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NCC > Neuro ICU Book > Flashcards

Neuro ICU Book Flashcards

1
Q

Most important step for a patient with high-grade acute SAH with poor mental status and IVH?

A

EVD

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2
Q

SAH with IVH cause of vertical eye movement impairment and depressed level of arousal

A

Acute obstructive hydrocephalus from mass effect on thalamus and midbrain

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3
Q

Independent risk factor for development of symptomatic vasospasm after SAH

A

IVH

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4
Q

Hunt and Hess SAH grade: asymptomatic or mild headache and slight nucal ridigity

A

Grade I

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5
Q

Hunt and Hess grade for SAH: moderate to severe headache, nucal rigidity, no neurologic deficit other than cranial nerve palsy

A

Grade II

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6
Q

Hunt and Hess grade for SAH: drowsiness, confusion or mild focal deficit

A

Grade III

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7
Q

Hunt and Hess Grade for SAH: stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances

A

Grade IV

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8
Q

Hunt and Hess Grade for SAH: deep coma, decerebrate rigidity, moribund appearance

A

Grade V

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9
Q

In patients with aneurysmal SAH, does initial GCS correlate with long-term outcome?

A

Yes

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10
Q

Fischer Scale of SAH: no detectable SAH on CT scan

A

1

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11
Q

Fisher Scale of SAH: diffuse SAH, no localized clot >3 mm thick or vertical layers >1 mm thick on CT scan.

A

2

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12
Q

Fisher Scale of SAH: localized clot >5 x 3 mm in subarachnoid space or >1 mm in vertical thickness.

A

3

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13
Q

Fisher Scale of SAH: Intraparenchymal or intraventicular hemorrhage with either absent or minimal SAH on CT scan.

A

4

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14
Q

Which Fisher group has the highest incidence of vasospasm?

A

3

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15
Q

Modified Fisher Scale with thick diffuse or localized thick SAH and IVH

A

4

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16
Q

Modified Fisher Scale with diffuse thick or localized thick SAH and absent IVH

A

3

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17
Q

Modified Fisher Scale with diffuse thin or localized thin SAH and IVH

A

2

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18
Q

Modified Fisher Scale with diffuse or localized thin SAH and absent IVH

A

1

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19
Q

Modified Fischer Scale with no SAH and IVH

A

2

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20
Q

Modified Fisher Scale with no SAH and no IVH

A

0

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21
Q

The quantitative blood volume in contact with the cisternal space (directly in cisternal subarachnoid or intraventricular space) acts as what type of burden? And what is the risk of DCI?

A

Cumulative blood burden
Increased risk of DCI

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22
Q

What is the most consistent predictor of vasospasm after SAH?

A

Amount of SAH on the post ictal CT scan (IVH also a risk but not as strong)

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23
Q

What is the step-wise progression for treating intracranial hypertension after SAH?

A

Surgical Decompression (EVD, decompressive craniotomy or craniotomy)
1. Sedation with short-acting agents (IV propofol, versed or fentanyl)
2. Hyperventilation and osmotic agents (hyperventilation, mannitol 1 - 1.5 g/kg, hypertonic saline 30 mL 23.4%/5 mins q4-6h PRN, avoid Na >155)
3. Barbiturate Coma (pentobarbital: 10 mg/kg over 1 hr then 1-3 mg/kg/hr to 1-2 burst per 10 sec suppression - causes cardiac suppression, t 1/2 = 15=50 hrs)
4. Therapeutic hypothermia (32-34 deg C)

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24
Q

What are antishivering methods for therapeutic hypothermia?

A
  1. Skin counterwarming (warm, forced-air blankets)
  2. IV magnesium (60-80 mg/kg then 2g/hr)
  3. Buspirone (20-30 mg TID)
  4. IV dexmetomidine (0.4 - 1.5 microgram/kg/hr)
  5. IV meperidine (0.4 mg/kg q4-6 h 0 usual dose: 25-50)
  6. IV propofol (50-100 mg rapid IV push, 0.3-3 mg/kg/hr maintenance)
  7. IV Clonidine (1-3 micro gm/kg prn)
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25
Q

Caution with labetalol after ICH

A

Bradycardia
CHF
Bronchospasm

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26
Q

Caution with esmolol after ICH

A

Bradycardia
CHF
Bronchospasm

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27
Q

Caution with nicardipine after ICH

A

Severe aortic stenosis
Myocardial Ischemia

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28
Q

Caution with Fenoldopam after ICH

A

Tachycardia
Headache
Nausea
Flushing
Glaucoma
Portal Hypertension

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29
Q

Caution with Nitroprusside after ICH

A

Increased ICP
Variable response
Myocardial Ischemia
Thiocyanate and cyanide toxicity

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30
Q

Agents for RSI that don’t affect ICP

A

Propofol
Etomidate
Cis-atricurium
Vecuronium

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31
Q

Mannitol dosing (initial and bolus) with goal mOsm/kg

A

Initial dose: 1.0 - 1.5 g/kg 20% solution
Bolus dose: 0.25 - 1.0 g/kg
Goal: 300 - 320 mOsm/kg

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32
Q

Admission hyperglycemia in ICH is a predictor of what?

A

30 day mortality (diabetics and non-diabetics)

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33
Q

Goal Na and mOsm with hyperosmolar therapy?

A

Na: 150 - 155
mOsm/L: 300 - 320

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34
Q

Treatment of seizures in ICH

A

Lorazepam 0.05 - 0.1 mg/kg -> loading phenytoin or fosphenytoin (20 mg/kg)
May benefit from seizure prophylaxis

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35
Q

Predictors of seizures in ICH

A

Lobar location
Small hematomas

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36
Q

Risk factors for ICH

A

Age
Male
African Americans
Japanese
HTN
CAA
Cocaine
Low cholesterol levels
Oral anticoagulants
Excessive Etoh abuse

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37
Q

First AED for seizures IV and if IV access can’t be established?

A

IV: Lorazepam
No IV access: midazolam (10 mg IM, buccal or intranasal) or diazepam (20 mg rectal)

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38
Q

What should all patients with GCSE get after benzo and why?

A

Second-line antieplileptic
Benzodiazepines are not long term therapy that prevent recurrence of SE - instead of first and second line in sequence, give second-line with benzo (do not delay second-line AED to see if patient responds to initial benzo) - the benzo is the first line therapy
Phenytoin/fosphenytoin, valproate, levetiracetam, lacosamide and phenobarbital

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39
Q

Treatment for RSE

A

Add third line AED
Rapid and aggressive escalation with continuous IV anethestics with intubation: midazolam, propofol, pentobarbitol
If unable to intubate: valproic acid if not already used as second line
Traditionally: phenobarbital load with escalation to cIV pentobarbital (however, with caveats of barbiturates, preference for versed/midazolam and propofol have emerged)

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40
Q

Status epilepticus titration goal for cIV propofol and barbiturates and midazolam

A

Propofol and barbiturates: burst suppression
Midazolam: seizure supression
Maintain for 24 hours while conventional AED levels are optimized

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41
Q

Definition of super refractory status epilepticus

A

SE that continues for 24 hours or more after initiation of anesthetic agents

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42
Q

What is the potential problem of using valproic acid and phenytoin at the same time?

A

Valproate produces inhibition of CYP2C9 that leads to inhibition of clearance of phenytoin
Valproate also displaces the drug from it’s protein binding sites -> increasing the free fraction and total amount of phenytoin present
Closely monitor and follow total levels and free levels of phenytoin

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43
Q

What drug can be used in RSE if a patient doesn’t have an ileum for prevention of breakthrough and withdrawal siezures during tapering cIV infections?

A

Enteric topic image
Dosage: 300 - 1600 mg/d to abort RSE

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44
Q

Meds that can be used in SE when weaning from cIV meds?

A

Lacosamide
Enteric topiramate
Oxcarbazepine
Fella ate
Pregabalin
Carbamazepine
Ketamine

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45
Q

Issues with using inhaled anesthetics (isoflurane, halothane and desflurane) in terminating refractor SE?

A

Hypotension
Logistic issues in ICU
Frequent seizure recurrence upon withdrawal

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46
Q

When do you see generalized periodic discharges and what should be done about them?

A

Range of periodic or rhythmic patterns that don’t meet formal seizure criteria and aer seen after convulsive or Nonconvulsive SE, can be lateralized, generalized, bilateral independent and multifocal locals with varying secondary terms (periodic discharge, rhythmic delta and spike and wave)
Consider treating if 2 or more per second or on the ictal-interictal continuum
Investigate the cause (imaging, etc…), give conventional AEDs, consider benzo trial to determine ictal nature, continue cEEG monitoring to ID definitive seizure or SE later during hospitalization
Long term management: if they resolve without seizures - taper AEDs after 1 month, if PDs with seizure: continue AED for 3-12 months

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47
Q

NCSE Treatment Protocol cIV and non continuous IV

A

Continuous infusion (respiratory depression): midazolam, propofol or pentobarbital, ketamine (only if failure of or contraindication to midazolam, propofol and barbiturates), hypothermia
Non continuous infusion (no respiratory depression): fosphenytoin/phenytoin or valproate, levetiracetam, lacosamide (only if failure or contraindications to the above agents), phenobarbital

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48
Q

NCSE Treatment Protocol cIV and non continuous IV

A

Continuous infusion (respiratory depression): midazolam, propofol or pentobarbital, ketamine (only if failure of or contraindication to midazolam, propofol and barbiturates), hypothermia
Non continuous infusion (no respiratory depression): fosphenytoin/phenytoin or valproate, levetiracetam, lacosamide (only if failure or contraindications to the above agents), phenobarbital

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49
Q

What do you need to know about myoclonus status epilepticus

A

Most frequently seen after cardiac arrest
Has epileptiform nature (versus status myoclonus EEG has slow waves or burst suppression patters without epileptiform discharges)
Subcortical white matter injury - corticospinal tract
Tx: symptomatic, benzos, valproic acid, levetiracetam
EEG: generalized poly-spike and wave complexes on a nearly flat background
Treat like other RSE (keep poor prognosis in mind)

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50
Q

What do you need to know about epilepsia partialis continua (subtype of focal motor SE)

A

Can be very persistent
Epilepticus focal jerking activity can last days, weeks or decades
Focal structural brain lesion: heterotopias, infectious lesions, vascular abnormalities, subdural hematomas, or neoplasms
Prognosis: depends on the underlying lesion
Can have long term morbidity from weakness, sensory deficits, language dysfunction or cognitive deficits
Tx: benzos can prevent secondary generalization but usually do not stop seizure activity, occasionally can resolve without reverent or surgical treatment may be needed for intractable cases
Note: Nonketotic hyperglycemia can be associated with EPC in patients with concomitant focal cerebral lesion and respond best to conventional AEDs in concert with correction of metabolic disorder)

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51
Q

What factors increase risk of seizure in neuotrauma and duration of prophylactic AED in neurotrauma

A

Risks: GCS <10, cortical contusions, depressed skull fractures, wounds with dural penetration, prolonged (>24 hr) coma post traumatic amnesia
Phenytoin x 7 days, some keppra (levetiracetam)

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52
Q

CRASH trial

A

Corticosteroids after TBI - no benefit, increased mortality

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53
Q

Brain tissue oxygen tension monitoring after neurotrauma

A

Provides insight into cerebral metabolism
Pbto2 <15 mmHg associated with poor outcome

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54
Q

Which neurotrauma patients get hypothermia?

A

Refractory to osmotic therapy or unable to receive osmotic therapy
Correct ABG for temp to assure accurate readings (solubility of gas in liquid increases with lowering temp) - lower temp means increased CO2 in blood -> can lead to hypercapnea, cerebral vasodilatation and increased ICP)

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55
Q

Mannitol Side effects

A

Significant diuresis
Acute renal failure
Hyperkalemia
Hypotension
Rebound increased ICP

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56
Q

Mannitol dosing

A

0.25 - 1.0 gm / kg

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57
Q

Why is sodium chloride a better osmotic agent than mannitol?

A

NaCl has a better reflection coefficient (1.0 vs 0.9)
Normalizes resting membrane potential and cell volume by restoring normal intracellular electrolyte balance in injured cells
Can also raise MAP

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58
Q

Medications for sympathetic storming?

A

Bromocriptine
Beta-blockers (propranolol)
Morphine
Dantrolene
Clonidine

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59
Q

Steroids in spinal cord injury level of recommendation?

A

Controversial, not standard of care
Can be considered if you can minimize the risk of high-dose steroids (option, not recommendation)

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60
Q

STASCIS trial

A

Surgical Timing in Acute Spinal Cord Injury Study: early decompression within 24 hours of injury has a higher odds of improving neurologic outcome by a 2-grade improvement on ASIA impairment scale at 6 month follow-up

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61
Q

Early signs of infarct on CT scan

A
  1. Loss of insular ribbon
  2. Sulcal effacement
  3. Loss of grey-white junction
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62
Q

Diagnosis

A

Dense middle cerebral artery sign - intravascular dense clot material

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63
Q

ASPECTS grading score

A

The Alberta Stroke Program Early CT Score (ASPECTS) is a scoring system used to evaluate the severity of acute ischemic stroke:

Scoring
A score of 10 indicates a normal CT scan, while 1 point is subtracted for each region that shows early signs of ischemia. A score of 0 indicates diffuse involvement throughout the MCA territory.

Interpretation
An ASPECTS score of 8–10 indicates greater benefit from IV thrombolysis, while a score of ≤7 predicts a worse functional outcome at three months and symptomatic intracerebral hemorrhage.

Variations
There are variations of the ASPECT scoring system for the posterior circulation, known as pc-ASPECTS.

Diabetic patients
Diabetic patients have lower ASPECTS scores than non-diabetic patients, indicating more extensive strokes.

Mechanical thrombectomy
According to current American and European guidelines, mechanical thrombectomy is recommended for patients with an ASPECTS score of 6 or higher.

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64
Q

Indications and Contraindications to rTPA for ischemic stroke

A
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65
Q

Dose of TPA

A

0.9 mg/kg with a 10% bolus over 1-2 minutes then rest over 60 minutes

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66
Q

Should GP IIb-IIIa inhibitors be used in ischemic stroke patients

A

No secondary to significant safety concerns

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67
Q

What can be used after acute CVA?

A

ASA mild benefit
Heparin mild benefit offset by hemorrhage risk but can consider in setting of post cardiac surgery stroke, in select patients with carotid dissection and those with mechanical valve
Short course DAPT

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68
Q

What has a clear benefit in secondary stroke prevention after ischemic stroke?

A

Statins (independent of serum lipid panel)

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69
Q

What can the BP be in ischemic stroke patients if they haven’t received thrombolysis?

A

220/120 mmHg

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70
Q

When should carotid revascularization be done after ischemic stroke?

A

Stenosis >70%

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71
Q

CEA vs CAS

A

Similar for CVA, MI, death
CAS higher periop stroke
CEA higher periop MI
<2 weeks (unless larger cerebral infarction to minimize risk of hemorrhagic conversion)

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72
Q

Treatment to prevent malignant cerebral edema after complete MCA infarct

A

In patients that are difficult to arouse with symmetric or dilated but reactive pupil:
Neuro checks q2-4 hrs
Hypertonic saline or mannitol
Hemicraniectomy within 72 hours

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73
Q

Myesthenia Gravis target and symptoms

A

Target: T-cell dependent response targeted to postsynaptic acetylcholine receptor or receptor associated proteins
Symptoms: voluntary muscles (spares smooth and cardiac muscles), respiratory insufficiency
Treat trigger, plasmapheresis, IVIg
Symptom tx: Pyridostigmine
CHronic: prednisone, azathioprine, mycophenolate, cyclosporoine, some tacrolimus
Surgery: thymectomy with thymoma or <50 years old, not for MUSK+ patients or isolated ocular myathenia

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74
Q

Cholinergic crisis target and symptoms, what should be avoided

A

Excess acetylcholine esterase inhibitor
Symptoms: SLUDGE (salivation, lacrimation, urination, diarrhea, GI upset and emesis), mioisis, bronchospasm, flaccid weakness
Avoid tensilon challenge (can be dangerous, can distinguish from MG)

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75
Q

Lambert-Eaton myesthenic syndrome target, association, symptoms, uncommon?

A

Target: presynaptic autoimmune attack of voltage-ated calcium channels
Association: cancer (typically SCLC)
Symptoms: limb symptoms more prominant than occular/bulbar symptoms, faciculation with exercuse, autonomic dysfunction, reduced reflexes
Respiratory failure is uncomon

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76
Q

Botulism etiology, target, symptoms, treatment

A

Etiology: clostridium botulinum neurotoxin
Target: permanent blockage of presynaptic acetylcholne release at neuromuscular junction
Symptoms: symmetric descending paralysis and DIALTED PUPILS, dysautonomia, no sensory deficit
Treatment: equine antitoxin

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77
Q

Tick paralysis location, tick, symptoms, cure

A

Target: presynaptic neuromuscular blockage
Ticks: Rocky mountain wood tick, american dog tick, lone star tick, black-legged tick, western black-legged tick, gulf coast tick, austrialian Ixodes holocyclus tick
Symptoms: ascending paralysis, opthalmoparesis, bulbar dysfunciton, ataxia, reduced reflexes, can be rapid, no sensory symptoms,
Cure: tick removal

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78
Q

Snake venom snakes, target, symptoms

A

Snakes: tiger snake taipan, brazilian rattle snake target presynaptic blockage
Snakes: krait, cobras, mambas, coral snake sea snakes target postsynaptic blockage from alpha-bungarotoxin
Snakes: copperheads, cottonmouths, moccasins, rattlesnakes, vipers, adders, boomslang, twig snake block neuromuscular junction
Initially affects cranial nerves -> ptosis, opthalmoplagia, dysarthria and dysphagia to progressive limb weakness

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79
Q

Organophosphate toxicity sources, target, symptoms, what can happen 2-3 weeks later, treatment, avoidance?

A

Source: malathion, parathion, sarin, soman
Target: inactivates acetylchoilnesterase
Symptoms: SLUDGE, miosis, bronchospasm, blurred vision, bradycardia, confusion, optic neuropathy, extrapyramidal effects, dysautonomia, fasciculatios, seizures, cranial nerve palsy, weakness from continued depolarization of the neuromusclar junction
Delayed polynuropathy 2-3 weeks after exposure
Treatment: atropine, pralidoxime (2-PAM), benzodiazepine
Avoid: succinylcholine

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80
Q

Miller-Fischer Variant of GBS

A

Peripheral nervous system
Symptoms:
- Ophthalmoplegia (weakness or paralysis of the eye muscles),
- Ataxia (lack of muscle coordination),
- Areflexia (absence of reflexes).

Unlike typical GBS, which often presents with progressive weakness, the Miller-Fisher variant tends to have a more distinct presentation. It is often associated with antibodies against GQ1b gangliosides, and the symptoms can develop relatively quickly.

Treatment: supportive, IVIg, plasmapheresis

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81
Q

Diphtheria cause, symptoms

A

Cause: corynebacterium diphtheriae
Symptoms: thick gray pharyngeal pseudomembrane, AV block, endocarditis, myocarditis, lymphadenopathy, neuropathy, craniopharyngeal involvement, proximal-to-distal weakness and decreased reflexes

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82
Q

GBS

A

Immune- mediated poly neuropathyies with motor, sensory and dysautonimic features, early loss of F waves on MEG
Molecular mimicry from recent infection produces an autoimmune humeral and cell-mediated response to the ganglioside surface molecules of peripheral nerves,
Acute ascending weakness (often begins in proximal legs)
Paretehsia of hands and feet, low back pain,, displopia, dysautonomia (tachycardia/bradycardia, wide swings in blood pressure, orthostasis, tonic pupils, urinary retention, ileus/constipation, hypersalvation, anhidrosis), respiratory fialure
LP - elevated protein levels without elevation in leukocytes

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83
Q

Arsenic, lead poisoning and porphyrias lead to what?

A

Acute motor polyneuropathies

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84
Q

What do n-haxane (glue sniffing), peripheral nerve vasculitis (PAN, Churg-Strauss, RA, lupus), lyme disease, sarcoidosis, paraneoplastic disease and critical illness polyneuropathy all cause?

A

Polyneuropathy

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85
Q

Ciguatera toxin from red snapper, grouper, barracuda

A

Targets: voltage-gated sodium channels of muscles and nerves
Symptoms: metallic taste, hot-cold reversal,

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85
Q

Where do MG, Lambert-Eaton mysathenic syndrome, botulisum, organophosphate toxicity, neurotoxic fish poisoning all affect and what do they NOT cause?

A

Neuromuscular junction
Do NOT cause sensory involvement

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85
Q

EMG: when is insertional activity increased?

A

Denervated muscle

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86
Q

EMG: when is insertional activity decreased?

A

Muscle replaced by fat

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87
Q

What does spontaneous fibrillation potentials and sharp waves suggest on EMG?

A

Recent denervation or muscle necrosis

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88
Q

When is recruitment decreased on EMG?

A

When rapid firing results in damage to axon, neuro or nerve conduction or as a result of the loss of large number of motor units

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89
Q

When does poor activation/recruitment on EMG occur?

A

Central disorders with a decreased number of motor units recruited and firing is slow rather than rapid

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90
Q

What does early recruitment on EMG mean?

A

Myopathies

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91
Q

What does long motor unit potential duration indicate?

A

Lower motor neuro disorders

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92
Q

What does short-duration motor units indicate?

A

Myopathies
Can be seen in neuromuscular disorders and in early phases of reinnervation after neuropathy

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93
Q

What does long-duration, high-amplitude motor units indicate?

A

chronic neurogenic disorders

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94
Q

What does small-amplutude, short-duration motor units indicate?

A

Myopathic disorders

95
Q

What does 5 or more phases constitute and what does it indicate?

A

Polyphasia
Myopathic and neurogenic disorders

96
Q

When do you intubate MG, GBS and CIM/CIP?

A

VC <10 to 15 mL/kg or <1L and/or NIF less than -20 or rapiduly worsening

97
Q

What is the problem with bulbar dysfunction and PFTs?

A

Can’t make proper seal

98
Q

Rapid therapy, symptomatic therapy, chronic therapy and surgery for MG?

A

Rapid: treat trigger of crisis, plasmapheresis, IvIg
Symptomatic: pyridostigmine
Chronic: prednisone, azathioprione, mycophenolate mofetil, cyclospoirine, select: prograf, methotrexate, rituximab
Surgery: thymectomy if thymoma or onset <50 years of age
NOT for MUSK+ patients or isolated ocular myasthenia

99
Q

Rapid therapy, symptomatic therapy, chronic therapy and surgery for GBS?

A

Rapid: Plasmapheresis, IvIg
Symptomatic: lacri-lube if 7th nerve palsy
Chronic: none necessary
Surgery: none

100
Q

Rapid therapy, symptomatic therapy, chronic therapy and surgery for CIP/CIM?

A

Rapid: treat trigger
Symptomatic: PT, avoid neuromuscular blockage agents and corticosteroids
Chronic: none
Surgery: none

101
Q

Chronic therapy for MG

A

Check: AChR- Ab, start pyridostigine, support, possibel thymectomy.
2nd tier: prednisone or azathioprine
3rd: mycophenolayte or rituximab
4th tier: methotrexate, cyclosproien, tacrolimus

102
Q

RSI meds in suspected elevated ICP and which neuromusclar blocking agent?

A

Propofol and etomidate - wont affect neuro exam
Nondepolarizing neuromoscular blocking agents - cisatracurium, rocuroinium or vecuronium

103
Q

Side effects of etomidate?

A

Nausea, vomiting, myoclonic movements, lowers seizure threshiold, adrenal suppression

104
Q

Side effects of versed?

A

ICP

105
Q

Side effects of succynylcholine?

A

Hyperkalemia, cardiac arrhythmias, exacerbation of neuropathy or myopathy, malignant hyperthermia, increased ICP in patients with intracranial mass lesions

106
Q

Bacterial meningitis CSF

A

Hypoglycorrhachia
Polymorphonuclear pleocytosis
Elevated protein
Glucose <34
CSF to serum glucose <0.23
Protein >22-
Pleocystosis >2000

107
Q

Viral meningitis CSF

A

Milder protein elevation
Normal glucose
Mononuclear pleocytosis - may initially have polymophonuclear predominace

108
Q

Duration of treatment of CNS infection

A

7 days minimum
3-4 weeks for listeria
Strep pneumo 10-14 days
Strep agalactiae 21 days
Neisseria meningitides and Haemophilus influenzae 7 days
Immunocompromised = longer depending on clinical response

109
Q

Steroids in CNS infections?

A

Dexamethasone to adults in developed countries - 0.15 mg/kg IV q6h for 2-4 days 10-20 minutes before antibiotics in infants, children and adults with suspected bacterial meningitis
NOT following antibiotics
D/C if CSF gram stain or blood cultures are negative for pneumococcal meningitis
Not for use in herpetic encephalitis

110
Q

Seizure prophylaxis in CSN infections?

A

No data

111
Q

Hypothermia in meningitis after v fib arrest?

A

In theory:
- Preserves BBB function
- Reduced release of excitatory amino acids
- Decreased CSF nitric oxide
- Decreased myeloperoxiade activity
- Reduced ICP
However, one study did not improve outcomes - but issues with study
Should target normothermia

112
Q

Nimodipine in meningitis

A

Bacterial meningitis
tPA and plasminogen activator inhibitor-1 increased usually suggesting decreased fibrinolysis in SAH
Nimodipine decreased PAI-1 levels in SAH
Neuroprotective and this data is speculative to help in bacterial meningitis as meningitis may also have impaired fibrinolysis and may be adjunctive therapy

113
Q

Statins in meningitis

A

Attenuate leukocyte invasion into CNS and abolish hyperthermia in bacterial meningitis
Downregulate the production of many acute-phase cytokines and chemokides (ex: TNF-alpha and the interleukins IL-1b and IL-6)
Stains increase the activity of endothelial NO synthase (eNOS) by upregulating eNOS expression and induce eNOS phosphorylation and activating eNOS directly - neuroprotective

114
Q

How can meningitis spread to other areas?

A

Cerebral abscess from direct or hematogenous spread
Direct spread: mastoiditis, otitis media, sinusitis, dental infections
Hematogenous seeding: multiple abscesses, bacterial endocarditis, abdominal infections, empyemas, skin infections can spread TO the CNS

115
Q

Bacteria for cerebral abscesses?

A

Most common: Staph Aureus and Strep Viridans
Also: Pseudamonas, Enterobacteriaceae, Clostridium, Haemophilus

116
Q

Duration of treatment of cerebral abscess?

A

6-8 weeks

117
Q

Epidural abscess location and cause

A

Virtual space between inner skull and dura
Secondary to skull fractures or seeded from frontal sinus infection

118
Q

Subdural empyema location and cause

A

Dura and arachnoid membranes
Sinus infections

119
Q

Suppurative intracranial thrombophlebitis location and cause

A

Septic thrombophlebitis of intracranial veins
Complications of meningitis, abscesses or empyemas

120
Q

Temporal lobe abnormalities with fevers

A

HSV encephalitis - temporal lobe abnormalities

121
Q

Basal ganglia, thalamus or brainstem abnormalities

A

Arbovirus - arthropod-born virus or eastern equine encephalitis and west nile infections

122
Q

Diagnosis with fevers

A

West-Nile Virus

123
Q

CSF lymphocytic predominance, elevated WBC, mild elevation in protein with normal glucose, possible erthrocytes diagnosis

A

Viral meningitis

124
Q

What labs and imaging should be done in viral meningitis

A

PCR is superior to culture
MRI

125
Q

Anterograde memory impairment (temporal lobe involvement), CSF with erythrocytes, occasionally xanthochromia, DNA PCR diagnosis, early unilateral temporal lobe to later bilateral/inferior/occipital, EEG with intermittent periodic lateralizing epileptiform discharges in temporal lobe diagnosis

A

HSV encephalitis

126
Q

Diagnosis (intermittent periodic lateralizing epileptiform discharges in temporal lobe)

A

HSV encephalitis

127
Q

Treatment for this MRI with fevers

A

HSV encephalitis
IV acyclovir 10-15 mg/kg TID for 14 days, may need prolongation to 14-21 days

128
Q

HIV or immunosuppressed patient with CSF with elevated protein and mononuclear predominance, + PCR diagnosis, MRI: asymmetric, multiple infarcts from angitis/vasulopathies

A

Varicella zoster virus
MRI diffuse sequences can show the ischemic and/or hemorrhagic strokes from VZA vasculopathies
Treatment: IV acyclovir 10-15 mg/kg TID x7 days
If vasculopathy suspected: add steroids

129
Q

Treatment of fevers with scattered ischemic strokes on diffusion MRI

A

Varicella Zoster Virus
IV acyclovir 10-15 mg/kg TID for 7 days
Steroids for the vasculopathy causing the strokes

130
Q

What are the risk factors for west nile virus?

A

Advanced age
Organ transplant or cancer

131
Q

Viral infection, meningitis, encephalitis or flaccid (asymmetric weakness) paralysis diagnosis? (MRI with anterior horn involvement)

A

West Nile Virus
Acute flaccid paralysis causing asymmetric weakness during first 48 hours after initial symptom onset

132
Q

Fevers, asymmetric weakness 1st 48 hours, CSF: elevated protein, lymphocytic predominance, MRI: diffuse and nonspecific, possible basal ganglia, thalamus, meninges, spinal cord, cauda equine and nerve root involvement diagnosis and treatment?

A

West Nile Virus
Supportive
Ribavirin, IvIg, Interferons - no strong evdience

133
Q

Most common fungal infection in immunocompromised patients?

A

Cryptococcus neoformans: Cryptococcus neoformans or C gattii
Usually from pulmonary spread

134
Q

Headache, fever, mailaise, meningismus, photophobia, vomiting and/or cranial nerve palsy over several weeks, CSF: WBC <50, mononuclear predominance with low glucose, protein mild elevation, MRI: meningeal enhancement with mid brain and basal ganglia involvement diagnosis

A

Cryptococcus Neoformans meningitis
MRI: focal, ovoid lesions with post contrast sequences ranging from non-enhancing to nodular enhancement around periphery

135
Q

HIV +, fevers, cranial nerve palsy changes over weeks diagnosis and treatment

A

Cryptococcal Neoformans
Three phase protocol:
1. Induction: amphotericin B (0.7-1 mg/kg/day) and 5-flucytosine (100 mg/kg/day) x 2 weeks
2. Consolidation: fluconazole (400 mg/d) x 8 weeks
3. Maintenance: fluconazole 200 mg/day x 6 - 12 month
If HIV + = continue maintenance until CD4 count >100 cells per microliter or viral load undetectable for very low for at least 3 months

136
Q

Fevers after visiting Southwest or South and Central America, inhalation spread, MRI: basilar leptomeningitis, risk of hydrocephalus, antibodies from CSF for diagnosis disease and treatment?

A

Coccidioides Immitis
Treatment: fluconazole
MRI: leptomeningeal enhancement of post-gadolinium images in the basal cisterns (can be diffuse)

137
Q

Fevers after visiting Mississippi Ohio River Valley with meningitis, encephalitis or abscess, CSF: lymphocyte pleocytosis, elevated protein, normal glucose, culture sensitivity low diagnosis and treatment?

A

Blastomyces dermatitidis
Treatment: Liposomal amphotericin followed by fluconazole x 12 months

138
Q

Fevers after visiting Mississippi Ohio River valley or great lakes, inhalation spread, immune-competent also, meningitis, cerebral embolism from endocarditis, encephalitis, myelopathy (possible), MRI: noncaseating ganulomas, CSF: lymphocytic pleocytosis and elevated protein diagnosis and treatment?

A

Histoplasma Capsulatum
Treatment: Liposomal Amphotericin B followed by Itraconazole for at least 1 year until CSF abnormalities resolve

139
Q

Goal Na and osm in elevated ICP

A

Na 150-155
Serum osm >320

139
Q

Diagnosis

A

Brain tumor
Calcified, hyperdense mass with surrounding edema

139
Q

Side effects of hyperosmolar therapy

A

Electrolyte abnormalities
Pulmonary edema (rapid intravascular volume expansion)
Coagulopathy
Intravascular hemolysis

140
Q

Why are posterior fossa, pineal region and third ventricles predisposed to hydrocephalus?

A

Obstruction of CSF outflow

141
Q

Association with Von-Hippel-Lindau disease

A

Hemangioblastoma (posterior fossa lesion)

142
Q

Treatment for edema associated with intracranial tumors?

A

Dexamethasone

143
Q

Workup of Von Hippel Lindau syndrome with hemangioblastoma?

A

Opthalmologic evaluation (retinal lesions)
TOtal spine MRI with and without contrast (spinal cord hemangioblastomas)
VMA and metanephrine levels (pheochromocytoma also associated with VHL)

144
Q

Management of hydrocephalus in perioperative period for resection of posterior fossa brain tumor?

A
  1. Endoscopic third ventriculostomy - short and long term control, passage through floor of third ventricle into prepontine cistern bypasses the obstruction at the 4th ventricle
  2. Placement of right frontal EVD
145
Q

How long is dexamethasone continued post operatively after resection of posterior fossa tumor?

A

2 week taper

146
Q

When is repeat imaging performed after resection of a posterior fossa tumor?

A

MRI with and without contrast at 72 hours to evaluate (waiting limits artifact from normal postoperative changes)
Can also get MRI total spine with and without contrast if that wasn’t done preoperatively

147
Q

ABRUPT-onset headaches, vision changes (diplopia, loss of visual acuity, restriction of visual fields), nausea, vomiting, vertigo and/or decreased level of arousal diagnosis? Treatment?

A

Pituitary Apoplexy (infarction or hemorrhage)
Commonly from pituitary adenoma
Treatment: surgery (if worsening visual acuity, expanding visual field deficits, declining levels of arousal or deteriorating oculomotor function) - 48 hrs to 1 week after symptom onset
Transsphenoidal -> may need crani if extensive of hemorrhage to hemisphere or poor aerated sphenoid sinus

148
Q

Concerns with pituitary apoplexy?

A

Adrenal crisis from panhypopituitarism
Tx: 100 mg IV hydrocortisone -> 100 mg IV q6-8 hours until surgery
Check for levels of hormones and electrolytes, CT and MRI

149
Q

Diagnosis with ABRUPT onset vision changes? Findings on T1, T2 and T1 with gadolinium?

A

Pituitary apoplexy
T1 - high signal intensity
T2 - low to high signal suggesting old and new hemorrhages, various patterns of peripheral and heterogenous tumoral enhancement of T1 with gadolinium

150
Q

What should be monitored for after resection of pituitary apoplexy?

A

Diabetes insipidus

151
Q

Cancers associated with hemorrhagic brain lesions

A

Lung (bronchogenic carcinoma)
Melanoma, renal cell, thyroid carcinoma, choriocarcinoma

152
Q

Treatment of hemorrhagic brain lesions

A

Corticosteroids (dexamethasone: 10 mg bolus then same dose in 2-4 divided daily dose)
Anticolvulsants - controversial, many stimulate p450 system -> increased cortocosteroid metabolism and certain chemo drugs - BUT with multiple lesions it’s unclear if you should use

153
Q

How do you taper dexamethasone after surgery for hemorrhagic brain mets?

A

Dexamethasone 10 mg oral q6h x 24 hours to 2 mg q6h for duration of whole brain radiation therapy

154
Q

Sudden onset headache, vomiting, collapse, CT scan with following, evidence of hydrocephalus/herniation on physical exam, what is the diagnosis and first step?

A

Colloid cyst
Benign, epithelial-lined lesions containing mucin, arise from roof of anterior third ventricle, can cause sudden onset obstructive hydrocephalus and herniation
First step: place EVD

155
Q

Operative options for following with evidence of hydrocephalus?

A

Colloid cyst -> resection or VP shunt with endoscopic fenestration of septum pellucidum

156
Q

Which demyelinating disease can progress over days, impair bulbar function, central and peripheral nervous system involvement possible?

A

Guillan-Barre Syndrome

157
Q

Which demyelinating disease involved ophthalmoplegia, ataxia, areflexia and encephalopathy and is associated with peripheral motor axonal demyelination and brainstem encephalitis with IgG GQ1b antibody?

A

Bickerstaff encephalitis (variant of GBS)

158
Q

ADEM versus GBS main difference?

A

ADEM - central nervous system
GBS - peripheral nervous system

159
Q

Miller-Fischer versus Bickerstaff encephalitis?

A

Miller Fisher syndrome (MFS) and Bickerstaff brainstem encephalitis (BBE) are both autoimmune diseases that can cause ophthalmoplegia and ataxia, but they differ in several ways:
Cause
MFS is caused by the immune system attacking peripheral nerves, while BBE is caused by an autoimmune response in the brainstem.
Symptoms
MFS is characterized by weakness in the eye muscles, limb coordination problems, and loss of reflexes. BBE is characterized by drowsiness, gait disturbances, diplopia, and disturbances of consciousness.
Prognosis
Most patients with either disease recover within six months, even without treatment.
Pathology
MFS is consistent with a peripheral nerve etiology, while BBE is consistent with a central pathology.
Blood-brain barrier
BBE sera can disrupt the blood-brain barrier, while MFS sera do not.

160
Q

Diagnosis and treatment?

A

ADEM - multifocal white matter demyelination
Large, multiple and asymmetric lesions of the subcortical and central white matter, grey-white junction in hemispheres, cerebellum and brainstem
Treatment: methylprednisolone 1 g/d x 3-5 days -> plasmapheresis x 5-7 sessions -> IvIg
Maybe cyclophosphamide, interferon-beta, glatiramer, acetate and rituximab

161
Q

ADEM vs MS involvement?

A

ADEM: can involve grey matter in caudate head, globs pallidus, putamen and thalamus
Onset
ADEM symptoms usually develop quickly over hours or days, while MS symptoms can include a rising sense of numbness in the legs.
Frequency of attacks
ADEM typically occurs once, while MS patients experience repeated attacks.
Brain lesions
ADEM lesions are usually more numerous, ill-defined, and more widely distributed than MS lesions, which are more well-defined and tend to be of varying ages.
MRI scans
ADEM brain MRIs usually show minimal progression over time, while MS MRIs often show new damage.

162
Q

ADEM versus PML?

A

Both affect central nervous system

ADEM:
Cause: Immune system overreacts to a viral or bacterial infection
Symptoms: irritability, sleepiness, vision problems, weakness, tingling, unsteadiness, seizures
Treatment: High dose corticosteroids
Imaging: Brain lesions are usually ill-defined and of similar age.

PML
Cause: Infection by the human polyomavirus, JC virus
Symptoms: Loss of coordination, clumsiness, memory loss, vision problems, weakness in the arms and legs, personality changes
Treatment: Treatment focuses on strengthening the immune system, such as antiretroviral therapy for people with AIDS
Imaging: Does not generally enhance on imaging.

163
Q

When should ADEM be biopsied and what is the hallmark?

A

When there is no response to conventional therapy and presentation is atypical
Biopsy: perivenous demyelination (vs confluent demyelination in MS)

164
Q

Fevers, chills unusual behavior, hallucinations, focal neurologic signs and seizures diagnosis and treatment?

A

HSV encephalitis (HSV-1 or HSV-2)
Treatment: Iv acyclovir

165
Q

Ab for SCLC or thymoma with brainstem encephalitis with bulbar signs and symptoms

A

Hu (ANNA1)

166
Q

Testicular cancer with limbic encephalitis, brainstem encephalitis, hypothalamic dysfunction antibody?

A

Ma2 (Ta)

167
Q

Antibody associated with lung carcinoma and memory loss, encephalopathy, seizures, and tendency to relapse?

A

AMPAR

168
Q

Antibody associated with multiple cancers with memory loss, encephalopathy and seizures?

A

VGKC

169
Q

Antibody associated with refractory epilepsy?

A

GluR3

170
Q

Antibody associated with breast or SCLC and brainstem syndrome (opsoclonus, myoclonus), cerebellar syndrome and Lambert-Eaton syndrome

A

Ri (ANNA2)

171
Q

Antibody associated with SCLC, thymoma, cerebellar ataxia, movement disorders and myasthenic syndromes?

A

CV2 (CRMP5)

172
Q

Antibody associated with breast and SCLC and peripheral neuropathy, stiff-person syndrome and myelitis?

A

Amphiphysin

173
Q

40 year old women, acute onset psychiatric symptoms, behavior changes, orofacial dyskinesia, seizure, encephalopathy, autonomic instability, respiratory failure and catatonic state diagnosis?

A

Anti-NMDA Receptor Encephalitis

174
Q

Tumor associated with Anti-NMDA Receptor Encephalitis

A

Ovarian Teratoma

175
Q

Disease causing prominent microgliosis and deposits of IgG in the hippocampus, forebrain, basal ganglia and spinal cord? Ab to what?

A

Anti-NMDA receptor encephalitis
Can find NMDAR-expressing neurons with inflammatory infiltrates in the teratomas

176
Q

Disease pathogenesis of Anti-NMDA receptor encephalitis?

A

Immunoglobulin-induced receptor internalization and downregulation of surface NMDARs
Highest levels in amygdala and hippocampus - also area where blood-brain barrier is the weakest

177
Q

Diagnosis young woman with psych issues and seizures

A

Ant-NMDA receptor encephalitis
Nonspecific or increased fluid-attenuated inversion recovery (FLAIR) or T2 signal in brain parenchyma
N-acetylaspartate levels in tghe basal ganglia and thalamus reduced during involuntary movement - decreased NA A: Cr ratio = diffuse brain dysfunction
MRI = hyperperfusion diffusely

178
Q

Diagnosis and what does this presence mean?

A

Extreme delta brush in anti-NMDAR syndrome -> presence may indicated a prolonged hospitalization, longer continuous EEG monitoring and a trend towards worse outcomes

179
Q

Diagnosis and treatment?

A

Anti-NMDAR encephalitis
Treatment: tumor resection (teratoma) and immune suppression (corticosteroids: methylprednisolone 1 g x5 days -> if no change after surgery in 1st few days -> PE x 5-7 sessions -> if no response IvIg
Can consider rituximab, cyclophosphamide, bleomycin, etoposide, cisplatin

180
Q

What can be done in anti-NMDA disease process if patient has refractory encephalitis?

A

Prophylactic bilateral oophorectomy (without evidence of teratoma)

181
Q

How should you treat the bizarre movements associated with Anti-NMDAR encephalitis?

A

Treat only if oyu have to
Symptoms: benzos, long-acting agents like clonazepam, haldol, seroquel, propofol and benzo induction can be used
Jaw clenching: may need botulinum injections

182
Q

Which cells are particularly sensitive to decreased cerebral blood flow?

A

CA 1 hippocampal pyramidal neurons
Cerebellar Purkinje neurons
Medium spiny striatal neurons
Pramidal neurons in layers 3, 5 and 6 of neocortex

183
Q

Which CPC is good cerebral performance, conscious, alert, able to work?

A

CPC-1

184
Q

Which CPC is moderate cerebral disability, conscious, can carry out independent activities?

A

CPC-2

185
Q

What CPC is severe neurologic disability, conscious, dependent on others for daily support?

A

CPC-3

186
Q

What CPC is coma or vegetative state?

A

CPC-4

187
Q

What CPC is dead?

A

CPC-5

188
Q

Goal Sjvo2 and Pbto2 to avoid secondary neurologic injury after cardiac arrest?

A

Sjvo2 > 60%
PbtO2 > 20 mmHg

189
Q

Describe Lundberg A, B and C waves

A

A- plateau waves, 5-10 mins, reduced cerebral compliance
B - smaller waves, compliance may be compromised
C - normal cardiac/pulmonary cycle interactions

190
Q

Herniation syndrome that causes ipsilateral cranial nerve palsy, contralateral or bilateral motor posturing

A

Uncal herniation (lateral transtentorial) from temporal lobe mass lesion

191
Q

Herniation syndrome that causes progression from bilateral decorticate to decerebrate posturing, rostral-caudal loss of brainstem reflexes?

A

Central transtentorial herniation from diffuse cerebral edema or hydrocephalus

192
Q

Herniation syndrome that causes asymmetric (contralateral > ipsilateral) motor posturing but preserved oculocephalic reflex

A

Subfalcine herniation from convexity (frontal or parietal) mass lesion

193
Q

Herniation syndrome that causes sudden progression to coma with bilateral motor posturing and cerebellar signs?

A

Cerebellar herniation (up or down) from cerebellar mass lesion

194
Q

Do steroids work on vasogenic or cytotoxic edema?

A

Vasogenic (ex: abscess or neoplasm) not cytotoxic (ex: acute ischemic stroke)

195
Q

IV infusion when hyperventilation and osmolar therapy doesn’t work for ICP elevation?

A

Pentobarbital
Reduces cerebral metabolic rate
Needs continuous EEG monitoring to burst suppression
Impairs neurologic exam

196
Q

What pressors should be used to maintain PbtO2 >20?

A

Levophed, neo

197
Q

Treatment for refractory symptomatic vasospasm?

A

Angiography and intraarterial vasodilators or balloon angioplasty

198
Q

Which pathway do somatosensory evoked potentials test?

A

Dorsal column-leminiscal system
Dorsal column of spinal cord to cuneate nucleus in lower brainstem to ventroposterior lateral thalamus to primary somatosensory cortex
Median and tibial nerve

199
Q

What are BAEPs (brainstem auditory evoked potentials)?

A

Produced by audible clicking stimulus
5-6 peaks labeled with roman numerals with recoding electrodes between Cz and ipsilateral ear
During a BAEP test, small electrodes are placed on the scalp and forehead, and a clicking sound is played in one ear at a time. The test records up to seven positive wave peaks, labeled I-VII, and negative troughs in between.

200
Q

What does an absent or delayed wave V BAEP with normal wave I latency mean?

A

Conduction abnormalities central to distal portion of CN VIII

201
Q

What does an absent wave I with preserved wave V mean in BAEPs?

A

Peripheral hearing apparatus or auditory nerve (most commonly technical issue)

202
Q

What does preservation of wave I but loss of waves II to V on BAEP indicate?

A

Functional disruption of brainstem

203
Q

What does unilateral abnormal BAEP’s indicate?

A

Ipsilateral brainstem damage

204
Q

What does bilaterally absent N20’s indicate ?

A

Poor prognosis after cardiac arrest if still comatose at 72 hours or within 1st week

205
Q

What are event-related potentials?

A

Long-latency potential from signal-averaging techniques of the EEG
Represent complex cognitive processing of a stimuli
N100 represents attention
P300 elicited by rare tasked-related stimulus
MMN is “oddball” sound in a sequence of sounds

206
Q

What is MMN useful for in coma?

A

Relatively high specificity for recovery of wakefulness (particularly in anoxic injury)

207
Q

What raises the hypothalamic temperature set point?

A

Cerebral prostaglandin E synthesis

208
Q

Where should and EVD be zeroed?

A

External auditory meatus (level of the foramen of monro)

209
Q

What antibiotic has been given via that intraventricular route the most? Which is contraindicated secondary to neurotoxicity?

A

Vanc and gent
Cephalosporins

210
Q

Factors associated with chronic hydrocephalus after SAH?

A

Old age
High HH grade
Female
Acute hydrocephalus
Posterior circulation aneurysm
Aneurysm >2.5 cm

211
Q

What factors for age, comorbidities, ICH, SAH grade, location, neck, morphology, dome to neck ratio, giant aneurysm, vascular anatomy, atherosclerosis of aneurysm or perianeurysmal atherosclerosis or severe vasospasm favor endovascular treatment of aneurysm?

A

Age >70
Severe comorbidities
Higher SAH grade
Posterior circulation, proximal location
Narrow neck
Unilobular
>1.5-2 dome to neck ratio
Aneurysm >25 mm (giant ones)
Nontortuous vascular anatomy
Nonatherosclerotic proximal vessels BUT atherosclerotic calcification of aneurysms and perianeurysmal atherosclerosis favor endovascular treatment
Severe vasospasm

212
Q

What factors for age, comorbidities, ICH, SAH grade, location, neck, morphology, dome to neck ratio, giant aneurysm, vascular anatomy, atherosclerosis of aneurysm or perianeurysmal atherosclerosis or severe vasospasm favor surgical treatment of aneurysm?

A

Younger
ICH present
Lower SAH grade
MCA, pericallosal or distal location
Wide neck
Unilobular of fusiform with arterial branches exiting from aneurysm sac
<1.5-2 dome to neck ratio
Tortuous or atherosclerotic proximal vessels (but not calcification of aneurysm or perianeurysmal atherosclerosis)

213
Q

Benefit of nimodipine in vasospasm?

A

Calcium channel blocker that improves outcomes, induces hypertension and provides excess volume

214
Q

Management of vasospasm refractory to nimodipine (medical management)?

A

Intraarterial vasodilator therapy: papave3rine (opium alkaloid), milrinone (PDE3 inhibitor), verapamil and nicardipine (calcium channel blockers)
Balloon angioplasty

215
Q

Results of IMCVS study?

A

Invasive endovascular treatment for CVS does not lead to a lower rate of DCI but might lead to poorer outcomes compared to induced hypertension. The potential benefits of endovascular treatment for CVS need to be addressed in further studies, searching for a subgroup of patients who may benefit.

216
Q

What does a daughter sac predispose an aneurysm to?

A

Rupture

217
Q

Stroke Counsel of AHA recommends screening who for aneurysms?

A
  1. Patients with ≥2 family members with IA or SAH should be offered aneurysmal screening by CTA or MRA. Risk factors that predict a particularly high risk of aneurysm occurrence in such families include history of hypertension, smoking, and female sex (Class I; Level of Evidence B).
  2. Patients with a history of autosomal dominant polycystic kidney disease, particularly those with a family history of IA, should be offered screening by CTA or MRA (Class I; Level of Evidence B), and it is reasonable to offer CTA or MRA to patients with coarctation of the aorta and patients with microcephalic osteodysplastic primordial dwarfism (Class IIa; Level of Evidence B).
218
Q

Who gets management for unruptured aneurysms?

A

Posterior circulation aneurysms
Anterior circulation aneurysms 7 mm or larger
Mass-effect causing cranial neuropathy
Growing
Worsening focal neurologic signs
Increased risk of rupture
History of SAH and a coexisting aneurysm

219
Q

What are the three Borden classifications of dural AV fistulas?

A

I - Draining into dural venous sinus or meningeal veins
II - Drainage into dural venous sinus with cortical venous reflux
III - Drainage directly into subarachnoid veins (cortical venous reflux only)

220
Q

Should dural AV fistulas be treated?

A

Yes because they have a more aggressive course

221
Q

History of stroke or head trauma within how many months is a contraindication to rtPA?

A

3 months

222
Q

Spetzler and Martin Grading System for AVM

A

Eloquent - yes = 1
Venous drainage - deep = 1
3-6 cm = 2
>6 cm = 3
I - IIIA = microsurgery and/or endovascular surgery
IIIB radiosurgery and/or endovascular surgery
IV - V = observation or individualized multimodal approach with staged therapy

223
Q

Cause of cerebral edema after CEA?

A

Cerebral hyperperfusion syndrome

224
Q

Results of the carotid occlusion surgery study?

A

The Carotid Occlusion Surgery Study (COSS) found that patients with hemodynamic cerebral ischemia and recently symptomatic AICAO did not benefit from EC-IC bypass surgery over medical therapy alone. The study’s results included:
The two-year rates for the primary end point were 21% for the surgical group and 22.7% for the medical group.
The 30-day rate for ipsilateral ischemic stroke was 14.4% in the surgical group and 2.0% in the nonsurgical group.
The trial was terminated early for futility.
The COSS study enrolled patients who had a history of at least one transient ischemic attack (TIA) or ischemic stroke ipsilateral to the occluded ICA within the 120 days prior to randomization.

225
Q

Diagnosis, etiology and management of a palpable, subcutaneous fluid collection after spinal canal surgery?

A

Pseudomeningocele
CSF leak
Increase steroids and observe
If no improvement and/or appears to threaten wound: reoperation

226
Q

Treatment of pneumocephalus post operatively?

A

Keep flat
100% supplemental oxygen via nonrebreather

227
Q

Most common bug in post-neurosurgical procedure meninigitis?

A

Staph Aureus

228
Q

Management of CSF leak

A

CT to eval for hydrocephalus (if sx or leak >1 week)
Bed rest, head elevation, avoidance of anything that increases ICP
Reinforce skin incisions if leaking
LP or spinal drainage
If 1-2 weeks or meningitis -> wound washout and repair

229
Q

Management of nosocomial meningitis

A

LP
Empiric vanc 1 gm q8h, ceftriaxone 2 gm q8hr 8-12 days
Add gent if concerned for pseudomonas
Change vanc to nafcillin or oxacillin if not MRSA
If aseptic meningitis - d/c abx, add corticosteroids

230
Q

Craniotomy/craniectomy SSI infection management

A

Remove bone flap
If deeper: debridement or discard flap
Vanc + 3rd generation cephalosporin
Replace vanc wit nafcillin or oxacillin if MRSA negative
6 weeks abx post operatively

231
Q

Management of cerebral abscess

A

MRI with and without contrast
Empiric antibiotics: ceftriaxone, vancomycin, flagyl or alternatively merrem
Biopsy if unable to determine neoplasm/mass versus abscess
Drainage if enlarging, symptomatic or abuts ventricle, treatment is drainage once definitively diagnosed

232
Q

Components of the FOUR score

A

Eye response
Motor response
Brainstem reflex (pupils)
Respiration
All scale of 0 to 4

233
Q

ASIA scale

A

0 - Flaccid paralysis
1 - visible movement
2 - movement without gavity
3 - antigravity movement
4 - antigravity movement with resistance
5 - full strenght
A - complete - no movement or sensation
B - incomplete sensation present
C - incomplete motor but >50% less than 3/5 strength
D - incomplete motor but >50% more than 3/5 strenght
E - normal

234
Q

Brown sequard

A

Loss ipsilateral motor and light touch
Loss contralateral pain

235
Q
A

NCC (5 decks)

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