Headache Flashcards

1
Q

Primary Vs. Secondary Headache

A

Primary
* not associated with other diseases
* migraine, tension, cluster
* neuro exam normal between HA
* during HA photophobia/phonophobia often noted with an otherwise normal neuro exam

Secondary
* Caused by other conditions and will not resolve until casue is treated
* Viremic or acute sinusitis HA most common 2ndary HA seen in primary care
* other casues: intracranial bleed, increased ICP, meningitis, accelerated HTN, gian cell arteritis, tumor - Neuro exam abnormalities

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2
Q

Headache Red Flags for determining 2ndary HA

A

SNOOP
* Systemic symptoms - fever, weight loss: infection (menengitis, encephalitis), inflammation, metastatic disease
* Secondary HA risk fators: HIV, malignancy, pregnancy, anticogulation, HTN >180/120
* Nerologic S/S: new finding including confusion, impaireed alertness/consciousness, nucal rigididty, papilledema, CN dysfunction, abnl motor function
* Onset - Sudden, abrupt, or split-second (thunderclap) = subarachnoid hemorrhage. Onset with exertion,sexual activity, coughing and sneezing is suggestive of increased ICP = mass
* Onset - older age - temporal/giant cell arteritis, younger may be mass
* Prior HA Hx: change in quality or frequency - med overuse, mass, subdural hematoma
* Positional: upright vs. laying down, neck position = intracranial hypotension, posterior fossa pathology
* Papilledema (optic disk swelling) - visual problems = encephalitis, meningitis, mass

CT without contrast - most common test for acute severe HA with new onset abnormality on neuro exam - detects hemmorrhage or stroke
CT with contrast - can detect tumor or abcess
MRI - can detect tumor

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3
Q

Tension type Headache Characteristics

A
  • 30 min -7 days
  • pressure, non-pulsitile pain
  • mild to mod intensity
  • usually bilateral
  • notation of 0-1 of the following (if >1 may be migraine)
    1. nausea, photophobia, or phonophobia
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4
Q

Migraine without Aura charachteristics

A
  • lasts 4-72 hrs with 2 or more of the following
    1. Usually unilateral, can be bilat
    2. Pulsating quality, mod to severe
    3. agrivated by normal activity or causes avoidance of normal activities
    4. Durring HA noting more than 1 of the following:
    -nausea/vomiting, photophobia, phonophobia
    5. positive family Hx in 70-90%
    6. often occur 1 wk prior to menses
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5
Q

Migraine with Aura characterisitcs

A

Migraine type HA occurs with or after aura
* focal dysfunction of cerebral cortex or brain stem causes 1 or more aura symptoms developing over 4 min, or 2 or more occur in succession
* Symptoms can include: feeling of dread/anxiety, unusual fatigue, nervousness/excitement, GI upset, visual or olfactory alteration
* Aura symtoms should not last more than 1 hour

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6
Q

Cluster HA characteristics

A
  • HA occurs daily in groups or clusters usually lasting several weeks to months, then disappear for months to years
  • usually occur at characterisitic times of year (vernal and autumnal equinox), 1-8 episodes/day at the same time of day, commonly about 1 hour into sleep (alarm clock)
  • often located behind 1 eye with steady intense sensation, severe pain in crescendo pattern lasting 15 min - 3 hrs. Accompanied by ipsilateral autonomic signs: lacrimation, conjunctival injection, ptosis, nasal stuffiness
  • Male>female, 20% with family hx
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7
Q

Acute HA therapy, analgesics

A

NSAIDS, actaminophen (aspirin, ibuprofen, naproxen, diclofenac, celecoxib): limit use to 2 treatment days per week to avoid rebound HA. may combine with triptan to enhance headache relief

Triptans potentially helpful in tension-type HA that do not respond to satndard analgesic therapy, also used in treatmetn of cluster HA. Avoid use in pregnancy, CVD, poorly ctrled HTN
* effective at relieving photo/phonophobias

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8
Q

Migraine acute therapy

A

Triptans (Selective serotinin receptor agonists)
* inhibit the release of vasoactivepeptides, promoting vasoconstriction and block pain pathways
* Sumatriptan, almotriptan, rizatriptan

Ergots
* 5HT 1B/D blocker, pain modulating pathway, also a weak vasoconstrictor
* dihyroergotamine - nasal spray or injection

Ditans
* lasmidian

gepants (CGRP antagonist, monoclonal antibody)
* urbogepant (Ubrelvy)
* newer class, does not cause vasoconstriction

  • triptans, ergots, ditans - avoid use in pregnancy, CVD, poorly ctrled HTN
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9
Q

Prophylactic migraine meds

A

Indication for prohylaxis
* 3 or more migraines per month and/or attacks interfere with daily routines even with acute treatment
* containdication, failure, or overuse of acute treatments
* acute treatments lead to adverse event

  1. Beta blockers: metoprolol, propranolol
  2. tricyclic antidepressants - amytriptaline, nor triptaline
  3. Antiepileptic drugs (AEDs) - divalproex sodium, sodoum valproate, topiramate
  4. nutritional supplements - magnesium, riboflavin, buterbur, feverfew, coenzyme q10
  5. Lithium - usually for cluster only)
  • 4-6 weeks of use to see effect

Clacitonin gene-related peptide antagonisis - (CGRP)
* monoclonal atibody
* quickest onset, well tolerated
* used if no or limited clinical response to 1st line prevention therapy
* expensive
* erenumab, fremanezumab, ubrogepant (Ubrelvey)

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10
Q

Migraine rescue therapy

A

for severe symptoms

antiemetics, short course of systemic corticosteroids

avoid opioids

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11
Q

Giant Cell Ateritis
Etiology

A
  • autoimmune vasculitis that effects medium and large sized vessels as well as the temporal artery
  • inflammation and swelling of arteries leads to decreased blood flow and associated symptoms
  • most common in 50=85 years, female>males, seen with polymyalgia rheumatica
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12
Q

Giant cell arteritis
presentation and DX

A
  • Tender nodular pulsless vessel (usually temporal artery acompanied by severe unilateral headache
  • 50% will experiance visual impairment, including transient visual blurring, diplopia, eyepain, or sudden loss of vision
  • CRP and ESR are markedly elevated
  • definitive dx involves superficial artery bx
  • color duplex US can be used as an alternative/compliment to bx
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13
Q

Giant cell arteritis intervention

A
  • tx aimed to reduce pain and minimize risk of blindness
  • High dose systemic corticosteroid therapy (1-2mg/kg prednisone) until disease is stable, followed by slow taper for 6 months to 2 years
  • Apirin can be used to redce stroke risk
  • GI cytoprotection with PPI and biophosphinate for bone protection to minimize adverse effects of long term corticosteroid therapy
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