Headaches Flashcards

1
Q

What nerve pain receptors are activated in migraine HA’s?

A

Trigeminal nerve

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2
Q

List the 5 main migraine triggers

A
  1. Emotional stress
  2. Hormones in women (estrogen): menstruation, menopause, pregnancy
  3. Diet: missing a meal
  4. Weather
  5. Sleep disturbances
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3
Q

Define osmophobia

A

Sensitivity to smells/odor

Migraine sx

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4
Q

Define cutaneous allodynia

A

Sensitivity to touch

Migraine sx

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5
Q

What type of migraine is a Migraine without aura?

A

Common= 75%

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6
Q

What type of migraine is a Migraine with aura?

A

Classic= 25%

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7
Q

Chronic migraine classification

A

> or equal to 8 days/month for >3 months

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8
Q

Define retinal migraine

A

Aura of fully reversible monocular positive and/or negative visual phenomena confirmed during an attack by either or both of:

  1. Clinical visual field examination
  2. Pt’s drawing of a monocular field defect
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9
Q

Define brainstem aura

A

Aura of fully reversible visual, sensory and/or speech/language sx’s, BUT NO motor or retinal

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10
Q

Define Hemiplegic Migraine

A

Aura consisting of both fully reversible:

  1. Motor weakness
  2. Visual, sensory and/or speech/language sx’s
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11
Q

What is first line treatment in abortive therapy for mild-moderate migraine HA’s?

A

NSAIDs

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12
Q

What is second line treatment in abortive therapy for mild-moderate migraine HA’s?Indications?

A

Acetaminophen

  1. Patient failed NSAIDs
  2. CI to NSAIS: HTN, Warfarin therapy, renal failure, GI issues, allergy
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13
Q

What is a common cause of medication-overuse headache?

A

ASA/Acetaminophen/Caffeine (Excedrin)–>only for intermittent use!

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14
Q

What is first line treatment in severe migraine attacks (abortive)?

A

Serotonin (5-HT1) Agonistis: “Triptans”

-Sumatriptan (Imitrex)

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15
Q

What is second line treatment in severe migraine attacks (abortive)?

A

Ergotamines

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16
Q

Ergotamines MOA

A

Non-selective serotonin (5HT1) agonists

  • Less effective
  • More adverse effects
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17
Q

What is last line treatment in severe migraine attacks (abortive)?

A

Opiods

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18
Q

Indication for migraine prophylaxis/prevention

A
  1. Migraine > or equal to 3 days/month
  2. Duration >48 hrs
  3. Acute tx CI, ineffective, or overused
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19
Q

What was recently approved by the FDA for chronic migraines?

A

Botulinum Toxin

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20
Q

Migraine prevention treatment

A
  1. Anti-HTN meds: BB (propanolol), CCB (Verapamil)
  2. Anticonvulsants: Valporic acid
  3. Antidepressants: Amitriptyline
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21
Q

What is the most common primary headache disorder?

A

Tension headaches

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22
Q

Tension HA clinical findings

A
  1. Daily or episodic HA that last from 30 min-7 days
  2. Bilateral location
  3. Pressing/tightening quality (non-pulsating)
  4. Not increased with basic activity
  5. N/V,photophobia/phonophobia are rare
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23
Q

What is first line treatment for tension-type HA’s?

A
  1. NSAIDS: Ibuprofen, Naproxen
  2. Acetaminophen
  3. ASA
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24
Q

Classification of chronic tension-type headaches

A

> 7-9 HA/mo

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25
Q

What is the most effective treatment for chronic tension-type HAs?

A

Amitriptyline

26
Q

Non-pharmacologic therapy for tension-type HAs

A
  1. Cognitive Behavioral Therapy
  2. Relaxation training
  3. EMG biofeedback
27
Q

What is the least common primary headache disorder?

A

Cluster headaches?

28
Q

Risk factors for for Cluster headaches

A
  1. MALE
  2. Cigarette smoking
  3. High alcohol consumption
  4. Type A personality
29
Q

Cluster HA presentation

A
  1. Severe unilateral, supraorbital and/or temporal HA attacks
  2. Lasts for 15-180 minutes up to 8x/day
  3. Pain peaks within 10-15 minutes after onset
30
Q

What is the MC form of cluster headaches?

A

Episodic:

  • Attack phases last 2-16 weeks
  • Followed by cluster free period of 6 mos.-1 yr
31
Q

List the sx’s that are present on the affected side (one must be present)

A

SLUDE:

  1. Conjunctival injection and/or lacrimation
  2. Nasal congestion and/or rhinorrhea
  3. Eyelid edema
  4. Sweating-Forehead and facial
  5. Miosis and/or ptosis
32
Q

What can a cluster headache be misdiagnosed with?

A

Horner’s Syndrome

33
Q

Cluster headache acute attack 1st line treatment

A
  1. 100% oxygen

2. Sumatriptan(Imitrex)/Zolmitriptan(Zomig) =only FDA approved med

34
Q

Who are Triptans CI in?

A
  1. HTN

2. Vascular dz

35
Q

Cluster Headache Prophylaxis

A

CCB Verapamil

36
Q

Verapamil contraindications

A
  1. Heart block

2. Arrhythmias

37
Q

what is the primary use of CT/MRI in the case of a concussion?

A

Rule out intracranial hemorrhage

38
Q

What are the variables that predict intracranial hemorrhage in pediatric patients?

A
  1. LOC
  2. GCS<15
  3. Skull fracture
  4. Focal neurological defect
39
Q

List the Diagnostic criteria for analgesic rebound headache

A
  1. Simple analgesic use >or equal to 15 days/mo x3months in a patient with a pre-existing HA disorder
  2. HA resolves/reverts to previous pattern within 2 months after discontinuation of analgesics
40
Q

What is the most significant factor in the development of rebound headaches?

A

Lack of awareness by HC practitioner and patient

41
Q

What is the other name for pseudotumor cerebri?

A

idiopathic intracranial hypertension

42
Q

Who do pseudotumor cerebri primarily affect?

A

Women of childbearing age

43
Q

What are the associated sx’s observed in pseudotumor cerebri?

A
  1. Transient visual obscurations: Dimming or blackout in one or both eyes
  2. Intracranial noises: Pulsatile tinnitus
  3. Photopsia
  4. Retrobulbar pain
  5. Back pain
  6. Diplopia
  7. Sustained visual loss
44
Q

pseudotumor cerebri physical exam findings

A
  1. Papilledema
  2. Visual field loss
  3. Abducens (CN VI) Palsy: Horizontal diplopia
45
Q

What are some conservative treatment options for pseudotumor cerebri?

A
  1. Wt loss for obese pt’s
  2. Decrease sodium intake
  3. Carbonic anhydrase inhibitors: Acetazolamide
  4. Loop Diuretics (adjunct)
46
Q

What is no longer recommended in pseudotumor cerebri?

A

Corticosteroids

47
Q

What are some more invasive treatment options for pseudotumor cerebri?

A
  1. Serial LP’s: temporary basis to help provide symptomatic relief
  2. Optic nerve fenestration: “Window” in optic nerve sheath
  3. CSF shunting
48
Q

Temporal arteritis etiology

A

Systemic inflammatory vasculitis of unknown etiology

49
Q

What is the peak age of incidence in Temporal arteritis?

A

70-79 y.o.

50
Q

Temporal arteritis clinical presentation

A
  1. Abrupt or insidious
  2. HA-Temporal or occipital area
  3. Polymyalgia rheumatic
  4. Jaw claudication
  5. Fever
51
Q

What is the hallmark of GCA?

A
  1. Elevated ESR

2. Elevated C-reactive protein

52
Q

What is the standard for making the diagnosis of temporal arteritis?

A

Temporal artery biopsy

53
Q

Temporal arteritis treatment

A

High-dose corticosteroids: Prednisone

54
Q

When can you start to taper the prednisone?

A
  1. Signs of clinical inflammation are suppressed

2. ESR and CRP remain low

55
Q

What is another name for Trigeminal Neuralgia

A

“Tic Douloureux”

56
Q

Who is Trigeminal neuralgia 20x more common in?

A

Multiple sclerosis patients

57
Q

What is the MC cause of Trigeminal neuralgia?

A

Compression of trigeminal nerve root by cerebellar artery or vein

58
Q

Describe clinical presentation of Trigeminal neuralgia?

A
  1. Sharp, electrical, shock, UNILATERAL facial pain lasting few seconds to several minutes
  2. Pain triggered by chewing, t talking, smiling, shaving, cold air
  3. Pain starts near mouth to angle of jaw
59
Q

What is first line treatment for Trigeminal neuralgia?

A

Anti-convulsant and antidepressant= Carbamazepine (Tegretol)

60
Q

What is the best long term outcome treatment for Trigeminal neuralgia?

A

Surgical decompression

61
Q

What is the majority of causes of subarachnoid hemorrhages?

A

Ruptured saccular aneurysms

62
Q

Risk factors for subarachnoid hemorrhages?

A
  1. Uncontrolled HTN
  2. Smoking
  3. Alcohol