بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم

2. Abdominal Migraine Wael. B . ElSebaie Consultant Ped&Ped neurology Cairo University

3. Recurrent abdominal pain is a common problem in children . Not uncommonly that despite extensive investigations no organic cause could be found .

4. In past, it was widely believed that childhood abdominal pain with no organic cause is commonly psychogenic ; this view did not pass unchallenged .

5. 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.

6. 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 .

7. In this way ; it might be possible to categorize subgroups of children with recurrent abdominal pain ; which in turn might facilitate management .

8. 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.

9. 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. “

10. Those children typically develop “adult migraine “.i.e. pattern changes from “bilious attacks” of early childhood to typically adult migraine .

11. 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.

12. 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.

13. 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.

14. 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.

15. Diagnosis is excluded if : • Mild symptoms not interfering with daily activities. • Burning pain. • Non midline abdominal pain. • Symptoms suggestive of food intolerance, or malabsorption or GIT troubles. • Less than one hour duration. • Persistence of symptoms in between attacks.

16. 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.

17. ?? Endogenous prostaglandin release ; leads to derangement of hypothalmic pituitary adrenal axis. • ?? Episodes of stress and frustration . • ?? Emotion, Hypoglycemia, irregular sleep, travel &bright light.

18. 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}.

19. 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.

20. 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.

21. 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.

22. Abdominal migraine or epilepsy[1] Link between epilepsy and migraine: • Both are familial, paroxysmal , associated with transient neurologic disturbances. • Increase incidence of migraine in epilepsy and vice versa. • Headache can be a seizure manifestation , the reverse is not . • Abnormal EEG in both; but: • Basilar migraine & Benign occipital seizures, and role of EEG. • Role of vagus stimulation in treatment of intractable seizures.

23. [2] Link between abdominal and childhood migraine : • Both occur in childhood. • Similar triggering and releasing factors. • Associated GIT, sensory,& vasomotor changes. • Anti migraine prophylaxis are efficacious in prophylaxis of abdominal migraine. • Patients with abdominal migraine have abnormal VEP.

24. [3]Abdominal migraine not abdominal epilepsy • Not associated with altered consciousness. • Precipitated by stress, loud noise, emotion, frustration or irregular sleep. • Not followed by tiredness or confusion. • Relieved -in attacks- by oral medications.

25. 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

26. 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.

27. Prophylaxis: • Amyltryptine. • Propranolol. • Cryoheptadine. • Pizotifen.

28. Thank you