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objectives 2 Flashcards

1
Q

teratogenic epileptic drugs

A

i. Valproate=neural tube defects
ii. Lamotrigdine & carbamazepine=oral/facial clefts
iii. Phenytoin=Fetal hydantoin syndrome

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2
Q

drugs for absence seizures

A

ethosuximide
lamotrigdine
valproate

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3
Q

drugs for partial seizures

A

carbamazepine, oxcarb, phenytoin

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4
Q

protocol for status epileptics

A
  1. lorazepam 0.1 mg/kg (4-8 mg) IV repeatable in 5-10 minutes if needed,

2, loading with either:

  • fosphenytoin 20 phenytoin equivalents (PE)/kg IV, no faster than 150 mg/min,
  • phenytoin 20 mg/kg IV, given in saline no faster than 50 mg/min.
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5
Q

LP indications

A

i. Suspected CNS infection
ii. Suspected demyelinating/inflammatory dz
iii. Suspected SAH
iv. Diagnosing Normal Pressure hydrocephalus and pseudotumor cerebri
v. CSF cytological analysis

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6
Q

contraindications to emergent LP

A

i. ICP!!! b/c of risk of brain herniation
ii. Coagulopathy (INR>1.5 or platelets <50,000, 6hrs from last Heparin, 5 days from last Clopidogrel).
iii. Spinal cord trauma
iv. Cardiorespiratory compromise
v. Overlying skin lesion/infx

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7
Q

CSF findings in bacterial meningitis

A

WBC>500-1000 (PMN’s),
Protein ↑
Glucose ↓

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8
Q

CSF findings in viral meningitis

A

WBC <500 (lympho’s),
Protein ↡/nl,
Glucose nl

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9
Q

CSF findings in TB meningitis

A

WBC <500 (lympho’s),
Protein ↡,
Glucose ↟

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10
Q

CSF findings in fungal meningitis

A

Fungus: WBC <500 (lympho’s),
Protein ↡
Glucose ↟

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11
Q

what to for suspected SAH with negative CT?

A

do tap to r/o low-volume SAH

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12
Q

SAH tap CSF vs traumatic tap

A

SAH: xanthrochromic and same # of RBC’s in tube 1 and 4

traumatic tap: NOT be xanthochromic, and # of RBC’s will drop from tube 1 to 4

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13
Q

What can reduce edema or herniation from certain cerebral lesions
(tumor, abscess or encephalitis) or spinal cord lesions (metastatic cord compression, myelitis),

A

IV dex (antinflammatory)

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14
Q

symptoms of herpes simplex encephalitis

A

aphasia, behavior change, memory deficits

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15
Q

MRI of herpes simplex encephalitis

A

bilateral/asymmetric involvement of inferior frontal and medial temporal lobes

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16
Q

treatment of herpes simplex encephalitis

A

IV acyclovir

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17
Q

MS presentation

A

Most common initial sx involve optic nerves (optic neuritis, INO) or LE motor deficits

Trigeminal neuralgia, (+) Lhermitte’s sign also common

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18
Q

MS timing

A

starts relapsing/remitting,

later secondary progressive phase w/o full recovery between episodes

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19
Q

MS dx

A

Multiple signs/sx separated by space and time

i. brain/spinal cord MRI, new/active lesions enhance w/contrast
ii. Oligoclonal bands in CSF (clones of Ab’s), increased Ig synthesis in CSF

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20
Q

MS treatments

A

i. High dose IV steroids for acute MS attacks

ii. Beta-interferon or Glatiramer acetate reduces severity/frequency of attacks, lessens future
cumulative neuro-disability in some

iii. Calfampridine (K-channel blocker) increases conduction speed, improves sx
iv. Natalizumab: Ab that blocks T-cell adhesion molecules to prevent BBB penetration

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21
Q

Abortive Migraine tx - if migraines are <1-2/month

A

i. NSAIDs, Analgesics (Tylenol, ASA) for mild migraine
ii. Triptans (can be IM, helpful if pt also has N/V)
iii. Dihydroergotamine (injection, nasal spray)

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22
Q

Prophylactic Migraine tx - for more frequent or more severe neurologic effects

A

i. Beta-blocker (Propanolol), CCB (Verapamil)
ii. TCA (amytriptyline)
iii. Anticonvulsants (Valproate, Gabapentin, Topiramate)

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23
Q

Tension HA tx:

A

NSAIDS, analgesics, TCA’s

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24
Q

Eval of HA d/t increased ICP

A

LP urgently to exclude meningitis, SAH

Get CT first in setting of papilledema to r/o mass lesions (brain tumor, abscess, intraparenchymal hemorrhage) that could cause brainstem herniation

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25
Q

tx for HA due to increased ICP

A

Mannitol, hypertonic saline to reduce edema,

if there’s an aneurysm, clip or coil it.

Craniotomy to relieve pressure

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26
Q

work up for altered mental status

A

MMSE

labs: CBC, CMP, TSH, B12

MRI: tumor, infarct, NPH, abscess, etc.

LP if HA/fever

if young –> HIV test

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27
Q

Dx Alzhemeirs

A

diagnosis of exclusion-

observations from family/friends

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28
Q

Wallerian degeneration:

A

axons/myelin degenerate distal to crushing/penetrating focal nerve injury

29
Q

Demyelination caused by

A

focal compression (carpal tunnel)

GBS, etc.

30
Q

Toximetabolic causes of polyneuropathies almost always cause

A

axonal degeneration, with secondary demyelination

31
Q

Multiple mononeuropathies can be d/t

A

systemic illness like SLE, Sarcoid, or

Leprosy

32
Q

Non-acute Polyneuropathy causes

A

**DM

but can be metabolic, autoimmune,cancerous, infectious

33
Q

what testing can elucidate which type of neuropathy?

A

EMG

34
Q

If EMG + clinical picture suggests inflammatory, immune-mediated, or vasculitic cause, get ____ biopsy to confirm dx

A

sural nerve

35
Q

neuropathy treatments

A

i. Chronic weakness: Braces/splints/cane/walker
ii. Chronic pain: Topical capsaicin or lidocaine patches

iii. Pain:
- Anticonvulsants (Gabapentin, Pregabalin, Carb),
- Antidepressants (Duloxetine, Amitriptyline)

36
Q

trigeminal neuralgia tx

A

Anticonvulsants like gabapentin and carbamazepine prevent the nerve from misfiring and producing the shock-like pain.

37
Q

postherpatic neuralgia tx

A

acylcovir asap!

for pain sxs: Topical capsaicin or lidocaine

38
Q

Topical capsaicin MOA

A

depletes substance P, a pain mediator

39
Q

radiculopathy (dorsal root inflamm) tx

A

Surgical removal of the inflammatory insult (if possible) is obviously the best way

Otherwise, analgesics, anti-inflammatory meds (steroids), and nerve block procedures help

40
Q

Polymyositis diagnosis

A

clinical: (“I am having difficulties climbing up stairs”, “I have troubles
with reaching to grab something off the top shelf”…aka proximal weakness).

Confirmed with an EMG, muscle biopsy showing inflammatory cells amongst necrotic/regenerating m. fibers.

41
Q

Polymyositis treatment

A

corticosteroids

42
Q

myasthenia gravis dx

A

clinical: (ptosis, dysarthria, dysphagia, diplopia all extremely common).

Tensilon test (pretty outdated though).

LOOK FOR THE AUTOANTIBODIES (anti-AChR).

43
Q

MG treatment

A

immunosuppression (steroids), AChE inhibitors (pyridostigmine), thymectomy

44
Q

ALS dx

A

clinical diagnosis (combined UMN+LMN, often unilateral to start off, purely motor deficits, fasciculations).

45
Q

ALS treatment

A

not much except RILUZOLE (NMDA-R antag.)

46
Q

myasthenia graves crisis presentation

A

profound weakness/quadriplegia and inability to speak, swallow or breathe

triggers: acute stressors like severe infection.

47
Q

myasthenia crisis management

A

Neuro emergency, admit to ICU, maintain on ventilator.

Treat current infection, immunosuppress if indicated.

48
Q

GBS (guillan barre syndrom) emergency presentation

A

Ascending paralysis that can often involve diaphragm.

49
Q

GBS management

A

Neuro emergency, admit to ICU, ventilator.

immunosuppression

50
Q

spinal cord syndrome management

A

Evaluate UMN, LMN signs to localize.

Evaluate dermatomal sparing to
determine intramedullary (suspended sensory level, sacral sparing, etc) or extramedullary (sacral
involvement) etiology.

Remove cause of compression if possible.

51
Q

Parkinsons pathophys

A

Progressive loss of dopaminergic neurons from SNc.

This means loss of direct pathway “stimulation” of the VL thalamus and increase in indirect pathway
“inhibition” of the VL thalamus.

52
Q

Parkinson best treatment and MOA

A

Levodopa + Carbidopa

(prevent peripheral DOPA decarboxylase
conversion)

53
Q

treatment of essential tremor

A 
beta blockers
(also barbs and booze, but don't do it)
54
Q

CJD on EEG

A

periodic sharp wave discharge

55
Q

neurological criteria for brain death

A

a. Known severe cause
b. No improvement despite treatment for over ~6 hours (extended for younger folk)
c. unresponsive to painful stimuli
d. All CNs/brainstem reflexes must be absent
e. No spontaneous respirations

56
Q

what test can confirm brain death?

A

RADIOISOTOPE BRAIN SCAN:

the absence of cerebral blood flow over a 10 min period.

57
Q

supportive care for ALS

A

oxygen, CPAP, BiPAP mask.

Aggressive = mechanical ventilation via trach
tube.

Many patients opt for death by respiratory failure or pneumonia at home…relief of anxiety of dyspnea = BENZOS.

58
Q

managing end-stage dementia

A

Constantly monitor behavioral changes. Constantly address nutrition, dressing, hygiene

59
Q

acute hemorrhage on T2 MRI

A

center of an acute hemorrhage is brighter,

with a darker periphery, which changes as the hematoma ages.

60
Q

acute infarction seen faster on which imaging?

A

MRI

61
Q

is acute infarction bright or dark on MRI and CT?`

A

MRI: bright
CT: dark

62
Q

edema is dark or bright on MRI and CT?

A

MRI: bright
CT: dark

63
Q

do abscesses, encephalitis, and myelitis dark or bright on T2 MRI?

A

bright

64
Q

MRI of meningitis description

A

contrast enhancement of leptomeninges

65
Q

metastatic brain tumors presentation

A

often multiple,

with surrounding edema,

usually found at the gray-white junction

66
Q

Epidural spinal cord metastases often arise from ______ and expand toward ____

A

vertebral bone

spinal cord

67
Q

MS plaques appear bright or dark in T2 MRI?

A

bright

68
Q

Degenerative spine disease (spondylosis, disc herniations, and central canal stenosis) and its relation to the spinal cord and nerve roots are best seen with…

A

MRI

second place: CT with intrathecal contrast

Neuro (22 decks)

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