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Neurology Lectures > Headache (Ferguson) > Flashcards

Headache (Ferguson) Flashcards

1
Q

____ of the population has >1 headache annually

  • 5-7% of the population seeks medical attention
  • Reason for 2% of doctor visits, 3% of ER visits
  • 15% women, 6% men, 4% children
  • 5.5-17 billion dollars lost in productivity
A

65-85%

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2
Q

Which structures of the brain are pain sensitive?

  • Pain is a normal response from a healthy nervous system
A
  • Scalp
  • Sinuses
  • Meninges
  • Pial arteries
  • Arteries and major veins
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3
Q

Which cranial structures are not pain sensitive?

A
  • Ventricles
  • Choroid
  • Brain parenchyma(except one part of midbrain)
  • Small parenchymal and dural veins
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4
Q

What are some anatomic etiologies for pain?

  1. distention, traction, dilation, irritation, contraction, displacement, inflammation, or activation of… (5)
A
  1. Vasculature
  2. Nerve
  3. Meninges - dura
  4. Muscles - cranial or cervical musculature
  5. Brain stem (small area near the dorsal raphe nucleus [high concentration of serotonin])
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5
Q

Headaches are classified by the ________

and classified as either: (3 types)

A

International Headache society

  • Primary HA
  • Secondary HA
  • Cranial neuralgias
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6
Q

What type:

  • Primary
    • benign reoccuring disorder that has associated symptoms which can include: photophobia, phonophobia, nausea, vomiting, worsening with exertion, neurologic sx.
A

Migraine

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7
Q

What is thought to be the current pathophysiology behind migraines?

A
  • Begin in the brainstem, with activation of cells that spreads peripherally to stimulate the trigeminal system
  • May also affect other local systems - chemoreceptors and autonomic nervous system
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8
Q

What kind of migrane?

  • unilateral, often descibed as a deep ache or throbbing sensation
  • Photophobia, phonophobia, nausea, vomiting
  • Worsened by exertion and relieved with rest
    • 30 minutes - 6 hours, can last longer
A

Migraine without aura

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9
Q

What kind of migraine?

  • unilateral, often descibed as a deep ache or throbbing sensation
  • Photophobia, phonophobia, nausea, vomiting
  • Worsened by exertion and relieved with rest
    • 30 minutes - 6 hours, can last longer
  • Preceded by aura up to 30 mins before, and up to 1 hr into the headache
A

Migraine with aura

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10
Q

What is an aura?

  • Types?
A

Perceptual disturbance experienced prior to headache and/or into headache that can manifest as:

  • Visual aura - eg scintillating scotoma, central scotoma, zig-zag lines, kaleidoscope, tunnel vision, vision loss
  • Sensory aura - pins & needles
  • Motor aura - focal weakness, paralysis
  • Auditory aura - buzzing, amplitude modulation, heightened sensitivity to sound
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11
Q

What kind of migraine?

  • dramatic, same as migraine with aura - but can last for an extended period of time
  • can ​mimic the appearance of STROKE
A

Complicated Migraine

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12
Q

What kind of migraine?

  • Have associated brainstem and posterior cerebral circulation symptoms: vertigo, diplopia, dysarthria, ataxia
  • Headache follows neurologic symptom after 20-30 mins; often occipital throbbing pain

BONUS: what type is the most severe form of this, with total blindness and admixtures of vertigo, ataxia, dysarthria, and tinnitus?

A

Basilar Migraine

BONUS: Bickerstaff’s migraine

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13
Q

What kind of migraine?

  • CLinically appears as repeated attacks of severe noncolicky midline abdominal pain
  • Associated with typical migraine prodromes and auras
    • 2-4% prevalence in children; uncommon in adults
A

Abdominal migraine

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14
Q

What is the non-pharmacologic approach to migraine treatment?

A

AVOID TRIGGERS - e.g. red wine, certain foods (chocolate, cheese, msg, processed meats, nitrites); increased hunger, sleep deprivation, stress

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15
Q

What are the abortive/rescue therapies used to treat migraines?

A
  • NSAIDS - ibuprofen, naprosyn, ketorolac
  • 5HT1 antagonists - sumatriptan (short acting), zolmitriptan (intermediate acting), frovatriptan (long acting)
  • Dopamine Agonists - metoclopramide, prochlorperazine
  • Combinations - excedrin, fiorcet, midrin
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16
Q

What are the prophylactic therapies used to treat migraines?

BONUS: when should these be used?

A
  • Beta-blockers - propranolol, atenolol
  • Calcium channel blockers - verapamil
  • TCA’s - amitriptyline, nortriptyline
  • Anticonvulsants - gabapentin, valprioic acid, topiramate, levetiracetam
  • Serotonergic drugs - cyproheptadine

BONUS: used when migraines are severe enough to cause functional impairment, and occur at least 3x/month

17
Q

What are the trigeminal autonomic cephalagias?

pathophysiology: ________ pathways are involved in pain modulation = evolution of the headache

  • _____ is a neuropeptide made in the hypothalamus
  • trigeminovascular and cranial parasympathetic pathways are responsible for the ipsilateral pain/autonomic features
  • Pain sensitive intracranial structures are innervated by ___________
A

headaches with autonomic features:

  • Cluster headaches
  • Paroxysmal hemicranias
  • SUNCT
  • Hemicrania continua
  • Orexinergic
  • Orexin
  • Ophthalmic branch of the Trigeminal nerve
18
Q

Which trigaminal autonomic cephalagia? (primary)

  • Uncommon, 0.1% of population, more males, 20% familial
  • Episodic headaches - 1 to 3 short duration (15 min to 3 hr) attacks of severe unilateral stabbing periorbital/temporal pain
  • Occur in groups for 3-6 weeks, with at least 1: conjunctival injection, lacrimation, miosis, ptosis, edema, rhinorrhea, congestion, persperation
  • CIRCADIAN rhythm - same time of day
A

Cluster headaches

19
Q

What are the Acute treatments of cluster headaches?

  • via? for how long?
  • what route?
A
  • OXYGEN 12 L/min via - non-rebreather face mask for 15 minutes (most affective abortive agent)
  • Instranasal, subcutaneous Triptan - short onset, short duration
20
Q

What agents are used prophylactically for Cluster headache treatment?

  • s
  • s
  • s
  • s
A
  • High dose steroids - prednisone (60-80 mg/day) 2 weeks + taper
  • Calcium channel blockers - verapamil, 160 - 480 mg CR daily; baseline EKG
  • Lithium - 300 - 1200 mg, check TSH and renal fxn
  • Valproic acid (250-750 mg bid), monitor CCP, CBC
21
Q

What type of trigeminal autonomic cephalagia? (primary)

  • Uncommon, episodic headache occurs at least 20x - severe unilateral, orbital/supraorbital/temporal pain lasting 2-30 minutes
  • Must have at least 1: conjunctival injection, lacrimation, edema, miosis, ptosis, rhinorrhea, congestion, persperation
  • CIRCADIAN rhythm - same time

Treatment: *** responds to Indomethacin 150 mg/day (25 tid to 50 tid, check baseline renal fxn, no skipping doses)

A

Paroxysmal Hemicrania

22
Q

Which type of trigeminal autonomic cephalagia? (primary)

  • Uncommon, the rarest
  • Ultra-brief paroxysmal headache lasting seconds, 1 second to 10 minutes
  • stabbing in nature
  • Recurs many times over several minutes and may be superimposed on a dull ha (100x per day)
  • Must have at least 1: conjunctival injection, lacrimation, tearing
  • Sx can mimic pathology of the posterior fossa or pituitary
A

SUNCT (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing)

23
Q

Treatment for SUNCT?

A

Lamotrigine - first line, 75% responder rate, 100-400 mg daily titrated slowly

24
Q

What type of primary headache?

  • Most prevalent headache syndrome - squeezing/pressure sensation, light and/or sound sensitive
  • Never have nausea/vomiting
  • Treatment:
    • Decrease stress, biofeedback, CBT, sleep
    • Abortive?
    • Prophylaxis?
A

Tension headaches

  • Abortive - Acetaminophen, NSAIDs
  • Prophylaxis - TCA’s, Antiepileptic - gabapentin
25
Q

What secondary headache disorder?

  • Predominantly affects obese women of childbearing age
  • 8:1 female to male ratio
  • Pathophysiology: obstruction of segments in the distal transverse sinus, increased venous pressure in the superior sagittal sinus - CSF production = CSF reabsorption, but higher pressure is needed to achieve this balance 2/2 increased resistance at arachnoid granulations
A

Idiopathic Intracranial Hypertension

26
Q

How does obesity contribute to IIH?

A

Increases intra-abdominal pressure, and raises cardiac filling pressures, lead to impeded venous return form the brain, with a subsequent elevation in intracranial venous pressure

* if not treated, interruption of the axoplasmic flow of the optic nerves with papilledema - may lead to irreversible optic neuropathy

27
Q

What are some symptoms of idiopathic intracranial hypertension?

  • kind?
  • what sound?

Signs: PAPILLEDEMA

A
  • Headaches - nonspecific with variable location, throbbing/pressure, worse with valsalva
  • Pulsatile tinnitus - whooshing sound
  • Vision impairment - flashes, floaters, diplopia (trochlear, abducens palsy), decreased acuity and impaired visual fields (nasal inferior quadrant, then loss of the central visual field), dimming with valsalva
28
Q

For IIH, disc edema necessitates neuroimaging with ____ and _____ to rule out mass or dural venous sinus thrombosis

  • What might you see on MRI?

For LP required pressures are? (CSF can be drained to normal closing pressures)

A
  • MRI
  • MRV
  • Normal-small slit like ventricles, enlarged optic nerve sheaths, empty sella

LP: > 250 mm H2O

29
Q

What are the non-pharmacologic treatments for Idiopathic Intracranial Hypertension?

  • failed medical management resulting in elevated ICP, progressive visual deterioration, worsening disc edema, necessitates?
  • CSF shunts - vp, lp
  • optic nerve sheath fenestration
A
  • Weight loss
  • Diet
  • Bariatric surgery
  • Surgical management
30
Q

What are some drug classes used to treat idiopathic intracranial hypertension?

A
  • Acetazolamide - 4g daily (start at 250 mg), helps improve visual outcome
  • Furosemide
  • Corticosteroids - transient use
  • Anticonvulsants - topiramate; weak carbonic anhydrase inhibitor, side effect of weight loss
31
Q

What are some alternate causes of idiopathic intracranial hypertension?

A
  • Vitamin A toxicity
  • Minocycline
  • Dural venous thrombosis
32
Q

Waht secondary headache disorder?

  • Vasculitis that is almost exclusively found in >50 year olds
  • Presents as progressive, unilateral, throbbing headache with tenderness of the temporal scalp area
  • Often complain of concomitant: jaw claudication, joint aches, visual disturbance, monocular transient vision loss
  • Elevated ESR, CRP
A

Giant Cell Arteritis

33
Q

What is the gold standard for diagnosis of giant cell arteritis?

Treatment?

A

Temporal artery biopsy

- Obtain a large section of artery, known to skip sections

  • Tx: high dose steroids (typically resolve in 3 days)
34
Q

Evaluation of this should hinge on obtaining a complete history and thorough neuro examination - urgent CT to rule out hemorrhage, large mass lesion, or hydrocephalus

  • MRI is much more sensitive to subtle pathology and should be considered
  • LP in setting of febrile illness, immunocompromised patient, and when hemorrhage is suspected even when CT is normal
A

Acute , new-onset, severe headache

Neurology Lectures (12 decks)

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