 2012).
In 1949, Moruzzi and Magoun discovered that the electrical stimulation of the reticular formation, a set of interconnected nuclei that
are located through the brain stem (Gleitman et
al 228), leads to a generalized arousal reaction
in the cortex of the brain, which is what they
found controls the sleep-waking cycle. Their
experiment results indicated that the interaction between the thalamus neurons and the cortex neurons produces these sleep-wake cycles.
Moruzzi and Magoun also identified the ascending reticular formation system, which sends electrical stimuli to produce wakefulness, and reduces electrical stimuli to produce sleep(Moruzzi et
al 1949).
There are four stages of sleep. In stage one, an
individual is in light sleep; light enough to be woken up by a sound. If stage one sleep is not
Volume 15
MEDICAL DIALOGUE REVIEW
25
Buttar
disrupted, sleep starts to deepen, and within an
hour that individual will go through stage two.
Stage two is characterized by rapid brain wave
activity called sleep spindles. The individual continues to fall into a deeper sleep as they move
through stage three, where slow, large waves
emerge in the electroencephalogram (EEG).
These large waves, known as delta waves, take
Figure 1. Each stage of sleep is defined
by brain wave patterns (Bryant et al 2004).
over and stage four occurs. Stages three and four
are referred to as slow-wave sleep (SWS). “Slow,
rolling eye movements, low cortical arousal, and
slowed heart rate and respiration,” characterize
sleep waves (Gleitman et al, 235).
SWS has been discussed in great deal,
and hypotheses have been made that show that
SWS can be triggered, and the enhancement of
those waves induce sleep (Roth 2009). The trigger mechanism involves interactions between
sleep inducing neurons in the ventrolateral prepotic area (VLPO), and wake inducing neurons
in the brainstem and hypothalamus (Anaclet et
al 2014). Researchers at University of Buffalo
School of Medicine and Biomedical Sciences
and Harvard School of Medicine have recently
discovered the second sleep node identified in
the mammalian brain. This sleep-promoting circuit, located deep in the parafacial zone (PZ) in
the brainstem, appears adequate and necessary
to produce deep sleep (Goldbaum, 2014). SWS
is crucial for deep sleep to occur, and the recently
discovered PZ GABAergic neurons have shown
to enhance and promote SWS waves. This new
GABA neuron, which makes the neurotransmitter gammaaminobutryic acid, is reported to be
26
MEDICAL DIALOGUE REVIEW
responsible for deep sleep (Goldbaum 2014).
Researchers at Harvard and University
of Buffalo tested the PZ GABAgeric neurons
in mice. Researchers injected a virus containing
an excitatory modified muscarinic G proteincoupled receptor, expressed in a Cre-dependant
manner, into the paraficial zone of Vgat-IREScre mice and their non-Cre-expressing littermates (Anaclet et al 2014). Vigorous cell-surface
expression of the G protein-coupled receptor
was exhibited on the GABA neurons of the
Vgat-IRES-cre mice, but was not detected in the
non-Cre-expressing mice. This data confirms
that Cre activity is required for receptor expression to be enabled in PZ GABAgeric neurons.
Although it was then demonstrated that without the agonist clozapine-N-oxide (CNO), a
chemical that binds to receptors to make them
effective, the mice with the G protein-coupled
receptors in their neurons did not show any different hourly sleep-wake, or difference in their
EEG, than the mice that did not express the G
protein-coupled receptors. Thus, it is apparent
that the ligand (CNO) is needed to bind with the
G protein-coupled receptors to induce PZ neuron activity. The induction of PZ neuron activity
releases the GABA neurotransmitter, and results
in deep sleep (Anaclet et al 2014).
These injections of CNO did not seem
to have an affect on the mice that did not express
the G protein- coupled receptors. To test the
effectiveness of the ligand CNO on the receptors, researchers first injected the mice with an
interaperitoneal (IP) vehicle injection, a solution
without CNO. Results following the injection
show high electromyogram (EMG) activity, and
low EEG slow wave activity (SWA). The higher
the EMG activity and the lower the SWA, the
more periods of wakefulness are occurring. Adversely, when the IP CNO was injected the mice
fell asleep in a short period of time and had low
EMG activity, along with high SWA. The slow
wave sleep occurred in bouts 1-10 minutes with
the IP vehicle injection, while the IP CNO mice
had SWS that occurred in bouts longer than 5
minutes, with 35% occurring in bouts longer
than 20 minutes. This shows that the activation
of PZ GABAergic neurons by CNO results in
higher SWS delta waves, which occur during sta-
Fall 2014
Buttar
ges three and four of sleep (Anaclet et al 2014).
Even though the location of this SWSpromoting/EEG-synchronizing circuitry is still
a mystery, the activation of this sleep node could
potentially allow scientists to discover a method
where humans can trigger their own SWS. As
more discoveries about the brain, such as this
sleep node, are revealed, humans will begin to
see that we are in control of our own bodies.
With the uncovering of only two sleep nodes
scientists are able to unlock many mysteries
about the brain—imagine what the discovery
of the rest of the brain will allow humanity to
achieve.
REFERENCES
Anaclet, Christell, Loris Ferrari, Elda Arrigoni, Caroline E. Bass, Cliford B Saper, Jun Lu, & Patrick M Fuller. “The GAB
Aergic parafacial zone is a medullary slow wave sleep-promoting center” Nature Neurosciene. 17.9 (2014): 1217
1224. Web. 18 Oct. 2013
Bjorness, Theresa E and Robert W Green. “Adenosine and Sleep”. Current Neuropharmacology. 7.3. (2009): 238-245. Web. 18.
Oct. 2014
Coulon, Philippe, Thomas Budde, and Hans-christian Pape. "The Sleep Relay--the Role of the Thalamus in Central and
Decentral Sleep Regulation." Pflügers Archiv - European Journal of Physiology 463.1 (2012): 53-71. ProQuest. Web. 18
Oct. 2014.
Goldbaum, Ellen. "No Sedative Necessary: Scientists Discover New “sleep Node” in the Brain." No Sedative Necessary:
Scientists Discover New "sleep Node" in the Brain. University of Buffalo News Center, 16 Sept. 2014. Web. 19 Oct.
2014.
Levi-Montalcini, Rita, Marco Piccolino, Nicholas J. Wade. “Giuseppe Moruzzi: A tribute to a ‘formidable’ scientist and a
‘formidable’ man.” European Brain Ressearch Institute. (2010). Web. 18. Oct. 2014
Roth, Thomas. “Slow Wave Sleep: Does It Matter?” J Clin Sleep Med. 5.2 (2009): S4-S5. Web. 18 Oct. 2014
Saddichha, Sahoo. “Diagnosis and treatment of chronic insomnia” Ann Indian Acad Neurol. 13.2 (2010): 94-102. Web. 18
Oct. 2014
Volume 15
MEDICAL DIALOGUE REVIEW
27
Robles-Long
From Degeneration to
Regeneration
By Mark Robles-Long
“Although the human brain appears to be this ominous, mysteriously
impossible object (which it undoubtedly is), it is nothing without its
equally divine counterpart in the central nervous system–
the spinal cord.”
An Introduction to Multiple
Sclerosis
The central nervous
system earns its name as the
core headquarters of the human body, regulating everything from voluntary movement of your eyes down the
width and length of this paper
to the involuntary retinal processing of these objects in the
thalamus and primary visual
cortex. It enables us as humans
to have the evolutionarily advanced ability to sense one
thing, visually, and then perceive it as much more than just
what it appears to be: seeing a
white object in the sky while
feeling a chilling sensation on
our noses and hands may induce nostalgia, reminiscence,
recollection of a past event in
our life and followed perhaps
by a discrete smile or laugh.
This is how we create our reality, through perception and
interpretation of the physical
world rather than simple sensation. Oftentimes, we create a
reality in which we feel invincible for we can conjure up profound, ethereal ideas. Although
28
the human brain appears to
be this ominous, mysteriously
impossible object (which it
undoubtedly is), it is nothing
without its equally divine counterpart in the central nervous
system–the spinal cord. It is
no breaking news the brain and
spinal cord communicate: receiving, processing, and sending signals that alert us of environmental cues, warnings or
rewards, and our own internal
disruptions. In fact, if it were
not for signaling at the microscopic, synaptic level, we would
not walk, sense the world, or
even breathe. Without axonaldendritic communication, that
is, the signaling of neuronal
cells that comprise the nervous system, we would not be
alive. Thus, rationally speaking,
neurodegenerative
diseases,
those that degrade these crucial neurons, cannot simply
be cured by a few therapy sessions, monthly prescriptions,
and hope; but rather, they necessitate a much more in depth
remedial process, one perhaps
characterized by rehabilitating the entire nervous system.
Neurodegenerative disease af-
MEDICAL DIALOGUE REVIEW
Fall 2014
ter all is a matter of life and
death...or so it appears. One
such disease is only a matter
of life and death in rare cases.
Multiple sclerosis makes it excruciatingly clear that neurodegenerative diseases are not explainable through a three-word
ultimatum–“life or death”.
Rather, MS expounds itself as
an autoimmune disease, akin
to a virus in that it destroys its
host’s human qualities such as
extremity comfort, articulation, sense of collectivity with
others, and a peace of mind
all without quite destroying its
host.
About the Disease
Multiple
sclerosis
translates to “many scars”.
These scars refer to lesions in
the brain comprising a path of
destruction created by the selfinflicting immune system as it
devours and degrades the myelin lining of axons, necessary
“insulation” of all axons that
allows saltatory conduction
of action potentials.1 Without
myelin, action potentials would
not propagate sufficiently
Robles-Long
down an axon, resulting in a
loss of signal. These lost signals could vary between not
feeling a prick of the finger
to developing problems with
simple or complex cognitive
processes. In this case, autoimmune reactions against myelin
are induced by inflammatory
cytokines, proteins involved in
signaling and thus stimulation
of T cell proliferation and differentiation.6 Proliferation and
differentiation of T cells are
typically beneficial and necessary aspects of a healthy, normal immune system. These
cells are involved in maintaining our well-being by engulfing bacteriophages that would
otherwise cause sickness. However, these processes are utterly
detrimental to humans plagued
with MS. These T cells attack
myelin sheaths and the oligodendrocytes, cells responsible
for myelination, thereby exposing delicate axons, which are
then damaged in the degenerative process.1 It only seems reasonable to find a solution using
one’s gut intuition: stop the cytokines. Inhibiting the true primary source of demyelination,
the cytokines, may seem like
a plausible and obvious solution; however, doing so would
decrease the proliferation of
T cells altogether. This would
perhaps result in a decrease of
demyelination, but more definitely a decrease in the formidability of the immune system,
leaving the patient vulnerable
and prone to disease. This approach is clearly ineffective
seeing as the patients are seeking an escape from an incapacitating disease rather than
a potential introduction to a
plethora of new ones.
Effects and Symptoms
MS entails an unmatched stock of its own sustained illnesses, ranging from
physical disability to cognitive
impairment. Trigeminal neuralgia is just one neuropathic pain
that accompanies multiple sclerosis. It affects the 5th cranial
nerve, the trigeminal nerve, as
a result of demyelination.7 This
particular nerve branches three
ways throughout the face, encompassing chin to forehead,
spanning countless amounts
of nerves. This neuralgia is described as both physically and
mentally incapacitating. To the
likeness of a toothache and
presumably a migraine, a bilateral effect can occur. This is
a combination of the extreme
and episodic pains of Type 1
and the atypical, persistent aching and burning sensations of
Type 2.7 This type of pain is
one of extreme magnitude, and
although not all pains caused
by MS are of the same scale,
the disease knows no limits and
grips nearly every facet of the
human body, even extending
into the human psyche.
According the National Multiple Sclerosis Society, MS affects virtually every
sensory system. Vision malfunction is oftentimes a very
first sign of MS. From temporary blurs to pain, seeing double to having trouble deciphering contrast,5 MS affects the
nerves and signaling involved
in sensing the world. Damage to nerves implies irregular
Volume 15
muscle function as well. This is
seen in the difficulties had with
speaking, swallowing, and even
breathing wherein MS patients
may articulate poorly or slur
their speech and have trouble
breathing as a result of nerves
that control chest muscles being damaged.5 As for extremity discomforts, damage to the
myelin sheath results in muscle
weakness (i.e. numbness), pain
and complications with preserving balance and hand-eye
coordination.5 In terms of
bladder and bowel function,
80% of MS patients struggle
with constipation, diarrhea, or
loss of bowel control.5 Additionally, damage to nerves may
lead to kidney or urinary tract
infections. While the reproductive and circulatory systems
are only rarely or not directly
affected at all, certain components are nonetheless affected,
invoking difficulties in experiencing orgasm/arousal or administering sufficient oxygen
to the brain.5 This insufficiency
is associated with the inability
to breathe deeply due to weak
chest muscles and therefore
prompts cardiac problems and
stroke.5
As is the case with
most diseases, while the physical body is barraged with symptoms and begins to gradually
decline in wellness, the emotional state follows in shadow
of it, becoming darker with
each new slope. Oftentimes,
patients with MS experience
depression or low-self esteem
as a result of their disabilities,
particularly sexual and/or hygienic. When we look toward
the child/adolescent popula-
MEDICAL DIALOGUE REVIEW
29
Robles-Long
tion of MS patients, there is
an increase in effects already
stated as well as on academic
performance and relationships
with either family or classmates.5 Having experienced
pre-teen years and the conventional rocky adolescent blossoming like the majority of
young adults, it is no surprise
younger MS patients may experience a phase of self-image
discontentment magnified tenfold.
Susceptibility and Risk Variability
Studying
children
typically provides insight to researchers as they seek to answer
questions pertinent to their
study; in the case of MS, these
questions are intricate and
abundant, probing deeply into
the core cause and early detection of neurodegeneration.
As we have seen already, neurodegenerative diseases know
no limits when it comes to the
human body or the human
soul; however, it is also true it
knows no age limits, targeting
children due to their immature
immune and nervous systems.
MS is thought to be a disease
dependent on demographics
such as age, gender, ethnicity,
and geography, rather than genetics like most other autoimmune diseases though genetics
does have its role in inferring
how MS comes about.8 While
Relapse-Remitting
Multiple
Sclerosis (RRMS) diagnosis
occurs between 20’s and 30’s,
this particular type of MS can
occur in childhood.5 Diagnosis
of children is even more prob30
lematic than diagnosing adults,
however, due to the ubiquitous irregularities associated
with childhood having similar
symptoms as MS (i.e. puberty,
growing pains, etc.). Relapses
of inflammation along with
more brain lesions containing
inflammatory cells characterize
RRMS.5 Children experience
more inflammation and relapse
responses than adults as well as
a slower disease progression,
which may cause a significant
disability accumulation.5 It is
also in this type of the disease
that developmental cognition
such as learning, memory, and
information processing is affected, hence the prevalence
among growing brains of
children. Statistically speaking, 18,000 to 25,000 children
have been diagnosed with MS
or have reported feeling symptoms resembling those of MS.5
Yet how exactly does MS target
the immature, vulnerable systems of children? The answer
is not clearly known. Research
suggests chemical exposure to
a certain environmental trigger
such as a virus during childhood, prior to the age of 15,
may determine risk of MS contraction.4 Since viruses play a
virulent, inflammatory role in
the destruction of myelin as
well as in autoimmune disease
(e.g. human immunodeficiency
virus preceding acquired immune deficiency syndrome), it is
likely a virus is responsible for
the onset of MS. Connecting
dots such as these, however,
does not establish causation; it
is necessary that a longitudinal
study be in practice in order to
help elucidate the mystery of
MEDICAL DIALOGUE REVIEW
Fall 2014
MS triggers.
What more might we
look toward to understand MS
triggers? The onset of MS is
popularly attributed to demographics: prevalent in the Pacific Northwest of the United
States,4 in areas of greater latitudes (regions away from the
equator) around the world,
among women versus men at a
ratio of 2-3:1, and most common among Caucasians of
Northern European descent.8
However, there are correlation conflicts. MS is not prevalent in areas like southernmost
New Zealand, and Norway of
northern Europe though the
two countries are exceedingly
distant from the equator and
Norwegians are Northern Europeans.8 While it is believed inhabitants of equatorial regions
are not susceptible to MS due
to Vitamin D sufficiency and
thus a year-round supported
immune system and protection
against autoimmune disease, it
is more likely geography acts
in hybridization with ethnicity
and other demographic variables8 to explain MS prevalence
around the world. Migration,
for example, show trends of
immigrants and their descendants taking on either higher
or lower risks of MS development depending on the area
to which they move.8 Childhood prevalence is exemplified further in these migratory
trends where if migration occurs early in childhood results
in immigrants taking on the
geographic-dependent chance
themselves whereas if it occurs
later in the life of an individual,
the risk factor is passed
Robles-Long
down to the next generation.8
As for the asymmetry between
men and women with MS, it is
supposed hormones may play
a role in the risk factor.8 Demographic trends even coincide with the genetic influence.
While an average American has
a 1% chance of disease development, a first-degree relative
to someone with MS, such as
a child or sibling, has an increased 2.5-5% chance.8 This
perchance is due to the likelihood of the environment in
which the family lives containing chemical triggers. One case
of reverse causation suggests
that a person may be born with
a genetic predisposition, such
as a weak immune system or
otherwise endangering trait,
that essentially makes him or
her a susceptible, vulnerable
target to MS development.8
who do not have MS as so.
Thus more people are diagnosed than actually have the
disease. This is not necessarily
a terrible situation. Relative to
the other option of diagnosing
fewer people than actually have
MS, this excessive diagnostic
technique is the safer option.
Though professionals know
what types of lesions demonstrate MS affliction such as
those of the corpus callosum,
to name one, other similar but
unrelated white matter lesions
may distort their view.13 Aside
from lesion congestion in MRI
scans, overlapping symptoms
of unrelated disease or disorders further convolute patient
examinations. This is particularly true, as stated earlier, for
children and teens experiencing drastic physical and emotional changes.5
Problematic Diagnoses
Stem Cell Therapy–A Potential Treatment
While deducing and
speculating the causes and triggers of MS seems a mess of
intermingled strings, connecting some things but not others, the actual diagnosis of MS
is even hazier. MRI scans display the residual “scars” of the
immune-mediated destruction,
the white brain matter lesions
indicative of MS whose degree
of spread and circulation aid in
professionals diagnostics. What
makes MRI a helpful yet inadequate method of detection
is its inability to detect lesions
necessarily caused by MS. The increase in sensitivity, diagnosing
people actually having MS correctly, results in a decrease of
specificity, diagnosing people
13
Undoubtedly, multiple sclerosis compromises
human functionality in nearly
every facet of the physical and
emotional body. Infiltration of
the delicate brain cells spells disaster for the misfortunate person living with MS. However,
with the relatively recent advent of stem cell therapy, this
disaster could not only be halted but also reversed with new
advances in oligodendrocyte
understanding. One neurology
department in Greece attempted to completely eradicate the
immune-mediated
reactive
cells via rabbit-derived antibodies against human T cells
(ATG–antithymocyte globulin)
Volume 15
and install a new immune system derived from an allogeneic
donor.2 The method used was
HSCT (hematopoietic stem
cell transplantation) in an autologous setting, where stem
cells from the patient’s peripheral blood were transplanted
into an MS patient, mobilized,
and their feasibility as appropriate MS treatment and toxicity assessed. The experimenters
utilized an autologous setting
rather than allogeneic due to
the potential GVHD (graftversus-host disease) problem,
where the donor cells attack a
new host. According to previous reports, autologous procedures involving BMT (bone
marrow transplant) resulted in
short and occasional long remissions; that is, malignancies
disappear temporarily. Thus
autologous HSCT was the safer alternative.
The transplantation
was performed in 15 patients,
8 male, 7 female, all in the
progressive phase of MS with
characteristic
abnormalities
on MRI scans, and only with
ineffective past therapy. Upon
mobilization, experimenters
closely observed the nervous
system to monitor toxicities,
intensification of either preexisting symptoms of MS or new
ones brought about as a result
of the transplantation. In order
to evaluate the wellbeing of the
subjects, two tests were used,
assessing impairments of daily
activities or overall improvement of disabilities. What
these experimenters found was
that aside from episodes of infection due to unrelated bacteria, no neurotoxicity or deaths
MEDICAL DIALOGUE REVIEW
31
Robles-Long
were noted, nor were any adverse effects lasting longer than
1-2 days and being more than
mild in their effects. There
were several cases of aggravation and allergic reactions due
to the transplant of both ATG
and stem cell infusion; however, no patient had been re-admitted to a medical facility for
a prolonged procedure-related
disorder. Experimenters noted
significant improvement in disability, especially in one patient
who continued to improve 9
and 15 months post-procedure, ranking a 2 on the EDSS
(Expanded Disability Status
Scale where 0 indicates no disability and 10 indicates death)
at 18 months from an original
entry ranking of 5. While worsening did occur on this scale,
no worsening occurred on the
SNRS (Scripps Neurologic
Rate Scale where 100 points
indicates maximum efficiency).
This scale is more reliable, according to researchers, due
to reliance on more than just
walking ability on which EDSS
solely relies. However, two
patients relapsed after having
improved on this scale. One
such relapse can be attributed
to the receipt of a minimal
dose of ATG. We might infer
the original, malignant T cells
still existed, reacting against
myelin and perpetuating MS.
32
Although economic feasibility
and late adverse effects must
be taken into account, these
researchers believe this therapy
can suppress MS progression,
reducing disability, or, in the
best case, totally eradicate the
disease.
One important finding of this experiment was
that MS progression depends
on the circulation of lymphocytes. This disease thrives on
the presence of intact, reactive
T cells as well as the presence
of myelinated axons. While
this study provides a possible
solution to fixing the immunemediated response, it does not
give insight into how damage
may be repaired. Neuroscience
researchers at the University
of California, San Francisco
have recently discovered an effective way to screen potential
therapeutic compounds for the
treatment of MS.3 Micropillar
arrays serve as a pseudoaxonal
substrate upon which myelination by oligodendrocytes can
occur. The real question is,
however, under what conditions does myelination occur
most efficiently. Upon screening of multiple compounds,
researches came to the conclusion that clemastine, an antihistamine, promotes differentiation of oligodendrocyte
precursor cells into oligoden-
MEDICAL DIALOGUE REVIEW
Fall 2014
drocytes, thereby promoting
remyelination in organisms by
inducing formation of concentric rings about the micropillars. Fortunately, clemastine is
an FDA-approved compound
and therefore reserves pharmaceutical potential.
A Valuable Foe
We, even in 2014, are
unclear about the vast majority of biological functions,
particularly dysfunctions and
malfunctions. Yet this fact does
not detract from the desire to
research and experiment. Multiple sclerosis, though a terrible
disease in some unparalleled
aspects, is more valuable than
it is detrimental. It not only
prompts rigorous study in the
medical field and public awareness, but it is one of the many
diseases that remind us that we
are not invincible. From physical disability to emotional incapacitation, MS usurps power
of the human body. However,
it is unlikely this disease will remain in reign much longer. The
scientific community remains
confident in the progressing interest, concern and subsequent
research in neurodegenerative
diseases, that it may one day
provide a remedy.
Robles-Long
REFERENCES
1: "About MS." National Multiple Sclerosis Society. N.p., n.d. Web. 14 Nov. 2014.
2: Fassas, A., et al. "Peripheral Blood Stem Cell Transplantation in the Treatment of Progressive Multiple Sclerosis: First Results of a Pilot Study." Bone Marrow Transplantation 20.8 (1997): 631-38. Web.
3: Mei, Feng, et al. "Nature Medicine." Micropillar Arrays as a High-throughput Screening Platform for Therapeutics in Multiple Sclero
sis (2013): n. pag. Web.
4: "Pediatric MS Cases Rise in the Northwest." InvestigateWest. N.p., n.d. Web. 14 Nov. 2014.
5: "Pediatric MS." National Multiple Sclerosis Society. N.p., n.d. Web. 14 Nov. 2014.
6: "TH1/TH2 Cytokine Profile in Relapsing-remitting Multiple Sclerosis Patients Treated with Glatiramer Acetate or Natali
zumab." BMC Neurology. N.p., n.d. Web. 14 Nov. 2014.
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Orthognathic Surgery 101
By William Pang
“Orthognathic surgery truly exemplifies the mission of oral & maxillofacial surgery: saving faces, changing lives.”
Orthognathic literally means straight
jaws. This particular type of surgery is unique
within Oral & Maxillofacial Surgery, a dental
specialty. Patients with misaligned bites that cannot be corrected by orthodontics alone are prime
orthognathic candidates. Orthognathic surgery,
or corrective jaw surgery, can be performed to
spatially manipulate the upper jaw(maxilla) and/
or the lower jaw(mandible) in order to improve
harmony between the jaws and the teeth in addition to the considerable enhancement in patients’ quality of life.
The maxillofacial region is comprised
of the face, mouth, tongue, and jaws. Many
deformities occur in this area as a result of heredity and/or environmental factors. The most
prevalent irregularities pertain to the congenital
jaw structure. Jaw discrepancies are largely due
to uneven growth in one or both jaws. This
misalignment of the jaws, or malocclusion, can
impair function and impact the patient’s appearance. Resulting functional problems include difficulty eating, speaking, and breathing properly.
In cases of slight deviation, orthodontics can
be used to treat the problem in its early stages.
However, if the occlusion or bite is deemed
too severe for conservative treatment, plans for
orthognathic surgery begin when the patient is
done growing. Usually growth plates fuse at age
16 for females and at age 20 for males.
Another benefit of orthognathic surgery is the improvement of facial aesthetics;
particularly of the lower third portion of the
face. Facial aesthetic is related to symmetry and
proportions. In regards to the frontal facial view,
a face that is more symmetric when split midsagittally, or into two halves between the eyes,
is universally deemed more attractive. This component also includes the dental midline. Teeth
appear most aesthetic when the maxillary and
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MEDICAL DIALOGUE REVIEW
mandibular midlines match each other.
It is very common for patients with jaw
deformities to exhibit various degrees of asymmetry. A maxillary cant, or a slight tilt in the
Figure 1. Vertical line divides the face into
two halves to assess symmetry.
maxillary occlusal plane, can affect the aesthetics
of the entire jaw. Since the mandible is the only
freely articulating, or moving, bone in the skull,
the maxillary cant is detrimental to the symmetrical development of the mandible. Since the dimensions of soft tissue are strongly correlated
to the underlying skeletal structure, maxillary
cants will often cause a crooked appearance of
the lips. Functionally, this can lead to a host of
problems including Temporal Mandibular Disorder (TMD) and bruxism, or aggressive clenching of teeth. TMD is a painful condition that
is localized at the Temporal Mandibular Joint
(TMJ). Symptoms include aching pain in the
maxillofacial region, jaw stiffness, and clicking
during elevation (opening) and depression (closing) of the mandible. The dysfunction in the jaw
joint is highly detrimental to a patient’s ability
to speak, eat, chew, breathe, and make facial expressions.
The patient featured in figure 2 exhibits a visible maxillary cant with mandible
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Pang
aesthetically favored. Convex profiles are characterized by a softer look, due to weak chin projection. Bart Simpson’s profile, for example, helps
demonstrate this characterization. Lastly, concave profiles display a prominent chin, which
juts anteriorly. A prime example of someone
who exemplifies this type of profile is Jay Leno.
The two major facial bones that oral
Figure 2. Cephalometric analysis.
Facial profile: (A) Convex, (B) Straight,
(C) Concave
Convex Profile - Lines form an angle
pointed away from the face.
Straight Profile - Lines form a straight
line.
Concave Profile - Lines form an angle
pointed towards the face.
Figure 3. Front view of soft tissue.
deviating to the left side. TMD symptoms are
present in the left condylar joint. As seen in figure 3, the soft tissue is reflective of the underlying skeletal discrepancies.
The facial profile is the side view of a
patient’s face. Three main facial landmarks along
with two straight lines are used in the assessment
of the profile. The landmarks include the soft
tissue nasion, subnasale, and soft tissue pogonion. The nasion is the point directly between the
eyes; the subnasale is the point below the base
of the nose; the pogonion is the most anterior
point of the chin. There are two lines that connect from the nasion/subnasal and subnasal/
pogonion segments with the resulting angle being the determinant for facial profile.
In classification, there are three main
facial profile categories: straight, convex, and
concave. A straight profile is aesthetically ideal
and can be characterized as being neither convex nor concave. Males with a straight profile
are considered most attractive. On the other
hand, females with a slightly convex profile are
and maxillofacial surgeons operate on in orthognathic surgery are the maxilla (upper jaw) and
the mandible (lower jaw). Each jaw contains certain unique features that are interconnected with
blood vessels and nerves. The most commonly
damaged nerve is the inferior alveolar nerve
(IAN). This sensitive nerve passes through the
mental foramen in the body of the mandible.
Injury or trauma to the IAN can cause pares-
Figure 4. The inferior alveolar nerve transverses through the mandibular canal.
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thesia or numbness of the lips, chin, and other
surrounding areas immediate to the mandible.
Such disturbances can have both functional and
psychological consequences that decrease quality of life. Careful measures, such as proper retraction and deliberate surgical instrumentation
must be used to protect this nerve during the
more invasive mandibular osteotomy (bone cut)
procedures.
Skeletal Disharmonies
Figure 5. I:Class I Occlusion; II1:Overbite with proclined anterior teeth;
II-2:Overbite with retroclined anterior
teeth; III:Underbite.
is when the mesiobuccal cusp of the upper 1st
molar lies anterior to the mesiobuccal groove of
the lower 1st molar. Typically, the mesiobuccal
cusp sits between the 1st mandibular molar and
2nd premolars. There are two subtypes of this
bite: division 1 and division 2. In division 1, the
anterior teeth are protruded or flared outwards.
In division 2, the anterior teeth are retroclined or
pointed into the mouth. Class II’s are usually accompanied by a weak chin projection and a relatively small mandible. They can be disguised or
even corrected by orthodontics if treatment is
done at a young age. However, for optimal longterm results, orthognathic surgery is usually recommended when the patient is done growing.
Class III: Underbite
Class III (prognathism) is the most
severe of the malocclusions. In this case, the
mesiobuccal cusp of the maxillary 1st molar lies
posteriorly to the mesiobuccal groove of the
mandibular 1st molar. In other words, the lower
teeth sticks out in front of the upper teeth. The
underlying culprit behind a Class III malocclusion is usually a large mandible and/or a short
maxilla.
Classifying occlusions is essential in treatment
planning, as it distinguishes the morphology
of dental and skeletal discrepancies from what
is considered normal. In modern day dentistry,
Angle’s classification of malocclusion is the gold
standard. This system is based on the location of
where the buccal groove of the mandibular 1st
molar makes contact with the mesiobuccal cusp
of the maxillary 1st molar.
Class I
Class I is representative of a normal
occlusion in regards to the maxillary first molar. However, there may be slight issues such as
spacing, crowding, and/or over/under eruption
of teeth. This occlusion is the most prevalent
and can be solely corrected with orthodontic
treatment.
Figure 6. Open bites exhibit a prominent
gap between front teeth.
Apertognathia Open Bite
An open bite is characterized by an
absence of anterior occlusion in addition to the
premature occlusion of posterior teeth. Early
childhood habits such as thumb sucking may
contribute to the formation this bite.
Class II: Overbite
Class II (retrognathism), or overbite,
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Figure 7. Cross bites appear crooked and
have uneven occlusal force.
Cross Bite
A cross bite is the lateral misalignment
of the maxillary and mandibular arches. It may
involve a single tooth or a set of teeth that are
skewed, thus placing tremendous stress on particular areas. This leads to an uneven distribution
of occlusal force and an unaesthetic smile.
Orthodontics
The presurgical phase begins with the
placement braces. The braces used to treat orthognathic patients aim to decompensate the
dentition. Over time, teeth tend to migrate or
compensate to touch their opposing side for
maximum surface area contact. In the case of
an underbite, the maxillary teeth will be proclined or flared out while the mandibular teeth
will be retroclined in order for the top and bottom teeth to meet each other. Proper orientation
of the teeth are pertinent during the final stages
leading to orthognathic surgery. Therefore, the
orthodontist will decompensate the bite, making
the patient’s condition appear even worse until
it is fixed by the surgeon. It may take anywhere
from 6 to 12 months for the patient’s bite to be
ready for surgery.
During the week before surgery, the
orthodontist will place surgical hooks between
the brackets to act as an anchor for the surgeon
to fixate wires onto in order to hold the splint
in place. The splint is a custom made wafer that
guides and stabilizes the patient’s new bite.
Orthodontic treatment continues after surgery
when the bones have been fully healed. This
phase lasts from 3 to 6 months before the braces can be removed, leaving behind an aesthetic
smile and functional bite.
Orthognathic Surgery
Usually, the patient’s General Dentist
will spot out the malocclusion and will refer the
case to an orthodontist. The orthodontist will
then determine if the irregular bite is the result
of a tooth or skeletal problem. More mild cases
such as Class I with crowding/spacing, Class II,
and crossbites, can be conservatively corrected
with dentofacial appliances such as braces or
headgear. Less commonly, severe Class II malocclusions, or overbites, and Class III malocclusions, or underbites, will require correction using orthodontic treatment in conjunction with
orthognathic surgery at the end of the patient’s
growth. Orthodontists will refer orthognathic
cases out to an oral & maxillofacial surgeon.
Oral & maxillofacial surgeons are specialists
who combine their expertise in both dentistry
and medicine to effectively treat patients with
skeletal abnormalities within the maxillofacial
region. Becoming a full-fledged OMFS is a long
and arduous journey with many rewards. College
graduates attend four years of dental school before training in OMFS at a hospital based residency program. There are two residency paths
that may be taken to be board certified: a fouryear certificate program or a six-year combined
MD/certificate program. Lately, there has been
a shift towards dual degree OMFS. With extensive training in anesthesiology, dentistry, ENT,
and plastic/reconstructive surgery, oral & maxillofacial surgeons are uniquely qualified to operate on the jaws.
Imaging
Radiology
Surgeons use imagery to observe the
nuances of the patient’s maxillofacial anatomy.
The position of surrounding structures, such as
the Inferior Alveolar Nerve, to the shape of the
mandible are crucial information that the surgeon will use to determine which surgical procedures will yield optimal functional and aesthetic
results.
CT scanning of the maxillofacial region allows the surgeon to see the skull in floating 3D format.
In a submentovertex radiograph, the
xray beam enters behind the chin and exits at
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Pang
Figure 8. The blue and red regions
highlight the maxilla and the mandible,
respectively.
Dolphin Imaging
Surgeons may use advanced software
to predict the final look of the patient. Skeletal movements of the jaws will lead to drastic
changes in facial appearance, and soft tissue
movement is often difficult to accurately predict
due to factors that include swelling and accumulation of fat tissue. It is expected for patients undergoing orthognathic surgery to look different
from before.
the top of the head as the patient looks up. The
Submentovertex view is used to see the curvature and thickness of the mandible in planning
for lower jaw surgery. For thinner mandibles that
require a setback, the surgeon will perform an
IVRO (intraoral vertical ramus osteotomy). Otherwise, BSSO (bilateral sagittal split osteotomy)
will be performed.
Models
The average time of pre-surgical orthodontics ranges from six to twelve months.
When the teeth are fully decompensated, the
orthodontist will meet with the surgeon to make
models of the patient’s bite. The surgeon will
then conduct a mock surgery on the models and
use CT guided imagery to fabricate an intermediate and final splint. The intermediate splint is
only used in double jaw surgery. It is placed on
the maxillomandibular occlusion immediately
following the first jaw that was operated on. The
final splint is placed at the end of the case to
maintain the occlusion. Depending upon the
procedures used, the splint may or may not be
removed for a set duration of time.
Figure 10. The purple wafer is the intermediate splint used to reposition the first
jaw. The blue wafer is the final splint used
to fixate the second jaw. These splints are
tied to the patient’s surgical hooks as the
jaws are being moved.
Figure 11. The innovation of Dolphin
allows patients to visualize their expected
outcome.
Figure 9. X-ray beam enters the posterior region of the mandible.
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MEDICAL DIALOGUE REVIEW
Procedures
Lefort I Osteotomy
The most commonly used procedure
of the maxilla is the Lefort I osteotomy. A transverse or horizontal bony cut is made in the maxilla until it separates from the skull. The surgeon
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Figure 12. The versatility of the Lefort
I osteotomy in maxillary repositioning
make it the primary option for upper jaw
surgery.
usually down-fractures the maxilla by gently ripping it towards the mandible with a figure-eight
motion. It is a versatile procedure that allows the
surgeon to rotate, advance, push back, and tilt in
varying degrees to give the patient optimal aesthetics and function of bite.
BSSO (Bilateral Sagittal Split Osteotomy)
Figure 13. Rigid fixation of titanium screws and plates are used
to stabilize the mandible during
healing. These metal components
remain in the patient’s face unless
an infection warrants its removal.
Bilateral means two sided, and sagittal refers to
the anatomical plane in which the osteotomy or
bone cut will be made. The tooth-bearing segment is split from the condyle-bearing segment
attached to the skull, akin to sliding open and
closing a drawer. The condyle-bearing segment
is lateral to the tooth-bearing segment. BSSO
may be used to correct Class II and Class III
malocclusions. Its versatility gives the surgeon
the option of advancing forward or pushing
backward the mandible. This flexibility of movement allows the BSSO to correct mandibular
asymmetries with great success.
The disadvantages of using BSSO to
move the mandible lie in the cuts’ close proximity to the IAN. BSSO procedures carry a 9-10%
incidence of permanent numbness. BSSO requires rigid fixation with titanium plates and
screws, which increase the rate of infection
post-op. However, this fixation allows the patient to open their mouths immediately following surgery. They may drink liquids and follow a
soft diet, unlike patients who have undergone an
IVRO.
IVRO (Intraoral Vertical Ramus Split Osteotomy)
Figure 14. The IVRO features an oblique
cut made in the ramus of the mandible,
completely avoiding the IAN. Surgical
hooks facilitate mandibulomaxillary fixation (MMF or wiring of the jaws) during
the healing process.
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Intraoral means inside the oral cavity.
Vertical refers to the anatomical plane through
which the osteotomy is made. In IVRO, the ramus is split down in the coronal or vertical plane.
Since this procedure is done far away from the
IAN, the incidence of permanent numbness
is much lower at 2%, compared to the 9-10%
BSSO. Unlike the BSSO, the jaws must be wired
shut for 6-8 weeks following IVRO due to the
lack of rigid fixation. Instead, the segment containing the mandibular condyle is everted or
flared outwards laterally to allow bony contact
with the mandible. Due to the dependency of
bony contact, the IVRO may only be used in
mandibular setbacks. Therefore, they are only
performed on prognathic patients who exhibit
Class III malocclusion. At least 3 months is required for full bony union following an IVRO. A
patient must take extreme caution and care during this vulnerable time as any trauma to the jaw
will require another operation to correct.
Figure 15. A horizontal cut is made across
the inferior border of the mandible.
Genioplasty
A genioplasty or chin osteotomy may
be done for purely cosmetic reasons. The chin is
a vital component of the face that helps balance
and frame the other features. A small chin may
accentuate the prominence of the nose, whereas,
a large chin may be too overbearing and masculine for female patients. The oral surgeon must
take into account the patient’s race and gender in
the determination of the chin’s final location. In
most cases, the navigation of this fine balancing
act is varied due to the patient’s and surgeon’s
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MEDICAL DIALOGUE REVIEW
Figure 16. Rigid fixation is used to secure
the newly positioned chin.
preference. The best genioplasty are the ones
that leave no indications of surgery and instead
appear natural to the public.
In the case of a Class III malocclusion,
the chin tends to lose its prominence due to
retraction of the mandible. Thus, a small osteotomy can be made at the inferior border of the
mandible to give the patient back his/her chin
projection.
Conclusion
Orthognathic surgery is a common
treatment modality used to correct skeletally
related jaw discrepancies such as overbites, underbites, open bites, and cross bites. Treatment
planning involves close collaboration between
the patient’s orthodontist and oral & maxillofacial surgeon. With the assistance of advanced
imaging, the oral & maxillofacial surgeon will
know which procedures to perform and the degree of movements required in repositioning the
patient’s jaw(s) for the final occlusion.
The orthognathic journey is long and
arduous, but worth it. The majority of orthognathic patients rave about its life changing effects.
Increases in quality of life due to optimal bite
functionality and closer symmetry in facial aesthetics are the two most noted differences that
are made. Gone are the times when their skeletal
disharmonies interfered with their livelihood.
Newly found comfort in smiling, chewing, and
interacting with peers have given patients their
confidence back. Orthognathic surgery truly
exemplifies the mission of oral & maxillofacial
surgery: saving faces, changing lives.
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Pang
REFERENCES
Aofoundation.org/wps/portal/surgery. Ed. Chris Colton, Steve Krikler, Joseph Schatzker, and Peter Trafton. Web.
<https://www2.aofoundation.org/AOFileServerSurgery/MyPortalFiles?FilePath=/Surgery/en/_img/
surgery/05-RedFix/95b/X300-SpecCond-PlanningOrthSurg/95_X300_i260_540.gif>.
"Dolphin Imaging & Management Solutions." Dolphin Imaging & Management Solutions. Web. <http://www.dolphinimaging.
com/3dsurgery.html>.
Gunson, Arnett. "Grafting Materials." Orthognathic Surgery. Web. <http://www.arnettgunson.com/technology/grafting-
materials>.
"Orthognathic Surgery, Education, and Research." Orthognathic Surgery. Web. <http://www.arnettgunson.com/>.
Premkumar, Sridhar. Prep Manual for Undergraduates: Orthodontics. New Delhi: Elsevier, 2008. 163.
ROBINSON, MD, DDS, RANDOLPH C., and REBECCA L. HOLM, RN, MSN, CNOR. "Orthognathic Surgery for Patients with Maxillofacial Deformities." AORN Journal 92.1 (2009): 28-49. Web. <http://isgweb.aorn.org/
ISGWeb/downloads/CEA10053-4017.pdf>.
Volume 15
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Fabbro
NYU’s Police Stress and Health
Program Gains Insight Into
Stressors Police Officers Face
By Rebecca Fabbro
“Can science tell us anything about how urban police departments can
better select and train police officers to make critical decisions, particularly when lives are at stake?”
On a hot August
night, a 28-year-old white police officer named Darren Wilson approached an unarmed
black teenager named Michael
Brown and shot him to death.
We do not know, and may never know, the details of what
transpired that night or exactly
what Darren Wilson was thinking when he pulled the trigger.
But as the impact of the tragedy continues to reverberate
beyond Ferguson, Missouri, it
underscores why it is so important to better understand
the stressors police officers
confront—and what departments can do to equip police
to make difficult decisions under pressure. Can science tell
us anything about how urban
police departments can better
select and train police officers
to make critical decisions, particularly when lives are at stake?
For the past eight
years, research into the unique
psychological and physiological
stressors police officers face—
as well as the protective factors
that equip some officers to
show resilience under stress—
has been taking place just a few
blocks northeast of NYU’s
main campus at NYU Langone
42
Medical Center (NYULMC).
Under the leadership of Lucius N. Littauer Professor Dr.
Charles R. Marmar, who also
serves as chair of NYLMC’s
department of psychiatry,
NYU’s Police Stress & Health
Program has been working in
collaboration with researchers
at the University of California, San Francisco to answer
four primary questions: what
are the unique stressors faced
by law enforcement professionals; what are the positive
and negative ways that officers
cope with duty-related stress;
is there a way to develop tools
to maximize the emotional
and physical health of police
officers; and is there a way to
test for genetic markers that
may indicate vulnerability to—
or resilience to—developing
stress-related disorders (Police
Stress & Health Program). Dr.
Marmar brings to this work a
quarter century of experience
in research on trauma and
PTSD with Vietnam and Iraq
War veterans, fire departments,
and disaster relief teams—including research on the prevalence of PTSD in 9/11 first responders. Like soldiers, Police
officers must maintain high
MEDICAL DIALOGUE REVIEW
Fall 2014
performance even in the face
of distressing events, making
them an especially important
group in which to understand
risk and resilience to stress-related disorders. This article will
focus on two of the center’s
many findings and will discuss
their implications for law enforcement personnel selection
and training.
Police Officers Face Particular Stressors
For the average student, taking final exams may
seem extraordinarily stressful,
but serving as a police officer
is without a doubt one of our
country’s most stressful occupations. Within their first year
on the job, New York’s new
police recruits are exposed to
potentially traumatic events,
and it’s no secret that an officer’s job description entails
the use of lethal force. In fact,
Weiss et al. found that a quarter of police officers reported
having to kill or seriously injure
someone during the course of
their careers (2010). Until the
past few years, little research
had been done on how this use
of force affected police office-
Fabbro
rs psychologically. Studies of
Iraq War veterans who have
killed in combat, however,
have found that an individual’s
prior use of deadly force can
increase his or her risk of developing some of the more
serious forms of PTSD (Maguen, 2014). In addition to
these risks, police officers on
active duty also face potential
threats to their own lives. The
prevalence of these stressors,
combined with a myriad of
others, takes a severe toll on
law enforcement professionals’ mental health. Between 7
to 15 percent of police officers develop duty-related Posttraumatic Stress Disorder over
the course of their lifetimes
with more showing symptoms
of pre-PTSD, compared to an
estimated 6.8 percent of individuals in the general population (Maia et. al, 2007; Kessler).
While a small percentage of
police exposed to critical incidents go on to develop PTSD,
the condition has serious repercussions; PTSD is correlated with increased likelihood
of divorce, inability to perform
job duties, lifetime suicidal ideation and other major impairments in life function (Maia et
al., 2007). To maximize the effectiveness of the police force,
therefore, it is critical that officials develop a better understanding of the factors that
protect recruits from stress-related mental health conditions.
Certain psychological factors predispose police officers to developing PTSD after critical incidents; others
appear to be protective
To help understand
which factors might predispose officers to developing
stress-related mental health
disorders--as well as which
factors promote resilience Dr.
Charles Marmar and colleagues
conducted one of the first longitudinal studies of police. The
research team followed 400
police officers in four cities—
New York, Oakland, San Francisco and San Jose—during
and after their academy training—and examined several factors (2010). One group, led by
Chengmei Yuan at the University of California, San Francisco assessed a subgroup of 233
officers to determine which
factors might promote resilience: the ability to “bounce
back from negative emotional
experiences and by flexible
adaptation to the changing demands of stressful experiences” (Tugade and Fredrickson,
2004). These are also known
as protective factors. Previous studies of protective factors in other subgroups have
found that certain personality
attributes, social networks and
skills, basic attitudes of an individual toward him/herself and
the world, and specific coping
skills can all be protective factors that promote resilience.
The research team set out to
see which, if any, of these factors demonstrated a protective
effect against stress in police.
Officers were assessed using the NEO FiveFactor Inventory to measure
five factors of personality: neuroticism, extraversion, openness, agreeableness and conscientiousness. They were also
Volume 15
assessed on the World Assumptions Scale, a 32-self-reported
questionnaire designed to assess an individual’s assumptions about his/her self-worth,
the benevolence of the world
and the meaningfulness of the
world (Yuan). Finally, officers
completed two measures of
social support and functioning:
The Sources of Social Support
Scale (SOS), a 10-item test to
measure social support previously used in the National
Vietnam Veterans Readjustment Study; and The Social
Adjustment Scale-Self Report
(SAS-SR), a measure of social
functioning. Two years later,
the team assessed the same officers for symptoms of PTSD
using the Civilian Mississippi
Scale, a revised version of the
Mississippi Scale for Combat
Related PTSD, designed to capture associated traits of PTSD
as specified by the DSM-III by
asking officers to rate how often they had thoughts such as,
“I have nightmares of experiences that happened during
my police service.” Officers
were also asked about their exposure to critical or traumatic
incidents during the past two
years, such as using lethal force
of witnessing a death during
duty.
After controlling for
demographic factors (a smaller
percentage of Caucasian police
officers, for example, go on to
develop PTSD than do officers of color), the researchers
determined several factors that
appeared to be promote resilience in all officers. Surprisingly, differences in personality
traits were not significantly co-
MEDICAL DIALOGUE REVIEW
43
Fabbro
rrelated with officers’ abilities
to cope. Other results were
less surprising. Officers with
lower exposure to “critical incidents” during duty, such as
having their life threatened,
watching someone die, or being involved in a car accident,
were predictably at less risk of
developing PTSD. But of the
officers exposed to traumatic
experiences, the two traits that
appeared especially protective
against stress-related disorders
were “greater assumptions of
benevolence in the world” and
“better social adjustment during training” (Yuan).
While these traits
promoted resilience, others
placed officers at greater risk
of developing PTSD and other
stress-related mental health
disorders. Another study associated with the longitudinal
study revealed several traits
that significantly increased the
likelihood that officers would
develop PTSD following a critical incident. The subgroups
most likely to develop PTSD
included: police officers with a
history of childhood trauma, a
family history of anxiety, a lack
of social support, a history of
mood disorders, or a history of
substance abuse (Johnson).
While these studies are some of the first into
which factors may increase the
risk of stress-related disorders
or promote resilience in police
officers, a few preliminary recommendations for police departments can be drawn. First,
police academies may be able
to better prepare officers from
stress by adding instruction to
help officers adjust socially dur44
ing training as well as to adopt
assumptions of benevolence;
previous studies have demonstrated that both traits are
malleable, given the right conditions (Yuan). Second, an assessment of whether or not an
officer candidate displays protective factors against or risk
factors for developing PTSD
could be conducted as additional criteria for place officers
in best fit roles. A person with
more protective factors against
developing PTSD might be a
better fit for a stressful active
duty post than someone without those protective traits.
One particular trauma that the researchers paid
special attention to is how killing and injuring others in the
line of duty affected police officers’ health. Komarovskaya et
al. assessed 400 police officers
of New York during academy
training, and again five times
during their first three years of
service (2011). During those
initial years, nearly 10 percent
of officers self-reported that
they had to kill or seriously
injure someone in the line of
duty and more than two thirds
of officers reported that they
had experienced at least one
event in which they felt a direct
threat to their own lives. After
36 months of duty, researchers
assessed officers’ mental health
symptoms using the Beck Depression Inventory-2nd edition to measure symptoms of
depression and the Mississippi
Combat Scale-Civilian Version for symptoms of PTSD.
They also conducted two tests
to measure levels of social adjustment and alcohol abuse.
MEDICAL DIALOGUE REVIEW
Fall 2014
Komarovskaya and colleagues
found that injuring or killing
another person in the line of
duty, while only marginally associated with depression symptoms, was significantly associated with developing PTSD (p
< .01). These results were the
first to highlight the severity
of the mental health impact
of killing or seriously injuring
someone in the line of duty.
Hopefully one result of the
study will be to draw greater
mental health services to officers following exposures.
Physiological risk factors
While mental health
conditions have long been
viewed as conditions of the
mind that do not manifest in
physical symptoms, we now
know that there are several
physiological signs of stress.
Dr. Marmar and his team have
recently focused on documenting physiological symptoms
of stress and studying their
connection to mental health
diseases in police. To do so,
Pole and others tested to see
how quickly officers in training would startle—and then
reassessed officers following
one year of duty (Pole et al.).
All participants were brought
into the laboratory and shown
videos of real-life, dangerous
police situations. Following
the viewing, several physiological reactions were measured,
including an individual’s tendency to blink, a person’s heart
rate, and changes in salivary
3-methoxy-4-hydroxyphenylglycol (MHPG) and cortisol
from the baseline, after contro-
Fabbro
lling for demographic factor.
At the start of the
study, none of the initial group
of 400 officers had a significant chronic axis 1 psychiatric disorder. During the years
covered by the study, the initial
recruits experienced several
critical events: subjects had an
average of seven potentially
traumatic incidents including
encountering a dead or dying
body (nearly 9 in 10 officers),
witnessing another officer’s
injury or death (more than 1
in 5), being seriously injured
(more than 1 in 10) and having
to shoot to kill. The research
team found that officers who
startled most easily during
training were more likely to develop PTSD, after controlling
for the number of incidences
they had encountered and for
other demographic factors.
The most profound
effect was seen in officer candidates who had been exposed to
trauma in childhood. Twentyfive percent of new police recruits had experienced trauma
prior to the age of 13, from
exposure to violence, abuse or
accident. While this rate was
similar to that measured in the
general population, the study
observed that recruits who
reported a history of trauma
in childhood showed initial
changes in psychological and
biological reactivity compared
to their peers, including a tendency to startle more quickly
when exposed to videos of
dangerous police situations,
that were predictive of developing PTSD 4 years later.
At the start of the study, new
recruits who had experienced
early childhood trauma already
showed upregulated endocrine
responses to the videos of
police trauma (including sustained 3-methoxy-4-hydroxyphenylglycol reactions and
elevations of salivary catecholamine). They were also more
likely to demonstrate a startle
response to sound in the form
of blinking eyes or increased
heart rate compared to officers who had not experienced
childhood trauma, even though
neither group had a measurable
psychiatric illness. When assessed four years later, the officers who had been exposed to
childhood trauma were more
likely to show a greater reactivity (as measured by adrenergic
and glucocorticoid reactivity)
to real-life trauma while on
duty. According to Johnson,
“Officers who followed trajectories of resilience and recovery over 4 years mounted
significant increases in cortisol
in response to the experimental
stressor, while those following
a trajectory of chronic increasing distress had no significant
cortisol change in response to
the challenge.” The team concluded that a “blunted cortisol
response to a laboratory stressor is a risk factor for later vulnerability to distress following
significant life stressors. This
is another trait that could be
measured by police academies
when determining where to
place officer candidates.
Some mental health
professionals have expressed
Volume 15
concern that data on which
factors predispose officers to
developing PTSD could be
used to “screen out” potential
officers from active duty. Associate Director of Clinical
Training at the University of
Pennsylvania's Department of
Psychology, Melissa Hunt, in
Philadelphia, expressed concern that, “ultimately, this kind
of research will be used for
screening people out of certain
professions: 'That kid shouldn't
be a Green Beret, maybe this
one shouldn't be a police officer’” (Johnson). However, Dr.
Marmar maintains that the aim
of the program is not to weed
out officers, but to provide
them with better training and
placement. As he explained the
aims at a conference for Anxiety Disorders of America in
2012, “I think the view is that
this kind of information could
be used not to exclude people
from service, but to provide
resilience-building
training
and/or triage people into different roles” (Johnson). At the
moment, the research continues, as officers continue to be
assessed later in their careers to
see if trends established during
their time in the academy and
several years out continue to
hold. The hope is that a better
understanding of the stressors officers face—as well as
the genetic, physiological and
psychological factors that allow them to be resilient despite
stress, will lead to healthier and
effective police departments
for our urban areas.
MEDICAL DIALOGUE REVIEW
45
Fabbro
REFERENCES
Brunet, A., Weiss, D., Metzler, T., Best, S., Neylan, T., Rogers, C., Fagan, J. & Marmar, C. The Peritraumatic Distress Inven
tory: a proposed measure of PTSD Criterion A2. Am J Psychiatry 2001; 158(9), 1480-5.
Galatzer-Levy, Isaac R. et al. Cortisol response to an experimental stress paradigm prospectively predicts long-term distress
and resilience trajectories in response to active police service. (2014). Psychiatric Research, 56(September 2014),
36-42. Retrieved November 18, 2014, from http://www.journalofpsychiatricresearch.com/article/S00223956(14)00133-2/abstract?showall=true=
Johnson, K. (2012, April 17). Childhood Trauma 'Profound' Predictor of PTSD. Retrieved November 18, 2014, from
http://www.medscape.com/viewarticle/762166
Kessler, R.C., Berglund, P., Delmer, O., Jin, R., Merikangas, K.R., & Walters, E.E. (2005). Lifetime prevalence and age-of
onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Archives of General
Psychiatry, 62(6): 593-602.
Komarovskaya I., Maguen S., McCaslin S. E., Metzler T. J., Madan A., Brown A. D., Galatzer-Levy I. R., Henn-Haase C.,
Marmar C. R. (2011).The impact of killing and injuring others on mental health symptoms among police of
ficers. Journal of Psychiatric Research, 45(10), 1332-1336. doi: 10.1016/j.jpsychires.2011.05.004
Maguen, S., Madden, E., Bosch, J., & Galatzer-Levy, I. (2013). Killing and latent classes of PTSD symptoms in Iraq and
Afghanistan veterans. Journal of Effective Disorders, 145(3), 344-348. Retrieved November 18, 2014, from
http://www.sciencedirect.com/science/article/pii/S0165032712005903
Maguen, S., Metzler, T.J., McCaslin, S.E., Inslicht, S., Henn-Haase, C., Neylan, T.C., & Marmar, C.R. (In press). Routine
Work Environment Stress and PTSD Symptoms in Police Officers. Journal of Nervous and Mental Disease.
1480-5.
Maia, D.B., Marmar, C.R., Metzler, T., Nobrega, A., Berger, W., Mendlowicz, M.V., Coutinho, E.S., Figueira, I., 2007. Post
traumatic stress symptoms in an elite unit of Brazilian police officers: prevalence and impact on psychosocial
functioning and on physical and mental health. Journal of Affective Disorders 97, 241–245.
Pole, N., Neylan, T., Best, S., Orr, S., & Marmar, C. Fear-potentiated startle and posttraumatic stress symptoms in urban
police officers. Journal of Traumatic Stress 2003; 16(5), 471-479.
Police Stress & Health Program. (n.d.). Retrieved November 18, 2014, from http://policestressandhealth.med.nyu.edu/
Tugade, M.M., Fredrickson, B.L., 2004. Resilient individuals use positive emotions to bounce back from negative emotional
experiences. Journal of Personality and Social Psychology 86, 320–333.
Weiss DS, Brunet A, Best SR, Metzler TJ, Liberman A, Pole N, et al. Frequency and severity approaches to indexing expo
sure to trauma: the critical incident history questionnaire for police officers. Journal of Traumatic Stress
2010;23: 734-43.
Yuan, C., Wang, Z., Inslicht, S.S., McCaslin, S.E., Metzler, T.J., Henn-Haase, C., Apfel, B.A., Tong, H., Neylan, T.C., Fang,
Y., & Marmar, C.R. (2010). Protective factors for posttraumatic stress disorder symptoms in a prospective study
of police officers. Psychiatry Research, 188(1), 45-50.
46
MEDICAL DIALOGUE REVIEW
Fall 2014
Popkova
The Ebola Epidemic and its
Fallout in West Africa
By Alina Popkova
“As of August 2014, only about 2200 medical staff were sent…by Doctors Without Borders, the World Health Organization, and the Center
for Disease Control and Prevention to work with local medical practitioners… this number is far from enough for the nearly 203 million
people who live in these countries and therefore some
Ebola patients go untreated.”
For the first time since its recognition as a virus more than 40 years ago, Ebola
has been confirmed in multiple countries. The
fear of contamination has increased coverage of
Ebola and has had a surging effect on its international response in West Africa from health agencies such as Doctors Without Borders. While
these efforts have had some successes, many of
the people in West Africa continue to die from
Ebola and the spread of the virus is nowhere
near diminishing.
It is believed that the Ebola virus first
spread from animals that were infected by contagious bats nearly 40 years ago and has been able
to infect humans by using a specific biomedical
Figure 1.
mechanism. In 2008, the researchers at the University of Texas Medical Branch at Galveston
were able to determine this mechanism. They
found that upon entering the body, the virus infects a host cell by activating the phophoinositide-3 kinase pathway on the cell membrane
which makes the cell draw in the virus in an endosome capsule. Once the virus is inside the cell,
it can replicate and then burst through at an appropriate time to infect others. Current research
focuses on developing an antibiotic against Ebola by blocking this PI3 kinase pathway so that
the virus becomes trapped inside its capsule and
cannot escape to replicate. However, there has
been little success in this endeavor.
One such treatment to stop the virus
once a patient is infected is ZMappTM. which is
currently being developed by Mapp Biopharmaceutical Inc. The drug, which was first identified
as a candidate against Ebola in January 2014, is
a combination of three monoclonal antibodies
that are grown by inserting the genes for the
antibodies into a DNA vector and developing
the DNA in the Nicotiana benthamiana plant. It
is believed that Zmapp works by binding to the
Ebola virus and stopping it from continuing
its infection of the patient. However, since the
drug is fairly new, not enough trials have been
run to know whether or not it is effective against
Ebola. Furthermore, only a small amount of the
drug had been manufactured and is available for
use on patients in West Africa so other methods
are used to prevent the spread of the virus.
Organizations such as Doctors Without Borders, the World Health Organization and
the United Nations have built up an international response in the form of doctors, medical
supplies and donations to West Africa to stop
Ebola’s spread in West Africa. Trained doctors
Volume 15
MEDICAL DIALOGUE REVIEW
47
Popkova
go on missions and visit villages in the West African countries affected by the Ebola outbreak
to isolate and treat the patients. They visit the
people who are suspected of having Ebola and
look for the symptoms associated with the disease such as severe hemorrhagic fever, muscle
pain, weakness, and vomiting which can show
up anywhere from 2 to 12 days after a patient
becomes infected. The patients then have to be
taken from their villages to specialized Ebola
hospitals where they are treated.
At the Ebola hospitals, the patients are
diagnosed using an array of tests such as the
ELISA, polymerase chain reaction or virus isolation method which can show if the virus is pres-
Figure 2.
ent in a blood sample belonging to the patient.
Once it is established that a patient does indeed
have Ebola, he or she is isolated and cared for
until the disease goes away. The doctors give
patients intravenous fluids, balance their electrolytes levels, maintain oxygen and blood pressure levels and cure them of any infections they
may have besides Ebola, since the symptoms of
other infections will have a cumulatively worse
effect on the patient’s health and chances of survival. Once the symptoms subside, the patients
are tested for antibodies against the Ebola virus
and if they do have them, then they are cured of
the virus and are returned home. The patients
are given a certificate proving that they are cured
so that the villagers will be more acceptable of
them and more likely to welcome them back.
Although this is how the procedure
used for containing Ebola is structured, in real
48
MEDICAL DIALOGUE REVIEW
life the response effort has had many setbacks.
Most of the organizations such as Doctors
Without Borders and the World Health Organization keep every doctor’s mission to West
Africa short, lasting only 6 to 8 weeks. This is
because the doctors can become fatigued, which
would not help the effort to fight the outbreak,
and there are not enough doctors to replace
those that return. As of August 2014, only
about 2200 medical staff were sent to regions
of Guinea, Sierra Leone, Liberia and Nigeria by
Doctors Without Borders, the World Health Organization, and the Center for Disease Control
and Prevention to work with local medical practitioners there. This number is far from enough
to for the nearly 203 million people who live in
these countries and therefore some Ebola patients go untreated.
Along with a limited amount of doctors willing to go, there is also a limit in the number of hospitals and supplies available to accommodate Ebola patients. According to the World
Health Organization, there are only 14 hospitals
and Ebola treatment centers available in Sierra
Leone, Liberia and Guinea, which is not enough
to account for the people living in the outbreak
regions. Ebola patients are being turned away
once hospitals become overcrowded. This again
leads to some Ebola patients who are missed by
the medical staff and go untreated. As for the
patients who are received by the hospitals, there
is not enough food and water available because
of the limited donations. This means that not
every patient in the hospital receives the care that
is necessary for full recovery from Ebola. The
cases where not enough medical staff, hospitals
or supplies are available to the Ebola patients
shows a major fault in the international healthcare and disease response system in its ability to
organize an effective response to an infection as
deadly as Ebola, for which the survival rate is
approximately 50%, according to the WHO.
Along with the setbacks in the international response to Ebola, there have been setbacks with gaining the trust and cooperation of
the people living in West Africa. Many of the
people do not understand the dangers of the
Ebola virus and the safety measures that should
be taken to prevent its spread. For example,
Fall 2014
Popkova
Figure 3.
some of the Ebola patients lie and say they do
not know others who are infected in order to
protect them. Although the Ebola patients have
a valid cause for this since as mentioned previously, the hospital conditions are very rough and
difficult to live in, the Ebola hospitals are also
the best possibility many of the people infected
with Ebola have for making a recovery.
Yet another example is that the villagers of West Africa are also not aware that their
daily routines can further spread Ebola. For example, the death burial rituals of many villages
require that the body be washed before burial
but this can spread the virus to living people.
The Ebola virus spreads from person to person
through contact with bodily fluids such as urine,
saliva or sweat or through contaminated objects
such as syringes. Here the health organizations
such as Doctors Without Borders can offer a
solution by increasing awareness of how the disease spreads and how to avoid infection.
This shows that the health organizations are able to isolate and treat present Ebola
patients and prevent new ones by informing the
people living in outbreak areas of ways they can
limit the infection spread. But this can only happen if they have the resources necessary to fund
their missions in West Africa. As of October
12, 2014, there have been 8,997 cases of Ebola
in West Africa and 4,493 reported deaths. This
is largely due to the lack of resources available
from the governments to provide the necessary
aid to the affected communities. This is where
government funds and private grants and loans
come into play to provide fiscal aid, such as
those just approved by the World Bank Group.
On September 16, 2014, the World
Bank Group approved the United States to provide $105 million for the Ebola containment effort in Sierra Leone, Liberia and Guinea. These
countries have been hit heaviest by the Ebola
outbreak and have no medical infrastructure to
fight the disease. For this reason, most of the
donations are expected to go towards funding
for an Outbreak Response Plans and towards
obtaining enough international workers to carry
out the health services.
Without aid, there were only 50 doctors available in Liberia alone to respond to
the beginning of the Ebola outbreak back in
March 2014. Liberia has been most affected by
the Ebola virus and shows just how insufficient
Figure 4.
the sources for aid to West Africa were. Since
March, international health organizations continue to send what resources they have, whether
it is workers, donations or medical supplies, to
West Africa in an effort to contain the outbreak.
As of now, it is clear that the Ebola outbreak is
nowhere near diminishing and a new approach
is needed towards containing and treating the
virus. At the end of this year, relief funds are
beginning to be sent to West Africa in an effort
to contain and treat patients who have Ebola.
Furthermore, there is now a push towards increasing the production and testing of the drug
ZMappTM so that it will hopefully become
available to patients in West Africa as another
resource. However, these efforts are new and it
is still unclear whether they will have a lasting
effect and end Ebola.
Volume 15
MEDICAL DIALOGUE REVIEW
49
Popkova
REFERENCES
"Africa." Ebola: Economic Impact Could Be Devastating. “http://www.worldbank.org/en/region/afr/publication/ebolaeconomic-analysis-ebola-long-term-economic-impact-could-be-devastating”
Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 16 Oct. 2014. “http://www.cdc.gov/
vhf/ebola/”
Ebola:World Bank Group Approves US$105 Million Grant for Faster Epidemic Containment in Guinea, Liberia, and Sierra Leone. “http://www.worldbank.org/en/news/press-release/2014/09/16/ebola-world-bank-group-approves-
grant-faster-epidemic-containment-guinea-liberia-sierra-leone”
James Harding Giahyue and Bate Felix. "Ebola Patients Keep Escaping Liberian Hospitals." Business Insider. Business Insider, Inc, 06 Sept. 2014. “http://www.businessinsider.com/r-ebola-outbreak-stirs-anger-in-fragilelibe
ria-2014-9”
“Mapp Bio.” Mapp Bio. Mapp Biopharmaceuticals, Inc., 2012 “http://www.mappbio.com”
Population of All Countries of the World / All National Populations Largest to Smallest - Worldatlas.com." Population of All Countries of the World / All National Populations Largest to Smallest - Worldatlas.com “http://www.worldatlas.
com/aatlas/populations/ctypopls.htm”
University of Texas Medical Branch at Galveston. "Ebola Cell-invasion Strategy Uncovered." ScienceDaily. ScienceDaily, 5 September 2008. www.sciencedaily.com/releases/2008/09/080903172428.htm
Weintraub, Karen. "Doctors and Nurses Risk Everything to Fight Ebola in West Africa." National Geographic. “http://
news.nationalgeographic.com/news/special/features/2014/08/140829-ebola-caregivers-doctors-nurses-
west-africa-sierra-leone/”
"What Is the Ebola Virus's Survival Rate? And Other Key Questions About the Epidemic." National Journal.
50
MEDICAL DIALOGUE REVIEW
Fall 2014
Martinez
Political Conditions on Humanitarian
Aid: How Health and Political Relations Mix and Why It Concerns You
By Andrea Martinez
“Why help anyone who hasn’t helped us? Why make it easy on a humanitarian aid organization that helps the people who killed, or will
kill, our own people?”
It seems as if anywhere we go, people ask for
money from us. On the streets,
we are asked for donations. A
cashier asks for money in exchange for a Big Mac. During
commercials of popular television shows, advertisements ask
for money. They do not ask
for much; some are even content with spare change. And
after we donate money, we feel
good about ourselves, as if we
are making an impact on the
world. Despite the existence
of humanitarian aid, issues like
poverty and world hunger remain unsolved. Even considering all the money we have seen
donated, it is almost as if nothing has been done in support
of these issues.
Recently the UN declared that the fight against
Ebola fell short of its fundraising goal. Out of the desired billion, only 250 million
dollars were collected. This
is interesting, as President
Barack Obama called Ebola “a
growing threat to regional and
global security”. A shortage of
money for humanitarian aid—
considering the amount of suffering and death West Africa is
experiencing—should come as
a surprise. Collecting from all
the major powers in the world
should be an easy task. Yet nobody should be surprised as to
why only 25% of the money
has been collected. This is not
the first time a fundraising goal
has not been met, and this will
certainly not be the last time.
The
International
Red Cross was founded in
1863, in Geneva, by Henry
Dunant and Gustave Moynier.
Dunant and Moynier strived
to create an organization that
preserved the lives and dignity of war victims. Today,
the International Red Cross
receives help from around 97
million volunteers around the
world. Médecins Sans Frontières (MSF) was founded over
one hundred years afterwards.
Even the United Nations (UN)
was created after World War II
to show international cooperation, a way to facilitate aid and
discussion in a peaceful setting,
but in the short years following its creation, the UN lacked
the proper administration to
be effective, even though it
was terribly needed right after a devastating war. Luckily,
the United States stepped in
and led the reconstruction of
Volume 15
Europe. Yet there was a more
insidious reason behind this
aid, for no country ever takes
an action without a higher motive. The Marshall Plan was
the United States’s response
to the growing threat of communism during the Cold War,
in which the United States gave
the equivalent of 160 billion
dollars in current dollar value
in economic support to help
rebuild European economies;
developmental and humanitarian assistance filled the void
left by the withdrawal of diplomacy. At one point, Soviet
deputy foreign minister Andrei
Vyshinsky said the Marshall
Plan violated the principles of
the UN, accusing America of
trying to impose its will on independent states by using economic resources distributed as
relief to needy nations as an
instrument of political pressure. Indeed, Vyshinsky was
not wrong in his assumption,
as the Marshall Plan countries
remained capitalist amidst the
growing amount of communist states in Eastern Europe.
Humanitarian aid not
only requires effort from the
volunteers and donations, but
there is also another side many
MEDICAL DIALOGUE REVIEW
51
Martinez
do not account for: politics.
Starting with the conflict in
Iraq, the Humanitarian Practice Network writes about the
conditions humanitarian agencies experience from security
crises to policy quandaries to
the need to interact with forces
that the international community deems as illegitimate.
Especially in areas like Iraq
and Afghanistan, humanitarian agencies are seen as taking
sides. This comes from their
unique political position, where
they need to work with an occupying power, which also happens to be the agency’s primary
funder as well. This is the main
issue dubbed as the Samaritan’s
Dilemma: can a humanitarian
aid agency be neutral? Fabric
Weissman, one of the co-authors of the book Humanitarian
Negotiations Revealed: The MSF
Experience, mentioned the reality in the Taliban-held Afghanistan, stating that they claim
responsibility of the goods
and services that humanitarian
groups are providing, which
allows the Taliban to appear
to the local population as effective governors. “On many
occasions,” Weissman continues, “the MSF, like other organizations, uses combatants to
ensure the safety of its teams
and convoys.” Just by existing
in areas of conflict, the agency
inadvertently influences the
behavior of policy decisionmakers, a coveted advantage
not many have. Added to the
fact that humanitarian agencies
need money from large benefactors, it seems as if we found
a match made in heaven. But
this assumption has complica52
tions.
The
humanitarian
principles of humanity, neutrality, and impartiality serve
to create an ethical framework
that defines and dictates the
humanitarian sphere in which
relief agencies operate. This
definition is then contorted
by the involvement of politics.
Once humanitarian aid covered
a narrow set of relief activities
carried out by a small group of
agencies. Now it has become a
more complex activity involving rehabilitation work. This
transformation created a whole
new set of standards for the
performance in the field, and
led to increasing uncertainties
on the quality of humanitarian responses and its accountability. This accountability has
even worsened in the advent
on 9/11. Since the “North”
becomes more focused on terrorism and its real or perceived
ramifications,
humanitarian
agencies are affected by the
double standards applied by
the North to the South. This is
how humanitarian agencies become extensions of the security and foreign policy objectives
of the North in crises such
as Afghanistan, Kosovo, and
Iraq. The “North” also makes
it hard for aid groups to fully
operate. US counter-terrorism
laws that have entangled humanitarian organizations in
a web of regulations and requirements, which add to their
costs, slow down their transactions, and sow distrust between
them and their local partners.
The laws further stipulate that
providing support resources to
terrorists, even if not for ter-
MEDICAL DIALOGUE REVIEW
Fall 2014
rorist purposes, could result in
criminal prosecution.
Humanitarian organizations are stuck between
a rock and a hard place. They
want to save lives, but saving
these lives involves having relationships with enemy organizations that the international
community may not agree
with. But if they don’t create
these relationships, the humanitarian aid will never actually
benefit the people who need
it. This entanglement is one
of the main reasons why not
many countries donate money
to these organizations, or why
the transactions to accessing
the money are so muddled in
paperwork and bureaucracy.
Though the Islamic
State of Iraq and the Levant
(ISIS) has stolen the spotlight
as the newest story from the
Middle East with their grotesque acts of violence, the
Syrian civil war is not over,
and the death count continues
to rise. Even if the conflict
is no longer at the forefront
of the media outlets, chilling
facts of humanitarian involvement still remain. Claimed to
be 60 percent underfunded in
2012 by the United Nations,
the Syrian Civil War is not
the only instance of catastrophes that receive minimal aid.
Even MSF complained about
lack of resources, citing that
medical assistance is at risk for
thousands of Syrians living in
overcrowded conditions, suffering psychological distress,
and unable to afford medical
care. But the Syrian Civil War is
not the only instance of underfunded aid. Iraq, South Sudan,
Martinez
Afghanistan, Colombia, Israel, and Myanmar are but the
few amount of examples of
countries with underfunded
aid. Many of the deaths the
Rwandan Genocide in 1994
could have been avoided if
the international response had
been better. What all of these
conflicts have in common is a
lack of resources, but the reason behind this lack is simply
politics and its influence on humanitarian aid.
Then again, we hear
stories about all this suffering
and, though a horrified reaction is perfectly normal, we
eventually move on and do not
think much about them until
the media bombards us with
images and videos and dollar
signs accompanied by trailing
zeroes and a body count. Why
should we care what is going
on outside of this country,
this continent? Each government only has an obligation
to its constituents, its citizens.
Syrians don’t pay taxes to the
American government. Afghani children won’t become
the next American soldiers,
doctors, engineers. American
history was not built by Colombians. Why help anyone
who hasn’t helped us? Why
make it easy on a humanitarian aid organization that helps
the people who killed, or will
kill, our own people? These are
perfectly reasonable questions
to have, and it isn’t inhumane
to think this way. Worrying
about a person thousands of
miles away over the person
standing next to you is almost
impossible for some of us. Yet,
with the advent of globalization, the people living in Iraq
are interconnected with us by
an invisible link. It’s impossible for us to see it or even
predict the ramifications, but
the link exists. We established
the link when we built ships to
sail the oceans, when we conquered the New World, when
we forcibly opened Japanese
harbors, when we connected
everyone with the Internet. As
much as we want to go back to
the days where we didn’t even
know what Saudi Arabia was,
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we live in an era in which children travel on airplanes before
they’re five and teenagers have
smartphones.
Recently people have
expressed much concern with
Ebola, a disease that surged in
West Africa and has started to
spread throughout the world.
Ebola is a link of globalizations whose effects we can see.
The media saturates us with
doomsday scenarios in America, but Ebola is not a problem
in developed countries, but
more of a problem in countries
that lack proper hygiene and
nutrition. West Africa needs
the money more than we need
it, and the money goes to save
lives, and we can see the effects
of our money because we are
interconnected. Disease is just
one of the effects globalization has brought, and it isn’t
the only one. Containment in
West Africa did not stop Ebola
from spreading, and at least
the disease can be monitored.
The seeds of hatred for our
Western lifestyle can only be
stopped by humanitarian aid.
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53
Martinez
REFERENCES
“AID POLICY: The Politics of Humanitarian Principle.” IRINnews. IRIN, 28 Oct. 2011. Web. 14 Nov. 2014.
Curtis, Devon. “Politics and Humanitarian Aid: Debates, Dilemmas and Dissension.” Politics and Humanitarian Aid: Debates, Dilemmas and Dissension - HPG Reports 10 - Research Reports and Studies (n.d.): n. pag. ODI. ODI, Apr. 2001. Web.
Donini, Antonio, Larry Minear, Peter Walker, and Feinstein International Famine Center. “Humanitarian Exchange Maga
zine.” Iraq and the Crisis of Humanitarian Action. Humanitarian Practice Network, 26 Mar. 2004. Web. 14 Nov. 2014.
Eriksson, John R., Tor Sellström, Howard Adelman, Astri Suhrke, Bruce Jones, John Borton, and Krishna Kumar. The In
ternational Response to Conflict and Genocide: Lessons from the Rwanda Experience. Copenhagen?: Steering Committee of the Joint Evaluation of Emergency Assistance to Rwanda, 1996. OECD. OECD, Mar. 1996. Web.
"Making US Humanitarian Aid to Syria a Political Tool Is Ineffective and Dangerous." The Christian Science Monitor. The Christian Science Monitor, 13 June 2013. Web. 14 Nov. 2014.
Mollins, Julie. "Cb1f21c7-7d98-4ea3-903f-c5de10e41700." Thomson Reuters Foundation. Thomas Reuters Foundation, 11 Sept. 2012. Web. 14 Nov. 2014.
Nakamura, David. "Obama: Ebola Is 'growing Threat to Regional and Global Security'" Washington Post. The Washington Post, 25 Sept. 2014. Web. 14 Nov. 2014.
Nelson, Anna. "Six Underfunded ICRC Operations." ReliefWeb. N.p., 26 June 2014. Web. 14 Nov. 2014.
Pallage, Stephane. Recognizing the Political Side of Humanitarian Aid Stéphane Pallage , ESG UQAM (n.d.): n. pag. CIR
PEE. CIRPEE. Web.
"Trust Fund Factsheet - Ebola Response MPTF." Trust Fund Factsheet - Ebola Response MPTF. United Nations, n.d. Web. 14 Nov. 2014.
Vynshinsky, Andrei. "Vyshinsky Speech to U.N. General Assembly." Vyshinsky Speech to U. CNN, n.d. Web. 14 Nov. 2014.
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Reztsova
The Ebola Time Bomb
By Mariya Reztsova
“It is apparent that without further intervention by the UN in partnership with nations around the globe, the epidemic can reach its tipping
point and can develop into a global problem.”
Abstract: The Ebola virus has made
headlines around the world with its gruesome
and shocking images. However, what the general public isn’t informed about is how the virus
outbreak occurred and how people got infected
in the first place. This article explored the virus
from its ancestry and structure to its effect on
impoverished countries of western Africa. It is
apparent that without further intervention by
the UN in partnership with nations around the
globe, the epidemic can reach its tipping point
and can develop into a global problem.
In recent news the Ebola virus seemed
to be holding the spotlight. With thousands
dead and the virus reaching American shores,
a growing panic has been brooding. But where
did this new virus come from? And how was it
able to become an epidemic? The Ebola virus
is not a newly discovered disease. According to
a report by Joseph McCormick in the Journal
of Infectious Diseases, it is one of the genera
of the Filoviridae viral family and has circulated
amongst primates and mammals in the central
African rain forests for many years. Ebola haemorrhagic fever, as the virus is formally known,
Figure 1: Ebola Virus Structure
(Source: Swiss Institute of Bioinformatics).
was discovered 30 years ago. The first genus of
the Filoviridae family, the Marburgvirus, was
discovered in 1967 during an outbreak in Marburg, Germany (CDC, “Outbreak of Ebola
Viral Hemorrhagic Fever”). At the time, laboratory workers were infected while working on
infected tissues recovered from the Circopithecus aethiops monkeys imported from Uganda
(McCormick, “Ebola Virus Ecology”). The
subtype filovirus the Ebola haemorrhagic fever, was discovered in 1976. Two outbreaks of
the disease occurred simultaneously in southern
Sudan and northern Zaire (now the Dominican Republic). It was ascertained later on that
the two outbreaks were caused by two different
species of Ebola, the Ebola-Sudan virus and the
Ebola-Zaire virus. Ebola-Zaire the more fatal of
the two had an 88% fatality rate and killed 280
people (WHO, “Ebola virus disease”). In 1994, a
third Ebola virus species was discovered in Cote
d’Ivoire. The virus was discovered in an ethnologist who was exposed to the virus while working
with chimpanzees in the Tai Forest reserve. As
scientists later discovered there was a recurring
theme of the filovirus spreading from primates
to humans through close contact with the tissues and fluids of infected primates. Though the
virus has infected humans, historically filovirus’
have wrecked havoc on populations of primates
such as the mandrills and baboons and causing outbreaks in remote areas of Africa (McCormick, “Ebola Virus Ecology”). The largest
outbreak of the Ebola virus in humans occurred
recently in Liberia, Sierra Leone, Guinea, and
Nigeria around March 2014. The current Ebola
virus shares 97% resemblance to Ebola-Zaire
strain first discovered in 1976 (Ansari A. “Clinical features and Pathobiology of Ebolavirus
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Figure 2: (Source: U.S. Centers for
Disease and Control & BBC).
infection”). According to the World Health Organization (WHO), thousands of people from
western Africa have been infected and with almost a 50% fatality rate.
Ebola virus is an RNA virus; its genome
contains only RNA strands and has a method
of infection and replication similar to HIV. The
structure of the virus is referred to as the virion
and consists of four parts: the nucleocapsid,
the matrix, the RNA polymerase complex, and
the lipoprotein membrane envelope (Figure 1).
The virion is rod-shaped and 650-14,000 nm in
length with a diameter of 80 nm (Konstantinov
I. et la. “The Ebola Virus”). The RNA of the
virus is transcribed into cDNA in the host cell
using an enzyme called Reverse Transcriptase.
The seven genes on the cDNA are then translated into four structural proteins (VP24, 30,
35, 40), an RNA polymerase (L), a glycoprotein
(GP), and a nucleoprotein (NP) that are all about
19,000 nucleotides in length (Ascenzi P. et la.,
“Molecular Aspects of Medicine”). The lipoprotein membrane of the virion contains multiple
copies of the glycoprotein (GP) which are seen
as spikes in X-ray analysis and NMR spectroscopy. It is this lipoprotein which allows the cell
to fuse into a host cell. The high lipid content
and glycosylation of the membrane also help in
penetration of the host cell by producing viral
proteins that contribute to suppressing the host’s
immune system (Ansari A., “Clinical Features
and Pathobiology of Ebolavirus infection”).
One of the staple characteristics of the virus
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that seems to contribute to its high virulence is
its ability to vary its shape and size in response to
environmental stimuli.
The Ebola virus enters a host when
there is direct contact with the body fluids (blood,
semen, mucus, urine, saliva, and feces) of an infected person (Ghayourmanesh S, & Hawley H.,
“Ebola virus”). Usually this occurs when eating
bush meat or wildlife meat that is infected, using
unsterilized needles, contact with dead infected
bodies, and unprotected sex. The route of infection is usually through mucosal surfaces, breaks/
abrasions in the skin, and/or pregnancy (Feldmann, Heinz, & Thomas W. Geisbert, "Ebola
Haemorrhagic Fever."). When the Ebolavirus
enters the body it disables the immune system
and the vascular system. It does this through
infecting important cells of the immune system
such as dendritic, macrophage, and endothelial
cells (Ansari A., “Clinical Features and Pathobiology of Ebolavirus infection”). The dendritic
cells are responsible for presenting antigens to
T-cells and lymphocytes in order to initiate an
immune response (Steinman, “Introduction to
Dendritic Cells”). When these cells are infected
it is difficult for the body to recognize infections
and create a rapid response to ward off the infection. Macrophage cells are immune cells that
function to recognize, engulf, and destroy target
cells. Macrophage cells are part of the body’s
second line of defense; they secrete a chemical
called cytokines to attract more macrophages
and inducing feverish symptoms (Mandal, A.
“What is a Macrophage?”). When these cells are
destroyed and infected by a virus the body cannot as effectively protect itself from virulent viruses or even simple infections. Endothelial cells
are cells that form the lining of blood vessels.
They function to provide blood to cells of the
body. When these cells are infected low blood
pressure and internal bleeding can occur within
the body (Alberts B, Johnson A, Lewis J, et al.,
“Blood Vessels and Endothelial Cells”).
According to the World Health Organization (WHO), once a human is infected by
the Ebola virus symptoms arise in 2-21 days.
Only when symptoms are onset can the virus be
transmitted on to others. The first sign of infection are usually symptoms of fever, headache,
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Reztsova
sore throat, muscle pain, and fatigue (WHO).
Since these symptoms are highly similar to the
flu the Ebola virus can be difficult to detect
without adequate blood tests for white blood
cell and platelet counts. The second and more
severe symptoms that follow are vomiting, diarrhea, impaired liver and kidney function, rash,
and in some cases internal and external bleeding
(Figure 2). In some cases severe symptoms such
as seizures, heavy bleeding, and brain damage
can occur. There is a 50% and higher mortality
rate once a person is infected.
The countries which currently have
critical outbreaks of the Ebola virus are Guinea, Sierra Leone, and Liberia (Figure 3). These
countries are highly impoverished with some
of the lowest PPP per capita in the world. For
example, Guinea is the fourth poorest country
in the world with a PPP per capita of $394.25
(Valentina Pasquali, Global Finance Magazine).
With high poverty rates and high corruption
these countries have inadequate health care systems to treat many diseases much less to deal
with critical outbreaks. Liberian President Ellen
Johnson Sirleaf stated “We were not prepared
to really fight this battle in terms of the material, the training, the people, the expertise,” (qt.
Time “Racing Ebola”). The inadequate health
care plus the close proximity within rural villages and the large populations living within villages created a dangerous scenario. Once a person developed Ebola it lit a spark that spread
through the country like wild fire. According to
The New England Journal of Medicine the first
person who contracted the disease, or Patient
Zero, was possibly a two year old boy from a
village in Guinea. How the disease was contracted in the first place is currently unknown. In a
TED talk called “Contagion,” Dr. Todd Disotell commented that the most common ancestry
of the current Ebola virus is the Zaire virus. In
fact the Ebola virus has a 97% resemblance to
the Ebola-Zaire strain first discovered in 1976
(Ansari A., Journal of Autoimmunity). According to Dr. Disotell the Zaire virus is most commonly found in bats and can spread to primates.
It has been known that some species of the fruit
bat carry the Ebola virus without exhibiting
any symptoms. It is theorized by scientist and
reported by Time magazine that the Ebola virus was contracted from the consumption of an
infected fruit bat, a type of bush meat eaten in
rural African countries. This created a spillover
event or the first animal-to-human transmission of the virus. According to Madison Park
a reporter for CNN, when the boy died on December 6, 2013 near Gueckedou, Guinea the virus spread to his family members. When these
family members died and had open funerals the
people who attended contract the virus from
the exposed dead bodies and spread it to people
within their villages. Without adequate treatment
and the isolation of the infected the virus spread
to Sierra Leone and Liberia.
There is currently neither a cure nor a
vaccine for Ebola. Infected individuals are put
on supportive therapy, a system maintenance
method in which doctors administer IV fluids
and try to balance the bodies electrolytes. Doctors try to maintain oxygen and blood pressure
levels and treat other present infections (CDC).
That is of course if there is an adequate medical facility available. In the majority of areas that
Ebola has affected do not. The only thing that
Figure 3: Map of Outbreaks (Western
Africa) (Source: U.S. Centers for Disease
Control).
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impoverished areas can do is try to contain the
disease so that it doesn’t spread farther. The
Centers for Disease Control (CDC) recommends that three steps should be taken to prevent the spread of an epidemic. First, infected
patients are isolated and their disease confirmed.
Then, people who have been recently in contact with the infected person are tracked down
Figure 4: Fighting Ebola (Source: Time
Magazine “Racing Ebola”).
and identified, a process known as contact tracing. Finally, the people who were in contact are
watched for symptoms. The incubation period
for Ebola is 21 days, so if the contact does not
exhibit symptoms in three weeks they’re released
(Time, “Now Arriving”). But even this process
is difficult to follow through because of the
densely populated areas of western Africa and
widespread confusion. Another problem is that
many people live in fear of the disease and try to
hide their sick loved ones (Time, “Racing Ebola”). This has caused many cases to go unreported and the virus to spread as uninformed people
handled infected bodies without protection and
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cared for sick loved ones, contracting the infection themselves. A late response to contain the
disease also allowed the Ebola virus to reach
epidemic levels. The virus first struck a Guinean
village in March 2014 but many health officials
believed the virus would stop on its own accord.
However, their latent response allowed the virus
to spread to Liberia and Sierra Leone. Just like
that an epidemic ensued.
By the time the UN, top officials
within the country, and nonprofit groups were
informed the virus was already in three countries infecting hundreds with a 50% fatality
rate. Panic spread, people locked infected individuals in empty buildings, and hospitals were
overwhelming with incoming cases. As nurses
treated the sick without adequate equipment,
they contracted the disease themselves and may
have spread it further. In September, the CDC
reported that if the amount of care given was
to continue, the amount of infected people
could double every 20 days and potentially infect 1.4 million people by mid-January (Figure
4; Time, “Racing Ebola”) President Obama issued a statement to the UN General Assembly
emphasizing the risk of not stopping the virus.
On September 25, Obama stated “If this epidemic is not stopped, this disease could cause
a humanitarian catastrophe across the region.
And in an era where regional crises can quickly
become global threats, stopping Ebola is in the
interest of all of us” (qt. Time). The thing that
has health officials around the globe worried is
that Ebola will reach its tipping point soon. According to epidemiologists there exists a tipping
point in all epidemics that point is reached when
the number of infected patients is so large that
no number of health workers could isolate each
person and stop the spread of the virus. Viruses
spread exponentially, for each person that is infected and not properly treated/ isolated a multiple more are infected.
According to the CDC, there is still
time for the Ebola virus epidemic to be extinguished. Currently Red Cross, the World Health
Organization (WHO), and many other nonprofit organizations are providing essential supplies
to countries affected by Ebola. However, though
there is no shortage of protective gear there is
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Reztsova
much more than supplies that are needed by the
countries to stop the epidemic. For example,
2,122 more beds for patients, 50 more deadbody management teams, and 734 million dollars in funds are needed. More crucially 500-600
more health experts are needed. Without expertise on how to deal with outbreaks and set up
treatment centers the epidemic has little chance
of being extinguished (Time, “Racing Ebola”).
The only silver lining of the Ebola epidemic seems to be what experts can learn from
the virus. As reported by Bryan Walsh and Alexandra Sifferlin for Time, one thing we can learn
is to be weary of diseases that can spread from
animals. These zoonotic diseases are currently
more frequently subject to spillovers, where the
virus spreads to humans. These spillover events
seem to occur more frequently as “deforestation
and development bring humans and animals
closer together” (Time, “After Ebola”). Another
pattern that was pointed out by Dr. Disotell in
his TED talk “The Contagion,” was that as the
Earth’s climate gets warmer more infectious
insects such as mosquitoes will migrate north
towards North America. In fact, recently there
has been a reemergence of highly infectious viral disease such as the Chikungunya virus and
other viral Caribbean viruses. Another lesson
from the virus is the need for research funding.
Consider this, in 2001 after 9/11 there were various research teams looking for a vaccine or cure
for the Ebola virus because they feared that it
could be used as biowarfare. However, because
the research was underfunded many of these
research laboratories had to scrap their work.
Another lesson to be learned is how critical a
quick response to an epidemic is needed. As Dr.
Disotell stated if the funds and supplies were
provided to the infected countries in April the
epidemic would have been distinguished by now.
A final note to take away from this is what can be
learned from the Ebola strain. How did it spread
from primates or fruit bats to humans? What
ancestry is it related to? These and many other
scientific inquiries can provide information for
current and future viral outbreaks.
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Fever." The Lancet 377.9768 (2011): 849-62.
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ence; 2002. Blood Vessels and Endothelial Cells.
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WHO. Ebola virus disease. World Health Organization. 2014.
Drehle, D. Now Arriving. Time . 2014;184(14):36-37.
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Artwork by Michelle Shi
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