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NCC > NCC Boards > Flashcards

NCC Boards Flashcards

1
Q

Narrowest part of CSF system?

A

Aqueduct of Sylvius
Cerebral Aqueduct (same thing)

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2
Q

Where are a line and ICP measured/calibrated?

A

Interventricular foramen of Monro

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3
Q

What creates and absorbs CSF?

A

Creates: choroid
Absorbs: arachnoids

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4
Q

Goal ICP to improve outcomes and what ICP worse outcomes?

A

Goal: <20 mmHg
Worse: >20

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5
Q

Brain trauma foundation treatment threshold for ICP?

A

> 22

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6
Q

Goal osmolar gap for ICP?

A

<20

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7
Q

CPP equation and goal?

A

MAP - ICP
Goal 50-70 mmHg

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8
Q

Mannitol dose for elevated ICP?

A

1 mg/kg

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9
Q

P1

A

Pressure through choroid plexus into ventricles

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10
Q

P2

A

Arterial pulse through parenchyma

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11
Q

P3

A

Closure of aortic valve (dicrotic notch)

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12
Q

P2 > P1

A

Reduced brain compliance
Impending herniation

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13
Q

Lundberg A Waves

A

Pathologic
Increased ICP for 5-10 minutes
“Plateau waves”
Reduced compliance
May indicated impending herniation
ICP can rise as high as 50-100 mmHg

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14
Q

Lundberg B Waves

A

Increase in ICP 0.5 - 2 x/min
Usually don’t exceed 30 mmHg
Indicator of poor compliance
Normal, ventilated, asleep

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15
Q

Steroid dose for brain mets (usually found at grey-white junction)

A

10 mg IV decadron then 4 mg IV q6h for acute event

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16
Q

what mimics tetanus?

A

Strychnine poisoning - check thin-layer chromatography on gastric aspirate and urine sample

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17
Q

Orthopnea definition and dx

A

SOB laying flat
Heart failure

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18
Q

Cheyne-Stokes definition and dx

A

Cyclic breathing pattern with apnea -> gradual increase in respiratory frequency and tidal volume -> gradual decline -> apnea
Heart Failure

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19
Q

Hyperpnea definition and dx

A

Increased depth and rate of breathing linked to increased oxygen demand or metabolic activity and ABG will be normal (versus hyperventilation doesn’t have increased oxygen demand or metabolic activity and will have decreased CO2).

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20
Q

Agonal breathing definition and dx

A

Irregular, gasping or labored breathing
Anoxic brain injury

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21
Q

Kussmaul respirations definition and dx

A

Deep, rapid and difficult breathing
Metabolic acidosis, uremia, toxic ingestions (etoh and salicylates)

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22
Q

Apneuristic breathing definition and dx

A

Prolonged, gasping inhalations then extremely short and inadequate exhalations
Upper pons injury (CVA, trauma) - signifies severe injury and poor outcome, temporary induction can happen with ketamine

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22
Q

Biot respiration definition and dx

A

Deep breaths interspersed with apnea -> increasing irregularity -> ataxic breathing
Damage to pons (CVA, trauma, uncal herniation), occ opiate intoxication

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22
Q

ALS

A

Upper and lower motor neuron, pyramidal Betz cells in motor cortex, anterior horn cells of spinal cord (retrograde axonal loss) and lower cranial motor nuclei of brainstem, gliosis replaces lost neurons, bunina bodies, sx: hand weakness, shoulder girdle weakness and foot drop; frontotemporal dementia, pseudobulbar palsy, autonomic symptoms, spectrum

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22
Q

Central neurogenic hyperventilation definition and dx

A

Persistent hyperventilation
Head trauma, brain hypoxia, or inadequate cerebral perfusion due to midbrain or upper pons

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22
Q

Lower motor neuro findings

A

Muscle atrophy and fasciculations, weakness

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22
Q

Central neurogenic hypoventilation definition and dx

A

Persistent hypoventilation
Medullary respiratory centers don’t respond appropriately to stimuli (head trauma, cerebral hypoxia and narcotic suppression)

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23
Q

Ondine’s curse

A

Hypoventilation due to impaired autonomic ventilation control while maintaining normal voluntarily breathing (forget to breathe while asleep, but ok when awake)
Congenital central hypoventilation syndrome, brainstem tumors or infarcts, and surgical manipulation of 2nd cervical vertebrae for intractable pain

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23
Q

Upper motor neuro findings

A

Hyperreflexia, poor dexterity, incoordination and spasticity, bulbar: dysarthria and dysphagia

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24
Q

Pick’s Disease

A

Frontotemporal dementia

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25
Q

Pseudobulbar palsy

A

Inappropriate periods of crying, laughing, or yawning from involvement of the frontopontine motor neurons

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26
Q

H/O OLT with multiple ring enhancing lesions, crescent-shaped with red staining nuclei organism and treatment

A

Toxoplasma Tachyzoites
Tx: pyrimethamine and sulfadiazine + corticosteroids for mass effect, leucovorin to reduce hematologic side effects of treatment, 6 weeks

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26
Q

Treatment of cryptococcal meningitis

A

Flucytosine and amphoteracin

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27
Q

Treatment of cytomegalovirus encephalitis

A

Antivirals

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28
Q

Immunocompromised HIV patient with ataxic gait, dysdiadochokinesia and dysmetria, MRI T2 hyperintense noncontrast enhancing lesion in right cerebellar peduncle and subcortical regions etiology and treatment.

A

Progressive Multifocal Leukoencephalopathy from papovavirus (BK, JC, SV40 strains)
Tx: reverse immunocompromised state

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29
Q

Conduction aphasia localization

A

Information can’t travel from Wernicke’s area to Broca’s area
Posterior aspect of left superior temporal gyrus, left supramarginal gyrus and underlying white matter (including arcuate fasciculus)

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30
Q

Brocas aphasia localization

A

Broca’s area
Left inferior frontal gyrus

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30
Q

Inability to name unique entities (ex: famous people) location

A

Left temporal pole

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31
Q

Transcortical motor aphasia localization

A

Left cingulum bundle

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32
Q

Neck pain, headaches and TIA symptoms name and etiology

A

Horner syndrome
Right ICA dissection > vertebral artery dissection

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33
Q

Causes of bacterial meningitis by age: 17-59 and >60

A

Neisseria meningitis
Strep pneumo

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34
Q

4th ventricle lesion with hydrocephalus, increased cell density in papillary fronds without nuclear pleomorphism and necrosis lesion

A

Choroid plexus papilloma

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35
Q

Meningioma: imaging, commonality, pathology, mutation, path and treatment

A

Homogenous enhancing, dural based
Infra or supratentorial, can be bifrontal, can be all over
MC primary tumor in adult, women > men,
Arachnoid cells, can be in NF2, Cowden and Gorlin syndrome
22q12
“whorl” of meningothelial cells, “psammoma bodies”
Tx: surgery > radiation (atypical, anaplastic, recurrent, surgically inaccessible), VEGF inhibitors

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36
Q

Glioma: imaging location, pathology, characteristics that portend better prognosis, treatment

A

Infra or supratentorial, can be bifrontal, can be mutliple
Astrocytes and/or oligodendrocytes, higher grade (GBM): atypia, hypercellular, increased mitotic rate/vascularity/necrosis
IDH-mutant type (vs. IDH-wildtype), MGMT promotion methylation, younger, lower grade = better prognosis than
Tx: surgery, radiation, temozolomide

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37
Q

CNS Lymphoma: imaging, epidemiology, symptoms, other tests, treatment

A

Wide imaging, diffusion weighted imaging, patchy on post contrast MRI
Increases with age, immunocompromised and immunocompetent
Neurocognitive/neuropsychiatric symptoms possible
Biopsy (large B cell = 90%), LP, optho slit lamp, PET scan, testicular US, bone marrow bx, steroids can obscure diagnosis (lymphotoxic)
Treatment: methotrexate, chemo + autologous stem-cell transplant

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38
Q

Metastatic brain tumors: location, prevalence, MC tumors, location, treatment, better prognosis, risk of recurrence after surgery

A

Isolation or with multiple lesions
10x’s more common than primary
MC: breast, lung and melanoma (can be any)
Grey-white junction
Treatment: surgery (dominant symptomatic lesion, up to 3 lesions), radiation (whole brain if multiple lesions), steroids (edema), chemo (CNS penetration: methotrexate, thiotepa, cytarabine, temozolamide, vinorelbine, capecitabine, carboplatin, topotecan), immunotherapy, AED (non-enzyme inducing: levetiracetam, lacosamide, zonisamide)
Better: younger, good functional status, solitary lesion
50-60% risk of local recurrence post-resection

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39
Q

Spinal cord tumors: intradural-extramedullary, intradural-intramedullary and extradural types

A

Intradural-extramedullary: meningioma, nerve sheath tumor
Intradural-intramedullary: ependymoma, astrocytoma
Extradural: metastasis, chordoma, ewing sarcoma/osteosarcoma, lymphoma

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40
Q

Benign spinal cord tumors

A

Meningiomas, nerve sheath tumors (schwannoma, neurofibroma, ganglioneuroma)

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41
Q

Malignant spinal cord tumors

A

Gliomas

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42
Q

Benign spinal column tumors

A

Hemangioma, osteoid osteoma, osteoblastoma

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43
Q

Malignant spinal column tumors

A

Chordoma, chondrosarcoma, Ewings sarcoma, lymphoma, metastasis (MC in adults), plasma cell neoplasms

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44
Q

Management of spinal cord tumors

A

Are there neurologic deficits for surgery?
Is the tumor sensitive to radiation or chemo?
Radiosensitive mets: lymphoma, myeloma, small cell lung cancer, germ cell, prostate and breast;
Radioresistant mets: melanoma, RCC, NSCLC, GI cancer, sarcoma;

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45
Q

Carcinomatous Meningitis

A

Imaging (Dural enhancement, enhancement of meninges, enhancement around brain stem) or LP
CN or radicular nerve deficits
CSF poor sensitivity (3 taps required), MRI brain + c/t/l spine: linear enhancing deposits in cerebellar folia, cortical sulci or cranial nerves; nodular enhancement of the cauda equina or coating of the spinal cord
Whole brain XRT or craniospinal XRT, systemic chemo with CNS penetration (EGFR TK inhibitors), intrathecal chemo (methotrexate, thitepa, cyterabine), palliative shunt placement (if obstructive hydrocephalus)

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46
Q

Paraneoplastic syndromes: ab location, panel location, number of techniques to dx, treatment

A

Antibodies to cell surface or synaptic antigen or intracellular antigens
Serum and CSF antibody panel - check panel before starting treatment (can be false neg or pos)
Confirm ab positivity with two separate assay techniques
Serial testing not useful
Negative ab test does not exclude a paraneoplastic neurologic disorder
Identify and treat any underlying cancer
Methylprednisolone 1 gm daily x 5 days then taper
IVIG or PLEX > Rituximab and/or cyclophosphamide

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47
Q

Acute complications of radiation therapy: timing, symptoms, treatment, mechanism and prognosis

A

Days to weeks: AMS, fatigue, worsening preexisting neurologic deficits
Tx: steroids
Potential mechanisms: cerebral edema, neuroinflammation, vascular toxicity, transient blood-brain barrier disruption
Prognosis: sx generally resolve with steroids

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48
Q

Early-delayed complications of radiation therapy: timing, symptoms, mechanism

A

Weeks to 6 months: cognitive symptoms, fatigue, headache, nausea and lethargy
Mechanism: transient demyelination

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49
Q

Late-delayed complications of radiation therapy:

A

Months to years: cognitive decline, possible focal findings
Imaging and path: leukoencephalopathy, tissue necrosis (can mimic tumor recurrence), brain volume loss, secondary tumors, vasculopathy (can cause ischemia or hemorrhage)
Mechanism: direct cytotoxic effects on various neural cells and their progenitors, chronic inflammation and neurovascular injury
Treatment: neurostimulants, shunt

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50
Q

HSV encephalitis population and treatment

A

Think about in patients with cancer undergoing whole brain radiation
Tx: acyclovir

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51
Q

Complications of chemotherapy: CNS

A

Acute (reversible) encephalopathy, subacute encephalopathy, chronic encephalopathy, reversible posterior (leuko)encephalopathy syndrome (PRES), multifocal leukoencephalopathy, thrombotic microangiopathy, cerebral infarcts, cortical blindness, optic neuropathy, visual disturbances, psedotumor cerebri, cerebral venous thrombosis, cerebellar dysfunction, seizures, aseptic meningitis

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52
Q

Complications of chemotherapy: PNS

A

Platinum compounds: cisplatin, oxaloplatin
Vinca alkaloids: vincristine, vinblastine, vindesine
Taxanes: paclitaxel, docetaxel
Bortezomib
Thalidomide
Suramin

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53
Q

CAR-T (tisagenlecleucel, axicabtagene, ciloleucel and brexucabtagene autoleucel) for leukemia and lymphoma CNS effects

A

Cytokine release syndrome and neurotoxicity
Immune effector cell-mediated neurotoxicity syndrome, ICANS
3-10 days after administration
Encephalopathy, behavior changes, headaches, tremor, seizures, coma
Cerebral edema
Steroids and supportive care
Tocilizumab: improves cytokine release syndrome but won’t impact neurotoxicity

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54
Q

Which patients with cancer and neurologic symptoms should get steroids?

A

ALL unless CNS lymphoma is on the differential

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55
Q

Data on phenytoin in SAH for seizure prophylaxis

A

Links between phenytoin and poor neurologic outcome
No change in rates of seizures, increased complications

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56
Q

What reduces neurologic symptoms associated with vasospasm and improves neurologic outcome after aneurysmal SAH? What is it’s effect on incidence of vasospasm?

A

Nimodipine (less stroke and poor neurologic outcome)
No decrease in incidence

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57
Q

Which part of triple H therapy increases cerebral blood flow after SAH?

A

Euvolemic hypertension

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58
Q

Elevated mean velocities versus global elevation with normal Lindegaard ratio meaning

A

Elevation in mean velocities can be a sign of cerebral vasospasm, however, if a global elevation with a normal Lindegaard ratio is more likely due to cerebral hyperperfusion

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59
Q

EEG findings with cerebral vasospasm after SAH

A

Decrease in alpha-delta variability
Periodic discharges = worse overall outcome

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60
Q

Acute severe headache, normal neurologic exam

A

Parimesencephalic SAH (PMSAH)
10% of all SAH
Hemorrhage anterior to midbrain or pons, no extension around brainstem, into supracellar cistern or proximal Sylvian fissure
DSA unlikely to show aneurysm
Good outcome, few complications

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61
Q

Confusion, seizures, hypertension

A

Posterior reversible encephalopathy syndrome

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62
Q

Hypotension, hyponatremia, increased urine sodium, increased urine output, and low cvp treatment

A

Cerebral Salt Wasting
Fluid bolus (1st line)
Can use fludricortisone and salt tabs

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63
Q

Normal to hypertensive, hyponatremia, low urine output, increased urine sodium treatment

A

Free water restriction (1st line)
Salt tabs
Can use tolvaptam (vasopressor receptor antagonists)

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64
Q

How does magnesium inhibit smooth muscle contractions?

A

Binds to voltage-dependent calcium channels to inhibit smooth muscle contraction
May also inhibit glutamate release

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65
Q

Milrinone mechanisms

A

Phosphodiesterase III inhibitor
Vasodilation and inotropic properties
Weak data shows some improvement in vasospasm

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66
Q

Intraventricular nimodipine

A

Reduced delayed cerebral ischemia
Rescue therapy

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67
Q

Hypothermia in delayed cerebral ischemia

A

Limited data
Decreases cerebral blood flow
Improves outcomes in high grade SAH (limited data)

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68
Q

Diagnosis

A

Vertebral artery aneurysm

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69
Q

Diagnosis

A

Anterior spinal artery aneurysm

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70
Q

Diagnosis

A

Posterior Inferior Cerebellar Artery Aneurysm (PICA)

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71
Q

Contralateral loss of pain and temp body, ipsilateral loss of pain and temp face, ipsilateral horners, ataxia, hearing loss and facial droop stroke - vessel?

A

AICA stroke
Lateral pons

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72
Q

Contralateral loss of pain and temp body, ipsilateral loss of pain and temp face, ipsilateral horners, ataxia, dysphagia, hoarseness, decreased gag stroke - vessel?

A

PICA stroke
Lateral medulla

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73
Q

Contralateral motor deficit, tongue deviation stroke - vessel?

A

Anterior spinal artery
Medial Medulla

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74
Q

Vertigo, nausea, vomiting, ipsilateral facial numbness, horners syndrome, dysphagia and ataxia stroke vessel

A

Lateral medullary or Wallenberg syndrome, superior cerebellar artery syndrome
Inferior posterior cerebellar hemisphere, inferior vermis, lateral medulla
PICA

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75
Q

Ipsilateral limb ataxia, vertigo, nystagmus, dsyarthria stroke vessel

A

Superior cerebellar artery syndrome
Dorsolateral upper brainstem and cerebellar and superior cerebellar peduncle
SCA

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76
Q

Ipsilateral ataxia, hearing loss, Horner’s syndrome, contralateral decreased temp and pinprick stroke vessel

A

Lateral pontine syndrome
Ipsilateral labrynth, lateral potine tegmentum
AICA

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77
Q

Somnolence, convergent nystagmus, skew deviation, vertical gaze paralysis, some components of proximal basilar/PCA stroke vessel

A

Top of the basilar syndrome
Midbrain, thalamus and mesial temporal lobes and occipital lobes
Top of basilar artery

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78
Q

Ipsilateral loss of facial sensation, ipsilateral ataxia stroke vessels

A

Lateral mid-pontine syndrome: Lateral and medial pontine perforators from mid-basilar artery

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79
Q

Ipsilateral ataxia, contralateral weakness, “wrong way” gaze deviation (pons ponders paresis)

A

Medial mid-pontine syndrome: Lateral and medial pontine perforators from mid-basilar artery

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80
Q

Quadriplegia, horizontal gaze paralysis, bifacial paralysis
May have preservation of vertical eye movements

A

Locked-in syndrome - bilateral lower pons from proximal basilar artery

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81
Q

Contralateral arm and leg weakness, ipsilateral tongue paralysis

A

Medial medullary or Dejerine syndrome
Medulla and cervical spinal cord
VA

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82
Q

Arteries for these three

A

PICA / AICA / SCA

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83
Q

Posterior cerebral vascular territories

A
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84
Q

Clinical features by vascular territory

A
85
Q

Imaging features by vascular territory

A
86
Q

EEG Findings in DCI in SAH

A

Earliest sign: loss of fast frequency (ex: alpha)
Alpha-delta ratio and alpha variability predict onset of vasospasm (up to 3 days before vasospasm)
Alpha/delta ratio: ischemia tends to reduce alpha frequencies and increase delta frequencies - Reductions in alpha/delta ratio suggest vasospasm, especially if reduction occurs focally in one hemisphere.
Relative alpha variability: Measurement of the normal fluctuation in alpha-activity over time. Decreased relative alpha variability may be a reflection of delayed cerebral ischemia.
(2) Worsening focal slowing or late-appearing epileptiform abnormalities (e.g., epileptiform discharges, periodic/rhythmic activity) may predict delayed cerebral ischemia

87
Q

Management of delayed cerebral ischemia

A

Treat hypovolemia and hypomagnesemia
MAP therapy (85) - levo or neo may be needed - brain lacks alpha-1 receptors
Lower opening pressure of EVD
IR for intra-arterial vasodilator and/or angioplasty
Intrathecal nicardipine for refractory vasospasm, systemic milrinone (MILRISPASM - improved functional outomes, Montreal Neurologic Hospital protocol)

88
Q

CRASH trial

A

High-dose methylprednisolone over 48-hours within 8 hours of TBI
Higher mortality at 2 weeks and 6 months

89
Q

CLEAR III Trial

A

Intraventricular TPA safe in IVH but no clinical benefit

90
Q

Goal PbtO2 in TBI (with goal ICP and CPP)

A

> 25 mmHg with ICP < 22 mm Hg and CPP 60 - 70 mm Hg

91
Q

IMPACT versus CRASH Head Injury Prognostic Models

A
92
Q

Risk factors for post traumatic seizures

A

GCS 10 or lower initially
Immediate seizures
Post traumatic amnesia lasting longer than 30 minutes
Linear or depressed skull fracture
Penetrating head injury
Subdural, epidural or intracerebral hematoma
Cortical contusion
Age 65 or younger
Chronic alcoholism

93
Q

Data on hypothermia in TBI

A

Not recommended for adults with diffuse injury
Peds without improvement in function, worse mortality

94
Q

Burr hole with drain placement in chronic subdural: effect on recurrence and 6 month mortality?

A

Decreased risk of recurrence
Decreased 6-month mortality

95
Q

Presence of sacral sparing (versus no sacral sparing) on initial evaluation in SCI?

A

More likely to make motor recovery with complete motor injury but sensory preservation on initial exam versus no sacral sparing

96
Q

Who should get a CT venogram in skull based fractures to evaluate for sinus thrombosis?

A

Fractures extending into transverse, sigmoid or jugular bulb petrous temporal bone (over fractures extending into superior saggital sinus)

97
Q

Retained fragments in this location increase the risk of seizures after penetrating trauma.

A

Eloquent cortex

98
Q

Rare life-threatening side effect of valproic acid?

A

Pancreatitis

99
Q
A
100
Q

Alcohol withdrawal seizures characteristics and timing

A

Seizure seizure of flurry of generalized tonic-clonic seizures within first 6-48 hours

101
Q

Diagnosis: delirium, agitation, tachycardia, hypertension, fever, 2-4 days after admission in alcoholic

A

Delirium tremens

102
Q

What is more effective in eclamptic seizures: magnesium, diazepam or phenytoin?

A

Magnesium

103
Q

Management of recurrent seizure in eclmepsia after 1st seizure treated with magnesium?

A

Benzodiazepine

104
Q

IV midazolam: loading, repeat dose, half-life, side effects/prolonged use

A

Loading: 0.2 mg/kg
Repeat: 0.2 - 0.4 mg/kg q5 mins until seizure stops
1/2 life: 1.5 - 3.5 hrs
Prolonged use: tachyphylaxis, prolonged half-life
Side effects: sedation, respiratory depression, hypotension

105
Q

IV Propofol: loading, repeat, contraindications, side effects, labs to monitor

A

Loading: 1 mg/kg
Repeat: 1-2 mg/kg bolus q5 mins until seizure stops
Contraindications: allergy to soybean oil, egg lecithin or glycerol, caution in combo with carbonic anhydrase inhibitors (ex: zonisamide and topiramate - risk refractory acidosis)
Side effects: sedation, large lipid load, occasional pancreatitis, dose-dependent hypotension, Propofol infusion syndrome (metabolic acidosis, rhabdo, ciculatory collapse -> death)
Monitor: CPK, triglycerides, amylase/lipase, blood gas, lactic acid

106
Q

IV Pentobarbital: loading, repeat, max bolus rate, half life, side effects, serum level target

A

Loading: 5 mg/kg
Repeat: 5 mg/kg until seizure stops
Max bolus rate: 20 - 50 mg/min
IV Dose: 1 mg/kg/hr (usual maintenance range: 0.5 - 10 mg/kg/hr)
Half life: 15-60 hrs
Side effects: prolonged coma (days after meds stopped), hypotension, myocardial depression, immune suppression, ileus, allergies (including Steven-Johnsons)
Target levels: ?

107
Q

Diagnosis and treatment: peripheral edema, blistering, pain and discoloration of extremity after IV phenytoin

A

Purple glove syndrome
Treatment: may need excision

108
Q

Young woman with mental disorder and new seizures and worsening hallucinations and dyskinesia EEG findings and diagnosis

A

Extreme delta brush (background delta slowing with overriding fast beta activity)
NMDA encephalitis

109
Q

Confusion, agitation and tonic-clonic seizures EEG findings and diagnosis

A

Temporal lateralized periodic discharges
HSV encephalitis

110
Q

Memory and behavior changes, coordination difficult, visual disturbances, rapid progression EEG findings and diagnosis

A

Generalized periodic discharges
Creutzfeldt-Jakob disease

111
Q

Treatment agent for cryptococcal neoformans meningitis that causes aplastic anemia? What is it’s mechanism?

A

Flucytosine (bone marrow suppression, pancytopenia, aplastic anemia, agranulocytosis), can also cause UC and bowel perforation
Inhibits RNA and DNA synthesis

112
Q

Dual treatment agents for cryptococcal neoformans meningitis and their increased toxicities?

A

Flucytosine and Amphotericin B
Hepatic, renal and hematologic toxicities

113
Q

What brain lesion has a CT finding of inner hypodense center and outer hyperdense rim? What is the first antibiotic regimen of choice?

A

Brain abscess
IV ceftriaxone (3rd generation cephalosporin) and flagyl

114
Q

EEG findings for Grade I - IV of anoxic encephalopathy

A

I: Alpha
II: Theta
III: Slow delta
IV: low-amplitude delta

115
Q

Anatomic site for CVA causing deviation of angle of mouth to left and left-sided weakness

A

Genu of internal capsule has motor fibers and corticobulbar fibers
Basal ganglionic bleeds can compress this area and lead to these symptoms

116
Q

What does infarct of the facial nucleus cause?

A

Crossed hemiplegia

117
Q

What does involvement of the facial nerve at the stylomastoid foramen or terminal branches lead to?

A

Lower motor pattern of facial nerve palsy without any motor weakness

118
Q

NMS toxicity meds and treatment

A

Dopamine-receptor antagonist or rapid withdrawal of dopaminergic meds
Dantrolene, dopamine agonists, benzodiazepines

119
Q

Fractures where cause purple tympanic membrane discoloration?

A

Basilar skull fx - petrous ridge of temporal bone

120
Q

What lab checks for CSF leak?

A

beta transferrin

121
Q

Pathology of HSV encephalitis
CSF: lymphocytes, high protein, inc RBCs, normal glucose

A

perivascular cuffs of lymphocytes with “owl’s eye” intranuclear inclusions, foamy macrophages and areas of hemorrhages

122
Q

Treatment of HSV encephalitis (dose and duration)

A

IV acyclovir: 10 mg/kg body weight q8 hrs for 14-21 days

123
Q

Versus acyclovir, what does valganciclovir treat?

A

Cytomegalovirus

124
Q

Diagnosis: progressive memory impairment over 6 months, reduced blinking, rigidity, arm tremors, decreased arm swinging with walking, dementia, liver firmness, palpable splenic tip, MRI with globus pallidus and putamen atrophy?

A

Wilsons disease

125
Q

Mutation that causes Wilson’s disease and treatment

A

ATP7B - copper incorporation into ceruloplasmin
Pencillamine

126
Q

What is a patient at risk for with immune reconstitution syndrome?

A

TB meningitis after starting antiretrovirals for HIV with history of TB exposure

127
Q

Diagnosis of CSF:
Pressure 5-20
Normal appearance
0.18 - 0.45 g/L protein
2.5 - 3.5 mmol/L glucose
Normal gram stain
Glucose - CSF to serum: 0.6
WCC <3

A

Normal CSF

128
Q

Diagnosis of CSF:
Pressure >30
Turbid appearance
> 1 g/L protein
> 2.2 mmol/L glucose
Gram stain positive
Glucose - CSF to serum: < 0.4
WCC >500
90% PMN

A

Bacterial meningitis

129
Q

Diagnosis of CSF:
Pressure: normal or mild increase (5-20 or min above)
Clear appearance
< 1 g/L protein
2.5 - 3.5 (normal) mmol/L glucose
Gram stain Normal
Glucose - CSF to serum: >0.6
WCC <1000
Monocytes
10% have >90% PMN
30% have >50% PMN

A

Viral meningitis

130
Q

Diagnosis of CSF:
Pressure: normal or mild increase (5-20 or min above)
Clear or fibrin web appearance
0.1 - 0.5 g/L protein
1.6-2.5 mmol/L glucose
Gram stain normal
Glucose - CSF to serum: < 0.4
WCC 100 - 500
Monocytes

A

Fungal meningitis

131
Q

Diagnosis: CSF slightly increased raised pressure, pleocytosis 25-500 with lymphocytic predominance, decreased glucose (20-40), increased protein, no growth on culture in patient with history of HIV who just started antiretrovirals?

A

TB meningitis

132
Q

Diagnosis: hydrophobia or aerophobia (spasm from stimulus), agitation, changes in mentation, autonomic dysfunction, increased DTR, nuchal rigidity, + Babinski sign, tachypnea, tachycardia, fever -> hyperactivity

A

Rabies from rhabdovirus (peripheral nervous system to central to encephalomyelitis then back to peripheral nerves)

133
Q

50-70% of meningitis after skull fracture are due to what organism?

A

Strep pneumoniae

134
Q

Does prophylactic antibiotics after CSF rhinorrhea decrease the risk of meningitis?

A

No

135
Q

Location of CVA causing dysphagia, dysarthria, nystagmus, right-sided horners syndrome, ipsilateral ataxia and loss of gag reflex with contralateral loss of pain and temperature

A

Posterior inferior cerebellar causing right-sided lateral medullary syndrome - Wallenberg syndrome
9th and 10th cranial nerves, sympathetic and spinocerebellar tract affects
Crossed signs

136
Q

What causes sudden lower extremity weakness, sensory deficit, episodic hypertension, profuse sweating, CSF with pleocytosis and elevated IgG, with MRI with local cord swellling?

A

Transverse Myelitis
Idiopathic (60%), other causes: viral infection (Herpes), immune system disorders (neuromyelitis optica) and demyelinating diseases (MS)
MC thoracic region

137
Q

What kind of paraplegia is copper deficiency and adrenoleukodytrophy associated with?

A

Spastic paraplegia

138
Q

What is albuminocytologic dissociation is characteristic of what disorder? What is it?

A

Guillain-Barre Syndrome
CSF has elevated protein and normal cell count

139
Q

What guarantees poor functional outcome or death if a patient is not cooled after cardiac arrest?

A
  1. Absent pupillary or corneal reflexes on day 3 (but not before)
  2. Bilateral extensor posturing or absent motor responses on day 3 (but not before)
  3. Myoclonus status epilepticus within 24 hours
  4. Serum NSE >33 on days 1-3
  5. Somatosensory evoked potentials (SSEPs) showing bilaterally absent negative responses 20 ms after stimulation (N20) on days 1-3
    Day 1: No brainstem reflexes = :(
    Day 1: Myoclonus status epilepticus = :(
    Day 1-3: Serum NSE > 33 = :(
    Day 3: Absent pupil or corneal reflexes; extensor or absent motor response = :(
    Day 1-3: SSEP absent N20 responses = :(
140
Q

When patients have hypothermia after cardiac arrest, what can NOT be used to provide prognostication?

A
  1. Motor examination
  2. Serum NSE
  3. Early myoclonus
  4. Corneal reflexes
  5. Myoclonus status
141
Q

When patients have hypothermia after cardiac arrest, what CAN still be used to provide prognostication?

A

SSEPs once rewarmed
Possibly bilaterally absent N20 on SSEPs, unreactive EEG or combination of early myoclonus and absent pupillary or corneal reflexes

142
Q

4 aspects of CAM-ICU

A
  1. Acute onset and fluctuating course
  2. Inattention
  3. Disorganized thinking
  4. Altered level of consciousness
143
Q

What can cause neuropsychiatric symptoms in the absence of focal motor deficits?

A

Acute infarct of the caudate nucleus

144
Q

An ischemic stroke where can cause receptive aphasia (fluent aphasia) and be misinterpreted as “confusion”?

A

Dominant left temporal lobe

145
Q

An ischemic stroke where can present with only altered mental status?

A

Thalamic lesion (even unilateral)

146
Q

What should be ordered with MRI if infection or neoplasm is on the differential?

A

Gadolinium

147
Q

Visual disturbances, seizures, headaches, altered mentation diagnosis and treatment?

A

PRES
Treatment: treat hypertension, tx seizures or coma
Stop immunosuppressants if trigger

148
Q

Mental deterioration, dementia, involuntary myoclonic jerks, anxiety, depression, OCD, psychosis, speech impairment, gait instability, lack of coordination diagnosis and treatment?

A

Creutzfeldt-Jakob Disease
Cause: prion
Treatment: none

149
Q

Confusion, seizures, speech difficulties, memory impairment, psychiatric manifestations with high atni-TPO or anti-M antibodies diagnosis and treatment?

A

SREAT (Steroid-responsive encephalopathy associated with autoimmune thyroiditis)
Treatment: steroids (like all steroid responsive encephalopathies), IvIg and Plasmapheresis
MRI: non enhancing MRI with increased intensity of T2 and fast fluid-attenuated inversion recovery (FLAIR) imaging in the white matter as well as dural enhancement

150
Q

What’s wrong with the “ICP” tracing?

A

P2 higher than P1 is a sign of problems with intracranial compliance and risk of elevated ICPs

151
Q

MRI findings in acute ischemic stroke

A

Hyperacute (24 hrs) and Acute (24 hours to 1 week)
1. DWI - focal area of restricted diffusion (high signal)
2. ADC - focal area of low intensity

Subacute and chronic
Hyperintense DWI - T2 shine through
ADC - moves from hypointense to hyperintense

152
Q

Adderall reacts with MAOIs (phenelzine), serotonergic meds (venlafaxine and amitryptiline, opiates, dextromethorphan, buspiron, lituium, LSD) and CyP2D6 inhibitors (bupropion, fluoxetine, paroxetine, terbinafine, methadone, levomepromazine, citalopram, quinidine) how?

A

MAOI: hypertensive crisis
Serotonergic meds: serotonin syndrome
CyP2D6 inhibitors: serotonin syndrome

153
Q

Diagnosis and treatment: seizures, behavioral changes with fevers in patient with HIV (CT hypodense with surrounding edema, MRI iso-hypointense on T1 and hypo to hyperintense on T2)

A

Cerebral toxoplasmosis
Treatment: sulfadizine (1000-1500 mg QID) + pyrimethamine (200 mg loading then 50-75 mg daily) + leucovorin (10-25 mg daily)
Alternative to sulfadiazine = clindamycin (600 mg IV or oral QID) + pyrimethamine (200 mg loading then 50-75 mg QID) + PO leucovorin
Alternative: atovaquone (1500 mg PO BID) + pyrimethamine (200 mg loaind then 50-75 mg daily) + leucovorin (10-25 mg daily)

154
Q

Drugs or other etiologies that can cause acute ophthalmoplegia, areflexia and ataxia with preceeding bacterial or viral illness? Can involve cranial nerves causing facial oculomotor or bulbar weakness that can extend to limbs, distal hyporeflexia, focal paresis, loss of light and vibratory sense in distal extremities with autonomic dysfunction? What is the diagnosis and treatment?

A

Heroine, suramin, streptokinase, isotretinoin, TNF-alpha antagonists (ex: adalimumab), autoimmune diseases (ex: RA)
Miller-Fisher Syndrome (variant of GBS)
Treatment: IvIg, plasmapheresis
Corticosteroids are not effective

155
Q

What tau level is diagnostic of CJD?

A

1150 pg/mL

156
Q

Source of ischemic stroke in patients with hereditary hemorrhagic telangiectasia with bubble study positive after 3 cardiac cycles? What if less than 3 cycles?

A

At least 3 cycles: DVT through pulmonary AV malformation
Before 3 cycles: DVT through PFO

157
Q

Where does dexmedetomidine bind?

A

Alpha-2 receptors

158
Q

What drug do the following conditions and drugs make people more resistant to?
- CP, burn injuries, hemiplegia, peripheral nerve injuries, chronic infections of botulism and tetanus
- Anticonvulsants: valproic acid and carbamazepine, anticholinesterase inhibitors: neostigmine and pyridostigmine

A

Nondepolarizing neuromuscular blockers (ex: rocuronium, pancuronium, vecuronium, atricurium)

159
Q

Complication after LP causing cauda equina syndrome? Treatment?

A

Epidural hematoma
Surgical decompression within 48 hours

160
Q

Corticospinal tract injury causes what?

A

Spastic paresis below injury

161
Q

Spinothalamic tract injury causes what?

A

Loss of temp and pain contralaterally

162
Q

Interruption of a sympathetic pathway in Brown-Sequard syndrome can cause what? (Ex: posterior stab wound to neck with hemitransection of cord)

A

Horners syndrome (ptosis, miosis and anhydrosis)

163
Q

Which arteries supply the nucleus responsible for vestibuloocular reflex (doll’s eyes)?

A

Anterior inferior cerebellar artery and posterior inferior cerebellar artery supply the vestibular nucleus in brainstem
Vestibulo-ocular reflex: moving head to left -> otoliths in semicircular canal of ear -> L vestibular N to vestibular nucleus -> activate contralateral nerve of eye: oculomotor, abducent and trochlear)

164
Q

What positioning do you put patients with pneumocephalus in?

A

30 degree Fowler position

165
Q

Which antibiotic can lead to neuromuscular blockade with impaired ventilation, acute respiratory failure, seizures, coma and death especially when administered with concomitant neuromuscular blocking agents? Treatment?

A

Gentamycin
Treatment: calcium

166
Q

Treatment of rhinoorbital cerebral mucormyocosis

A

Amphotericin B and surgical debridement (and reverse immunosuppressed state)

167
Q

What causes man in a barrel syndrome?

A

Watershed infarcts of zones between anterior and middle cerebral artery distributions

168
Q

Cause of internuclear ophthalmoplegia?

A

Lesion in the medial longitudinal fasciculus (CN III and VI)

169
Q

Cause of ipsilateral fixed and dilated pupil?

A

Edinger-Westphal nucleus lesion(parasympathetic efferent of the eye)

170
Q

Cause of down and out gaze, ptosis and absent light reflex?

A

CN III lesion

171
Q

Cause of palsy of the superior oblique muscle of the eye

A

Trochlear nerve lesion

172
Q

What is the frequency of the breach rhythm?

A

6-11 Hz mixed with waves of higher and lower frequencies, including beta, mu or theta activity
Can be high amplitude spiky or sharply contoured activity similar to epileptiform activity, pure breach rhythms do not have an after-going slow wave and doesn’t spread to rest of brain
Sleep recordings can differentiate between breach rhythm and epileptiform activity (breach can affect both sleep and wake sleep rhythms)

173
Q

Causes of hyperdensities in dentate nucleus of cerebellum

A

INH
Flagyl
Metabolic disorders: maple syrup urine disease, canavan’s disease, glutaric-aciduria-type-1

174
Q

Transfuse for eptifibatide bleeding?

A

DDAVP
Cryo

175
Q

What happens when merrem and valproic acid are taken together?

A

Decreased valproic serum concentrations

176
Q

what can be used to temporize an aneurysm in SAH until it can be clipped?

A

TXA or amicar
Limit risk of rebleeding

177
Q

What medication for intubation causes fatal side effects in the neuro ICU?

A

Succinylcholine - fatal hyperkalemia in patients with neuromuscular disorders, prolonged immobilization or issues with spinal cord
Short acting, depolarizing paralytic

178
Q

Fever, thrombocytopenia, microangiopathic hemolytic anemia (shistocytes), neurologic symptoms and renal insufficiency diagnosis and treatment

A

TTP
Plasma exchange until platelet count normalizes
Refractory cases: rituximab

179
Q

Dysautonomia with CSF with albuminocytologic dissocation diagnosis and treatment?

A

Guillain Barre Syndrome
Plasma exchange, IvIg

180
Q

Diagnosis of neurologic changes with Horner’s syndrome during CEA

A

Carotid dissection

181
Q

What reflex can you skip during the brain death exam and still declare the patient brain dead?

A

Oculocephalic reflex IF oculovestibular reflex is absent

182
Q

Treatment of nonthyroidal illness?

A

Continue current care

183
Q

Treatment of sinking flap syndrome

A

Clamp VP shunt
Trendelenburg position
Hydration
Stop hyperosmolar therapy
Need to raise ICP to counteract external atmospheric pressure and herniation

184
Q

Treatment of CAR T-cell therapy neurotoxicity

A

High-dose glucocorticoids (dexamethasone)
Can add acetazolamide to reduce elevated ICP (or other methods to reduce ICP) and control cerebral edema

185
Q

Signs of recovery despite post anoxic myoclonus on EEG?

A

EEG reactivity
Time-locked midline-maximal spines over a continuous background

186
Q

Thunderclap headaches with or without other symptoms with segmental constriction of cerebral arteries? Diagnosis and time to resolution? What can they have? Treatment?

A

Reversible Cerebral Vasoconstriction syndrome (aka: postpartum angiopathy, migrainous vasospasm, drug-induced crebral vasculopathy or benign angiopaty of the central nervous system)
Resolves in 3 months
Associations: Unruptured aneurysms and convexity/sulcal SAH
Treatment: calcium channel blockers (resolves)

187
Q

Mirgrains with aura, relapsing TIAs and ischemic strokes with subcortical infarcts, psychiatric symptoms, gradual cognitive impairment to severe dementia with leukoencephalopathy diagnosis? Most common cause of what? Gene involved?

A

Cerebral Autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)
MC cause of stroke in adults younger than 65
NOTCH3 gene on chromosome 19

188
Q

Ischemic strokes and hemorrhagic strokes, seizures, headaches and cognitive impairment diagnosis and vessels involved and treatment?

A

Moyamoya disease (disease = bilateral, syndrome = can be unilateral)
Terminal portion of ICA and associated abnormal vascular network at base of the brain
Treatment: ASA (prevent stroke but no evidence this helps), surgical revascularization

189
Q

How does ketamine raise BP?

A

Antagonist of NMDA receptor (avoid in patients that have uncontrolled hypertension)

190
Q

Drowsiness, encephalopathy, ocular changes, and renal failure with severe anion-gap metabolic acidosis diagnosis and etiology of toxicity? Antidote and treatment if evidence of end organ damage?

A

Methanol toxicity
Methanol metabolized into formaldehyde to formic acid and formate causes elevated anion gap with neurologic, renal and ocular toxicity
Fomepizol (works for ethylene glycol also)
End-organ damage = add HD

191
Q

What is contraindicated in TTP?

A

Platelet transfusion - increases risk of arterial thrombosis and mortality

192
Q

TTP versus ITP

A

Cause
ITP is an autoimmune disorder that occurs when the body produces antibodies that destroy platelets. TTP is caused by a deficiency in the enzyme ADAMTS13, which controls blood clotting.
Treatment
Corticosteroids and rituximab can be used to treat both ITP and TTP, but plasma exchange therapy (PEX) is the first-line treatment for TTP, while corticosteroids are the first-line treatment for ITP.

193
Q

Size cut off for observing post-catheter femoral pseudoaneurysms intervention? 1st line treatment? Treatment if complicated?

A

> 3 cm or growing on serial imaging (q1-2 weeks)
Treatment: US guided thrombin injection
Treatment if complicated (hemodynamic instability, expanding hematoma, neurovascular deficit, localized cellulitis or severe pain): open surgical repair

194
Q

What does amantadine do in TBI?

A

Improves rates of recovery in vegetative or minimally conscious states
The 2012 study “Placebo-controlled trial of amantadine for severe traumatic brain injury” concluded that amantadine increases the rate of recovery after severe TBI in patients in a vegetative or minimally conscious state. The 2018 Guidelines on Disorders of Consciousness recommend amantadine 100-200 mg bid started 4-16 weeks post-injury. Some early observational studies showed improvement in Disability Rating Scale in patients treated with amantadine, but significant improvement in final functional outcome has yet to be confirmed in a randomized controlled trial.

195
Q

Rescue ICP and DECRA takehome

A

Rescue ICP and DECRA demonstrated that early surgical intervention did not improve outcomes or mortality, though ICP was controlled. The better approach was to use the medical management of ICP for as long as possible (randomized to early (less than 72 hours) versus late (greater than 72 hours)). Once ICP’s became refractory to conservative medical management, a large frontotemporal decompressive craniectomy was recommended both for ICP control and improvement of outcomes.
Level IIA–to improve mortality and overall outcomes
1. NEW–Secondary DC performed for late refractory ICP elevation is recommended to improve mortality and favorable outcomes.
2. NEW–Secondary DC performed for early refractory ICP elevation is not recommended to improve mortality and favorable outcomes†.
3. A large frontotemporoparietal DC (not less than 12 × 15 cm or 15 cm in diameter) is recommended over a small frontotemporoparietal DC for reduced mortality and improved neurological outcomes in patients with severe TBI.

196
Q

SMART trial takehome

A

The SMART trial demonstrated improved outcomes in the general ICU population when treated with a balanced solution compared with NaCl 0.9%.

197
Q

Locked-in syndrome injury location, cause, characteristics?

A

The locked-in syndrome is caused by an insult to the ventral pons, most commonly an infarct, hemorrhage, or trauma. The characteristics of the syndrome are quadriplegia and anarthria with preservation of consciousness. Patients retain vertical eye movement and upper eyelid function, facilitating non-verbal communication.

198
Q

Data on ICP and PbtO2?

A

More studies are needed to fully evaluate the safety as well as efficacy of treatment-directed protocols based on both ICP and PbtO2 as compared to ICP monitoring and treatment alone.

199
Q

SUP-ICU and PEPTIC trial takehome

A

The SUP-ICU Trial is a multi-national, randomized trial comparing pantoprazole vs placebo in critically ill patients in the ICU. The trial concluded that among adult patients in the ICU who were at risk for gastrointestinal bleeding, mortality at 90 days and the number of clinically important events were similar in those assigned to pantoprazole and those assigned to placebo.

The PEPTIC trial investigated the comparative efficacy of pantoprazole versus H2 blockers in mechanically ventilated critically ill patients and did not find a significant difference in any of the outcomes studied.

200
Q

Data on BP management post-thrombectomy for acute ischemic stroke with large vessel occlusion

A

Neither AHA/ASA and NCS have any statements or guidelines with definite guidance on the issue of post-thrombectomy blood pressure management. While the optimal BP targets remain uncertain some guidance can be found in emergent thrombectomy trials. In a single-center analysis of 217 patients who underwent thrombectomy, a 10-mmHg increment in maximum SBP during the first 24 hours post-thrombectomy was associated with a lower likelihood of functional independence and a higher likelihood of mortality at 3 months. In the MR CLEAN Trial, higher baseline SBP was associated with a higher risk of symptomatic intracranial hemorrhage, the investigators also found a U-shaped association because both low and high baseline SBP was associated with poor functional outcome. Therefore, in the setting of a successful thrombectomy with TICI 3, it is most reasonable to keep the SBP between 140-160.

201
Q

Treatment of BP after rtPA

A

The current 2019 AHA/ASA Acute Ischemic Stroke guideline recommends that BP be <185 mm Hg systolic and <110 mm Hg diastolic before treatment with alteplase and <180/105 mm Hg for the first 24 hours after treatment

202
Q

Mechanism of clopidogrel

A

ADP/P2Y12 irreversible inhibitor
Hepatic metabolism to active drug and clearance
Poor metabolizers exist

203
Q

the Salzburg criteria to diagnose non-convulsive status epilepticus

A

EEG should demonstrate
(1) more than 25 epileptiform discharges (ED) per 10-second epoch, i.e., >2.5/s
(2) patients with EDs ≤ 2.5/s or rhythmic delta/theta activity (RDT) exceeding 0.5/s
AND at least one of the additional criteria:
(3a) clinical and EEG improvements from antiepileptic drugs (AEDs)
(3b) subtle clinical phenomena
(3c) typical spatiotemporal evolution

204
Q

Weight loss, cough, lymphadenopathy, joint pain, altered mental status with PRES electrolyte abnormality?

A

Hypercalcemia (sarcoidosis with PRES)

205
Q

Diagnosis hyporeninemic hypoaldosertonism with hyperkalemia, metabolic acidosis and acidic urine and cause?

A

Type 4 RTA can be caused by diabetic nephropathy and medications: heparin and heparin analogs, spironolactone

206
Q

What antiepileptic can cause pancytopenia rarely?

A

Levetiracetam

207
Q

Reversal of warfarin bleeding?

A

PCC (superior to FFP) and vitamin K

208
Q

Electrolyte abnormalities in tumor lysis syndrome

A

HYPOcalcemia
Hyperkalemia, hyperphosphatemia, hyperuricemia

209
Q

Intervention for this disease?

A

Moyamoya disease
Endovascular stenting contraindicated - rapid restenosis
Superficial temporal artery bypass to MCA (EC-IC bupass)

210
Q

PATCH trial

A

Platelet transfusion in Cerebral Hemorrhage - platelet transfusion inferior to standard care for patients on antiplatelet therapy before ICH
More serious side effects during hospital course

211
Q

STICH trial

A

Surgical Trial in Intracerebral Hemorrhage
No benefit in surgical evacuation of ICH, early evacuation worse outcomes

212
Q

When should cerebellar hemorrhage have intervention?

A

Neurologic deterioration
Brainstem compression
Hydrocephalus from ventricular obstruction

213
Q

CLEAR III trial

A

Clot Lysis Evaluation of Accelerated Resolution of Intraventricular Hemorrahge III - RCT, double-blind, placebo-controlled, multiregional trial
IVH + EVD - intraventricular alteplase does not improve functional outcome at the modified Ranking Score (mRS) 3 versus irrigation with saline

214
Q

Diagnosis and at risk patients for CT with dilated cortical veins, cortical SAH, dense appearing cerebral sinus that becomes an empty delta sign with contrast? What is the treatment?

A

Cerebral venous thrombosis
Pregnancy
Other risks for venous thrombosis: hematologic, oncologic, autoimmune
Head trauma
Recent intrathecal or spinal procedures
Treatment: anticoagulation (heparin gtt)

215
Q

Diagnosis, affected nerves and treatment?

A

Carotid-cavernous fistula causing chemosis (fluid-buildup)
CN III and IV -> opthalmoplegia
Treatment: endovascular occlusion of fistula

216
Q

CADISS trial

A

Cervical Artery Dissection in stroke Study
Randomized, end-point blinded study
No different in efficacy of antiplatelet and anticoagulant drugs in preventing stroke and death in patients with symptomatic carotid and vertebral artery dissection
Coumadin contraindicated in pregnancya

217
Q

Dabigatran reversal

A

Idrucizumab

218
Q

Seizure prophylaxis in stoke patients?

A

No data

219
Q

Thunderclap headache diagnosis? Other names? Associations? Progression? Complications?

A

Reversible cerebral vasoconstriction syndrome
Pseudovasculitis
Associated with drugs, pregnancy and other headache types
Self-limited, may be complicated by seizures or cerebral ischemia

220
Q

Interventions for spinal cord infarction?

A

Placement of lumbar drain - reduces intrathecal pressure and allows for increased spinal cord perfusion
DO not lower MAP
Use distal bypass during surgery to restore cord perfusion in segments disrupted by grafting

221
Q
A

NCC (5 decks)

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