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Foundations-Neuro > Headaches > Flashcards

Headaches Flashcards

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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
What is the most effective treatment for chronic tension-type HAs?
Amitriptyline
26
Non-pharmacologic therapy for tension-type HAs
1. Cognitive Behavioral Therapy 2. Relaxation training 3. EMG biofeedback
27
What is the least common primary headache disorder?
Cluster headaches?
28
Risk factors for for Cluster headaches
1. MALE 2. Cigarette smoking 3. High alcohol consumption 4. Type A personality
29
Cluster HA presentation
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
What is the MC form of cluster headaches?
Episodic: - Attack phases last 2-16 weeks - Followed by cluster free period of 6 mos.-1 yr
31
List the sx's that are present on the affected side (one must be present)
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
What can a cluster headache be misdiagnosed with?
Horner's Syndrome
33
Cluster headache acute attack 1st line treatment
1. 100% oxygen | 2. Sumatriptan(Imitrex)/Zolmitriptan(Zomig) =only FDA approved med
34
Who are Triptans CI in?
1. HTN | 2. Vascular dz
35
Cluster Headache Prophylaxis
CCB Verapamil
36
Verapamil contraindications
1. Heart block | 2. Arrhythmias
37
what is the primary use of CT/MRI in the case of a concussion?
Rule out intracranial hemorrhage
38
What are the variables that predict intracranial hemorrhage in pediatric patients?
1. LOC 2. GCS<15 3. Skull fracture 4. Focal neurological defect
39
List the Diagnostic criteria for analgesic rebound headache
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
What is the most significant factor in the development of rebound headaches?
Lack of awareness by HC practitioner and patient
41
What is the other name for pseudotumor cerebri?
idiopathic intracranial hypertension
42
Who do pseudotumor cerebri primarily affect?
Women of childbearing age
43
What are the associated sx's observed in pseudotumor cerebri?
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
pseudotumor cerebri physical exam findings
1. Papilledema 2. Visual field loss 3. Abducens (CN VI) Palsy: Horizontal diplopia
45
What are some conservative treatment options for pseudotumor cerebri?
1. Wt loss for obese pt's 2. Decrease sodium intake 3. Carbonic anhydrase inhibitors: Acetazolamide 4. Loop Diuretics (adjunct)
46
What is no longer recommended in pseudotumor cerebri?
Corticosteroids
47
What are some more invasive treatment options for pseudotumor cerebri?
1. Serial LP's: temporary basis to help provide symptomatic relief 2. Optic nerve fenestration: "Window" in optic nerve sheath 3. CSF shunting
48
Temporal arteritis etiology
Systemic inflammatory vasculitis of unknown etiology
49
What is the peak age of incidence in Temporal arteritis?
70-79 y.o.
50
Temporal arteritis clinical presentation
1. Abrupt or insidious 2. HA-Temporal or occipital area 3. Polymyalgia rheumatic 4. Jaw claudication 5. Fever
51
What is the hallmark of GCA?
1. Elevated ESR | 2. Elevated C-reactive protein
52
What is the standard for making the diagnosis of temporal arteritis?
Temporal artery biopsy
53
Temporal arteritis treatment
High-dose corticosteroids: Prednisone
54
When can you start to taper the prednisone?
1. Signs of clinical inflammation are suppressed | 2. ESR and CRP remain low
55
What is another name for Trigeminal Neuralgia
“Tic Douloureux”
56
Who is Trigeminal neuralgia 20x more common in?
Multiple sclerosis patients
57
What is the MC cause of Trigeminal neuralgia?
Compression of trigeminal nerve root by cerebellar artery or vein
58
Describe clinical presentation of Trigeminal neuralgia?
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
What is first line treatment for Trigeminal neuralgia?
Anti-convulsant and antidepressant= Carbamazepine (Tegretol)
60
What is the best long term outcome treatment for Trigeminal neuralgia?
Surgical decompression
61
What is the majority of causes of subarachnoid hemorrhages?
Ruptured saccular aneurysms
62
Risk factors for subarachnoid hemorrhages?
1. Uncontrolled HTN 2. Smoking 3. Alcohol

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