Pt is a 28 yo female with chronic Hx of recurrent nonaural HA which are unilateral to ? side and lasts 48 hr. HA usually began at start of menstrual cycles or were due to other triggers, and were characterized by throbbing, nausea, vomiting, photophobia, and phonophobia.

Comment: good summary, though left out fh of hemiplegic migraine

Head: meninges and cerebral blood flow, vasoconstriction (aura) or vasodilation (migraine) of arteries within and outside the brain. Aura associated with vasoconstriction and reduction in cerebral blood flow (hypoperfusion and ischemia). Migraine associated with vasodilation and increase in blood flow. Mother and sisters Sx appear also have cortical involvement.

The physical signs do not tell you there is vasoconstriction though you are right that the hx in the mother and sister does suggest hemispheric, likely cortical involvement. The symptoms and the physical exam suggest involvement of cranial nerv V, involvement of arteries (blood vessels carry pain fibers).

Dilation leading to increase blood flow, and pulsation of cerebral blood vessels lead to Sx of migraines, especially throbbing. Migraines may also involve the release of serotonin by the neurons of the dorsal raphe.

Comment: you comment on the pathogenesis but do not answer the question: i.e. what clues do you get from the onset and course. The sudden onset suggests vascular or electrical; the recurrence with paroxysms suggests a channelopathy.

Common migraine (no aura, most prevalent)
Classic migraine (with aura: aphasia, scotoma, fortification spectrum, stars, sparks)
Complicated migraine (focal deficits of ischemic origin) Also need to R/O: cluster HA and tension HA. Tension HA can be initiated by stress and last for days.
Often times with migraines, you can sleep off the HA. Migraine HA has strong Fam Hx. Pediatric migraines may be diffuse and not confined to hemisection.

the question asks for one clinical dx. you give several; one answer is migraine with a family hx of familial hemiplegic migraine. List of alternative dx could include tension h/a, cluster h/a, symptomatic headache secondary to local pathology, hypoglycemia, infection, tumor

CT (or MRI) to R/O intracranial lesions: epidural, subdural, subarachnoid hemorrhages Blood glucose (hypoglycemia can initiate a migraine HA) and electrolytes. If this patient were a regular patient of yours, her negative general and neurological examination would most likely obviate the need for further tests. ER patient may require above (and more) workup.

the question asks for 2 tests: you give several; the tests are designed to confirm or refute your clinical dx i.e. migraine. an imaging study would not help confirm or refute migraine. clinical follow up with a therapeutic trial of antimigraine medication would constitute one such test. I like the test you suggest for hypoglycemia. this test may help confirm the dx of symptomatic migraine

Main complications are the social and economic costs (work hours lost) of migraines. Another complication is that the ischemic events (aura) that the mother and sister experiences can lead neural cell necrosis and result in permanent neurological deficits.

good one; i agree with the cost of migraine; and i agree you can get strokes as a consequence of complicated migraine; another potential complication is narcotic addiction

Two strategies: Abortive therapy (treat acute migraine) or Prophylaxis therapy

Abortive Therapy
Analgesics to reduce pain and inflammation Sumatriptan works by affecting vascular supply or stabilizing serotonin release, therefore need to give at START of migraine Cafergot: ergotamine + caffiene. Ergotamine is also thought to reduce serotonin release. Cell bodies of serotonergic neurons are found in and around the midline raphe nuclei of the brain stem.

Prophylaxis Therapy
Avoid Triggers: exertion, EtOH, stress, hunger, lack of sleep, and oral contraceptives Beta blockers: mode of action unknown

good; note sumatriptan is a 1B/D serotonin receptor agonist. Calcium channelopathies cause complicated migraine and calcium channel blockers are effective prophylactic agents and potentially cause vasodilation. Paradoxically ergots are serotonin antagonists (including to type 2 serotonin receptors) and cause vasoconstriction and can be used as abortive therapy. They are avoided in complicated migraine because they tend to exacerbate the vascoconstriction and may cause a cerebral infarct in migraine patients.

This is a 28 y/o female, presenting with recurrent unilateral, throbbing headache with associated nausea, vomiting, and sensitivity to light and sounds. Headaches cycle with the menstrual period and began at the age of 13.

Data regarding location of the headache may be informative. If the source is an extracranial structure, as in giant cell arteritis, the correspondence with the site of pain is fairly precise. Lesions of paranasal sinuses, teeth, eyes, and upper cervical vertebrae induce less sharply localized pain, but that pain that is still referred in a regional distribution. Intracranial lesions in the posterior fossa cause pain that is usually occipitonuchal, and supratentorial lesions most often induce frontotemporal pain.” (Harrisons Textbook of Internal Medical Online, Part 2, Chapter 15, Raskin.)

Migraine headaches are a result of vascular constriction (thought to cause the aura) and vascular dilation (thought to cause the pain associated with migraines). Migraines have three components: 1) vasculomotor component, 2) mid-brain trigger, and 3) activation of the trigeminal system. For this particular patient, the migraines are associated with her menstrual periods. Periods often cause water retention in women, causing tissue edema, which may include brain tissue. The edema may increase intracranial pressure, causing pressure on the blood vessels, thus triggering migraines.

A. Migraines
B. Cluster headaches with chronic paroxysmal hemicrania
C. Tension headaches
D. Trigeminal neuralgias
E. Brain tumor
F. Giant cell vasculitis
G. Idiopathic headache

Migraines are diagnosed based on clinical judgement, but genetic studies are beginning to identify gene loci in some cases.

Like the patients mother and sister, complications of migraine include hemiplegic migraines.

PET studies of a patient taken during migraine showed a depression of cerebral blood flow beginning at the occipital poles and spreading bilaterally up to the central fissure. The management of the patient depends on the causes of the migraine, which is thought to be due to Calcium channel disorders. Prophylactic use of Calcium channel blockers is commonly prescribed as treatment.

SOURCES:
1. Harrisons Textbook of Internal Medicine Online.
2. Robert C. Collins “Neurology”, 1997, pg.45-46.
3. Lindsay & Bone, Neurology and Neurosurgery Illustrated, Third
edition, 1997, pg. 66-70.

I liked your answers. I have some comments on the case. The pathophysiology could have included info on serotonin receptors, calcium channelopathy. Your summary is good and concise. Localization should be shorter. the pathogenesis question is getting to how the course helps us with clues for pathophysiology i.e. paroxysmal and recurrent suggestive of a vascular or ion channel problem.

A 44 yo woman presents with acute symptoms of severe headache, stiff neck and loss of consciousness. On physical exam, she can only react to strong pain stimuli, and with reduced right-sided movement.

Lesion localization based on PE:
1. Meninges (PE findings: stiff neck, positive Kernig)
2. left motor cortex (PE findings: reduced movement on right with pain stimulation)
3. bilateral hemisphere/brainstem (PE findings: coma)

note: coma is caused by disruption in either the global hemispheres or the reticular activating system (sleep center).

Pathogenesis: SUDDEN
In order of likelihood:
1. Vascular: onset is minutes to hours
2. Seizure: onset is seconds to minutes
3. Infection: onset is hours to days

Diagnosis: SUBARACHNOID HEMORRHAGE

In order of likelihood:
1. Vascular: This patient could have hemorrhaged in to her meninges.
Most likely, this is a subarachnoid hemorrhage since you don't bleed in sub-pia space and bleeding in the sub-dural space is caused by trauma (bridging veins damaged). Hemorrhage could be caused by A-V malformation or a ruptured aneurysm. 2. Seizure: this can not explain the lesions stated in #2.
3. Infection: Could be abscess or meningitis. Least likely because the patient's onset was sudden and fever was low.

Tests:
1. CT to visualize blood in subarachnoid.
2. Lumbar puncture to test glucose and protein levels. If the patient has bacterial meningitis, her glucose would be low and proteins would be high. Probably would do CT first because lumbar puncture can cause herniation if patient has increased intracranial pressure.

Relevance of pathophysiology: as listed in complications. Underlying anatomical defect of ruptured aneurysm or an AV malformation. Acutely, concern with rebleeds (increasing intracranial pressure) and vasospasm. After surviving the acute episode, a surgical intervention probably is necessary to prevent a reoccurance.

Good job. You were one of the few people whose summary was appropriately concise. You are a bit skimpy on the pathophysiology question, (see my comments on the posted case). Pathophys discussion could include comments on the vasospasm secondary to blood in the subarachnoid space thought to be secondary to oxyhemoglobin, and also to using hypervolemic and hypertensive measures of maintaining cerebral perfusion. For question 2 the lesion could be in the left hemisphere not necessarily the left cortex.