Neuro ICU Book Flashcards
Most important step for a patient with high-grade acute SAH with poor mental status and IVH?
EVD
SAH with IVH cause of vertical eye movement impairment and depressed level of arousal
Acute obstructive hydrocephalus from mass effect on thalamus and midbrain
Independent risk factor for development of symptomatic vasospasm after SAH
IVH
Hunt and Hess SAH grade: asymptomatic or mild headache and slight nucal ridigity
Grade I
Hunt and Hess grade for SAH: moderate to severe headache, nucal rigidity, no neurologic deficit other than cranial nerve palsy
Grade II
Hunt and Hess grade for SAH: drowsiness, confusion or mild focal deficit
Grade III
Hunt and Hess Grade for SAH: stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances
Grade IV
Hunt and Hess Grade for SAH: deep coma, decerebrate rigidity, moribund appearance
Grade V
In patients with aneurysmal SAH, does initial GCS correlate with long-term outcome?
Yes
Fischer Scale of SAH: no detectable SAH on CT scan
1
Fisher Scale of SAH: diffuse SAH, no localized clot >3 mm thick or vertical layers >1 mm thick on CT scan.
2
Fisher Scale of SAH: localized clot >5 x 3 mm in subarachnoid space or >1 mm in vertical thickness.
3
Fisher Scale of SAH: Intraparenchymal or intraventicular hemorrhage with either absent or minimal SAH on CT scan.
4
Which Fisher group has the highest incidence of vasospasm?
3
Modified Fisher Scale with thick diffuse or localized thick SAH and IVH
4
Modified Fisher Scale with diffuse thick or localized thick SAH and absent IVH
3
Modified Fisher Scale with diffuse thin or localized thin SAH and IVH
2
Modified Fisher Scale with diffuse or localized thin SAH and absent IVH
1
Modified Fischer Scale with no SAH and IVH
2
Modified Fisher Scale with no SAH and no IVH
0
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?
Cumulative blood burden
Increased risk of DCI
What is the most consistent predictor of vasospasm after SAH?
Amount of SAH on the post ictal CT scan (IVH also a risk but not as strong)
What is the step-wise progression for treating intracranial hypertension after SAH?
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)
What are antishivering methods for therapeutic hypothermia?
- Skin counterwarming (warm, forced-air blankets)
- IV magnesium (60-80 mg/kg then 2g/hr)
- Buspirone (20-30 mg TID)
- IV dexmetomidine (0.4 - 1.5 microgram/kg/hr)
- IV meperidine (0.4 mg/kg q4-6 h 0 usual dose: 25-50)
- IV propofol (50-100 mg rapid IV push, 0.3-3 mg/kg/hr maintenance)
- IV Clonidine (1-3 micro gm/kg prn)
Caution with labetalol after ICH
Bradycardia
CHF
Bronchospasm
Caution with esmolol after ICH
Bradycardia
CHF
Bronchospasm
Caution with nicardipine after ICH
Severe aortic stenosis
Myocardial Ischemia
Caution with Fenoldopam after ICH
Tachycardia
Headache
Nausea
Flushing
Glaucoma
Portal Hypertension
Caution with Nitroprusside after ICH
Increased ICP
Variable response
Myocardial Ischemia
Thiocyanate and cyanide toxicity
Agents for RSI that don’t affect ICP
Propofol
Etomidate
Cis-atricurium
Vecuronium
Mannitol dosing (initial and bolus) with goal mOsm/kg
Initial dose: 1.0 - 1.5 g/kg 20% solution
Bolus dose: 0.25 - 1.0 g/kg
Goal: 300 - 320 mOsm/kg
Admission hyperglycemia in ICH is a predictor of what?
30 day mortality (diabetics and non-diabetics)
Goal Na and mOsm with hyperosmolar therapy?
Na: 150 - 155
mOsm/L: 300 - 320
Treatment of seizures in ICH
Lorazepam 0.05 - 0.1 mg/kg -> loading phenytoin or fosphenytoin (20 mg/kg)
May benefit from seizure prophylaxis
Predictors of seizures in ICH
Lobar location
Small hematomas
Risk factors for ICH
Age
Male
African Americans
Japanese
HTN
CAA
Cocaine
Low cholesterol levels
Oral anticoagulants
Excessive Etoh abuse
First AED for seizures IV and if IV access can’t be established?
IV: Lorazepam
No IV access: midazolam (10 mg IM, buccal or intranasal) or diazepam (20 mg rectal)
What should all patients with GCSE get after benzo and why?
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
Treatment for RSE
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)
Status epilepticus titration goal for cIV propofol and barbiturates and midazolam
Propofol and barbiturates: burst suppression
Midazolam: seizure supression
Maintain for 24 hours while conventional AED levels are optimized
Definition of super refractory status epilepticus
SE that continues for 24 hours or more after initiation of anesthetic agents
What is the potential problem of using valproic acid and phenytoin at the same time?
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
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?
Enteric topic image
Dosage: 300 - 1600 mg/d to abort RSE
Meds that can be used in SE when weaning from cIV meds?
Lacosamide
Enteric topiramate
Oxcarbazepine
Fella ate
Pregabalin
Carbamazepine
Ketamine
Issues with using inhaled anesthetics (isoflurane, halothane and desflurane) in terminating refractor SE?
Hypotension
Logistic issues in ICU
Frequent seizure recurrence upon withdrawal
When do you see generalized periodic discharges and what should be done about them?
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
NCSE Treatment Protocol cIV and non continuous IV
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
NCSE Treatment Protocol cIV and non continuous IV
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
What do you need to know about myoclonus status epilepticus
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)
What do you need to know about epilepsia partialis continua (subtype of focal motor SE)
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)
What factors increase risk of seizure in neuotrauma and duration of prophylactic AED in neurotrauma
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)
CRASH trial
Corticosteroids after TBI - no benefit, increased mortality
Brain tissue oxygen tension monitoring after neurotrauma
Provides insight into cerebral metabolism
Pbto2 <15 mmHg associated with poor outcome
Which neurotrauma patients get hypothermia?
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)
Mannitol Side effects
Significant diuresis
Acute renal failure
Hyperkalemia
Hypotension
Rebound increased ICP
Mannitol dosing
0.25 - 1.0 gm / kg
Why is sodium chloride a better osmotic agent than mannitol?
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
Medications for sympathetic storming?
Bromocriptine
Beta-blockers (propranolol)
Morphine
Dantrolene
Clonidine
Steroids in spinal cord injury level of recommendation?
Controversial, not standard of care
Can be considered if you can minimize the risk of high-dose steroids (option, not recommendation)
STASCIS trial
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
Early signs of infarct on CT scan
- Loss of insular ribbon
- Sulcal effacement
- Loss of grey-white junction
Diagnosis
Dense middle cerebral artery sign - intravascular dense clot material
ASPECTS grading score
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.
Indications and Contraindications to rTPA for ischemic stroke
Dose of TPA
0.9 mg/kg with a 10% bolus over 1-2 minutes then rest over 60 minutes
Should GP IIb-IIIa inhibitors be used in ischemic stroke patients
No secondary to significant safety concerns
What can be used after acute CVA?
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
What has a clear benefit in secondary stroke prevention after ischemic stroke?
Statins (independent of serum lipid panel)
What can the BP be in ischemic stroke patients if they haven’t received thrombolysis?
220/120 mmHg
When should carotid revascularization be done after ischemic stroke?
Stenosis >70%
CEA vs CAS
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)
Treatment to prevent malignant cerebral edema after complete MCA infarct
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
Myesthenia Gravis target and symptoms
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
Cholinergic crisis target and symptoms, what should be avoided
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)
Lambert-Eaton myesthenic syndrome target, association, symptoms, uncommon?
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
Botulism etiology, target, symptoms, treatment
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
Tick paralysis location, tick, symptoms, cure
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
Snake venom snakes, target, symptoms
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
Organophosphate toxicity sources, target, symptoms, what can happen 2-3 weeks later, treatment, avoidance?
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
Miller-Fischer Variant of GBS
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
Diphtheria cause, symptoms
Cause: corynebacterium diphtheriae
Symptoms: thick gray pharyngeal pseudomembrane, AV block, endocarditis, myocarditis, lymphadenopathy, neuropathy, craniopharyngeal involvement, proximal-to-distal weakness and decreased reflexes
GBS
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
Arsenic, lead poisoning and porphyrias lead to what?
Acute motor polyneuropathies
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?
Polyneuropathy
Ciguatera toxin from red snapper, grouper, barracuda
Targets: voltage-gated sodium channels of muscles and nerves
Symptoms: metallic taste, hot-cold reversal,
Where do MG, Lambert-Eaton mysathenic syndrome, botulisum, organophosphate toxicity, neurotoxic fish poisoning all affect and what do they NOT cause?
Neuromuscular junction
Do NOT cause sensory involvement
EMG: when is insertional activity increased?
Denervated muscle
EMG: when is insertional activity decreased?
Muscle replaced by fat
What does spontaneous fibrillation potentials and sharp waves suggest on EMG?
Recent denervation or muscle necrosis
When is recruitment decreased on EMG?
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
When does poor activation/recruitment on EMG occur?
Central disorders with a decreased number of motor units recruited and firing is slow rather than rapid
What does early recruitment on EMG mean?
Myopathies
What does long motor unit potential duration indicate?
Lower motor neuro disorders
What does short-duration motor units indicate?
Myopathies
Can be seen in neuromuscular disorders and in early phases of reinnervation after neuropathy
What does long-duration, high-amplitude motor units indicate?
chronic neurogenic disorders
What does small-amplutude, short-duration motor units indicate?
Myopathic disorders
What does 5 or more phases constitute and what does it indicate?
Polyphasia
Myopathic and neurogenic disorders
When do you intubate MG, GBS and CIM/CIP?
VC <10 to 15 mL/kg or <1L and/or NIF less than -20 or rapiduly worsening
What is the problem with bulbar dysfunction and PFTs?
Can’t make proper seal
Rapid therapy, symptomatic therapy, chronic therapy and surgery for MG?
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
Rapid therapy, symptomatic therapy, chronic therapy and surgery for GBS?
Rapid: Plasmapheresis, IvIg
Symptomatic: lacri-lube if 7th nerve palsy
Chronic: none necessary
Surgery: none
Rapid therapy, symptomatic therapy, chronic therapy and surgery for CIP/CIM?
Rapid: treat trigger
Symptomatic: PT, avoid neuromuscular blockage agents and corticosteroids
Chronic: none
Surgery: none
Chronic therapy for MG
Check: AChR- Ab, start pyridostigine, support, possibel thymectomy.
2nd tier: prednisone or azathioprine
3rd: mycophenolayte or rituximab
4th tier: methotrexate, cyclosproien, tacrolimus
RSI meds in suspected elevated ICP and which neuromusclar blocking agent?
Propofol and etomidate - wont affect neuro exam
Nondepolarizing neuromoscular blocking agents - cisatracurium, rocuroinium or vecuronium
Side effects of etomidate?
Nausea, vomiting, myoclonic movements, lowers seizure threshiold, adrenal suppression
Side effects of versed?
ICP
Side effects of succynylcholine?
Hyperkalemia, cardiac arrhythmias, exacerbation of neuropathy or myopathy, malignant hyperthermia, increased ICP in patients with intracranial mass lesions
Bacterial meningitis CSF
Hypoglycorrhachia
Polymorphonuclear pleocytosis
Elevated protein
Glucose <34
CSF to serum glucose <0.23
Protein >22-
Pleocystosis >2000
Viral meningitis CSF
Milder protein elevation
Normal glucose
Mononuclear pleocytosis - may initially have polymophonuclear predominace
Duration of treatment of CNS infection
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
Steroids in CNS infections?
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
Seizure prophylaxis in CSN infections?
No data
Hypothermia in meningitis after v fib arrest?
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
Nimodipine in meningitis
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
Statins in meningitis
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
How can meningitis spread to other areas?
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
Bacteria for cerebral abscesses?
Most common: Staph Aureus and Strep Viridans
Also: Pseudamonas, Enterobacteriaceae, Clostridium, Haemophilus
Duration of treatment of cerebral abscess?
6-8 weeks
Epidural abscess location and cause
Virtual space between inner skull and dura
Secondary to skull fractures or seeded from frontal sinus infection
Subdural empyema location and cause
Dura and arachnoid membranes
Sinus infections
Suppurative intracranial thrombophlebitis location and cause
Septic thrombophlebitis of intracranial veins
Complications of meningitis, abscesses or empyemas
Temporal lobe abnormalities with fevers
HSV encephalitis - temporal lobe abnormalities
Basal ganglia, thalamus or brainstem abnormalities
Arbovirus - arthropod-born virus or eastern equine encephalitis and west nile infections
Diagnosis with fevers
West-Nile Virus
CSF lymphocytic predominance, elevated WBC, mild elevation in protein with normal glucose, possible erthrocytes diagnosis
Viral meningitis
What labs and imaging should be done in viral meningitis
PCR is superior to culture
MRI
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
HSV encephalitis
Diagnosis (intermittent periodic lateralizing epileptiform discharges in temporal lobe)
HSV encephalitis
Treatment for this MRI with fevers
HSV encephalitis
IV acyclovir 10-15 mg/kg TID for 14 days, may need prolongation to 14-21 days
HIV or immunosuppressed patient with CSF with elevated protein and mononuclear predominance, + PCR diagnosis, MRI: asymmetric, multiple infarcts from angitis/vasulopathies
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
Treatment of fevers with scattered ischemic strokes on diffusion MRI
Varicella Zoster Virus
IV acyclovir 10-15 mg/kg TID for 7 days
Steroids for the vasculopathy causing the strokes
What are the risk factors for west nile virus?
Advanced age
Organ transplant or cancer
Viral infection, meningitis, encephalitis or flaccid (asymmetric weakness) paralysis diagnosis? (MRI with anterior horn involvement)
West Nile Virus
Acute flaccid paralysis causing asymmetric weakness during first 48 hours after initial symptom onset
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?
West Nile Virus
Supportive
Ribavirin, IvIg, Interferons - no strong evdience
Most common fungal infection in immunocompromised patients?
Cryptococcus neoformans: Cryptococcus neoformans or C gattii
Usually from pulmonary spread
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
Cryptococcus Neoformans meningitis
MRI: focal, ovoid lesions with post contrast sequences ranging from non-enhancing to nodular enhancement around periphery
HIV +, fevers, cranial nerve palsy changes over weeks diagnosis and treatment
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
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?
Coccidioides Immitis
Treatment: fluconazole
MRI: leptomeningeal enhancement of post-gadolinium images in the basal cisterns (can be diffuse)
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?
Blastomyces dermatitidis
Treatment: Liposomal amphotericin followed by fluconazole x 12 months
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?
Histoplasma Capsulatum
Treatment: Liposomal Amphotericin B followed by Itraconazole for at least 1 year until CSF abnormalities resolve
Goal Na and osm in elevated ICP
Na 150-155
Serum osm >320
Diagnosis
Brain tumor
Calcified, hyperdense mass with surrounding edema
Side effects of hyperosmolar therapy
Electrolyte abnormalities
Pulmonary edema (rapid intravascular volume expansion)
Coagulopathy
Intravascular hemolysis
Why are posterior fossa, pineal region and third ventricles predisposed to hydrocephalus?
Obstruction of CSF outflow
Association with Von-Hippel-Lindau disease
Hemangioblastoma (posterior fossa lesion)
Treatment for edema associated with intracranial tumors?
Dexamethasone
Workup of Von Hippel Lindau syndrome with hemangioblastoma?
Opthalmologic evaluation (retinal lesions)
TOtal spine MRI with and without contrast (spinal cord hemangioblastomas)
VMA and metanephrine levels (pheochromocytoma also associated with VHL)
Management of hydrocephalus in perioperative period for resection of posterior fossa brain tumor?
- Endoscopic third ventriculostomy - short and long term control, passage through floor of third ventricle into prepontine cistern bypasses the obstruction at the 4th ventricle
- Placement of right frontal EVD
How long is dexamethasone continued post operatively after resection of posterior fossa tumor?
2 week taper
When is repeat imaging performed after resection of a posterior fossa tumor?
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
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?
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
Concerns with pituitary apoplexy?
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
Diagnosis with ABRUPT onset vision changes? Findings on T1, T2 and T1 with gadolinium?
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
What should be monitored for after resection of pituitary apoplexy?
Diabetes insipidus
Cancers associated with hemorrhagic brain lesions
Lung (bronchogenic carcinoma)
Melanoma, renal cell, thyroid carcinoma, choriocarcinoma
Treatment of hemorrhagic brain lesions
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
How do you taper dexamethasone after surgery for hemorrhagic brain mets?
Dexamethasone 10 mg oral q6h x 24 hours to 2 mg q6h for duration of whole brain radiation therapy
Sudden onset headache, vomiting, collapse, CT scan with following, evidence of hydrocephalus/herniation on physical exam, what is the diagnosis and first step?
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
Operative options for following with evidence of hydrocephalus?
Colloid cyst -> resection or VP shunt with endoscopic fenestration of septum pellucidum
Which demyelinating disease can progress over days, impair bulbar function, central and peripheral nervous system involvement possible?
Guillan-Barre Syndrome
Which demyelinating disease involved ophthalmoplegia, ataxia, areflexia and encephalopathy and is associated with peripheral motor axonal demyelination and brainstem encephalitis with IgG GQ1b antibody?
Bickerstaff encephalitis (variant of GBS)
ADEM versus GBS main difference?
ADEM - central nervous system
GBS - peripheral nervous system
Miller-Fischer versus Bickerstaff encephalitis?
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.
Diagnosis and treatment?
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
ADEM vs MS involvement?
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.
ADEM versus PML?
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.
When should ADEM be biopsied and what is the hallmark?
When there is no response to conventional therapy and presentation is atypical
Biopsy: perivenous demyelination (vs confluent demyelination in MS)
Fevers, chills unusual behavior, hallucinations, focal neurologic signs and seizures diagnosis and treatment?
HSV encephalitis (HSV-1 or HSV-2)
Treatment: Iv acyclovir
Ab for SCLC or thymoma with brainstem encephalitis with bulbar signs and symptoms
Hu (ANNA1)
Testicular cancer with limbic encephalitis, brainstem encephalitis, hypothalamic dysfunction antibody?
Ma2 (Ta)
Antibody associated with lung carcinoma and memory loss, encephalopathy, seizures, and tendency to relapse?
AMPAR
Antibody associated with multiple cancers with memory loss, encephalopathy and seizures?
VGKC
Antibody associated with refractory epilepsy?
GluR3
Antibody associated with breast or SCLC and brainstem syndrome (opsoclonus, myoclonus), cerebellar syndrome and Lambert-Eaton syndrome
Ri (ANNA2)
Antibody associated with SCLC, thymoma, cerebellar ataxia, movement disorders and myasthenic syndromes?
CV2 (CRMP5)
Antibody associated with breast and SCLC and peripheral neuropathy, stiff-person syndrome and myelitis?
Amphiphysin
40 year old women, acute onset psychiatric symptoms, behavior changes, orofacial dyskinesia, seizure, encephalopathy, autonomic instability, respiratory failure and catatonic state diagnosis?
Anti-NMDA Receptor Encephalitis
Tumor associated with Anti-NMDA Receptor Encephalitis
Ovarian Teratoma
Disease causing prominent microgliosis and deposits of IgG in the hippocampus, forebrain, basal ganglia and spinal cord? Ab to what?
Anti-NMDA receptor encephalitis
Can find NMDAR-expressing neurons with inflammatory infiltrates in the teratomas
Disease pathogenesis of Anti-NMDA receptor encephalitis?
Immunoglobulin-induced receptor internalization and downregulation of surface NMDARs
Highest levels in amygdala and hippocampus - also area where blood-brain barrier is the weakest
Diagnosis young woman with psych issues and seizures
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
Diagnosis and what does this presence mean?
Extreme delta brush in anti-NMDAR syndrome -> presence may indicated a prolonged hospitalization, longer continuous EEG monitoring and a trend towards worse outcomes
Diagnosis and treatment?
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
What can be done in anti-NMDA disease process if patient has refractory encephalitis?
Prophylactic bilateral oophorectomy (without evidence of teratoma)
How should you treat the bizarre movements associated with Anti-NMDAR encephalitis?
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
Which cells are particularly sensitive to decreased cerebral blood flow?
CA 1 hippocampal pyramidal neurons
Cerebellar Purkinje neurons
Medium spiny striatal neurons
Pramidal neurons in layers 3, 5 and 6 of neocortex
Which CPC is good cerebral performance, conscious, alert, able to work?
CPC-1
Which CPC is moderate cerebral disability, conscious, can carry out independent activities?
CPC-2
What CPC is severe neurologic disability, conscious, dependent on others for daily support?
CPC-3
What CPC is coma or vegetative state?
CPC-4
What CPC is dead?
CPC-5
Goal Sjvo2 and Pbto2 to avoid secondary neurologic injury after cardiac arrest?
Sjvo2 > 60%
PbtO2 > 20 mmHg
Describe Lundberg A, B and C waves
A- plateau waves, 5-10 mins, reduced cerebral compliance
B - smaller waves, compliance may be compromised
C - normal cardiac/pulmonary cycle interactions
Herniation syndrome that causes ipsilateral cranial nerve palsy, contralateral or bilateral motor posturing
Uncal herniation (lateral transtentorial) from temporal lobe mass lesion
Herniation syndrome that causes progression from bilateral decorticate to decerebrate posturing, rostral-caudal loss of brainstem reflexes?
Central transtentorial herniation from diffuse cerebral edema or hydrocephalus
Herniation syndrome that causes asymmetric (contralateral > ipsilateral) motor posturing but preserved oculocephalic reflex
Subfalcine herniation from convexity (frontal or parietal) mass lesion
Herniation syndrome that causes sudden progression to coma with bilateral motor posturing and cerebellar signs?
Cerebellar herniation (up or down) from cerebellar mass lesion
Do steroids work on vasogenic or cytotoxic edema?
Vasogenic (ex: abscess or neoplasm) not cytotoxic (ex: acute ischemic stroke)
IV infusion when hyperventilation and osmolar therapy doesn’t work for ICP elevation?
Pentobarbital
Reduces cerebral metabolic rate
Needs continuous EEG monitoring to burst suppression
Impairs neurologic exam
What pressors should be used to maintain PbtO2 >20?
Levophed, neo
Treatment for refractory symptomatic vasospasm?
Angiography and intraarterial vasodilators or balloon angioplasty
Which pathway do somatosensory evoked potentials test?
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
What are BAEPs (brainstem auditory evoked potentials)?
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.
What does an absent or delayed wave V BAEP with normal wave I latency mean?
Conduction abnormalities central to distal portion of CN VIII
What does an absent wave I with preserved wave V mean in BAEPs?
Peripheral hearing apparatus or auditory nerve (most commonly technical issue)
What does preservation of wave I but loss of waves II to V on BAEP indicate?
Functional disruption of brainstem
What does unilateral abnormal BAEP’s indicate?
Ipsilateral brainstem damage
What does bilaterally absent N20’s indicate ?
Poor prognosis after cardiac arrest if still comatose at 72 hours or within 1st week
What are event-related potentials?
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
What is MMN useful for in coma?
Relatively high specificity for recovery of wakefulness (particularly in anoxic injury)
What raises the hypothalamic temperature set point?
Cerebral prostaglandin E synthesis
Where should and EVD be zeroed?
External auditory meatus (level of the foramen of monro)
What antibiotic has been given via that intraventricular route the most? Which is contraindicated secondary to neurotoxicity?
Vanc and gent
Cephalosporins
Factors associated with chronic hydrocephalus after SAH?
Old age
High HH grade
Female
Acute hydrocephalus
Posterior circulation aneurysm
Aneurysm >2.5 cm
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?
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
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?
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)
Benefit of nimodipine in vasospasm?
Calcium channel blocker that improves outcomes, induces hypertension and provides excess volume
Management of vasospasm refractory to nimodipine (medical management)?
Intraarterial vasodilator therapy: papave3rine (opium alkaloid), milrinone (PDE3 inhibitor), verapamil and nicardipine (calcium channel blockers)
Balloon angioplasty
Results of IMCVS study?
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.
What does a daughter sac predispose an aneurysm to?
Rupture
Stroke Counsel of AHA recommends screening who for aneurysms?
- 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).
- 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).
Who gets management for unruptured aneurysms?
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
What are the three Borden classifications of dural AV fistulas?
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)
Should dural AV fistulas be treated?
Yes because they have a more aggressive course
History of stroke or head trauma within how many months is a contraindication to rtPA?
3 months
Spetzler and Martin Grading System for AVM
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
Cause of cerebral edema after CEA?
Cerebral hyperperfusion syndrome
Results of the carotid occlusion surgery study?
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.
Diagnosis, etiology and management of a palpable, subcutaneous fluid collection after spinal canal surgery?
Pseudomeningocele
CSF leak
Increase steroids and observe
If no improvement and/or appears to threaten wound: reoperation
Treatment of pneumocephalus post operatively?
Keep flat
100% supplemental oxygen via nonrebreather
Most common bug in post-neurosurgical procedure meninigitis?
Staph Aureus
Management of CSF leak
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
Management of nosocomial meningitis
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
Craniotomy/craniectomy SSI infection management
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
Management of cerebral abscess
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
Components of the FOUR score
Eye response
Motor response
Brainstem reflex (pupils)
Respiration
All scale of 0 to 4
ASIA scale
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
Brown sequard
Loss ipsilateral motor and light touch
Loss contralateral pain
