Migraine Headache
 

Headache
Pathophysiology
Classification
Approach to Patients
Migraine Headache
Primary Headache Syndromes
Secondary Causes
Cranial and Facial Pain Disorders
References

Table of Contents

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Epidemiology

5% in males, 17% in females

Peaks around 40 YO and gradually declines

 

Pathophysiology

Abnormal Vasculature

  • Vasoconstriction being responsible for aura and rebound vasodilatation the cause of the pounding headache

Primary Brain Disorder

  • Response of brain tissue to some trigger
  • Secondarily disordered activity of blood vessels

Aura

  • Primary neuronal dysfunction
  • Slowly spreading wave of neuronal hypoactivity traveling across brain tissue
  • Corresponding decrease in local blood flow (not follow vasoconstriction territories)

Headache

  • Pain-sensitive Intracranial structures largely supplied by sensory axons of trigeminal ganglion in the supratentorium, while the upper cervical roots innervate the posterior fossa
  • Related to activation of these sensory axon
  • Sterile neurogenic inflammation and promotes local vasodilatation
  • Release of peptides and the resulting inflammation and extravasation can be blocked by ergots, indomethacin, Triptans (+vasoconstriction effect)

No understood neurophysiologic pathways linking between aura and headaches

Enhanced excitability of occipital cortex neurons in migraine patients is a possible trigger

 

Clinical Features

85% of migraine sufferers have no aura with the event.

Duration is typically four to seventy-two hours.

Common Migraine

Accurate diagnosis of migraine without aura requires at least two of the following four characteristics. (not sens or sp)

  • Unilateral Position
  • Pulsating Quality
  • Moderate to Severe Quality
  • Aggravated by Activity

In addition, at least one of the following criteria is required:

  • Nausea or Vomiting
  • Photophobia or Phonophobia

Classical Migraine

In order to fill this criteria, at least three of the following four characteristics must be present.

  • Reversible Aura Symptoms Indicating Brain Dysfunction
  • At Least 1 Aura Develops Gradually Over 4 Minutes
  • No Single Aura Lasts More Than 60 Minutes
  • Headache Follows Aura With a Free Interval Less Than 60 Minutes

Visual aura are the commonest, usu consisting of scintillating scotoma or flashing lights

Virtually any neurologic symptom or sign can occur

Typical auras : hemiparesthesia, hemiparesis, aphasia, other speech difficulties

Rare type : basilar migraine (brainstem symptoms), lasting longer than 60 min (prolonged aura), migraine aura without headache

Auras should be distinguished from prodromes : Lethargy, hyperactivity, yawning, depression, food craving, polyuria, fluid retention

Less Forms of Migraines

Ophthalmoplegic migraine : Paresis of CN III, IV, VI

Retinal migraine : Monocular scotoma or blindness

 

 

 

Childhood Periodic Syndrome

Migraine equivalents

Ill-defined syndromes ass with migraine

Abdominal pain or vomiting without headache

 

Migrainous Infarction

Complicated migraine

Aura lasting more than 7 days or neuroimaging evidence of cerebral infarction

Migraine with focal deficit

Diagnosis of exclusion

  • Hx of previous similar migraines including neuro deficit
  • Normal results of prior Ix

Aura and deficits rarely last more than 60 min, expected to resolve prior to discharge

 

Treatment

Drugs which block the stimulation of the trigeminovascular system, tachykinin release, or neurogenic inflammation can all be used to treat migraine.

Agents which stop tachykinin release, (i.e., Sumatriptan, Ergotamine), or neurogenic inflammation (i.e., NSAID) should be used for acute migraine therapy.

Those agents which inhibit trigeminovascular stimulation (i.e., beta blockers, calcium blockers, anti-depressants) are useful in preventing migraines.

Wide spectrum of clinical practice

No clear consensus on the best therapy

No migraine treatment has been shown to be superior in all respects

Factors : efficacy, ability to abort migraine, CI, relief of other symptoms, ADR, cost, ease of administration, time to return to normal activities

DHE (CHS)

5-HT 1D receptor agonist

Highly effective in relieving headaches

Appropriate fist-line therapy

ADR : vomiting (other 5-HT + DA receptor)

Pretreated with metoclopramide or prochlorperazine

Sumatriptan (CHS)

More selective agonist

Effective and less N/V

Frequent but short-lived minor ADR (sc form) : sensations of heat, tingling, chest discomfort, injection site reaction

More costly, higher 24-hr recurrence rate

Useful for migraines unresponsive to other medications, not given within 24hr of DHE (vasoconstriction)

Other drugs studied in ED-based RCT

  • Metoclopramide
  • Chlorpromazine
  • Prochlorperazine
  • Ketorolac
  • Dexamethasone 20 mg IV
    • One ED-based RCT  reduce rate of 48 to 72 hr recurrent migraine compared to placebo
  • Meperidine and Opioids
    • Less effective than other agents but still used, May exacerbate headache in chronic use

 

 

Adjunctive Treatment

Placed in a darkened, quiet area

IV rehydration

 

Migraine Triggers

Sleep deprivation/excess

Caffeine ingestion or caffeine withdrawal
Wine, especially red, & alcohol in general
Fasting

Sex hormones

Most migraines have no trigger

Strong familial pattern

 

Migraine in Pregnant

Nonpharmacologic, rest and ice, should be tried first

Medication if intractable or N/V

Acetaminophen and NSAIDs are class B by US FDA

NSAID may inhibit labor and decrease mniotic fluid

Metoclopamide (class B) can be very useful esp if significant N/V

 

Prophylaxis

  • B-blocker without intrinsic sympathomimetic activity
  • CCB
  • TCA
  • NSAID

Titrated for several months before concluding that ineffective

Withdrawn slowly to prevent rebound headaches

 

Summarized By Thirayost Nimmanon

โดย ธีรยสถ์ นิมมานนท์

 

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