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Neuro > Lecture 2: Headaches > Flashcards

Lecture 2: Headaches Flashcards

1
Q

What are the 3 primary headache syndromes?

A
  • Migraine
  • Tension
  • Cluster

90% of all headaches

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2
Q

What are the secondary classes of headaches?

A
  • Meningitis
  • Intracranial mass
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3
Q

What are the danger signs of a HA?

A
  • Systemic symptoms, illness, or condition
  • Neurologic symptoms or abnormal signs
  • Onset is new or sudden (> 40 or thunderclap)
  • Other associated conditions & features
  • Previous HA history with progression

SNOOP

Other:
Head trauma
Illicit drug use
Awakens from sleep
Worse with Valsalva
Precipitated by cough, exertion, or sex

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4
Q

What are the danger neurologic signs?

A
  • Confusion
  • ALOC
  • Papilledema
  • Meningismus (nuchal rigidity, light reaction)
  • Focal neurologic deficits
  • Seizures
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5
Q

What are the other features that suggest a secondary source for headache?

A
  • Impaired vision, Halos around lights (glaucoma)
  • Visual field defect
  • Sudden, severe, unilateral vision loss
  • Blurring of vision on forward bending or HA upon awakening
  • N/V, worsening of HA with body position change
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6
Q

What PE systems should we do for every headache patient?

A
  • HEENT
  • Neurological
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7
Q

What features would suggest that we order imaging for headaches?

A
  • Age of onset > 40
  • Focal neurologic S/S
  • Onset of headache with exertion, cough, or sexual activity
  • Change in pattern
  • Cancer, lyme disease, or HIV
  • Progressive worsening despite adequate therapy
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8
Q

When is a LP recommended for headache?

A
  • Meningismus
  • Subarachnoid hemorrhage

Measure opening pressure for SAH

Opening pressure MUST BE MEASURED LATERALLY

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9
Q

What is the preferred imaging study for HA?

A

MRI

Hard to do in kiddos

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10
Q

What are specifically NOT common causes of recurrent headaches?

A
  • Acute/chronic sinusitis
  • Poor vision/eye strain
  • HTN (unless in crisis)
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11
Q

When is admittance suggested for headache?

A
  • Need for repeated parenteral pain meds
  • Facilitate/expedite imaging/consults
  • Monitoring when ER workup is inconclusive
  • Pain severe enough to impair activities
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12
Q

What is the most common type of migraine?

A

Without an aura

MC in women also

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13
Q

What are the 4 classic phases of a migraine?

A
  1. Prodrome (common)
  2. Aura (uncommon)
  3. Headache
  4. Postdrome
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14
Q

What S/S are common in a prodrome for migraines?

A
  • Euphoria
  • Depression
  • Irritability
  • Food cravings
  • Constipation
  • Neck stiffness
  • Yawning
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15
Q

How does a classic headache associated with migraine typically present?

A
  • Unilateral
  • Throbbing/pulsatile
  • Associated anorexia, N/V, cutaneous allodynia, vision blurring, hyperalgesia
  • Aggravated with routine physical activity

Can be bilateral in 40% of cases

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16
Q

What is the diagnostic criteria for a migraine without aura?

A

If you have an aura, only 2 attacks instead of 5!

seems importante

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17
Q

What are the mainstays of migraine treatment?

A
  • Preventative: meds, avoiding triggers
  • Abortive/symptomatic: NSAIDs, triptans, ergotamines, antiemetics
  • Resting in a quiet, darkened room with cold washcloth to head.
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18
Q

If a patient is unable to tolerate one NSAID for their migraines, what should we recommend next?

A

Trying a different one :)

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19
Q

What is the first-line prescribed medication for migraines?

A

Triptans

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20
Q

MOA and use of triptans?

A
  • MOA: 5-HT 1b/1b agonists
  • Use ASAP at start of headache
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21
Q

What are the 3 most successful Triptans and what other medication shows good efficacy together with them?

A
  • Rizatriptan
  • Eletriptan
  • Almotriptan
  • NAPROXEN!!!!!!

ARE Naproxen

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22
Q

What is the only injectable triptan?

A

Sumatriptan

Suma SubQ

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23
Q

What is the general protocol regarding triptan use?

A
  1. If you fail one, try it at least 3 times before switching to a different one
  2. Use < 10 times a month to prevent overuse
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24
Q

What are the contraindications to triptan use?

A
  • CAD, peripheral vascular disease
  • Familial hemiplegic migraine and basilar migraine
  • Ischemic stroke or risk factors for stroke
  • IHD
  • Prinzmetal’s angina
  • Patients taking ergot compound meds
  • Avoid in patients > 65

Refer to neuro if using triptan in child.

Ischemic conditons + ergots + weird migraines

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25
Q

What should we be cautionary of when prescribing a triptan?

A
  • Patient on HR-lowering meds
  • Patients on SSRI’s or SNRI’s
  • Patients using CYP3A4 inhibitors with eletriptan in 72 hrs
  • Avoid breastfeeding 12 hrs after use. Preg C.
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26
Q

What patient education should be provided regarding triptans?

A
  • DNU if MAOi used in past 2 weeks
  • DNU within 24 hrs of migraine med
  • Wait 2 hours in between dosages
  • Only use sumatriptan once the headache begins
  • Do not breastfeed within 12 hours of use
  • Only for patients 18-65
  • May impair decision-making/driving.
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27
Q

What are ergotamines derived from?

A

Fungi

Shrooms are the cure

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28
Q

What are the BBW of ergots?

A
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29
Q

Who are ergotamines contraindicated in?

A
  • Peripheral vascular disease
  • CAD
  • HTN
  • Renal impairment
  • Hepatic impairment
  • Sepsis
  • Pregnancy
  • Breastfeedings
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30
Q

For a mild-mod migraine, what are the recommended med classes?

A
  • Simple analgesics
  • NSAIDs
  • Combo drugs (Excedrin migraine)
  • Antiemetic for N/V
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31
Q

What are the meds within excedrin migraine?

A
  • ASA
  • Caffeine
  • Acetaminophen
32
Q

For a mod-severe migraine attack, what is the first-line therapy?

A

Oral migraine-specific agents, usually triptans.

33
Q

What is an analgesic overuse headache?

A

Overuse of opioids or excedrin > 15 times a month.

34
Q

What is the primary benefit of ditans over triptans?

A

No vasoconstrictor activity, so people with CVD risk factors can take it.

5-HT1F receptor agonist.

35
Q

What are gepants?

A

Calcitonin GEne-related Peptide ANTagonists

Zavegepant is FDA approved as a nasal spray.

36
Q

What is the MOA of a gepant?

A

Blocks CGRP protein that carry pain signals.

37
Q

What are the differences between gepants and CGRP MABs, which are used for prophylaxis?

A
  • Oral vs injection
  • Elimination in days vs longer
  • Do not cause med overuse headaches
38
Q

What factors may indicate need for prophylaxis for migraines?

A
  • Recurring migraines (>= 4 migraine HAs a month)
  • CI to acute therapy or overuse
  • Adverse events
  • Patient preference

1 month followup

39
Q

If a med is helping with preventing migraines, what is the minimum amt of time we should stay on it?

40
Q

What non-pharm treatments are used for migraine prophylaxis?

A
  • Botox type A injections (FDA approved)
  • Acupuncture
41
Q

What medications are specifically used for the prophylaxis of migraines?

A
  • Topiramate
  • Valproic acid
  • BBs (timolol or propranolol)
  • Amitriptyline
  • Venlafaxine
  • Botox A
  • Riboflavin
  • CGRP MABs (injectable and takes months to be eliminated)
42
Q

What is the most common type of headache disorder?

A

Tension

tension is top

43
Q

What muscular/psychogenic factors contribute to tension headaches?

A
  • Stress
  • Poor posture
  • Depression
44
Q

Describe how a tension headache typically presents.

A
  • Mild-mod pain that is generalized, bilateral, and non-pulsatile.
  • Band-like/vise-like
  • Stress is the most common trigger

Stress Tension = ST

45
Q

What drugs are generally last resort in tension headache treatment?

A
  • Triptans
  • Ergot

TightEnds are bad tension

46
Q

What is the theory behind cluster headaches?

A

Activation of cells in the ipsilateral hypothalamus with secondary triggering of trigeminal autonomic vascular system.

cluster causes a cluster of symptoms

47
Q

What are the risk factors associated with cluster headaches?

A
  • Middle-aged men
  • Small amounts of vasodilators (+ heavy ETOH use)
  • Tobacco use
  • Family Hx
  • Hx of head trauma/surgery
48
Q

How does a cluster headache typically present?

A
  • Severe unilateral temporal HAs in grouped attacks/episodes
  • Occurs over weeks to months
  • Occurs at night and wakes patient
  • Ipsilateral autonomic S/S
  • Alcohol is the common trigger

Cluster has a C like alcohol

49
Q

What are the ipsilateral autonomic S/S associated with cluster HAs?

A
  • Horner syndrome
  • Lacrimation
  • Conjunctival injection
  • Rhinorrhea
  • Nasal congestion
50
Q

What imaging is good for initial evaluation of cluster headaches?

A

MRI w/ and w/o con

51
Q

What are the primary treatments for cluster HAs?

A
  • 100% O2 at 7-12L/min over 15 min via NRB
  • Contralateral admin of nasal sumatriptan
  • DHE (ergot derivative)
  • Preventative stuff
52
Q

What would prompt referral for a cluster HA?

A
  • Thunderclap onset
  • Increasing HA unresponsive to simple measures
  • Hx of trauma, HTN, fever, visual changes
  • Presence of neurologic S/S or scalp tenderness
53
Q

What is benign intracranial hypertension (BIH)?

A

Syndrome of increased ICP without space occupying lesion

54
Q

Who is BIH MC in?

A

Obese, postpubertal, white, non-hispanic women

55
Q

What are the underlying factors for BIH?

A
  • Excessive CSF and extracellular edema
  • Increased venous sinus pressure
  • Defective CSF absorption
56
Q

Regarding children specifically, what is the concern with BIH development?

A
  • It can occur after thrombosis of a dural sinus
  • Often can occurs after OM or mastoiditis, which increases venous sinus pressure
57
Q

What are the S/S of BIH?

A
  • Throbbing HA that worsens on strain
  • Visual disturbances, uni or bi
  • Tinnitus
  • N/V
  • Papilledema on fundoscopy
58
Q

What CSF pressure is considered a positive finding for BIH?

A

> 250 mm Hg

59
Q

What is the purpose of a MRI/CT in BIH?

A
  • R/o mass or sinus obstruction
  • Ventricles should be normal.
60
Q

What medications are indicated for the treatment for BIH?

A
  • Acetazolamide (diuretic to reduce formation of CSF)
  • Topiramate (carbonic anhydrase inhibitor)
  • Furosemide
  • Methylprednisolone for visual changes only
61
Q

What are the other treatments to help with BIH?

A
  • Repeated LP to lower ICP
  • Wt loss and low salt
  • Optic nerve sheath decompression, LP shunt
62
Q

What is a spontaneous cause of SAH?

Subarachnoid hemorrhage?

A

Berry aneurysm or A-V malformation rupture

63
Q

What is the common demographic for SAH?

A
  • Older
  • Female
  • Non-white
  • HTN
  • Tobacco use
  • Excessive alcohol use
64
Q

What are the S/S of SAH?

A
  • Sudden, severe HA never experienced by patient before
  • Patient in/out of consciousness
  • N/V, confusion, agitation, and nuchal rigidity
65
Q

What is the primary imaging modality for SAH?

A
  • CT angiogram
  • LP if CT is negative
66
Q

What CSF findings suggest SAH?

A
  • Blood
  • Xanthochromia (yellow)
67
Q

What is the treatment for SAH?

A
  • Hospitalize for 2 weeks on bedrest
  • Neuro consult
  • Treat underlying condition
68
Q

How does a mass occupying lesion typically present?

A
  • HAs that worsen upon awakening or laying down.
  • Awakes person at night
  • New onset at 40-50
  • Fever, night sweats, immunocompromised, Hx of malignancy
69
Q

What imaging study is most important in locating a mass-occupying lesion?

70
Q

What is giant cell arteritis/temporal arteritis?

A

Chronic vasculitis of large and medium sized vessels

71
Q

What are the S/S of temporal arteritis?

A
  • HA
  • Jaw claudication
  • Scalp tenderness
  • Visual abnormalities
  • Temporal artery may be nodular, tender, or pulseless
72
Q

What is the common factor seen in most cases of temporal arteritis?

A

VZV antigen

73
Q

How do we diagnose temporal arteritis?

A
  • Elevated ESR > 50
  • Anemia
  • Elevated CRP and ALP
  • Temporal artery biopsy
74
Q

How do we treat temporal arteritis?

A

High dose corticosteroids

75
Q

What are the S/S of a CNS infection?

A
  • Fever
  • HA
  • Nuchal rigidity
76
Q

How do we diagnose and treat a CNS infection?

A
  • LP is routine
  • Admit with IV ABX and steroids

Neuro (17 decks)

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