آمال و طموح

Migraine in few words

نشر في 16 يونيو 2009 في المجلس الطبّي بواسطة ONE

بسم الله الرحمن الرحيم
الشقيقة او الصداع النصفي صُنف بمنظمه الامم المتحده للصحه بثالث مرض يعيق عمل النسان ويفقد ساعات العمل اليوميه وقدرت هذه الساعات بالمليارات في كل سنه فقط في الولايات المتحده الامريكيه.. وباختصار:انواع الصداع حسب تصنيف جمعيه الصداع الامريكيه بحوالي 999.9 تصنيف واهمها الصداع النصفي المعروف بدون اي اعراض تنبيهيه ومنها مايصاحبها التنبيهيه مثل زغلله النظر او مايسمى نبضات نظر برقيه قبل حدوث الصداع بساعه تقريبا. قديما يعتقد ان الصداع صادر عن انقباضات ومن ثم ارتخاء شرايين غشاء الدماغ والان نتجه الى ان نظريه تهيج العصب الخامس ومن ثم تهيج الشرايين اقرب علميا حسب التجارب المكثفه وخواص الادويه خلال سبر اسرار الصداع النصفي. وكما ذكرت سابقا بان انواع الصداع كثيره ويختلف علاجها من نوع الى آخر وحتى الشقيقه لها عده انواع منها مايتم علاجه “بالتربتانات” ومنها من يحظر تناول “التربتانات” في حالات خاصه. اعراض الصداع تختلف من شخص لآخر ولكن تم عمل خواص محدده لتشخيصه ومنها, 5 حالات تكرار للصداع النصفي العام مصاحب باي من :الغثيان او الرجاع او الانزعاج من الضوء المباشر وايضا ازدياد النوبه باي مجهود عضلي يتسبب برغبه المصاب للاسترخاء في غرفه مظلمه. يشعر المصاب باله “نبضي في جانب الراس في اغلب الحالات . اما في حاله الصداع مع التنبيه المسبوق: فيشعر المريض بزغلله نظر او احيانا تنميل في اطراف الجسم او نادر ظعف في الاطراف ويتبعه الصداع خلال فتره لاتزيد عن ساعه ويتكفي نوبتين مشابهه لتشخيصه. ولا ننسى بان هناك انواع من الاطعمه تزيد من الصداع النصفي للذين لهم قابليه , مثلا:الاطعمه المبخره مثل البيتزاء والمشاوي, واطعمه المعلبات , والادخنه ايضا تثير المصاب , وللنساء في فتره العاده الشهريه. نعتقد ان منشأ الصداع في الفص الخلفي بعد كشف نشاط في هذه لمنطقه بواسطه الرنين المغناطيسي الحيوي ,واعراض النظر اكدت المسبب ولان مركز النظر في هذه المنطقه. في الاطفل يختلف الصداع في فتره حدوثه ولكن لايختلف كثيرا عن الذكور في العلاج والاعراض. من انواع العلاجات : علاج فوري وهي “ايبوبروفين” او البندول لكن بجرعات كبيره تصل الى 1200 كل 4 ساعات او اما بحقن المصاب تحت الجلد او العضل او الفم او الانف بدواء “التربتان” وتحت الجلد اكثر فعاليه. وايضا العلاج بواسطه “ارجوتامين” التربتان والارجوتامين يمنع استخدامه في حالتين: الصداع مع اعراض تنبيهيه طويله الاجل اي اكثر من 24 ساعه. ويمنع مع اي صداع مصاحب لها ضعف في الاطراف ولايعطى الدوائين مجتمعين لخطورتهما معا. وعلاج مزمن لمن يتعرض للصداع متكرره اسبوعيا ويفقد كثير من اوقات العمل فيتم التدريج بالادويه حتى تصل لمنسوب معين في الدم ومنها خاصه لمرض الصرع وهي ناجحه بالصداع مثل “فاربوريك اسد” وادويه خاصه بالقلب مثل “بروبانلول ونها ادويه خاصه للاكتئاب.. كثير من الاشخاص يستخدمون ادويه لزملاء لهم على اساس ان لديهم صداع وهذا خطأ, مثلا هناك صداع اكثر في لنساء ويسمى” هيمي مايجرين كونتونيا” اي صداع نصفي متكرر وعلاج ببساطه “الاندوسيد. فرساله موجهه للجميع:الصداع النصفي علاجه سهل ويزيد في الفئات العمريه الصغيره وهناك فتره راحه للصداع , فالدواء مؤقت وليس مزمن وليس له علاقه باي مرض خبيث. ويستحسن عمل تصوير مغناطيسي مره واحده خاصه لصغار السن للتاكد من عدم وجود مايشكك بالصداع . وهذا مختصر مفيد ولم اتطرق كثيرا في دوره الصداع كما في الرسم لصعوبه ترجمه المصطلحات الانجليزيه. ونتمنى لكم حياه خاليه من الصداع. اضغط على الصور للتكبير MIGRAINE always click on figure to enlarge
Migraine Pathophysiology

Vascular Theory
-migraine is thought be a vaso-spastic disorder that is initiated by vasoconstriction in the cranial vasculature.
-vasoconstriction appears to be associated with migraine aura.
-after early vasoconstrictive, intracranial or extracranial blood vessels dilate
-blood vessel dilation activates the trigeminal sensory nerves that surround the meningeal blood vessels (these BV show a high level of sensory innervation), causing pain
-activation of trigeminal nerves also causes the release of vasoactive neuropeptides that further contribute to dilation and worsen pain.
FOR: 1)Studies show the occurrence of oligemia during the aura phase of a migraine, and an increase in blood flow during the headache phase. 2)When a patient with a headache is given a vasodilator such as a nitrate, the headache intensifies, whereas when a patient is given a vasoconstrictor such as a 5-HT agonist, the headache is usually alleviated.
AGAINST: 1) Question whether the measured decreases in cerebral blood flow during the aura phase are sufficient to cause the aura symptoms (e.g., visual disturbances) that some migraineurs experience 2) Vasodilation alone cannot explain the local swelling and tenderness of the head that generally accompany migraine 3)The oligemia that spreads across the cerebral cortex at a rate of 2-3 mm per minute does not conform to discrete vascular territories, making unlikely the theory that vasospasm of individual cerebral arteries with subsequent cerebral ischemia is the source of the aura.
Cortical spreading depression theory
-more aptly described as spreading activation, followed by a wave of spreading depression.
-begins with a brief wave of excitation, followed by a prolonged period of neuronal depression, associated with disturbances in nerve cell metabolism and regional reductions in blood flow -support the clinical observation of “positive” visual scintillations followed by a “negative” visual scotoma or by the march of positive sensory (paresthesia) symptoms. -suggest that the changes in blood vessel caliber and blood flow may be due to a primary neuronal event, triggered by enhanced neuronal excitability and susceptibility to spontaneous depolarization, resulting in prolonged hypometabolism because of an impairment in energy metabolism caused by mitochondrial dysfunction.

Neurovascular Hypothesis
-migraine triggers or cortical spreading depression can activate trigeminal nerve axons
-neurons release neuropeptides (substance P, neurokinin A, and CGRP) from axon terminals near the meningeal and other blood vessels. -cause vasodilation and promote the extravasation of plasma proteins and fluid from nearby meningeal blood vessels. -CGRP does not promote plasma extravasation, but it is a potent vasodilator. -produce an inflammatory response in the area around the innervated blood vessels – “sterile neurogenic perivascular inflammation” -neuropeptides may also sensitize nerve endings, providing a mechanism for sustaining the headache. -trigeminal nerve also transmits pain impulses to the trigeminal nucleus caudalis, which relays pain impulses to higher centers of the brain.
-according to the neurovascular theory, vasodilation is not the cause of migraine headaches but is an accompanying phenomenon attributable to trigeminal nerve activation.
-cause of this activation is not known – it may be due to ionic and metabolic disturbances in brain function or abnormal activity in brain stem sensory nuclei causing antidromic activation of trigeminal sensory pathways.

Integrated Hypothesis
-attempt to consolidate various theories -triggers such as stress, glare, noise, the patient’s internal clock, the dilation of the carotid arteries, or other factors may activate specific centers in the brainstem. -constriction of cerebral blood vessels may cause a localized deficiency in blood flow, provoking cortical spreading depression, which, in turn, stimulate trigeminovascular fibers, eliciting neurogenic inflammation and headache pain. -the locus ceruleus (epinephrine), the dorsal raphe nucleus (serotonin), and the trigeminal nerve cause a stimulation of cranial nerves that dilate both cerebral and extracranial blood vessels. -dilation of meningeal vessels contributes to pain generation. -locus ceruleus also sends fibers to higher centers of the cerebral cortex, where it may influence state of arousal and awareness and descending projections of pain control mechanisms. -dorsal raphe nucleus sends fibers to blood vessels the cerebral cortex to help regulate sleep and neuroendocrine functions. Also connected with the lower brainstem and the hypothalamus.
-disruption in the normal function of the hypothalamus may be responsible for prodromal signs and symptoms of migraine such as mood changes, food cravings, drowsiness, thirst, and yawning. These signs and symptoms may occur several hours, or even one day, before headache pain begins.

Migraine Treatment in kids
Diagnostic Criteria italics: different from adult criteria -≥5 attacks fulfilling features B-D -Headache attack lasting 1 – 72 hours 4-72 hours -Headache has at least 2 of the following
-Either bilateral or unilateral (frontal/temporal) location unilateral only
-Pusating quality
-Moderate to severe intensity -Aggravated by routine physical activities or causing avoidance of routine physical activity -At least 1 of the following accompanies headache
*Nausea and/or vomiting
*Photophobia and phonphobia (may be inferred from their behaviour)
Acute Treatment
*Ibuprofen 10mg/kg
*Acetaminophen 15mg/kg
-note: at two hour end point for with reduction ≥ 2 points on 5 point scale, ibuprofen = acetominophen > placebo (56-53-36%), BUT for complete resolution of headache, ibuprofen> acetominophen>placebo (60-39-28%), and reduction in moderate to severe headache by ≥ 2 grades after 2 hours was 2X more likely with acetominophen and 3X more likely with ibuprofen
* Sumatriptan spray 10-20mg
-note: at 2 hour end point, a reduction of ≥ 2 points on 5 point scale 64%vs39% drug vs placebo
*No evidence for or against oral triptans
5) Inadequate evidence for SC sumatriptan.
Preventative Therapy
* Flunarizine 5mg is probably effective *There is insufficient evidence for cyporheptadine, amitriptyline, divalproex sodium, topriamate, or levetiracetam *Pizotifen, clonidine and nimodipine are not recommended From: Practice Parameter; Pharmacological Treatment of migrains headache in children and adolescents: Report of the American Acaemy of neurology Quality Standards Subcommitte and the Practice Committee of the child Neurology Society 2004
Sytematic review published by Damen et al, Pediatrics 2005 had the same conclusions
Practice Parameter: Evidence-based guidelines fro migraine headache(an evidence based review): Report of the Quality Standards Subcomitte of the AAN Neurology 2000 55:754-762.
Recommendations for acute treatment
-For mild to moderate migraine, NSAIDS and combination analgesics containing caffeine are a reasonable first line (level A)
-Triptans (naratriptan, rizatiptan, sumatriptan and zolmitriptan) are effective and safe for acute treatment of migraine in and are an appropriate initial treatment choice in moderate to severe migraine (Level A)
DHE nasal spray is safe and effective for the treatment of acute migraine and should be considered in moderate to severe migraine (level A)
-Ergotamine PO/PR (and caffeine combination) may be considered in the treatment to of moderate to severe migraine (Level B)
-Metoclopraminde IM/IV is an adjunct to control nausea (level C) and may be considered as IV monotherapy for migraine pain relief (level B)
Procholrperazine IV, IM, and PR may be a therapeutic choice for migraine (level B)
-Acetominophen alone is not recommended for migraine (level B)
5)Corticosteroids are a treatment choice for rescue therapy in status migrainosis (level C)
Recommendations for preventative Treatment
- Medications with proven efficacy and mild adverse events: Amitriptyline, Divalporex sodium, Propranolol
- Medications with lower efficacy and mild to moderate AEs: Other B-blockers, Ca-blockers (nimodipine, verapamil), NSAIDS, Gabapentin, Fluoxetine
- Medications w/o RCT evidence that show efficacy: SSRI/SNRIs, cyproheptadine, diltiazem, Topiramate
-Medications that have efficacy but frequent or severe AEs: Methysergide
- Medications with limited to no efficacy:Carbamazepine, Clomipramine, Clonazepam, Nifedipine, Indomethacin Figure
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