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
What should we be cautionary of when prescribing a triptan?
* 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.
26
What patient education should be provided regarding triptans?
* 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.
27
What are ergotamines derived from?
Fungi | Shrooms are the cure
28
What are the BBW of ergots?
29
Who are ergotamines contraindicated in?
* Peripheral vascular disease * CAD * HTN * Renal impairment * Hepatic impairment * Sepsis * Pregnancy * Breastfeedings
30
For a mild-mod migraine, what are the recommended med classes?
* Simple analgesics * NSAIDs * Combo drugs (Excedrin migraine) * Antiemetic for N/V
31
What are the meds within excedrin migraine?
* ASA * Caffeine * Acetaminophen
32
For a mod-severe migraine attack, what is the first-line therapy?
Oral migraine-specific agents, usually triptans.
33
What is an analgesic overuse headache?
Overuse of opioids or excedrin **> 15 times a month.**
34
What is the primary benefit of ditans over triptans?
No vasoconstrictor activity, so **people with CVD risk factors can take it.** | 5-HT1F receptor agonist.
35
What are gepants?
Calcitonin GEne-related Peptide ANTagonists | Zavegepant is FDA approved as a nasal spray.
36
What is the MOA of a gepant?
Blocks CGRP protein that carry pain signals.
37
What are the differences between gepants and CGRP MABs, which are used for prophylaxis?
* Oral vs injection * Elimination in days vs longer * **Do not cause med overuse headaches**
38
What factors may indicate need for prophylaxis for migraines?
* Recurring migraines (>= 4 migraine HAs a month) * CI to acute therapy or overuse * Adverse events * Patient preference | 1 month followup
39
If a med is helping with preventing migraines, what is the minimum amt of time we should stay on it?
8 weeks
40
What non-pharm treatments are used for migraine prophylaxis?
* Botox type A injections (FDA approved) * Acupuncture
41
What medications are specifically used for the prophylaxis of migraines?
* Topiramate * Valproic acid * BBs (timolol or propranolol) * Amitriptyline * Venlafaxine * Botox A * Riboflavin * CGRP MABs (injectable and takes months to be eliminated)
42
What is the most common type of headache disorder?
Tension | tension is top
43
What muscular/psychogenic factors contribute to tension headaches?
* Stress * Poor posture * Depression
44
Describe how a tension headache typically presents.
* Mild-mod pain that is generalized, bilateral, and non-pulsatile. * **Band-like/vise-like** * Stress is the most common trigger | Stress Tension = ST
45
What drugs are generally last resort in tension headache treatment?
* Triptans * Ergot | TightEnds are bad tension
46
What is the theory behind cluster headaches?
Activation of cells in the **ipsilateral hypothalamus** with secondary triggering of trigeminal autonomic vascular system. | cluster causes a cluster of symptoms
47
What are the risk factors associated with cluster headaches?
* **Middle-aged men** * Small amounts of vasodilators (+ heavy ETOH use) * **Tobacco use** * Family Hx * Hx of head trauma/surgery
48
How does a cluster headache typically present?
* 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** ## Footnote Cluster has a C like alcohol
49
What are the ipsilateral autonomic S/S associated with cluster HAs?
* Horner syndrome * Lacrimation * Conjunctival injection * Rhinorrhea * Nasal congestion
50
What imaging is good for initial evaluation of cluster headaches?
MRI w/ and w/o con
51
What are the primary treatments for cluster HAs?
* 100% O2 at 7-12L/min over 15 min via NRB * **Contralateral admin of nasal sumatriptan** * DHE (ergot derivative) * Preventative stuff
52
What would prompt referral for a cluster HA?
* Thunderclap onset * Increasing HA unresponsive to simple measures * Hx of trauma, HTN, fever, visual changes * Presence of neurologic S/S or scalp tenderness
53
What is benign intracranial hypertension (BIH)?
Syndrome of increased ICP **without** space occupying lesion
54
Who is BIH MC in?
Obese, postpubertal, white, non-hispanic women
55
What are the underlying factors for BIH?
* Excessive CSF and extracellular edema * Increased venous sinus pressure * Defective CSF absorption
56
Regarding children specifically, what is the concern with BIH development?
* It can occur after thrombosis of a dural sinus * **Often can occurs after OM or mastoiditis**, which increases venous sinus pressure
57
What are the S/S of BIH?
* Throbbing HA that worsens on strain * Visual disturbances, uni or bi * Tinnitus * N/V * Papilledema on fundoscopy
58
What CSF pressure is considered a positive finding for BIH?
> 250 mm Hg
59
What is the purpose of a MRI/CT in BIH?
* R/o mass or sinus obstruction * Ventricles should be normal.
60
What medications are indicated for the treatment for BIH?
* Acetazolamide (diuretic to reduce formation of CSF) * Topiramate (carbonic anhydrase inhibitor) * Furosemide * **Methylprednisolone for visual changes only**
61
What are the other treatments to help with BIH?
* Repeated LP to lower ICP * Wt loss and **low salt** * Optic nerve sheath decompression, LP shunt
62
What is a spontaneous cause of SAH? | Subarachnoid hemorrhage?
Berry aneurysm or A-V malformation rupture
63
What is the common demographic for SAH?
* Older * Female * Non-white * HTN * Tobacco use * Excessive alcohol use
64
What are the S/S of SAH?
* Sudden, severe HA never experienced by patient before * Patient in/out of consciousness * N/V, confusion, agitation, and nuchal rigidity
65
What is the primary imaging modality for SAH?
* **CT angiogram** * LP if CT is negative
66
What CSF findings suggest SAH?
* Blood * Xanthochromia (yellow)
67
What is the treatment for SAH?
* Hospitalize for 2 weeks on bedrest * Neuro consult * Treat underlying condition
68
How does a mass occupying lesion typically present?
* 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
What imaging study is most important in locating a mass-occupying lesion?
MRI
70
What is giant cell arteritis/temporal arteritis?
Chronic vasculitis of large and medium sized vessels
71
What are the S/S of temporal arteritis?
* HA * Jaw claudication * Scalp tenderness * Visual abnormalities * Temporal artery may be nodular, tender, or pulseless
72
What is the **common factor seen in most cases** of temporal arteritis?
VZV antigen
73
How do we diagnose temporal arteritis?
* Elevated ESR > 50 * Anemia * Elevated CRP and ALP * Temporal artery biopsy
74
How do we treat temporal arteritis?
High dose corticosteroids
75
What are the S/S of a CNS infection?
* Fever * HA * Nuchal rigidity
76
How do we diagnose and treat a CNS infection?
* LP is routine * Admit with IV ABX and steroids