Download Abdominal Migraine - Dr Wael B. El Sebaie Integrated Pediatric

Abdominal Migraine
Wael. B . ElSebaie
Consultant Ped&Ped neurology
Cairo University
Recurrent abdominal pain is a common
problem in children . Not
uncommonly that despite extensive
investigations no organic cause could
be found .
In past, it was widely believed that
childhood abdominal pain with no
organic cause is commonly
psychogenic ; this view did not pass
unchallenged .
It has recently been shown that , many such
children come from families that display
high level of maternal neuroticism ; and
go onto suffer increased prevalence of
psychiatric disorders in adults.
It is of course inherently unlikely that
children with unexplained or recurrent
abdominal pain ,comprise a homogenous
group . Even in absence of an organic
cause , it is important to define symptom
complex as accurately as possible .
In this way ; it might be possible to
categorize subgroups of children with
recurrent abdominal pain ; which in
turn might facilitate management .
One sub group is
“ Abdominal Migraine”
Where as children suffer from severe
recurrent abdominal pain .
Of course not every child with recurrent
severe abdominal pain diagnosed as
abdominal migraine; in fact very few do so.
We highly suspect diagnosis of abdominal
migraine when there is:
+ve F. H of migraine& relief of symptoms
with specific anti-migraine therapy.
Pain is described as “ prolonged bouts of
severe incapacitating pain, accompanied
by feeling of intense misery together with
symptoms like aura ; and completely free
in between attacks. “
Those children typically develop “adult
migraine “.i.e. pattern changes from
“bilious attacks” of early childhood to
typically adult migraine .
This view would imply that diagnosis
can not be made at time of complaint
when child is suffering ; thus denying
child treatment that shown to be
effective.
IHS put criteria for diagnosis as
follow:
1.Pain is severe enough to interfere with
normal daily activity: child is unable to
continue with normal classrooms or
leisure activities and is generally
incapacitated. At school he or she
generally has to leave classroom and lay
down . Most children describe their mode
as intense misery.
2 .Pain is preumbilical or poorly localized ; vague
central motion of hand centered around
umbilicus .
3.Pain is described as dull or sore in nature ; no
words to describe it ,it is just sore.
4.Pain is associated with some of : pallor( color
drained from face, dark shadow under eyes or
flushing {predominant vasomotor changes}
anorexia, nausea, vomiting.
5. Each attack lasts for at least one
hour, in practice usually 3-4hours.
6. Complete resolution in between
attacks.
7.Attacks occur at least twice a year.
Diagnosis is excluded if :
1. Mild symptoms not interfering with daily
activities.
2. Burning pain.
3. Non midline abdominal pain.
4. Symptoms suggestive of food intolerance, or
malabsorption or GIT troubles.
5. Less than one hour duration.
6. Persistence of symptoms in between attacks.
Etiology
• ??Food allergy plays a role; allergic
irritants to intestine transmitted to
Trigeminal V cranial nerve and triggers
imbalance of circulation to head .Those
irritants include the 5C [ Chocolate, coffee,
citrus, cola &claret].
• ?? Mitochondrial DNA mutation
(cytopathy).
• ?? Corticotropin releasing factors.
?? Endogenous prostaglandin release ;
leads to derangement of hypothalmic
pituitary adrenal axis.
• ?? Episodes of stress and frustration .
• ?? Emotion, Hypoglycemia, irregular
sleep, travel &bright light.
Pathophysiology
Fatigue, nervousness, and emotional factors
produce changes in motor activity of GIT
which results in duodenal stasis ; this
promotes absorption of allergens to which
patient reacts in his inherent pattern of
migraine.
It is unclear how to conceptualize between
vascular phenomenon and nervous
manifestation { like in migraine}.
cont
ENS:
Is an extensive network of neurons widely
dispersed through out the gut, that coordinate
together to regulate GIT events such as:
peristalsis ,blood flow, secretion & absorption.
ENS may play a role in neurologic disorders, as it
influences CNS through nerve reflexes and
production of neuropeptides.
It is estimated that 80% of vagal fibers [the main
parasympathetic are visceral afferents.
GIT symptoms :
Discharge arising in the amygdalla can be
transmitted to gut via dense direct
projection to dorsal motor nucleus of
vagus.
Sympathetic pathways from amygdalla to
GIT can be activated via hypothalamus.
Sensory pathways from bowel via vagus
nerve to solitary nucleus of medulla which
is heavily connected to amygdalla.
Stimulation of vagus nerve is used now for
intractable seizures.
It is stated that:
Abdominal migraine & headache are two
faces of one coin :
If sympathetic pathways dominate;
headache results with flushing as an
autonomic manifestation.
If vagus dominate ,abdominal migraine
occurs with vomiting as main symptom.
Abdominal migraine or epilepsy
[1]
Link between epilepsy and migraine:
1. Both are familial, paroxysmal ,
associated with transient neurologic
disturbances.
2. Increase incidence of migraine in
epilepsy and vice versa.
3. Headache can be a seizure
manifestation , the reverse is not .
4. Abnormal EEG in both; but:
5. Basilar migraine & Benign occipital
[2]
Link between abdominal and childhood
migraine :
1. Both occur in childhood.
2. Similar triggering and releasing factors.
3. Associated GIT, sensory,& vasomotor
changes.
4. Anti migraine prophylaxis are efficacious
in prophylaxis of abdominal migraine.
5. Patients with abdominal migraine have
abnormal VEP.
[3]
Abdominal migraine not abdominal
epilepsy
1. Not associated with altered
consciousness.
2. Precipitated by stress, loud noise,
emotion, frustration or irregular sleep.
3. Not followed by tiredness or confusion.
4. Relieved -in attacks- by oral medications.
Abdominal migraine not epilepsy
[cont]
5. Prophylaxis therapy is effective.
6. Ictal EEG is different.
7. + F H of migraine or develop migraine in
later life.
8. Not accompanied by elevation of
enzymes such as CPK or Prolactin
Management
In acute attacks:
• Stay in bed; better in dark quit room.
• I.V fluids containing glucose to prevent
catabolic state.
• Analgesics, antacids & anti-emetics.
Prophylaxis:
•
•
•
•
Amyltryptine.
Propranolol.
Cryoheptadine.
Pizotifen.