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Flashcards in HA, Cohen Deck (58)
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1
Q

Primary HA

A

no obvious pathologic cause

migraine, cluster, tension type

2
Q

secondary HA

A

pathological cause: tumor hemorrhage infection

3
Q

warning signs and Sx of secondary HA

A
single HA
sudden onset
onset HA after age 50
recent onset HA <6 mo
systemic disease
change in HA pattern
neuro Sx or abnormal neuro exam
4
Q

PE for HA

A

general appearance
fever or abnormal vital signs, supple neck
mental status, speech, LOC
vision and retinal discs, pupils, EOMI, papilledema
asymmetry of strengths or reflexes
babinski

5
Q

imaging for recurrent migraines

A

no CT or MRI unless recent change in HA pattern, focal neurologic signs or Sx

6
Q

imaging for nonmigraine HA

A

CT MRI role unclear

7
Q

imaging more likely to show cause for HA

A

MRI

8
Q

imaging for HA in pregnancy

A

MRI w/o contrast

9
Q

LP necessary for

A

Dx meningitis or encephalitis or possible carcinomatous meningitis
confirm subarachnoid hemorrhage but no blood on CT or MRI

10
Q

increased opening pressure in LP

A

it can help Dx pseudotumor cerebri or idiopathic intracranial HTN

11
Q

Dx primary headache syndrome

A

clinical features

12
Q

characteristics of migraine features

A
sick HA with light and sound sensitivity
worse with activity
build up intensity
 4-72 hours
aura or sensory or motor deficits before pain
13
Q

migrain criteria

A
>5 attacks
>2 of following:
-unilateral
-pulsating
-mod- severe intensity
-aggravation routine physical activity
>1 of following:
-nausea and/or vomiting
-photophobia, phonophobia
No evidence of Hx or exam of disease that might cause HA
14
Q

most common HA type that patients seek medical care

A

migraine

15
Q

migraine demographics

A

W>africans>asians

16
Q

genetics in migraines

A

possible 80% close family members with migraines too

17
Q

transmission of migraine genetics

A

mother to daughter

18
Q

mutations for familial hemiplegic migraine

A

Na and Ca Channels in neurons

19
Q

causes of migraines

A

environmental factors “triggers”
psychiatric disorders
hormones: migraines can end with menopause

20
Q

triggers for migraines

A

fasting, medication, circadian rhythms, environment, hormones, stress/overexertion

21
Q

visual auras before migraines

A

blurred vision or blind spots
seeing flashing lights
seeing jagged lines
difficulty in focusing

22
Q

sensory or motor changes before migraines

A

numbness or tingling of lips, face of hands on one side body

weakness in arms or legs, usually one side body

23
Q

speech or language changes before migraines

A

inability to understand words

loss of speech or inability to speak normally

24
Q

wolff concluded migraine pain from

A

reduction blood flow to occipital Cx in visual aura and the frontal or parietal cortices with other auras
actual pain from increase blood to brain

25
Q

cortical spreading depression

A

sudden brief depolarization of cortical neurons, followed by reduction in neuronal depolarization and synaptic transmission

26
Q

pain for migraine on PET

A

region of pons active up to 30 minutes before there is an increase in blood flow to brain

27
Q

increased activity to CN V leads to what

A

secondary vasodilation and inflammation of dura mater

“trigeminovascular activation”

28
Q

what NT are released from pons in migraine

A

serotonin
CGRP
substance P
NO

29
Q

what is increased in urine from migraine attack

A

increased 5-hydroxyindoleacetic acid in urine from increased release serotonin 5-hydroxytyptamine

30
Q

migraine ends with what

A

when neurons stop releasing more serotonin

31
Q

sumatriptan

A

serotonin 1b 1d agonist

effective in stopping migraine attack by binding these inhibitory serotonin autoR

32
Q

what is in migraine center

A

dorsal raphe nucleus

locus coeruleus

33
Q

antagonists to what molecule help stop migraine

A

CGRP

help show not purely vascular process because CGRP has no role in vasoconstriction

34
Q

most common type HA

A

tension type

35
Q

clinical features tension type HA

A

dull, b/l, squeezing, tight
non pulsating
routine physical acitivty does not aggravate pain
no vomiting and more than one of : nausea, photophobia, phonophobia
MSK component, cervicogenic
medication seldom necessary

36
Q

average length chronic tension type HA

A

> 15/mo

avg duration >4 hr/day if untreated and history >6 mo

37
Q

chronic tension type HA should not take what

A

more than one analgesic a week

38
Q

common findings with tension type HA

A
HTN
depression
anxiety
insomnia
DM/hypoglycemia
39
Q

pain pills in people with frequent HA

A

cause increase frequency

40
Q

cluster HA characteristics

A

brief 15 minutes-2 hours
one sided around eye
often 1 hr after falling asleep
occur daily or multiple times a day for weeks or mo at a time “season”

41
Q

intense unilateral HA causing patient to bang head on wall

A

cluster HA

42
Q

autonomic features of cluster HA

A
conjunctival injection
lacrimation
congestion
rhinorrhea
swelling
miosis
ptosis
eyelid edema
43
Q

weight gain abnormal vision and HA

A

secondary HA

44
Q

pseudotumor cerebri

A

idiopathic intracranial HTN

45
Q

signs pseudotumor cerebri

A

-progressive diffuse HA with intermittent loss of vision in 1+ eyes especially with eye movements
- obese young women!! E and P maybe or acutane
- increased intracranial P, from overproduction CSF
opening P >25
papilledema

46
Q

what can occur in idiopathic intracranial HTN if not Dx early

A

irreversible loss of visual acuity
often extraocular palsy
CN VI III IV

47
Q

Dx idiopathic intracranial HTN

A

spinal tap P and imaging

48
Q

Tx idiopathic intracranial HTN

A

weight loss, corticosteroids, carbonic anhydrase inhibitors, topiramate

49
Q

Trigeminal neuralgia

tic douloureux

A

brief shooting pain lasting only a sec
triggered by facial contact
one branch CN V

50
Q

triggers for trigeminal neuralgia

A

touching face
eating
shaving
applying lipstick or makeup

51
Q

causes trigeminal neuralgia

A

idiopathic

52
Q

age of trigeminal neuralgia

A

uncommon under 50 y.o

unlesss brainstem lesion, MS tumors

53
Q

Giant Cell Arteritis

A

temporal
example of vasculitis
non-infectious inflammation of aa leading to gradual occlusion
involves superficial temporal a (off external carotid a)

54
Q

temporal arteritis can spread how leading to what complication

A

to adjacent internal carotid a

reaching ophthalmic a and cause complete visual loss via ischemia

55
Q

other Sx temporal arteritis

A

fatigue
difficulty chewing
pain in neck and shoulders

56
Q

giant cell arteritis component of

A

polymyalgia rheumatica

57
Q

Dx temporal arteritis

A

ESR and CRP

confirmed by superficial temporary artery biopsy

58
Q

cure for temporal arteritis

A

prednisone within 1st weeks of onset!!

typically 60 mg per day then gradually and slowly dec over mo