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Neuro 2 > Headache > Flashcards

Headache Flashcards

1
Q

International Headache Society Classification

A
  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)
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2
Q

Temporal Mode of onset/progression of signs/symptoms

A
  • headaches of acute onset (abrupt-onset, rapid worsening)

- headaches of subacute onset (gradual onset, progressive buildup)

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3
Q

Pathophysiology Common Among Headaches

A

-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

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4
Q

How is headache pain transmitted?

A
  • 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
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5
Q

Headache Pain Red Flags

A
  • 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”
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6
Q

Primary Headaches: Migraine

A

-chronic neurological disorder causing recurrent headaches w/some or all of the following:
frequently unilateral (may switch sides)
pulsating
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

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7
Q

Stages of Migraine

A
  • Preheadache (prodrome & aura)
  • headache
  • post headache
  • begin or stop at any stage
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8
Q

Migraine Prodrome

A

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

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9
Q

Migraine Aura

A

-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
(20%)

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10
Q

Migraine Epidemiology

A
  • lifetime prevalence ~15-20% of pop.
  • women 10-15%, men 5-10%
  • begins before age 20
  • dec. occurrence after age 25
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11
Q

Migraine Genetics

A
  • family history
  • polygenic - one loci at 10q23
  • familial hemiplegi migraine (dominant gene)
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12
Q

Anatomical Substrate for Migraine

A
  • 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
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13
Q

Brain Stem Nuclei important for Migraine

A
  • magnus raphe, locus ceruleus, dorsal raphe nuclei

- connection b/w trigeminal nucleus caudalis and superior salivatory nucleus

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14
Q

Migraine Pathogenesis

A

-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

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15
Q

Migraine Pathogenesis: Cortical Spreading Depression

A
  • wave of brief neuronal excitation
  • prolonged depolarization
  • moves across cortex at 2-5mm/min
  • brief hyperemia with excitation
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16
Q

Migraine Pathogenesis: Migraine Aura

A
  • 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
17
Q

Chemicals Irritate Trigeminal Nerve

A

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)

18
Q

Role of CGRP

A
  • 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
19
Q

Migraine Treatment: Triptans

A
  • sumatriptan first approved for migraine

- agonists at serotonin or 5HT1 receptors, inhibits release of GCRT

20
Q

Migraine Treatment: Gepants

A

-CGRP antagonists

21
Q

Primary Headaches: Cluster

A
  • 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
22
Q

Cluster Headache: Treatment

A 
-acute Rx: nasal oxygen at 8-10l l/min
                subcutaneous Sumatriptan
-Prophylaxis: calcium channel blockers (Verapamil)
                    lithium
                    valproic acid
                    prednsone
23
Q

Primary Headaches: Episodic/Chronic Tension

A
  • 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
24
Q

Episodic/Chronic Tension Headaches: Pathophysiology

A

-complex & multifactorial

25
Q

Episodic/Chronic Tension Headaches: Treatment

A
  • 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
26
Q

Secondary Headache: Idiopathic Intracranial HTN

A 
-IIH (Pseudotumor Cerebri)
Features:
-headache of varying character
-papilledema
-transient visual obscurations
-diplopia secondary to CN VI paresis
-Tinnitus 
-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***
27
Q

Idiopathic Intracranial HTN Classification

A
  • 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
28
Q

Idiopathic Intracranial HTN Pathogenesis

A

-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

29
Q

Idiopathic Intracranial HTN: Diagnosis

A
  • 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
30
Q

Secondary Intracranial Hypertension: Treatment

A
  • (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
31
Q

Secondary Headaches: Giant Cell (temporal) arteritis

A
  • autoimmune, systemic vasculitis causing granulomatous infiltration & occlusion of medium/small elastic arteries
  • Headache: usually unilateral, chief complaint in >70%
  • point scalp tenderness over temporal artery
  • visual symptoms - monocular obscurations leading to blindness secondary ophthalmic artery occlusion
  • associated polymyalgia rheumatica ~50% with jaw claudication, malaise, fever, weightloss, myalgias
  • Stroke: particularly involving vertebral arteries
32
Q

Giant Cell (temporal) arteritis: lab & Rx

A
  • no single test but ESR inc. in 75%
  • C-reactive protein also elevated
  • temporal artery biopsy - may be - in 1/3 because of “skip” lesions
  • inflammation & multinucleated giant cells in elastic laminae of medium/small arteries
  • Medical/Neurological emergency (acute onset of monocular blindness)
  • Corticosteroids should be started immediately with temporal artery biopsy performed ASAP

Neuro 2 (16 decks)

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