Headache (Ferguson) Flashcards

(34 cards)

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
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**
Idiopathic Intracranial Hypertension
26
How does obesity contribute to IIH?
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
What are some symptoms of idiopathic intracranial hypertension? * kind? * what sound? * Signs: **PAPILLEDEMA**
* 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
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)
* MRI * MRV * Normal-small slit like ventricles, enlarged optic nerve sheaths, empty sella LP: \> 250 mm H2O
29
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
* Weight loss * Diet * Bariatric surgery * Surgical management
30
What are some drug classes used to treat idiopathic intracranial hypertension? * * * *
* 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
What are some alternate causes of idiopathic intracranial hypertension?
- Vitamin A toxicity - Minocycline - Dural venous thrombosis
32
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
Giant Cell Arteritis
33
What is the gold standard for diagnosis of giant cell arteritis? Treatment?
**Temporal artery biopsy** **-** Obtain a large section of artery, known to skip sections * Tx: high dose steroids (typically resolve in 3 days)
34
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
Acute , new-onset, severe headache