Neuro Objectives 25

1. Primary headache disorder (Tension, cluster, migraine): stable, non-progressive, intermittent, hemicranial, can alternate size, normal neurological exam

Secondary headache disorder (Increased ICP, tumor, vascular problem): weakness, first severe headache, progressive course, triggered by something, meningismus (stiffening of neck from meningitis), papilledema (optic nerve swelling)

Migraine symptoms: hemicranial with unilateral pounding/pulsating; prodrome (vague feeling of difference) → aura (visual differences) → headache → postdrome (washed out, low pain)

·  Note: Pain is mediated by the trigeminal nerve in the dura and has poor localization due to variability of nerve endings

2. Migraine aura: strange visual sightings that increase in size over 15-20 minutes; tingling in other areas may be present

Theories of aura:

a.  Constriction of blood vessels → ischemia → aura

b.  Spreading depression → wave of excitability over occipital cortex → aura

3. Evidence of brainstem involvement: symptoms of CN deficiencies are common in migraine, increased activity in trigeminal/dorsal Raphe nuclei (even when symptoms are treated), sleep aborts migraine

Evidence of serotonin involvement: drop in serotonin can trigger a migraine, during attack serotonin levels rise, serotonergic drugs are effective in treatment, serotonin causes inflammation (axon reflex) and vessel dilation (both cause indirect nociception by swelling against trigeminal nerve endings in dura)

·  Note: 5-HT1B, 1D autoreceptor agonists work by inhibiting reuptake and rerelease of serotonin

·  Note: 5-HT2 receptor antagonists shut off serotonin activity

·  Note: there are many classes of 5-HT receptors each with different signaling events and consequences