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Setha: Neuro > Handler: Headaches > Flashcards

Handler: Headaches Flashcards

1
Q

4 primary types of headaches?

A

Migraine

Tension

Cluster

Chronic daily headache

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2
Q

4 secondary headaches?

A

Post-traumatic (post concussion)

Space occupying lesions (tumors)

Assocaited with cerebrovascular disease

Hypertensive encephalopathy

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3
Q

Patients present not only for the headaches, but back fear of _______

A

brain tumor

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4
Q

Triggers, aura, self-treatment, diet (food, caffeine, etoh), sleep, relation to menses, childhood assocaitions

OPQRSTA

HA diary

A

Headache history

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5
Q

BP

Head

Vision, visual fields, EOMs, funduscopic exam (papilledema)

Brief neuro exam (language, gait, motor, reflexes)

A

PE for HA

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6
Q

If history is characteristic, no focal neuro findings and gait is normal

It is unlikely a _________

A

brain tumor

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7
Q

Do patients with primary headache disorders that you were able to obtain a good history require imaging studies?

A

No!

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8
Q

___% have absence of aura

___% have presence of aura

with migraine headaches

A

85%

15%

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9
Q

Onset in adolescence and early adulthood

peak ages 30-45

A

Migraine headaches

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10
Q

Infantile colic

Motion sickness with nausea and vomiting

Menstrial headaches

HA that worsen with physical activity

HA post consumption of small amounts of colored wine or liquor

Caffeine withdrawal HA

Water diving HA

After certain foods (chocolate, peanuts, caffeine)

These are called?

A

“Migraineurs”

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11
Q

2nd most common headache disorder

Prevalence 12%

18% in women and 6% in men

A

Migraine headaches

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12
Q

Pathophys unclear

End pathway: activation of afferent sensory fibers that innervate meningeal/cerebral blood vessels

Fibers arise from Trigeminal nerve

A

Migraine headaches

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13
Q

Pathophys: mirgraines have ______ and ______ components

No identifiable cause

A

Infammatory, vascular

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14
Q

Vasodilators (NTG) can trigger migraine headaches

Substances that cause vasoconstriction (erotamine) abort headaches

This is the ________ theory

A

Vasogenic

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15
Q

brain activates or sensitizes trigeminal nerve fibers within the meninges initiating the headache via neurogenic inflammation. The vascular changes that occur during the attack are the result of vascular inflammation

_______ theory believed by most neurologists

A

Neurogenic

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16
Q

Sx: photophobia, phonophobia, nausea, vomiting cannot be explained by vasogenic theory alone

Aural sx: visual hallucincations that cannot be explained by vasoconstriction or vasodilation alone

Seen in the _____ theory

A

Neurogenic

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17
Q

Neurotransmitter which activates pain fibers in the brainstem and contributes to vasoconstrictiopn and inflammation

Release of peptides and neurotransmitter at trigeminal nerve branches leads to inflammation and vasodilation of meningeal and dural blood vessels

A

Serotonin

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18
Q

Drugs that are _____ for serotonin receptors abort headaches when taken early

Example: 5-hydroxy tryptamine analogs

A

agonists

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19
Q

Transient (15-30”) epiosodes of focal neurologic dysfunction that appear before the headache phase begins

A

Aura

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20
Q

Expanding scotoma (blind spot) with scintillating margin: visual hallucinations with stars, sparks, and zigzags of light

Visual field defects

Unilateral paresthesias

Numbness

Weakness

Dysphagia

A

Aura

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21
Q

_____ symptoms suggest decreased blood flow in the distribution of the internal carotid artery mimicking TIA’s

Uncommonly involve distribution of basilar artery leading to vertigo, ataxia, tinnitis, and hearing loss

A

Aural

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22
Q

activation of a wave of electrical activity that spreads throughout the brain, depressing cortical activity and resulting in visual and other symptoms; initiated by the CNS. “Spreading depression of Lao” seen on PET scans.

What does this contribute to?

A

Mirgraine Aura

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23
Q

Can be lateralized to one side or generalized

Usually throbbing (mod-severe) and worse with physical activity

Develop gradually and last several hours

Associated sx: nausea, photophobia, phonopobia

Spectrum can vary and is a continum that might include aura, lateralization, varying length

A

Headache phase

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24
Q

Prolonged aura with neurologic deficits lasting

1 hour –> week

Uncommon

What type of migraine?

A

Complex

25
Q

Rarely there are permanent neuro deficits consistent with localized stroke (with defect on CT or MRI) in the distribution of the internal carotid but neuro-imaging or angiography do not show occlusion or fixed stenosis of intracerebral vessles

Seen with what type of mirgraine?

A

Complex

26
Q

Avoid triggers if identifiable (foods, additives, caffeine, strong smells, response to stress, sleep cycles)

Preventative treatment for what?

A

Migraines

27
Q

Bed rest in dark room

Mild attacks: ASA, NSAIDS effective if taken early but may need to be combined with other meds

Abortive therapy for ____?

A

Migraines

28
Q

Older migraine medication

Potent serotonin agonist and vasoconstrictor

caution in patients with HTN, Hx of CAD or stroke

Less selective/ safe than the new agents

A

Ergotamine

29
Q

Older treatment for migraines

Ergotamine 1mg and caffeine 100mg

A

Cafergot

30
Q

One of the top 5 diagnosies that PCP’s see in the office

A

Headaches

31
Q

Newer treatment for migraines

high affinity for serotonin receptors in trigeminal nerve branches with additional vasoconstrictive effects (see below): Sumatriptan (Imitrex), Zolmitriptan (Zomig) and others; similar efficacy.

Very few S/E and very safe

Avoid in patients with CHF

A

5-HT1 receptor agonists

32
Q

5-HT1 receptors are the predominant serotonin receptors in the CNS. Many of them function as presynaptic autoreceptors whose activation inhibits the release of serotonin and related neurotransmitters that cause vasodilation, inflammation and pain.

Activation of these receptors in pial/dural vessels leads to __________

A

Vasoconstriction

33
Q

Injected (auto-injector_ subcutaneous sumatriptan most effecti in aborting HA (oral meds poorly absorbed)

Also intra-nasal sumatriptan an alternative: less predictable

Used for acute _________?

A

severe headaches

34
Q

Usually treated in the ED with injectable dihydroergotamine and effective hours into an attack. Essential to pre-treat with anti-nauseant/emetic agent like metoclopramide.

Injectable narcotic, often Meperidine, combined with an anti-emetic (ED only).

Treatment for what type of HA?

A

Severe intractable migraine headaches

35
Q

What very potent NSAID can be used to prevent relapse of acute HA?

A

Indomethacin

36
Q

What is another drug that can be used to treat migraines that is effect and is used for a short course?

A

Steroids (glucocorticoids)

37
Q

HA’s limit work or daily activity 3 or more days/month

Sx of HA are severe or prolonged

Previous migraines were associated with a complication (complex migraine or stroke)

Treatment is empirical

A

Indication for migraine prophylaxis

38
Q

Beta adrenergic blockers: propranolol, metoprolol and others that cross BBB

Tricyclic antidepressants: amitriptylene, nortriptylene

Calcium channel blockers: verapamil, others.

Anticonvulsants: gabapentin, valproic acid, topiramate (Topamax)

Botulinum toxin type A- local injection into scalp

Used for what?

A

Migraine prophylaxis

39
Q

Most common type of HA

Females>males

Usually begin in 3rd decade

A

Tension HA

40
Q

Poorly understood

includes vascular, muscular & myofascial components

Pathophys of ________?

A

Tension HA

41
Q

Which type of HA has genetic predisposition?

A

Migraine HA

42
Q

Episodic and chronic forms

Symmetric tightness/pressure

Mild/mod pain that lasts min-days

DO NOT worsen with PE

no nausea or vomiting or ofther neuro sx

Associated sx: poor concentration, stress, fatigue, noise, glare, depression

A

Tension headaches

43
Q

Acetaminophen, NSAIDS

Meds for migraines may also be effective but NOT 1st line

A

Treatment for tension headaches

44
Q

Relaxation techniques

Biofeedback

Prevention for what type of headache?

A

Tension headache

45
Q

What is the other name for cluster headaches?

A

Migrainous neuralgias

46
Q

Much less common than migraines or tension HA’s

Males 6x> females

3rd-6th decade

A

Cluster headaches

47
Q

Poorly understood

Likely vascular with activation of trigeminal-vascular system

Pathogensis of what type of headaches?

A

Cluster headaches

48
Q

Watery eye, dropping eyelid, runny nose

Horner’s syndrome

Seen with what type of HA?

A

cluster headaches

49
Q

Recurrent episodes of intense unilateral orbital, supraorbital, or temporal head pain along with ipsilateral partial cervical sympathetic paralysis (conjunctival injection, lacrimation, rhinorrhea, nasal congestion, eyelid edema, loss of facial sweating); last 15” to 2 hrs and recur daily for days to weeks.

Triggers: ETOH, stress, glare, foods

A

Cluster HA’s

50
Q

100% O2 x 15”- very effective for long duration (1-2 hrs) HA’s

Oral drugs often not as effective as other routes: nasal, rectal or injection.

Acute attacks: Ergotamine tartrate, Sumatriptan, butorphanol, others ).

Prophylaxis: Verapamil, Ergotamine.

Tx for what type of headache?

A

Cluster headaches

51
Q

Any headache occurring > 15 days/month (often for 3 mos or more). Often develops over time in a patient with intermittent HA’s.

Includes tension, cluster, migraine, and other vascular headaches.

A

Chronic daily headaches

52
Q

What is the most common contributing factor to chronic daily headaches?

A

Medication overuse

53
Q

Often requires combination pharmacologic and behavioral interventions: biofeedback, massage, acupuncture, relaxation and physical therapy. Reduction of meds (if taking several) and caffeine often beneficial.

Often difficult

Treatment for what type of headache?

A

Chronic daily headaches

54
Q

A variety of neoplasms (benign and malignant) can cause headaches related to displacement of vascular structures.

A

Intracranial mass lesions

55
Q

Sx: usually dull bifrontal or occipital headaches that begin in the a.m., are worsened by exertion or postural changes and may be associated with N & V.

Clues: new onset HA’s in patients >45 y.o. Usually associated with other neurologic findings, focal or diffuse (generalized disturbance of cerebral function).

A

Intracranial mass lesions

56
Q

___% of intracranial mass lesions are gliomas

remainder are meningiomas, astrocytomas, acoustic neuomas

A

50%

57
Q

Signs: Neuro defects, papilledema, personality changes, intellectual decline, seizures and emotional lability.

Dangers: Brain Hernation through tentorial hiatus due to incrased pressure, leading to stupor and coma often followed by death.

A

Intracranial mass lesions

58
Q

How do you diagnose a intracranial mass lesion?

A

CT or MRI scans

59
Q

Treatment of intracranial mass lesions depends on ________?

A

pathology

Setha: Neuro (9 decks)

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