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ABIM > Neurology > Flashcards

Neurology Flashcards

1
Q

pupil size in coma:

  • one dilated, nonreactive or sluggish pupil
  • cause
  • examples
A
  • cause: parasympathetic nerve problem
  • oculomotor nerve compression from uncal herniation
  • aneurysm of posterior
  • communicating artery
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2
Q

pupil size in coma:

  • one pinpoint pupil (miosis)
  • cause
  • examples
A
  • cause: sympathetic nerve problem (Horner)

- lateral medullary syndrome- hypothalamus injury- Pancoast tumor- carotid dissection

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3
Q

pupil size in coma:- two midpoint, nonreactive pupils- cause- examples

A
  • cause: parasympathetic and sympathetic nerve destruction- midbrain disruption (can affect one or both pupils)- anoxia- hypothermia- anticholinergics- severe barbituate overdose
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4
Q

pupil size in coma:- two dilated, nonreactive pupils- examples

A
  • anoxia- hypothermia- anticholinergics- severe barbituate overdose
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5
Q

pupil size in coma:- two dilated, nonreactive pupils- examples

A
  • opiates- pontine destruction
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6
Q

what is a seizure?

A
  • paroxysmal electrical discharges of brain that cause LOC- alteration of perception or impairment of psychic function- convulsive movements- disturbance of sensation- or some combination thereof
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7
Q

what is epilepsy?

A

recurrent, unprovoked seizures

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8
Q

what is status epilepticus?

A
  • prolonged or repetitive seizures- life-threatening
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9
Q

what are triggers for seizures in susceptible individuals?

A
  • alcohol- cocaine- intense emotions- strobe lighting- loud music- stress- menstruation- lack of sleep
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10
Q

seizures are categorized into what 2 categories?

A
  • GENERALIZED- FOCAL
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11
Q

focal seizures involve how many sides of the brain, and motor activity is noted on how many sides?

A
  • 1 hemisphere- usually 1
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12
Q

generalized seizures involve how many sides of the brain, and motor activity is noted on how many sides?

A
  • both hemispheres- usually both, but not necessarily
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13
Q

focal (partial) seizures are further classified into what categories?

A
  1. simple partial: no LOC2. complex partial: LOC3. partial w/ secondary generalization
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14
Q

generalized seizures are further classified into what categories?

A
  1. nonconvulsive: absence seizure2. convulsive:2a. myoclonic2b. clonic2c. tonic-clonic2d. atonic
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15
Q

focal seizures are commonly d/t what?

A

focal brain lesions

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16
Q

primary generalized seizures are more typically d/t what?

A

genetics

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17
Q

if PNES (psychogenic nonepileptic seizures) are suspected or when the events do not respond to tx and the dx is not clear, what should be ordered?

A

video EEG monitoring

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18
Q

what percentage of pts w/ PNES (psychogenic nonepileptic seizures) also have epilepsy?

A

20%

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19
Q

what is an aura?

A

perceptual disturbance that may precede a FOCAL seizure

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20
Q

auras may precede what type of seizure?

A

FOCAL seizures

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21
Q

auras do NOT occur w/?

A

PRIMARY generalized seizures

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22
Q

how can auras manifest?

A
  • SENSES- MOTOR
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23
Q

auras are thought to be produced by?

A

EARLY seizure activity

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24
Q

describe generalized tonic-clonic seizures

A
  • involve both hemispheres- BILATERAL motor involvement- LOC- pronounced postictal period
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25
Q

describe absence seizures

A
  • nonconvulsive- no aura- no postictal symptoms- sudden interruption of consciousness- can be induced by HYPERVENTILATING- 3-per-second spike and wave pattern on EEG
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26
Q

what number of children outgrow absence seizures?

A

2/3

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27
Q

describe focal (aka simple partial) seizures

A
  • no LOC- symptoms depend on affected region of cortex
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28
Q

describe focal seizures w/ diminished consciousness (aka complex partial): temporal lobe type

A
  • aura may hallucination- altered behavior/consciousness- amnesic- automatisms: lip-smacking, chewing or swallowing movements, salivation, fumbling of hands, shuffling of feet
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29
Q

definition of status epilepticus

A
  • seizure lasting > 30 minutes- 2 or more seizures WITHOUT regaining consciousness in between
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30
Q

when should you be aggressive when treating seizures and use abortive therapy?

A

when seizure lasts 5 minutes or more

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31
Q

what are possible causes of status epilepticus?

A
  • stroke- alcohol- drugs- stopping or changing AEM’s- hypoxia- CNS infection- metabolic causes- tumor- trauma
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32
Q

seizure management: history

A
  • alcohol use- drug use- head injury- sleep deprivation- diabetes- thyroid or parathyroid surgery
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33
Q

seizure management: laboratory tests

A
  • glucose- Na+- Ca++- Mg++- transaminases- BUN- LP for VDRL if meningeal sxs
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34
Q

seizure management: best neuroimaging test

A

MRI (to r/o structual abnormality)

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35
Q

seizure management: can confirm dx of seizures and localize the origin

A

EEG

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36
Q

can a NORMAL EEG exclude the dx of epilepsy?

A

NEVER

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37
Q

after initial seizure, RISK OF RECURRENCE increases w/ the following:

A
  • abnormal EEG- h/o prior neurological injury- family h/o seizures- 1st seizure is a FOCAL seizure- MRI shows abnormality
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38
Q

ACUTE TX OF SEIZURES

A

IV benzos

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39
Q

typical tx of status epilepticus in adults

A
  1. thiamine, and 1 amp of D50 if blood glucose is low2. LORAZEPAM x 2 doses3. loading dose of PHENYTOIN/fosphenytoin
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40
Q

tx of status epilepticus if pt continues seizing after initial tx

A
  1. 3rd dose of lorazepam2. maximize phenytoin dose3. proceed to barbiturate or propofol4. +/- ET intubation and ICU care (generally needed if first 2 doses and dose of phenytoin don’t work)
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41
Q

mainstay of chronic tx of seizures

A

AEDs, w/ monotherapy as the preferred goal

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42
Q

PRIMARY DRUG for: focal

A

carbamazepine

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43
Q

advantage of carbamazepine

A

toxicity is UNcommon

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44
Q

disadvantages (adverse effects) of carbamazepine

A
  • hyponatremia- leukopenia- thrombocytopenia- aplastic anemia- hepatotoxicity- teratogenic- liver inducer; reduces OCP efficacy
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45
Q

PRIMARY DRUG for: generalized tonic-clonic

A

valproic acid

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46
Q

advantages of valproic acid

A
  • wide spectrum- good efficacy- IV form available
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47
Q

disadvantages (adverse effects) of valproic acid

A
  • GI side effects- can rarely cause BM suppression and hepatotoxicity/liver failure- teratogenic (neural tube defects)- tremor- weight gain- hair loss
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48
Q

PRIMARY DRUG for: absence (only)

A

ethosuximide

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49
Q

disadvantage (adverse effects) of ethosuximide

A

BM suppression (rare)

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50
Q

tx for absence (short-term adjunctive use only)

A

clonazepam

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51
Q

disadvantages (adverse effects) of clonazepam

A

loses efficacy

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52
Q

advantages of levetiracetam

A
  • well tolerated in elderly- safe in Asian pts w/ HLA-B*1502 (increased risk of SJS)- renally excreted so no interaction w/ levels of other AEDs
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53
Q

disadvantages (adverse effects) of levetiracetam

A
  • depression- fatigue- irritability- increased infections
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54
Q

advantages of gabapentin

A
  • one AED w/ NO significant drug interactions- renally excreted so useful in pts w/ liver disease
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55
Q

disadvantages (adverse effects) of gabapentin

A
  • ataxia- amnesia- limited efficacy
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56
Q

advantages of lamotrigine

A
  • wide spectrum- good efficacy- well tolerated in elderly
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57
Q

disadvantage (adverse effects) of lamotrigine

A

severe rash and SJS w/ rapid titration

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58
Q

last choice tx for focal siezures

A

phenobarbital

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59
Q

disadvantages (adverse effects) of phenobarbital

A
  • sedation in adults- hyperactivity in children- teratogenic- liver inducer; reduces OCP efficacy- DECREASES levels of other AEDs
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60
Q

advantages of topiramate

A
  • weight loss- headache ppx if present
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61
Q

disadvantages (adverse effects) of topiramate

A
  • kidney stones- increased glaucoma- weight loss- paresthesias- cognitive dysfunction- teratogenic- reduces OCP efficacy
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62
Q

which AEDs can be used to tx focal seizures?

A

ALMOST ALL AEDs, EXCEPT ethosuximide

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63
Q

tx for generalized seizures (tonic-clonic)

A
  • TOPIRAMATE- LAMOTRIGINE- VALPROATE- levetiracetam- felbamate- funinamide- zonisamide
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64
Q

tx for generalized seizures (absence)

A
  • lamotrigine- ethosuximide- valproic acid
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65
Q

when can you STOP AEDs?

A

individualized for each pt

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66
Q

tx options for INTRACTABLE EPILEPSY

A
  • resective surgery- vagus nerve stimulation- ketogenic diet (works well in children)
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67
Q

which AEDs reduce OCP efficacy? (6)

A
  • phenytoin- phenobarbital- carbamazepine- lamotrigine- oxcarbazepine- topiramate (higher doses)
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68
Q

uncontrolled seizures during pregnancy can cause

A
  • placental abruption- early labor- premature delivery
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69
Q

AEDs are still used in pregnancy bc the risk of complications from uncontrolled seizures is even GREATER than

A

risk of teratogenicity

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70
Q

tx strategy for seizures during pregnancy

A
  • control seizures as much as possible- MONOTHERAPY- LOWEST DOSE possible
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71
Q

MOST LIKELY AED to cause NEURAL TUBE defects

A

valproic acid

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72
Q

teratogenic risk of AEDs is DECREASED by

A

FOLIC ACID

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73
Q

should prophylactic VITAMIN K be given during the last MONTH of pregnancy in pts on AEDs bc of reports of increased bleeding?

A

no, currently not enough evidence

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74
Q

what is the definition of dementia?what is the definition of mild cognitive impairment?what is the clinical triad in NPH?how is AD diagnosed?1st line tx for AD

A
  • chronic cognitive decline w/ or w/o behavioral impairment- PROGRESSIVE- INTERFERES w/ normal daily functioning- NOT d/t DELIRIUM or PSYCHIATRIC D/O
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75
Q

dementia is diagnosed ONLY after completion of the following 3 tasks

A
  1. thorough H&P2. neuropsychiatric testing3. objective cognitive assessment (MMSE or MOCA)
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76
Q

how many abnormalities needed to diagnose dementia?

A

2 OR MORE out of 5 DOMAINS

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77
Q

which 5 domains may be impaired in pts w/ dementia?

A
  1. memory2. executive function3. perception4. language5. behavior
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78
Q

typical feature of advanced dementia

A

PSYCHOSIS refractory to treatment

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79
Q

what is the dx?- when only ONE OR MORE of the DOMAINS is in decline- impairment does NOT significantly impact daily functioning

A

mild cognitive impairment (MCI)

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80
Q

what are the 2 types of mild cognitive impairment (MCI), and which is more common?

A
  • amnestic and nonamnestic- AMNESTIC
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81
Q

at what rate does mild cognitive impairment (MCI) progress to dementia?

A

5-10% per year

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82
Q

what are reversible causes of dementia that need to be r/o when evaluating dementia?

A
  • medications- vitamin B12- hypothyroidism- chronic subdural hematomas- normal pressure hydrocephalus- tumors- infection/inflammation (AIDS, neurosyphilis, neurosarcoidosis, chronic meningitis, lupus cerebritis, vasculitis, autoimmune encephalopathy (such as Hashimoto encephalopathy))- heavy metal poisoning (arsenic, mercury, lead)
83
Q
  • enlargement of ventricles w/o obstruction of aqueduct (ie “COMMUNICATING HYDROCEPHALUS)- NO cerebral atrophy
A

normal pressure hydrocephalus (NPH)

84
Q

NPH often occurs after…

A
  • head TRAUMA- MENINGITITS- SUBARACHNOID HEMORRHAGE
85
Q
  • NORMAL intracranial pressure- NO papilledema- NO headache
A

normal pressure hydrocephalus (NPH)

86
Q

classic triad of normal pressure hydrocephalus (NPH)

A
  1. gradually worsening dementia2. gait apraxia; “magnetic gait”3. urinary incontinence
87
Q
  • must differentiate this from NPH- more common in pts w/ HTN or DM- can present w/ the SAME clinical TRIAD as NPH
A

diffuse white matter disease

88
Q

treatment for NPH

A

VENTRICULOPERITONEAL or VENTRICULOATRIAL SHUNT

89
Q

MC of dementia AFTER 60 YEARS OF AGE

A

Alzheimer disease (AD)

90
Q

diagnosis for Alzheimer disease (AD)

A
  • INSIDIOUS- PROGRESSIVE- 2 or more impaired domains (memory, executive functioning, perception, language, behavior) causing SIGNIFICANT IMPAIRMENT in normal daily functioning
91
Q

do NOT use these for definitive dx of Alzheimer disease (AD)

A
  • MRI- PET scan- CSF tau measurements
92
Q

why should MRI, PET scan, and CSF tau measurements NOT be used for dx of Alzheimer disease (AD)?

A

NOT SPECIFIC ENOUGH

93
Q

when should a dx of Alzheimer disease (AD) NOT be made?

A
  • h/o cerebrovascular disease- clinical features of frontotemporal dementia- clinical features of dementia w/ Lewy bodies- evidence of another psych or neuro illness- takes meds that cause cognitive impairment
94
Q

what are the main diagnoses to consider in elderly pt w/ dementia w/o movement d/o?

A
  • Alzheimer dz- VASCULAR dementia- MIXED dementia (w/ both neurodegenerative and vascular components)
95
Q

1st line tx for Alzheimer dz

A
  • CHOLINESTERASE INHIBITORS (CIs)- donepezil (Aricept)- rivastigmine (Exelon)- galantamine (Razadyne)
96
Q

what ADDITIVE drug tx can be used for Alzheimer dz?

A

memantine (Namenda)(N-methyl-D-aspartate receptor antagonist)

97
Q

what is better for tx of Alzheimer dz, especially advanced AD?

A

COMBINATION of CI and memantine

98
Q

can you use cholinesterase inhibitors and memantine for MCI?

A

NO

99
Q

what are the cholinergic sxs d/t adverse effects of cholinesterase inhibitors?

A
  • anorexia- nausea- diarrhea- bradycardia
100
Q

which atypical antipsychotics can used to tx agitation, insomnia, delusions, aggression, and wandering, but can INCREASE MORTALITY?

A
  • olanzapine- quetiapine- risperidone- clozapine
101
Q

what are the 2 general categories for dementia caused by cerebrovascular dz?

A
  1. MULTI-INFARCT dementia2. DIFFUSE WHITE MATTER disease (Binswanger dz)
102
Q

characteristics of multi-infarct dementia

A
  • d/t several strokes (large or small) in different brain regions- have prominent motor, reflex, visual, and gait abnormalities- do NOT have difficulty NAMING objects- ABRUPT onset- STEPWISE deterioration of mental function- different from ALZHEIMER’S which is SLOW and steady
103
Q

MCC of diffuse white matter dz

A

chronic HTN

104
Q

similar in presentation and course to Alzheimer dz

A

frontotemporal dementia (previously Pick dz)

105
Q

difference between frontotemporal dementia and Alzheimer dz

A
  • MORE RAPID- DISINHIBITION- LANGUAGE DEFICITS- onset in 5th to 6th decade of life- males > females
106
Q

CT or MRI scan results of ALzheimer pt

A

diffuse brain atrophy

107
Q

CT or MRI scan results of frontotemporal dementia pt

A

MORE FOCAL ATROPHY of frontal and temporal lobes

108
Q

only sure way to differentiate between Alzheimer and frontotemporal dementia pts

A

histologically at autopsy

109
Q

one of the very rare PRION dzs

A

Creutzfeldt-Jakob disease (CJD)

110
Q

how is Creutzfeldt-Jakob disease (CJD) subdivided?

A
  • SPORADIC (most typical, 95%)- FAMILIAL (about 5%)- IATROGENIC- VARIANT
111
Q

when does sCJD (sporadic Creutzfeldt-Jakob disease) usually present, and what causes it?

A
  • 55-65 yoa- we have no idea!
112
Q

when you see CJD in younger pts, think of

A

iCJD or vCJD

113
Q

what is believed to be the cause of vCJD?

A

prion causing “MAD COW DISEASE” (bovine spongiform encephalopathy)

114
Q

what causes iCJD?

A
  • receipt of infected human tissues (dural grafts, corneal transplant, or liver transplant)- receipt of infected hormones (eg GH, or gonadotropins)- exposure to contaminated surgical instruments)
115
Q

characteristics of Creutzfeldt-Jakob disease (CJD)

A
  • RAPIDLY PROGRESSIVE dementia (weeks, not years)- startle MYOCLONUS (startle to loud noises)
116
Q
  • changes in behavior- changes in emotional response- changes in intellectual function- ataxia- visual distortions- confusion- hallucinations- delusions- agitation- dementia- muteness
A

Creutzfeldt-Jakob disease (CJD)

117
Q

younger pts w/ vCJD have dementia w/ what predominant features?

A

PSYCHOTIC

118
Q

gold standard for diagnosing Creutzfeldt-Jakob disease (CJD)

A

brain BIOPSY

119
Q

other supportive studies for diagnosing Creutzfeldt-Jakob disease (CJD)

A
  • MRI- EEG- 14-3-3 PROTEIN in CSF
120
Q

mortality rate of Creutzfeldt-Jakob disease (CJD)

A

fatal in < 1 yr in > 90% of pts

121
Q

treatment for Creutzfeldt-Jakob disease (CJD)

A

none

122
Q

cause of Parkinson dz (PD)

A

loss of dopaminergic neurons in substantia nigra

123
Q

what percentage of Parkinson dz (PD) develop dementia?

A

80%

124
Q

dementia in Parkinson dz (PD) pts primarily affects what?

A
  • EXECUTIVE FUNCTIONS- ATTENTION
125
Q

when dementia PRECEDES or develops w/i 1 year after onset of motor dysfunction, it is referred to as

A

DEMENTIA W/ LEWY BODIES (DLB)

126
Q

clinical features of dementia w/ Lewy bodies (DLB), besides dementia

A
  • spontaneous motor features of parkinsonism- recurrent, vivid visual hallucinations- prominent fluctuations of attention and cognition
127
Q

which med spares D2 dopamine receptor and can be helpful in PDD and DLB?

A

CLOZAPINE

128
Q

which meds are not good for dementia w/ Lewy bodies (DLB)?

A

older antipsychotic drugs; haloperidol and chlorpromazine

129
Q

which meds are under FDA SAFETY ADVISORY bc they are associated w/ an INCREASED RISK OF DEATH in elderly pts w/ dementia, especially DLB?

A

antipsychotic drugs

130
Q
  • dementia- usually occurs in 6th decade of life- GAZE PALSY- abrupt falls
A

progressive supranuclear palsy (PSP)

131
Q
  • DEMENTIA- MOVEMENT DISORDER- autosomal dominant w/ complete penetrance
A

Huntington disease

132
Q

what gene is responsible for Huntington disease (HD)?

A

HTT gene on chromosome 4p

133
Q

when does Huntington disease (HD) occur?

A

LATE 30s

134
Q

what are sxs of Huntington disease (HD)?

A
  • dementia- CHOREA- psychiatric disturbances (personality changes, depression, and PSYCHOSIS)
135
Q

dx for Huntington disease (HD)

A
  • positive family hx- clinical features- genetic testing for HTT gene
136
Q

imaging finding in Huntington disease (HD)

A

caudate nuclei atrophy (“boxcar” ventricles)

137
Q

cure for Huntington disease (HD)?

A

none, FATAL

138
Q

tx for MILD CHOREA in Huntington disease (HD)

A

tetrabenazine

139
Q

adverse effects of tetrabenzapine

A
  • depression- sedation- bradykinesia
140
Q

MCC of dementia in younger pts

A

AIDS

141
Q
  • cognitive impairment- movement d/o- depression- HIV
A

HIV-associated dementia (HAD)

142
Q

what is “pseudodementia?”

A

significant cognitive dysfunction in pts w/ MAJOR DEPRESSION

143
Q

what is one differentiating feature seen in moderate or advanced dementia, but NOT pseudodementia?

A

FRONTAL LOBE release signs (grasp, suck, rooting, and palmomental reflexes)

144
Q

is commonly poor in depression d/t attentional dysfunction, but good in dementia pts

A

immediate recall

145
Q

what is delirium?

A
  • acute, often transient, altered mental status- typically occurs w/i hours to days
146
Q

in whom and where is delirium most commonly seen?

A
  • hospitalized elderly pts- ICU pts
147
Q

dx delirium

A
  • clinical- decreased attention span- varying states of confusion
148
Q

most crucial aspects in dx type and etiology of a headache

A

history and physical

149
Q

what history must be determined when dx a headache?

A
  • QUALITY of pain (dull, sharp, throbbing, constant)- LOCATION- DURATION- EXACERBATING factors- ALLEVIATING factors- associated sxs
150
Q

how are headaches classified?

A

primary or secondary

151
Q

what are the primary types of headache? (5)

A
  1. migraine2. tension-type headache3. cluster headache4. other trigeminal autonomic cephalgias5. other headaches
152
Q

what are the characteristics of primary headache?

A
  • chronic- recurrent- w/o signs of neurologic dz
153
Q

what are the secondary types of headache? (10)

A
  1. d/t hemorrhage2. head/neck trauma3. benign intracranial HTN4. brain tumors5. cranial/cervical vascular d/o6. substance abuse/withdrawal7. infection8. homeostasis d/o9. facial pain10. psychiatric d/o
154
Q

what hemorrhage can cause severe headache?

A

subarachnoid

155
Q

what are some examples of cranial/cervical vascular d/o that can cause headache?

A
  • carotid dissection- sinus venous thrombosis- giant cell arteritis
156
Q

what are some examples of substances or their withdrawal that can cause headache?

A
  • nitrates- EtOH- caffeine
157
Q

what are some examples of infection that can cause headache?

A
  • meningitis- encephalitis
158
Q

what are some examples of homeostasis d/o that can cause headache?

A
  • HTN- hyperviscosity
159
Q

what are some examples of facial pain that can cause headache?

A
  • cranium- neck- eyes- sinuses- teeth- trigeminal neuralgia- herpes zoster
160
Q
  • typical- largely familial d/o- periodic- often U/L- pulsatile (throbbing) pain- begin in childhood, adolescence, or early adulthood, and diminish in frequency w/ age
A

migraine headache

161
Q

definition of EPISODIC migraine headache

A

< 15 headaches/month

162
Q

definition of CHRONIC migraine headache

A

> 15 headaches/month x 3 months

163
Q

triggers for migraine headaches

A
  • emotional stress- foods (eg chocolate, AGED CHEESE, foods rich in tyramine- alcohol- menstruation- glare- strong sensory stimuli (eg perfume)- rapid changes in barometric pressure
164
Q

what % of migraine headaches have an aura?

A

25%

165
Q

most common visual sxs in migraine w/ AURA

A
  • sparkling lights (scintillating scotomata)- jagged zigzag lines (fortification spectra)
166
Q

how long do migraine auras last?

A

5-60 minutes

167
Q

what do longer than usual migraine auras represent?

A

complicated migraine or concern for stroke

168
Q

how much more typical is a migraine withOUT aura than one w/?

A

5x

169
Q
  • visual phenomena that occupy BOTH visual fields (temporary cortical blindness)- vertigo- dysarthria- INCOORDINATION of limbs- diplopia- tingling- headache that affects BRAINSTEM
A

basilar migraine

170
Q
  • migraine w/o headache- abnormal transient neurologic dysfunction
A

acephalic migraine

171
Q

multiple or virtually continuous headaches w/ scalp tenderness, > 72 hours

A

status migrainosus

172
Q

diagnosis for migraine headache

A

HISTORY

173
Q

if pt presents w/ typical migraine sxs, next step?

A

FIRST give TREATMENT TRIAL

174
Q

initial study for migraine w/ atypical sxs, HA pattern change, seizure, or focal neurologic sxs

A

CTH w/ and w/o contrast

175
Q

what is ACUTE tx for migraine headache?

A

any tx given WITHIN FIRST HOUR of HA

176
Q

what are some effective txs for acute migraine?

A
  • acetaminophen- aspirin- NSAIDs
177
Q

1st line treatment for migraine

A

TRIPTANS(sumaTRIPTAN, zolmiTRIPTAN, rizaTRIPTAN, naraTRIPTAN, almoTRIPTAN, eleTRIPTAN, frovaTRIPTAN)

178
Q

which triptan works the fastest?

A

rizaTRIPTAN

179
Q

which triptan has 3 methods of delivery, injection, intranasal, and PO?

A

sumaTRIPTAN

180
Q

which tx combination for migraine HA works synergistically and better than taking either as monotherapy?

A

sumaTRIPTAN and naproxen

181
Q

when are triptans CI bc of r/o inducing ischemia?

A
  • complicated or basilar migraines- CHD or Prinzmetal angina- h/o stroke- uncontrolled BP- pregnancy
182
Q

which 2 medications are effective for termination of migraine in pts who present to the ER w/ VOMITING?

A
  • PROCHLORPERAZINE- METOCLOPRAMIDE
183
Q

if pts take migraine headache medications too fequently, what can happen?

A

medication overuse headaches

184
Q

American Heart Association/American Stroke Association 2014 Guideline for Prevention of Stroke in Women recommend PROPHYLAXIS for women w/ frequent migraines w/ aura if, what?

A
  • GREATER THAN 55 YOA, especially if, taking OCPs
185
Q

what are the major categories of migraine prophylaxis?

A
  • BB
  • TCA
  • AED
  • CCB
  • ACEI/ARB
  • NSAID
  • botulinum toxin
186
Q

which BBs are FDA-approved for migraine prophylaxis tx?

A

propranolol and timolol

187
Q

when are propranolol and timolol NOT recommended for migraine prophylaxis tx?

A
  • GREATER THAN 60 YOA

- and/or SMOKERS

188
Q

distinct headache syndrome that responds to O2 tx

A

cluster headaches

189
Q

how often do cluster headaches usually occur?

A

several times/day for a few weeks

190
Q

cluster headaches are more common in which sex?

A

MALES (5:1)

191
Q

what’s a common trigger of cluster headaches?

A

ALCOHOL in 70% of pts

192
Q

cluster headaches description

A
  • UNIlateral
  • severe
  • ICE PICK or HOT POKER
  • PERI- or RETRO-ORBITAL
193
Q

when do cluster headaches usually occur?

A

night 1-2 hours after sleep onset, or several times throughout night

194
Q

what are the associated vasomotor phenomena of cluster headaches?

A

IPSIlateral blocked nostril, rhinorrhea, lacrimation, miosis, flush, and edema of that cheek

195
Q

best acute treatment for cluster headaches?

A

OXYGEN (6 L/min x 15 minutes) is commonly RAPIDLY ABORTIVE

196
Q

what tx can be combined w/ O2 for acute tx for cluster headaches?

A

SC or IN triptans

197
Q

DOC for cluster headache prophylaxis after 1st episode

A

verapamil (PO up to 480mg)

198
Q

adverse effects of verapamil if dose higher than 240mg

A
  • bradycardia

- heart block

199
Q

MC variety of headache

A

tension headache

200
Q

tension headache characteristics

A
  • pain that is chronic
  • B/L
  • constant
  • nonthrobbing
  • “SQUEEZING”
  • no migraine/cluster headache features
201
Q

duration of tension headaches?

A

can be present throughout the day for long periods of time

202
Q

1/3 of pts w/ chronic tension headaches have sxs of?

A

depression

203
Q

treatment for acute tension headaches

A
  • acetaminophen

- NSAIDs

204
Q

when should you consider PREVENTION medication for tension headaches?

A

if attacks occur > 2 days per week

ABIM (9 decks)

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