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Intern Year > Neuro PPMC > Flashcards

Neuro PPMC Flashcards

1
Q

1/5 of cardio emboli strokes are PCA. Otherwise more likely to be Anterior circulation due to vessel size (ACA)

A

4/5 cardio emboli strokes

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2
Q

Treat cardioembolic stroke:

A

.

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3
Q

Biggest risk factor for cardiogenic stroke:

A

A fib, and biggest risk factor for Agin is age

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4
Q

TPA definitely effective. Acute use of heparin not overall helpful for “all comer” patients. However in special cases we do heparinize.

A

So: all tPa candidates get heparin, aspiring should be given to everyone, and heparin or LMWH should NOT be used unless clear indication for urgent anticoagulantion exists

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5
Q

Long term anticoagulantion

A

Risk stratification
High risk e.g. Afib

Low risk e.g. PFO

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6
Q 
Chads2vasc most useful for helping to decide between aspirin and anticoagulantion 
Score of (one or) 2 or higher warrants anticoagulantion

2/3 risk

A

2/3 risk reduction from anticoagulantion, vs 20%?risk reduction with anti platelet

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7
Q

Cryptogram it TIA: rhythm monitoring, then vitamin k antagonist or NOAC for all non-valvular Agin

A

Anticoagulation in strokes risks of novel agents seems to come down

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8
Q

After large stroke, wait 10-14 days to anticoagulant

A

For smaller strokes can anticoagulantion pretty quick

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9
Q

Pradaxa/dabigatran is direct thrombin inhibitor; apixiban and rivaroxaban are 10-a inhibitors (upstream from factor 2 thrombin)

A

NOAC

Apixiban is only one with significant (if small) survival benefit over warfarin (ARISTOTLE trial)

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10
Q

In elderly people, aspirin may be just as dangerous as warfarin

A

Another European trial

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11
Q

For primary prevention, no benefit in anticoagulation for low-EF CHF

A

Also no need to close PFO.

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12
Q

AVERRROSE and ARISTOTLE are two stroke trials, older/sicker vs healthier

A

Need to have 200 falls to outweigh risk of anticoagulation

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13
Q

4-factor PCC is expensive and not yet proven to improve survival

A

4-factor reversal of warfarin vs FFP

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14
Q

After TPA, wait 24 hours to give aspirin

A

TPA might not be enough for thrombi that are not purely blood (e.g. Lipid and calcium), so sometimes we wait for endovascular clot busting–all the trials came out in 2015

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15
Q

PCA supplies thalamus

A

Intended stroke patient–could be top-of-the-arteries

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16
Q

Septic strokes tend to be smaller, more cortical-looking than clot-type thrombi

A

Think of the lady who had serratia endocarditis and bilateral blindness. Differential is carotid cavernous fistula with bleed into the cavernous sinus causing the really bloody eyes

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17
Q

4 lacunae syndromes with their corresponding arteries:

Pure motor hemiparesis-internal capsule/coronaradiata
Pure sensory -thalamic perforator its-PCA
Sensorimotor-thalamus plus internal capsule
Ataxic-cerebellar perforator a
Dysarthria/clumsy hand-uppersub thalamic and putaminal/Palladian posterolateral thalamus

A

MCA-lenticular trustee
PCA-thalamic perforators
Basilar-paramedian pontine perforator a
PICA/AICA-cerebellum perforators

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18
Q

Ddx stroke causes: tele, EKG, TTE, TEE, (CE), carotid ultra sound, CTA/MRA, angiogram for vasculitis or AVM

Stroke labs: lipids, A1C, ESR, RPR, LDL<70, BNP

A

CT:
MRI: DWI bright with ADC dark correlate suggests stroke
MRI: bFLAIR is T2 with CSF subtracted fluid attenuated
GRE gradient echo sequence-looks for blood-if you suspect amyloid

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19
Q

Stroke etiologies

A 
Small vessels -hTN
Cardiogenic -Afib, MI, Endocarditis, myxomatosis, fibrobroelastoma
Large vessel disease (carotid, verts)
Paradoxical embolus (DVT PFO , Pulm AVM)
Vasculitis
Malignancy
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20
Q

Stroke secondary treatment by etiology:

A

Afib-rate control, warfarin, DOAC
CHF 30% (global hypokinesis, regional wall motion abnormality)
Endocarditis-antibiotics
Carotid stenosis: endarterectomy for plaque, or stent
Small vessel-blood pressure control (130/80)
Cryptogenic-event recorder
Paradoxical: AC, filter, PFO closure,
Factor 5 Leiden, prothrombin mutation, anti cardiologist antibody. -anticoagulation
Malignancy-lovenox 1.5mg/kg per day

21
Q

One vessel supply for thalamus–Percheron artery
Can cause infarct
It also venous Thrombosis can cause back-up infarction

A

G

22
Q

Paraneiplastic treatment: Rituximab for shutting down antibodies: CD-20 specific, works just on B cells
Cyclophosphamide could also work
Steroids short term

A

Paraneiplastic treatment
Hold off on steroids if lymphoma because it responds well
Primary CNS lymphoma around ventricles, metastatic from systemic lymphoma is more in cortex

23
Q

Reading an MRI:

  1. Start with DWI/ADC to look for restricted diffusion (bright/dark). For stroke, but also seizure, inflammation, etc.
  2. FLAIR (water/dense bright, but with CSF subtracted). T2 good for pathology; T1 good for anatomy
  3. Post-contrast
  4. GRE to look for blood-pretty rapid, due to hemosiderin depositing
A

DWI/ADC
FLAIR
Post-contrast (T1)
GRE-pretty quick for blood (hemosiderin deposition) but get a head CT if you need immediate confirmation

24
Q

Hold off on steroids if lymphoma because it responds well

Primary CNS lymphoma around ventricles, metastatic from systemic lymphoma is more in cortex

A

CNS lymphoma

25
Q

Lateral medullary stroke (Wallenberg syndrome)

Upper medulla; facial fibers cross upper medulla, contra lateral body fibers cross lower
Vestibular problems
Dysarthria
Horners because affected down going sympathetic tract

A

Crossed sensory deficits

Lateral medullary

Or CN6 nucleus with Facial Nerve involvement (CN7 wraps around CN 6 nucleus

26
Q

Medial medullary: Dejerine’s syndrome

Contra lateral weakness (corticospinals)
sensory deficits (medial lemniscus)
Tongue deviates toward the lesion (lick your wounds)

A

CN 3, 6, and 12 come out in the middle

27
Q

Copaxone MS drug

Side effect-lipoiatrophy or atrophy

A

Glatiramer acetate, formerly known as copolymer-1, exerts its effects in Multiple Sclerosis (MS) patients through a mechanism of action that is not fully understood. It is believed to modify immune processes or functions which are thought to be liable for MS pathogenesis. In vitro studies suggest that glatiramer acetate-specific suppressor T-cells are induced and activated in the periphery .

28
Q

gerstmann syndrome

A

Gerstmann syndrome is characterized by four primary symptoms:

  1. Dysgraphia/agraphia: deficiency in the ability to write[2][3]
  2. Dyscalculia/acalculia: difficulty in learning or comprehending mathematics[2][3]
  3. Finger agnosia: inability to distinguish the fingers on the hand[2][3]
  4. Left-right disorientation[2][3]
29
Q

gelastic seizures

A

hypothalamic hamartoma

30
Q

catamenial seizure

A

menstrual synchronization

31
Q

Weber stroke syndrome

A

midbrain - Ipsilateral CN III palsy; contralateral hemiparesis

32
Q

Wallenberg stroke syndrome

A
  • vestibular symptoms (vertigo, diplopia, nystagmus, vomiting)
  • ataxia
  • myoclonus
  • contralateral pain and temperature deficits in body
  • ipsilateral pain and temperature deficits in face -dysphagia
  • hoarseness, dysphonia, dysarthria
  • diminished gag reflex
  • ipsilateral Horner’s syndrome
33
Q

Williams Syndrome

A

n

34
Q

Sternback vs Hunter criteria for serotonin syndrome

A

cognitive/behavioral, autonomic, movement

35
Q

afferent pupil reflex - CN 2 (afferent limb)
dolls eyes - CN 3, 4, 6, 8
corneal reflex - CN 5, 7
gag reflex CN 9, 10

A

Brainstem Exam

36
Q

Vertebral artery stroke syndrome

A

Lower cranial nerve deficits (dysphagia, dysarthria, tongue/palate deviation) and/or ataxia with crossed sensory deficits of the face and body, stupor, coma (+/- the rest of Wallenberg)

37
Q

Basilar artery stroke syndrome

A

Oculomotor deficits and/or ataxia with “crossed” sensory/motor deficits of the face and body; stupor, coma.

38
Q

Posterior cerebral artery stroke syndrome

A

Contralateral visual field deficits (homonymous hemianopia). Cortical blindness (Anton’s syndrome) and paresthesias may also be seen (e.g. visual hallucinations with insight and without sound)

39
Q

first-line treatment for primary generalized seizures

A

“Broad-spectrum” anticonvulsants such as valproic acid, topiramate, and lamotrigine are considered first-line treatment for 1° generalized seizures.

40
Q

tx for juvenile myoclonic epilepsy

tx for absence epilepsy

A

Two unique types of generalized epilepsy are juvenile myoclonic epilepsy,
which is best treated with valproic acid, and absence epilepsy,
which is classically treated with ethosuximide.

41
Q

stroke work up: diagnosis

stroke tx: TPA, thrombectomy, or ASA/clopidogrel

A

Workup for ischemic stroke: CT and/or MRI, carotid ultrasound, TTE/TEE, EKG, Heart monitor

42
Q

Drugs that induce the liver cytochrome

P-450 system (eg, phenytoin and carbamazepine) can lead to ↓ effectiveness of OCPs

A

carbamazepine and phenytoin

43
Q

Oculocephalic reflex: CN 8 progects cross-wise to 6, then CN 6 goes through MLF to CN 3 crossing back, and also goes directly to lateral rectus.

A

Direction of nystagmus (fast beat) is COWS cold opposite warm same
Cold water inhibits:
–>slow phase toward instilled ear (intact brainstem)
–>fast phase away (intact cortex providing corrective nystagmus
Warm water activates:
–>slow phase away from instilled ear
–>fast phase toward instilled ear

44
Q

Oculocephalic reflex: CN 8 progects cross-wise to 6, then CN 6 goes through MLF to CN 3 crossing back, and also goes directly to lateral rectus.

A

Direction of nystagmus (fast beat) is COWS cold opposite warm same.
Cold water inhibits:
–>slow phase toward instilled ear (intact brainstem)
–>fast phase away (intact cortex providing corrective nystagmus)
Warm water activates:
–>slow phase away from instilled ear
–>fast phase toward instilled ear

45
Q

Stages of Sleep:
Awake: small squiggle
Eyes closed: small tighter squiggles (alpha)
N1 - loss of alpha, looks kind of like awake again
N2 - larger amplitude, Spindles
N3-4 - Sawtooth
REM - looks a little like awake, check EMG tone

A

REM sleep: autonomic instability, poor thermoregulation, increased cortrical metabolism, penile tumescence, atonia, PGO (pontine geniculate occipital) waves

46
Q

orexin = hypercretin

orexin activates LV, raphe, and TMN

A

dopamine is wake-promoting
SNRIS are also rake-promoting
haloperidol also blocks dopamine to promote wakefulness
benztropine blocks ACh wake-promoting effects
GABA-A drugs (e.g. benzos) may mimic effects of GABA released from VLPO
Caffeine blocks sleep-promoting effects of adenosine

47
Q

hyperventilation brings out absence seizures
photic stimulation brings out juvenile myoclonic seizures
sleep deprivation brings out any kind of seizure
alcohol brings out any kind of seizure

A

Listeria, legionnaire’s, mycoplasma, and TB all like the brainstem (rhomboencephalitis)

48
Q

NMO: 3 vertebral segments plus aquaporphorin antibodies plus eye

A

brainstem press

Intern Year (3 decks)

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