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Flashcards in Headache Deck (32)
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International Headache Society Classification

1. Primary - without identifiable structural cause
(migrain, cluster, tension (episodic & chronic), miscellaneous)
2. Secondary - Headaches with underlying structural/metabolic cause
(brain tumor, meningitis/encephalitis, idiopathic intracranial HTN (pseudotumor cerebri), subarachnoid hemorrhage, giant cell (temporal) arteritis, cerebral vein thrombosis, post-traumatic headache)


Temporal Mode of onset/progression of signs/symptoms

-headaches of acute onset (abrupt-onset, rapid worsening)
-headaches of subacute onset (gradual onset, progressive buildup)


Pathophysiology Common Among Headaches

-inflammation or physical traction of pain sensitive nerve fibers underlies all types of headaches
Pain sensitive structures:
-dura & meninges at base of brain
-large arteries at base of brain, meningeal arteries
-scalp muscles
-upper cervical muscles
-periosteum of the skull
-facial & head structures/organs (skin, eyes, teeth, nasal sinuses, muscles)

-brain parenchyma has no sensory receptors & is thus INSENSITIVE to pain


How is headache pain transmitted?

-centrally via CNs V, VII, IX, X, and the upper cervical nerve roots C2-3
-ophthalmic branch of CN V innervates pain sensitive structures of the anterior/middle fossa and scalp; CN IX & X and cervical nerve roots C2 and C3 innervate the posterior fossa, the cervical muscles & posterior scalp
-pain sensitive nerve fibers synapse in trigeminal nucleus caudalis & dorsal horn of the upper cervical spine
-central pain fibers synapse in VPL & VML nucleus of thalamus and then onto sensory cortex


Headache Pain Red Flags

-red flag due to "secondary" etiology
-abrupt onset, recent head trauma, fever, Hx of immunosuppression, altered consciouses, focal neurologic signs/symptoms, new onset >50, neck pain or stiffness, anticoag use, headache progression over days, recently altered cognition, "worst headache of my life"


Primary Headaches: Migraine

-chronic neurological disorder causing recurrent headaches w/some or all of the following:
frequently unilateral (may switch sides)
moderate to severe intensity
duration of 4-72hr
nausea with or without vomiting
photophobia and/or phonophobia
may be preceded by prodromal phase
may be preceded by an aura in ~20% migraineurs
"triggers" or precipitating factors are frequent
family history


Stages of Migraine

-Preheadache (prodrome & aura)
-post headache
-begin or stop at any stage


Migraine Prodrome

in ~40% of migraineurs
-vague constellation of symptoms: mood swings (depression, anxiety, irritability), odd food cravings, malaise or vague feeling of un-wellness, fatigue, muscle aches & stiffness


Migraine Aura

-visual disturbance with precedes headache (no more than 60min)
-begin near center of visual field as small gray area with indefinite boundaries
-in minutes, gray expands into horseshoe with bright zigzag lines
-lines grow as a blind (scotoma) area expands and moves outward toward periphery of visual field


Migraine Epidemiology

-lifetime prevalence ~15-20% of pop.
-women 10-15%, men 5-10%
-begins before age 20
-dec. occurrence after age 25


Migraine Genetics

-family history
-polygenic - one loci at 10q23
-familial hemiplegi migraine (dominant gene)


Anatomical Substrate for Migraine

-Trigeminovascular System involving CN V1 innervation of pain receptors located in the dura, meninges, and medium/large cerebral arteries & veins that lie on the surface of the brain & above the tentorium
-C2 (back of head)
-CN VII & parasympathetic innervation of Superior salivatory nucleus (vasodilation & other parasympathetic symptoms associated w/migraine reflect central connections b/w pain pathways from CN V & superior salivatory nucleus


Brain Stem Nuclei important for Migraine

-magnus raphe, locus ceruleus, dorsal raphe nuclei
-connection b/w trigeminal nucleus caudalis and superior salivatory nucleus


Migraine Pathogenesis

-Central Sensitization (brain stem, thalamus)
to central pain (thalamus, cortex, limbic, parasym.)
-Internal, External Triggers (emotional, physical, chemical) to Central Generator (brain stem) or to Aura (cortical)
-Both go to Neurogenic Inflammation (triminovascular system) to central pain


Migraine Pathogenesis: Cortical Spreading Depression

-wave of brief neuronal excitation
-prolonged depolarization
-moves across cortex at 2-5mm/min
-brief hyperemia with excitation


Migraine Pathogenesis: Migraine Aura

-brief scintillations at leading edge
-move across the visual field that correspond to movement across cortex at 2-5mm/min
-scintillations replaced by scotoma
-CBF measurements in humans during aura show oligemia in affected territory


Chemicals Irritate Trigeminal Nerve

2 important neurotransmitters
1) Calcitonin gene related peptide (CGRP)
2) Substance P (SP)
-trigeminal ganglion may function as afferent system and efferent system (sending action potentials from neuron body orthodromically to the sensory nerve terminals where a variety of neurotransmitters chemicals may be released (CGRP and SP into dural & meningeal blood vessels, both vasodilators)


Role of CGRP

-mediate neurogenic inflammation & pain in migraine (37 AA peptide)
-CGRP receptors present on dural & cerebral vascular smooth muscle
-potent vasodilator
-causes mast cell degranulation
-serum plasma levels elevated during migraine
-triptans block CGRP release
-CGRP give iv causes migraine like headache


Migraine Treatment: Triptans

-sumatriptan first approved for migraine
-agonists at serotonin or 5HT1 receptors, inhibits release of GCRT


Migraine Treatment: Gepants

-CGRP antagonists


Primary Headaches: Cluster

-Chronic Neurological disorder causing recurrent headaches with some or all of:
-pain always unilateral, frontal, retro-orbital
-unilateral conjunctival infection & rhinorrhea
-unilateral Horner's syndrome & lacrimation
-Constant, severe, non-pulsing pain
-duration of minutes (3 hrs)
-daily attacks for weeks/months, remission for yrs
-men to women: 4:1
-~25yrs at onset
-"triggers" are alcohol & tobacco
-rare family history


Cluster Headache: Treatment

-acute Rx: nasal oxygen at 8-10l l/min
subcutaneous Sumatriptan
-Prophylaxis: calcium channel blockers (Verapamil)
valproic acid


Primary Headaches: Episodic/Chronic Tension

-chronic neurological disorder causing recurrent headaches with some or all or:
-pain bilateral & bandlike
-not associated with auras, nausea/vomiting, photo or phonophobia
-duration - 3 hrs
-daily attacks < 15 days/month = episodic
-daily attacks > 15 days/month = chronic


Episodic/Chronic Tension Headaches: Pathophysiology

-complex & multifactorial


Episodic/Chronic Tension Headaches: Treatment

-episodic tension headaches are most common form of headache & rarely prompt an office visit
-self medicate with over-the-counter analgesics

-chronic tension headaches require a careful & lengthy patient evaluation & followup
-best referred to neurologist or headache expert for diagnosis & treatment


Secondary Headache: Idiopathic Intracranial HTN

-IIH (Pseudotumor Cerebri)
-headache of varying character
-transient visual obscurations
-diplopia secondary to CN VI paresis
-constriction of visual fields, enlarged blind spots
-Female: Male 9:1
-age 20-45
-overweight, typically by 20% over normal body weight
***emergency, may cause loss of vision***


Idiopathic Intracranial HTN Classification

-Primary Idiopathic - cause unidentified
-Primary Symptomatic - cause related to underlying metabolic abnormality that alters CSF production or reabsorption
-Secondary - cause related to underlying process that physically blocks CSF circulation &/or absorption


Idiopathic Intracranial HTN Pathogenesis

-Primary Idiopathic - unknown, inc. CSF production
dec. CSF reabsorption
-Primary Symptomatic - hypervitaminosis A
antibiotics (tetracycline)
steroid withdrawal
-Secondary - Venous sinus thrombosis
Chronic meningitis
Chiari malformation


Idiopathic Intracranial HTN: Diagnosis

-clinical presentation
-MRI & MRV (both should be normal, images r/o masses or venous sinus thrombosis
-LP - opening pressure > 250 mm H2O is diagnostic in presence of normal MRI/MRV; pressures b/w 200-250 mm H2O are consistent with Dx but obese people may have CSF pressures normally in this range
-Visual Fields - to establish baseline against which to measure treatment success or disease progression


Secondary Intracranial Hypertension: Treatment

-(Pseudotumor Cerebri)
-weight loss most effective but difficult
-reduce CSF production - Acetazolamide, Furosemide
-Repeat LPs
-Surgical - Optic Nerve Fenestration
- Lumbar or ventricular peritoneal shunts
-monthly follow up to assure visual system is stable