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Neuro: Clin Med IIB > Headache > Flashcards

Headache Flashcards

1
Q

classification of headaches

A
  1. Primary: HA syndromes unto themselves (90%)
    - Migraine
    - Tension
    - Cluster
  2. Secondary: sx of other illness
    - Meningitis
    - Intracranial Mass
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2
Q

Most Important Questions for HA?

A
  1. Is this headache new or old?
  2. If old, is the headache typical?
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3
Q

what MHx/conditions are important for making a HA diagnosis?

A

HIV
Cancer
Pregnancy
HTN
Anxiety/Depression
FHx of HA disorders
Med Review: Overuse headache
Clues to other diagnosis

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4
Q

Danger signs of HA

A

SNOOP

  1. Systemic sx, illness or condition
    - F, wt loss, cancer, pregnancy, immunocompromised
  2. Neurologic sx or abnormal signs
    - Confusion, altered consciousness, papilledema, meningismus, focal neuro signs, seizures
  3. Onset - new or sudden
    - >40 y/o or “thunderclap”
  4. Other conditions or features
    - Head trauma, illicit drug use, awakens from sleep, worse with Valsalva, precipitated by cough, exertion, or sexual activity
  5. Previous HA hx with progression
    - Change in frequency, severity, or clinical features
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5
Q

Other Features Suggesting Secondary HA Source

A
  1. Impaired vision: halos around lights
  2. Visual fields defect
  3. Sudden, severe, unilateral vision loss
  4. Blurring of vision on forward bending or HA when awakening
  5. N/V, worsening with changes in body position, an abnormal neurologic exam, changes in pattern
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6
Q

PE for HA

A
  1. vitals - temp, BP, pulse
  2. HEENT
    - Sinus tenderness
    - Neck pain or stiffness, scalp tenderness, meningismus, muscle spasms
    - Palpate temporal arteries and TMJ
    - Signs of trauma
    - Listen for bruits
    - Examine spine and neck muscles
    - Otoscope
  3. eyes
    - Fundoscopic exam
    - Visual acuity
    - EOM, Visual fields, Pupillary defects
  4. Neuro
    - Mental status testing
    - Cranial nerves
    - Symmetry on motor, reflex, cerebellar (coordination), and sensory
    - Gait
    - Walking on tiptoes, heals, tandem gait, and Romberg
    - Reflexes
    - Pronator drift
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7
Q

diagnostic studies for HA

A
  1. Most primary HA need no studies, esp normal neuro exam
  2. Used to r/o secondary or life-threatening causes
  3. neuroimaging if warranted
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8
Q

Clinical features which warrant neuroimaging

A
  1. Age of onset >40
  2. Focal neurologic s/s
  3. Onset of HA with exertion, cough, or sexual activity
  4. Change in pattern of HA
    - Frequency or severity
  5. has cancer, Lyme, or HIV
  6. worsening despite therapy
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9
Q

imaging choice for HA?
others?

A
  1. MRI - most sensitive and preferred
  2. CT may be used in ED setting or if r/o sinusitis or head injury
  3. LP if signs of meningitis or subarachnoid hemorrhage
    - Measure opening pressures with suspected subarachnoid hemorrhage
  4. Basic lab studies
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10
Q

Misconceptions about HAs

A
  1. Acute/chronic sinusitis is an uncommon cause of recurrent HA
  2. Poor vision, or eye strain, is also rarely a cause of chronic HA
  3. HTN is not a likely cause of HA, unless the patient is in a HTN crisis
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11
Q

When to Hospitalize for HA

A
  1. Need for repeated doses of parenteral pain med
  2. expedited work-up requiring sequence of neuroimaging and procedures
  3. Monitoring progression and neurologic consultation when initial ER work-up is inconclusive
  4. Pain severe enough to impair ADLs or limit participation in f/u appointments or consultations
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12
Q

possible pathophys of migraines

A

neuronal dysfunction in trigeminal system
–> release of vasoactive neuropeptides (calcitonin gene-related peptide)
–> neurogenic inflammation, sensitization, and HA

(not the vasodilation/vasoconstriction theory)

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13
Q

epidemiology of migraines
MC type?
triggers for migraines?

A
  1. Affects up to 12% of the general population
    - 10% of school aged children suffer from migraines
  2. Women 3x; 25 – 55 y/o MC
  3. 90% +FHx
  4. Migraine w/o aura - MC type – 75%
  5. Triggers: stress, menstruation, visual stimuli, weather changes, nitrates, fasting, wine, sleep disturbances, aspartame
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14
Q

4 phases of migraines

A
  1. prodrome
  2. aura
  3. HA
  4. postdrome
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15
Q
  1. 60% of those with migraines report this phase
  2. Affective sx 24 – 48 hrs prior to next phase
    - Euphoria, depression, irritability, food cravings, constipation, neck stiffness, and increased yawning

what is this phase of migraine?

A

prodrome

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16
Q
  1. Occur in 25% of migraines
  2. Attributed to cortical spreading depression
  3. Transient neurologic sx
    - MC visual, but may be sensory, verbal, or motor
  4. Develop gradually and typically last no longer than hr

what is this phase of migraine?

A

aura

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17
Q
  1. Unilateral, throbbing or pulsatile in quality
    - may be bilateral or generalized in 40%
  2. Associated sx
    - Anorexia, N/V, photophobia, phonophobia, cognitive impairment, cutaneous allodynia and blurring of vision, hyperalgesia, blurred vision
  3. Lasts hrs-days
    - Typically 4 – 72 hours
  4. Aggravated with routine physical activity

what phase of migraine is this

A

HA

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18
Q

Patient often feels drained or exhausted, but some report a feeling of mild euphoria

what is this phase of migraine

A

postdrome

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19
Q

what can lead to the triggering of a pain response from stimuli which do not normally provoke pain

A

allodynia

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20
Q

The ICHD-3 criteria for migraine w/o aura are the following:

A

(w/ aura - only 2 attacks for dx)

  1. At least 5 attacks fulfilling criteria B through D
  2. HA attacks lasting 4-72 hrs
  3. HA has at least 2:
    - Unilateral location
    - Pulsating quality
    - Moderate/severe pain intensity
    - Aggravation by/causing avoidance of activity
  4. During HA, at least 1 of the following:
    - N and/or V
    - Photophobia and phonophobia

Not better accounted for by another ICHD-3 diagnosis

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21
Q

general management for migraines

A
  1. Preventative strategies
    - Meds
    - Avoiding triggers
  2. Abortive (symptomatic) tx
    - NSAIDS
    - Triptans
    - Ergotamines
    - Antiemetics
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22
Q

types of NSAIDs for migraines

A
  1. OTC and inexpensive
    - Acetaminophen
    - ASA
    - Ibuprofen
  2. Ketorolac (Toradol)
  3. Naproxen (Naprosyn, Anaprox)

If one does not work, may try another

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23
Q

what medication has agonistic effects on serotonin 5-HT1b (meningeal arteries) and 5-HT1d (trigeminal nerve) receptors in cranial blood vessels.
They also inhibit proinflammatory neuropeptide release

A

5-HT1b/1d receptor agonists

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24
Q

what medication is Used at the start of the headache phase to abort attack

A

5-HT1b/1d receptor agonists

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25
Q

dosing routes for 5-HT1b/1d receptor agonists?
which is fastest?

A

SubQ: 10 – 15 min
nasal spray: 15 – 30 min
oral: 30 min

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26
Q

5-HT1b/1d receptor agonists have Greater benefit when used with ?

A

Naproxen (500 mg orally)

  • Treximet (sumatriptan + naproxen sodium) - tab
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27
Q

what are the 5-HT1b/1d receptor agonists

A
  1. Sumatriptan (Imitrex), also (Sumavel DosePro) - SubQ (auto injection device), nasal spray, rectal supp, tab, oral susp
  2. Zolmitriptan (Zomig) - Nasal spray, rapidly dissolving wafer, tab
  3. Rizatriptan (Maxalt) - Rapidly dissolving wafer, tab
  4. Eletriptan (Relpax) - tab
  5. Naratriptan (Amerge) - tab
  6. Frovatriptan (Frova) - tab
  7. Almotriptan (Axert) - tab
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28
Q

which 5-HT1b/1d receptor agonists provide the highest likelihood of consistent success

A
  1. Rizatriptan (Maxalt)
  2. Eletriptan (Relpax)
  3. Almotriptan (Axert)
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29
Q

Contraindications for triptans

A
  1. CAD, peripheral vascular disease
  2. Familial hemiplegic migraine and basilar migraine
  3. Ischemic stroke or RF for stroke (uncontrolled HTN, DM, prior TIA, hypercholesterolemia, obesity)
  4. IHD
  5. Prinzmetal’s angina
  6. taking Ergot compound meds
  7. > 65 y
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30
Q

cautions with triptans

A
  1. meds lowering HR(CCB, BB, MAOI’s)
  2. SSRI’s or SNRI’s = Serotonin Syndrome
  3. eletriptan with CYP3A4 inhibitors (ketoconazole) - don’t use w/n 72 hrs
  4. Preg Cat C – avoid breastfeeding for 12 hrs after tx
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31
Q

pt education for triptans

A
  1. Injectables – pain at site, tingling 30 min
  2. Do not use if had MAOI w/n 14 d
  3. Do not use w/n 24 h before or after using another migraine med
  4. Wait 2 hrs after taking another
    - Do not exceed 200 mg in 24 hrs.
    - Do not exceed 40 mgin 24 hrs (nasal spray)
  5. only tx the HA once it has begun, not prophylaxis
  6. may breastfeed 12 hrs after dose but discard any milk expressed within 12-hr span
  7. Avoid <18 or > 65
  8. impair thinking or reactions - caution with driving
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32
Q

Alkaloid obtained from ergot, derived from a fungus

what med?

A

Ergotamine (Ergots)

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33
Q

MOA of Ergotamine (Ergots)

A
  • Acts as an agonist, producing peripheral vasoconstriction and decreased blood flow, but in large amounts, may be a vasodilator.
  • structurally related to biogenic amines - norepinephrine, epinephrine, dopamine, and serotonin
  • also acts upon serotonin receptors to cause vasoconstriction as well
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34
Q

what are the 3 ergotamines

A
  • Cafergot (ergotamine tartrate 1m with caffeine 100 mg)
  • Migergot with caffeine
  • Dihydroergotamine (DHE) - ergotamine derivative
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35
Q

dosing for ergotamines

A
  • 2 mg SL followed by 1-2 mg q 30 min until attack abated
  • don’t exceed 6 mg/day and >10 mg/week (injection is 1 mg, repeat in 1 hr with no more than 6 mg/d)
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36
Q

SE of ergots

A

HTN, coronary vasospasm, peripheral vascular ischemia, dependency, headache exacerbation and rebound headache (with overuse and prolonged use), valvulopathy, N/V, abd pain, leg weakness, myalgia, numbness, intermittent claudication, photosensitivity

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37
Q

which medication has a BBW for peripheral ischemia when combined with potent CYP3A4 inhibitors?
why does this happen?

A

Cafergot (ergotamine/caffeine)
CYP3A4 - protease inhibitors and macrolide antibiotics

CYP3A4 inhibition elevates serum levels of Cafergot - risk for vasospasm –> cerebral ischemia and/or ischemia of extremities is increased

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38
Q

CI for ergots

A

Peripheral vascular disease, CAD, HTN, renal impairment, hepatic impairment, sepsis, pregnancy (previously Cat X), breastfeeding

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39
Q

caution with triptans in who?

A

Elderly
Those with cardiac disease risk
Those with valvular heart disease

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40
Q

Ondansetron (Zofran)

A

Antiemetics

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41
Q

Promethazine (Phenergan)

A

Antiemetics

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42
Q

Metoclopramide (Reglan)

A

Antiemetics

43
Q

Chlorpromazine (Thorazine)

A

Antiemetics

44
Q

Prochlorperazine (Compro)

A

Antiemetics

45
Q

Guidance to therapy for mild-moderate attack

A
  1. Simple analgesics recommended
  2. NSAIDS (ASA, ibuprofen, naproxen, ketorolac)
  3. Combo drugs (Excedrin Migraine – ASA, caffeine, acetaminophen)
  4. Antiemetic if associated N/V
46
Q

guidance to therapt for mod-severe attack

A
  1. Oral migraine-specific agents are first-line, including oral Triptans and the combination of sumatriptan-naproxen
    - May use SubQ if N/V severe or nasal route
  2. Antiemetic agents are usually necessary
47
Q

guidance to therapy in emergency setting

A
  1. the same but may easily use parenteral forms with faster bioavailability
  2. HA are typically severe if requiring ED visit
48
Q

guidance to therapy of Medication Overuse HA

A

AKA: Analgesic rebound headache

  1. MC opioids and ASA/caffeine/acetaminophen combos
  2. Limit to 10 – 15 d / mo
  3. If have more frequent HA - preventative therapies early to prevent MOHs
49
Q

what med does not have the vasoconstrictor activity of other triptan meds

A

5-HT1F receptor agonist

Lasmiditan (Reyvow) - 50, 100, 200 mg tab form only - do not exceed 1 dose in 24 hrs
Can be given to those w/ CVD risk factors

50
Q

what med blocks the CGRP protein that carry pain signals along nerve endings that cause the pain associated with migraines

A

Calcitonin Gene-related Peptide Antagonists - CGRP

Rimegepant, atogepant, ubrogepant, zavegepant

51
Q

how do Calcitonin Gene-related Peptide Antagonists differ from CGRP monoclonal antibodies used for prophylaxis

A
  1. Oral form vs. injection
  2. Eliminated from system w/in days
  3. Do not cause medication overuse HA
52
Q

goals of preventive migraine therapy

A

Reduce frequency, severity and duration of attacks
Improve responsiveness to treatment of acute attacks
Improve function and reduce disability
Avoidance of trigger factors (regular sleep, meals, etc. with headache diary)

53
Q

The following factors may indicate need for migraine prophylaxis

A
  • Recurring migraines (>4 migraine HA days a month) that significantly interfere with daily routine in pts opinion despite acute tx
  • CI to or failure or overuse of acute therapies
  • Adverse events with acute therapies
  • Patient preference
54
Q

Once a drug has been found to help for preventive therapy, it should be continued for how long?

A

several months (at least 8 weeks)

If remains HA free, the dose may be tapered and the drug eventually withdrawn

55
Q

what are the other tx regimes for preventive migraine therapy?

A

Botulinum toxin type A injections approved by FDA for migraine prevention
Acupuncture

56
Q

preventive meds for migraine

A
  1. Antiepileptic (AED)
    - Topiramate
    - Valproic acid
  2. Beta-blockers
    - Timolol
    - Propranolol
  3. Antidepressant
    - Amitriptyline (TCA)
    - Venlafaxine (SSRI)
  4. other
    - Botulinum toxin A
    - riboflavin
57
Q

SE of Topiramate

A

somnolence, nausea, dyspepsia, irritability, dizziness, ataxia, weight loss

58
Q

SE of Valproic acid

A

N/V/D, drowsiness, alopecia, weight gain, hepatotoxicity

Avoid during pregnancy

59
Q

SE of propranolol

A

fatigue, dizziness, hypotension, bradycardia

60
Q

SE of Amitriptyline

A

sedation, dry mouth, constipation, weight gain, blurred vision, edema, hypotension, urinary retention

61
Q

SE of Venlafaxine

A

nausea, somnolence, dry mouth, dizziness, diaphoresis, sexual dysfunction, anxiety, weight loss

62
Q

SE of Botulinum toxin A

A

injection site reaction, hypersensitivity, muscle weakness

63
Q

SE of riboflavin

A

yellow-orange discoloration of urine

64
Q

upcoming txf or migraine prevention

A

Eptinezumab (Vyepti) - IV every 3 mos
Erenumab (Aimovig) - SQ monthly
Fremanezumab (Ajovy) - SQ monthly
Galcanezumab (Emgality) - SQ daily X 2 days; then monthly

65
Q

Most common type of HA disorder?

A

tension HA

migraine is the MC diagnosed in pts presenting with HA

66
Q

pathophys of tension HA

A

Multifactorial

  1. Muscular and psychogenic factors
    - Stress
    - Poor posture
    - Depression
  2. Recent study revealed that those w/ chronic tension headaches >5 years had lower cortisol levels noticed through hippocampus atrophy from chronic stress
  3. Patients also have increased myofascial pain sensitivity, along with a multitude of other associated neurological stimuli
67
Q
  1. Mild-moderate pain, generalized, bilateral, non-pulsatile, and may be most intense about the neck and/or back of head
  2. Constant, daily HA with band-like/vise-like or tight in quality pain
  3. No associated focal or neurological complaints

these s/s are of which type of HA?

A

tension HA

May have pericranial tenderness, poor concentration, and other nonspecific sx
Frequently confused with migraine

68
Q

MC trigger of tension HA?

A

stress

can be exacerbated by stress, fatigue, noise, or glare

69
Q

tx for tension HA

A
  1. Analgesics - NSAIDS / acetaminophen
  2. tx anxiety or depression is important
  3. Relax
70
Q

pathophys of cluster HA

A

Idiopathic
Theory only: activation of cells in ipsilateral hypothalamus (area in charge of circadian rhythm) with secondary triggering of trigeminal autonomic vascular system

71
Q

risk factors of cluster HA

A
  1. Predominantly affect middle-aged men (30 – 50 years old)
  2. Small amounts of vasodilators
    - ETOH - 50% have hx of heavy use
  3. Tobacco use - > 80% are heavy smokers
  4. Family hx
  5. Hx of head trauma / surgery
72
Q
  1. Minutes to hours of severe unilateral temporal headaches in grouped attacks over a period of weeks to months
  2. Attacks usually last 15 – 180 minutes
  3. associated with ipsilateral autonomic s/s
  4. Episodes occur at night
  5. Spontaneous remission until next attack
  6. Patient is restless and agitated during attack

these s/s are associated with what type of HA

A

cluster HA

73
Q

what type of ipsilateral autonomic s/s of cluster HA can be seen?

A

Ptosis
Miosis
Lacrimation
Conjunctival injection
Rhinorrhea
Nasal congestion
Horner syndrome

74
Q

what is the common trigger of cluster HA

A

alcohol

75
Q

initial workup for cluster HA

A
  • MRI w/ + w/o contrast for the initial evaluation
  • Lab work and other studies not helpful
76
Q

management for cluster HA

A
  1. 100% Oxygen - 7 – 12 L/min x 15 min w/ non-rebreather mask
  2. Sumatriptan - contralaterally to side of HA
  3. DHE (Ergot derivative)
    - Triptans and ergots used with metoclopramide
77
Q

what preventative meds are indicated to reduce medication overuse in cluster HA

A

Lithium
Verapamil
Topiramate (Topamax)
Valproate (valproic acid, Depakote)
Prednisone
Ergotamine rectal supp
CGRP monoclonal antibody: galcanezumab (Emgality)

78
Q

when to refer for cluster HA

A
  • Thunderclap onset
  • Increasing HA unresponsive to measures
  • Hx of trauma, HTN, fever, visual changes
  • Presence of neurologic signs or of scalp tenderness
79
Q

Defined as a syndrome of increased intracranial pressure without a space occupying lesion

A

Benign Intracranial Hypertension
AKA Pseudotumor Cerebri

80
Q

epidemiology of Benign Intracranial Hypertension

A
  1. Affects 0.9 per 100,000 of general population
    - ages 20 - 44 y/o
    - > 20% over ideal body weight
    - Women 9x > men
81
Q

pathophys of Benign Intracranial Hypertension

A
  1. Precise mechanism unknown
  2. Several factors
    - Excessive CSF and extracellular edema
    - Increased venous sinus pressure
    - Defective CSF absorption
  3. ventricles nml on imaging - MRI and CT scan
  4. Children may develop increased ICP after thrombosis of +1 dural sinuses, after OM or mastoiditis = increase venous sinus pressure
82
Q

begnin intracrainal HTN is MC in who?

A

Obesity, postpubertal white, non-Hispanic, female

83
Q

causes of benign intracranial HTN

A
  1. Meds
    - Retinoic acid
    - abx - tetracycline, nitrofurantoin, fluoroquinolones
    - Hormones - steroid use, OC, thyroxine
    - Vit A
    - Lithium
    - Immunizations - DTaP
  2. Refeeding and wt gain in nutritionally deprived
  3. Endocrine abnormalities - adrenal, Addison’s
  4. OSA
84
Q

Throbbing headache - worse on straining
Visual disturbances - unilateral or bilateral; diplopia
Tinnitus
Nausea and/or vomiting
Papilledema on fundoscopic exam

s/s are for what dx?

A

Benign Intracranial Hypertension

85
Q

labs for benign intracranial HTN

A
  1. Labs
    - LP - Pressure >250 mmHg (+)
  2. Imaging
    - MRI or CT scan - show normal ventricles but needed to r/o mass or sinus obstruction
86
Q

medications for benign intracranial HTN

A
  1. Acetazolamide (Diamox) - diuretic
    - Reduces formation of CSF
  2. Topiramate (Topamax) - carbonic anhydrase inhibitor
    - Similar mechanism as above with added wt loss
  3. Furosemide (Lasix) - diuretic
  4. Corticosteroids - methylprednisolone
    - used only with visual changes to improve Sx
87
Q

other tx for Benign Intracranial Hypertension besides pharm

A
  1. Repeated LP to lower ICP
  2. Weight loss and low sodium diet
  3. Surgery - optic nerve sheath decompression, LP shunt
88
Q

Spontaneously caused by rupture of arterial saccular (‘berry”) aneurysm or A-V malformation

A

Subarachnoid Hemorrhage

Traumatic most common but may be spontaneous

89
Q

demographics of Subarachnoid Hemorrhage

A

Older, female, non-Caucasian, HTN, tobacco use, excessive alcohol use

90
Q
  • Sudden, severe HA never experienced before
  • Pt may be in and out of consciousness
  • N/V (bending forward, etc.. increased ICP), confusion, agitation and nuchal rigidity (meningeal signs)

these s/s are for what dx?

A

Subarachnoid Hemorrhage

91
Q

dx work-up for Subarachnoid Hemorrhage

A
  1. CT scan (with angiography if available)
  2. If CT negative, immediate LP
    - Looking for presence of blood or xanthochromia
92
Q

tx for Subarachnoid Hemorrhage

A
  • Hospitalize with bedrest and no exertion for at least 2 weeks
  • Neurology consult
  • Treat underlying condition
93
Q
  • HA that are typically worse upon awakening or lying down
  • May awaken person at night
  • New onset HA over the age of 40 or 50
  • fever, night sweats, immunocompromised or history of malignancy

this presentation is associated with which dx?

A

Mass Occupying Lesion

94
Q

most important study for Mass Occupying Lesion

A

MRI

95
Q

what is Temporal Arteritis (Giant cell arteritis)

A

Chronic vasculitis of large and medium sized vessels

96
Q

what antigen is found in nearly 75% of the temporal arteries of affected patients?

A

varicella-zoster

97
Q
  • HA, jaw claudication, scalp tenderness, visual abnormalities
  • Temporal artery may be normal to nodular, tender, or pulseless

these s/s are for which dx?

A

Temporal Arteritis (Giant cell arteritis)

Incidence steadily rises with age (seldom occurs under age 50)

98
Q

dx work-up for Temporal Arteritis (Giant cell arteritis)

A
  1. Labs:
    - elevated ESR (over 50 typical) and anemia;
    - may have elevated CRP and liver enzymes (alk phos)
  2. intervention: Temporal artery biopsy
99
Q

tx for Temporal Arteritis (Giant cell arteritis)

A

High dose corticosteroids

100
Q

what pathogen can cause CNS infection?

A

viral or bacterial

101
Q

presentation of CNS infection

A
  1. Fever, HA and nuchal rigidity
  2. Routine lab work
    - WBC may be high or low; platelets may be low
102
Q

dx work-up for CNS infection

A
  • Blood cx
  • Lumbar puncture
  • CT scan not necessary in a majority of patients
103
Q

tx for CNS infection

A

Admit with IV antibiotics and steroids if indicated

Neuro: Clin Med IIB (13 decks)

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