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 Migraine Disorder –  Pain Sensitive Structures in the Brain 

1. Dura

2. V Nerve  

3. IX Nerve  

4. X Nerve  

5. Blood Vessels   

Migraine  

a.  It is an episodic Throbbing, Pulsatile headache that is associated with certain features such as sensitivity to light, sound, or movement (formication); nausea and vomiting often accompany the headache. patient may see ZIG – ZIG lines in front of eyes (Formification)


 b.  Patient may have aura (classical migraine) or may not have aura (common migraine)

 

c.  Time to Maximum Pain (3 To 72 Hours)  

Extra Edge:- Mechanism of migraine = It is initially vasoconstriction followed by vasodilation then pain.                        


Triptan cause vasoconstriction   Associated symptoms include:

  a. Paraesthesia with tingling and numbness 

 b. Other focal neurological symptoms such as clumsiness and weakness.

 c. Pathogonomic Aura = Scintillation Scotomas 

 

Variants of Migraine

 A- Ophthalmoplegic migraine  - 

It is characterized by a recurrent transient third nerve palsy which begins after the headache. (NEET 2017) ( USMLE 2016 )

 

B- Familial hemiplegic migraine - 

Is characterized by hemiplegia,  full recovery within 24 hours (Hemiplegia  with headache , recovery with in 24 hrs.) 


C - Basilar migraine - (NEET 2018) 

Occurs in children It is characterized by a typical migrainous aura associated with numbness and tingling of lips and extremities which is often bilateral  Ataxia of gait with occasional impairment of consciousness  

 Basilar migraine  

1. Basilar migraine is the diagnosis in patients in whom brain stem symptoms predominate. 

 2. In many patients, basilar attacks are intermingled with more typical migraine attacks. 

 3. Dizziness is frequently reported as a feature of an otherwise typical attack of migraine without an aura. 

4. Bilateral paresthesias can also occur with anxiety and hyperventilation


Diagnosis criteria :-

Repeated attacks of headache lasting 4–72 h in patients with a normal physical examination, no other reasonable cause  for the headache, and: 

At least 2 of the following features:

 1. Unilateral pain

 2. Throbbing pain

3.aggravated by movement 

4. Moderate or severe intensity

Plus at least 1 of the following features

1. Nausea/vomiting  

2. Photophobia and phonophobia 

  

 Triggers

 a. Migraine has its activators, referred to as triggers.

 b. Triggers are:  bright lights, sounds, hunger; excess stress; physical exertion; barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; oral contraceptive cheese, caffeine, and alcohol, Chocolate 

  

Recent Advances:

 Vasoactive neuropeptides, calcitonin gene–related peptide (CGRP) plays a very important role in the pathogenesis of migraine.   


Treatment of Migraine Acute Attack  

1. NSAIDs are the drug of choice for early migraine 

2. 5-HT1 Agonists: 

 a. Stimulation of 5-HT 1B/1D receptors can stop an acute migraine attack. 

 b. Ergotamine and dihydroergotamine are nonselective receptor agonists.  

c. The triptans are selective 5-HT 1B/1D receptor agonists.

  d. Triptans affect Blood flow by decreasing cerebral vasodilatation. Example of triptans (e.g naratriptan, rizatriptan, eletriptan, sumatriptan, zolmitriptan, almotriptan, frovatriptan). 

 

3. Dopamine antagonists  

Chlorpromazine, Prochlorperazine, Metoclopramide.   


Extra Edge: 

Drug of choice of early stage acute attack of migraine = NSAID  


 Preventive treatments in migraine  

1. Beta blocker: Propranolol (NEET 2017)

 2. Tricyclic: amitriptyline Dothiepin, Nortriptyline  

 3. Anticonvulsants: Topiramate, Valproate,   Gabapentin

 4. Serotonergic drugs: Methysergide 

 5. Other class: Flunarizine, candesartan 

6. For chronic migraine – Onabotulinum toxin type A .


Migraine – Disorder

 Migraine Disorder –  Pain Sensitive Structures in the Brain 

1. Dura

2. V Nerve  

3. IX Nerve  

4. X Nerve  

5. Blood Vessels   

Migraine  

a.  It is an episodic Throbbing, Pulsatile headache that is associated with certain features such as sensitivity to light, sound, or movement (formication); nausea and vomiting often accompany the headache. patient may see ZIG – ZIG lines in front of eyes (Formification)


 b.  Patient may have aura (classical migraine) or may not have aura (common migraine)

 

c.  Time to Maximum Pain (3 To 72 Hours)  

Extra Edge:- Mechanism of migraine = It is initially vasoconstriction followed by vasodilation then pain.                        


Triptan cause vasoconstriction   Associated symptoms include:

  a. Paraesthesia with tingling and numbness 

 b. Other focal neurological symptoms such as clumsiness and weakness.

 c. Pathogonomic Aura = Scintillation Scotomas 

 

Variants of Migraine

 A- Ophthalmoplegic migraine  - 

It is characterized by a recurrent transient third nerve palsy which begins after the headache. (NEET 2017) ( USMLE 2016 )

 

B- Familial hemiplegic migraine - 

Is characterized by hemiplegia,  full recovery within 24 hours (Hemiplegia  with headache , recovery with in 24 hrs.) 


C - Basilar migraine - (NEET 2018) 

Occurs in children It is characterized by a typical migrainous aura associated with numbness and tingling of lips and extremities which is often bilateral  Ataxia of gait with occasional impairment of consciousness  

 Basilar migraine  

1. Basilar migraine is the diagnosis in patients in whom brain stem symptoms predominate. 

 2. In many patients, basilar attacks are intermingled with more typical migraine attacks. 

 3. Dizziness is frequently reported as a feature of an otherwise typical attack of migraine without an aura. 

4. Bilateral paresthesias can also occur with anxiety and hyperventilation


Diagnosis criteria :-

Repeated attacks of headache lasting 4–72 h in patients with a normal physical examination, no other reasonable cause  for the headache, and: 

At least 2 of the following features:

 1. Unilateral pain

 2. Throbbing pain

3.aggravated by movement 

4. Moderate or severe intensity

Plus at least 1 of the following features

1. Nausea/vomiting  

2. Photophobia and phonophobia 

  

 Triggers

 a. Migraine has its activators, referred to as triggers.

 b. Triggers are:  bright lights, sounds, hunger; excess stress; physical exertion; barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; oral contraceptive cheese, caffeine, and alcohol, Chocolate 

  

Recent Advances:

 Vasoactive neuropeptides, calcitonin gene–related peptide (CGRP) plays a very important role in the pathogenesis of migraine.   


Treatment of Migraine Acute Attack  

1. NSAIDs are the drug of choice for early migraine 

2. 5-HT1 Agonists: 

 a. Stimulation of 5-HT 1B/1D receptors can stop an acute migraine attack. 

 b. Ergotamine and dihydroergotamine are nonselective receptor agonists.  

c. The triptans are selective 5-HT 1B/1D receptor agonists.

  d. Triptans affect Blood flow by decreasing cerebral vasodilatation. Example of triptans (e.g naratriptan, rizatriptan, eletriptan, sumatriptan, zolmitriptan, almotriptan, frovatriptan). 

 

3. Dopamine antagonists  

Chlorpromazine, Prochlorperazine, Metoclopramide.   


Extra Edge: 

Drug of choice of early stage acute attack of migraine = NSAID  


 Preventive treatments in migraine  

1. Beta blocker: Propranolol (NEET 2017)

 2. Tricyclic: amitriptyline Dothiepin, Nortriptyline  

 3. Anticonvulsants: Topiramate, Valproate,   Gabapentin

 4. Serotonergic drugs: Methysergide 

 5. Other class: Flunarizine, candesartan 

6. For chronic migraine – Onabotulinum toxin type A .


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