neuro critical care board review book – Flashcards
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localization of lesion causing cheyne-stokes respiration
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bihemispheric or diencephalic
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localization of lesion causing tachypnea hyperventilation
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midbrain
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localization of lesion causing apneustic breathing
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pons
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localization of lesion causing cluster respirations
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lower pons
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localization of lesion causing ataxic breathing
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medulla
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evidence of seizure activity to look for on exam of comatose patient
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tongue biting, urinary incontinence
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direction of tonic deviation of eyes in cold water calorics
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toward cold ear
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brain reason for midposition fixed pupils
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diffuse midbrain lesion or midbrain damage from transtentorial herniation, resulting in impairment of sympathetic and parasympathetic innervation.
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brain reason for pinpoint pupils
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pontine lesion, can also come from lesion above red nucleus due to disruption of sympathetic outflow
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localizing areas for gaze preference
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pons or frontal cortex
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relation btwn gaze preference and corticospinal tract damage
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patients look toward the side of hemiparesis
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gaze preference direction with frontal lobe lesion resulting in damage to motor strip
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patients look away from hemiparetic side
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localiization of skew deviation
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can localize to midbrain
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nature of periodic alternating gaze
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eyes deviate from side to side
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localization of periodic alternating gaze
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bilateral cerebral hemisphere dysfunction
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localization of lesion causing ocular bobbing
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can localize to pons
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labs to check on comatose pt
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lytes, cbc, ca, mg, NH3, drug levels, coags, glucose, ABG
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supportive measures for new comatose pt
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Thiamine 50-100 mg, glucose D50 (at least 25 ml) naloxone 1 ampule IV
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positive apnea test
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PaCO2 is above 60 with no spontaneous respirations
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caveat with apnea test
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chronic CO2 retainers may have false positives
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rate of increase of PaCO2 in apneic pt
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3-6 mmHg/min
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age up to which 2 confirmatory apnea tests are necessary
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2 months (separated by 48 h)
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age up to which one confirmatory apnea test is necessary
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one year (separate by 24 h)
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usual locations of hypertensive hemorrhages (5)
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deep locations: basal ganglia, subcortical white matter, cerebellum, thalamus, pons
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usual location of hemorrhage due to amyloid angiopathy
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lobar intraparenchymal
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things to watch for in intraparenchymal cerebral hemorrhage
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rebleed in 1st 12 h after sx, edema causing clinical deterioration btwn 24 and 72 h
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use of gradient echo sequence in question of hemorrhage
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may reveal silent hemorrhage in pts with amyloid or cavernous malformations
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target bp in people with intraparenchymal hemorrhages
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Below 120-130
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predictors of poor outcome in intraparenchymal hemorrhage
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volume less than 60 ml or GCS less than 8
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usual location for bleed in Moyamoya syndrome
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basal ganglia
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4 metastatic tumors that bleed easily
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renal cell, melanoma, lung cancer, choriocarcinoma
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usual location for venous hypertension and infarct
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usually cortical
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Terson's syndrome
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vitreal hemorrhage with SAH
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time by which CT findings normalize in SAH
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10% in day 3 and 50% by day 7
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type of SAH that has a more benign prognosis and is not associated with aneurysm
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perimesencephalic SAH
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Typical # of erythrocytes to leukocytes in traumatic tap
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750-1000:1
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protein per erythrocytes in traumatic tap
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1 mg/dl:1000 erythrocytes
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indication for angiography in SAH
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Non-traumatic SAH
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risk of rebleeding after SAH
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4% in 1st 24h, 1% daily thereafter for 1st 2 weeks
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risk of hydrocephalus in SAH
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20-25%
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timing of vasospasm after SAH
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4 to 14 days
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risk of vasospasm and resulting infarct in SAH
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50%, 15-20% with infarct
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effect of nimodipine on vasospasm
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reduces cerebral infarction rate due to vasospasm but doesn't affect incidence of vasospasm
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endovascular treatment for vasospasm
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angioplasty or intraarterial papaverine
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cardiovascular complications of SAH
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U waves, arrhythmia, myocardial stunning (possibly due to catecholamine surge)
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incidence of sz in SAH
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10-20%, more common if associated intracerebral hemorrhage
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timing and incidence of hyponatremia in SAH
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2-10 days after onset of sx, 10-30% of patients
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mortality rate of SAH
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30.00%
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% of population with an unruptured aneurysm
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3-5%
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% of population with multiple aneurysms
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20-30%
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location (anterior v posterior) of unruptured aneurysms
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90% in anterior circ, (acomm and pcomm are most common); 5-10% in posterior circ
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risk factors for aneurysm
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female, htn, smoking, stimulants, connective tissue disease, fam hx of 2 or more relatives, polycystic kidneys
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5 medical conditions predisposing to intracranial aneurysm
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aortic coarctation, pseudoxanthoma elasticum,ehler danlos type IV, marfan and NF
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common causes of symptoms in unruptured aneurysms
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compression and ischemic stroke
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patients with very low risk of aneurysm rupture
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anterior circulation aneurysm less than 7 mm with no previous hx of rupture
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% of aneurysms that are infectious in nature
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3.00%
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% of pts with infectious endocarditis who develop infectious aneurysms
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20-12%
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most common 2 bacteria in nfected aneurysms
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Strep (1), S. aureus
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best modality for finding aneurysms in head (esp infectious)
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conventional angiography
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risk factors for fusiform aneurysm
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smoking, htn, male, elderly
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most common location (anterior v posterior) for fusiform aneurysms
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posterior circulation
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range of cerebral perfusion pressure over which brain's autoregulation can compensate (ie, cerebral blood flow doesn't change)
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60-160 mmHg, but curve is shifted to the right with longstanding HTN
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nature of cytotoxic edema
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fluid accumulation within cells
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nature of vasogenic edema
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proteinaceous fluid leaks in extracellular space from capillaries
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formula for CBF
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CBF=CPP/CVR
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nl range for adult MAP
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70-110 mm Hg
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formula for MAP
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DBP + 1/3(SBP-DBP)
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nature of interstitial brain edema
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CSF pushed in extracellular space in periventricular white matter in hydrocephalus
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GCS score suggesting a need for ICP monitoring (if brain trauma is suspected)
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less than 8
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nature of plateau waves wrt ICP
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sudden surges in ICP to 50 to 80 mmHg lasting 5-20 minutes
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nature of B waves wrt ICP
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smaller surges in ICP to 20 mmHg for 1 to 2 minutes
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problem suggested by presence of A waves
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failing compliance of the brain to ICP and risk for ischemia
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usual cause of subfalcine herniation
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generally occurs with unilateral space-occupying mass in a cerebral hemisphere
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3 bad results of central (diencephalic) herniation
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Duret hemorrhages of brainstem, pituitary stalk shearing, and bilateral occipital infarctions from compression of posterior cerebral artery
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cause of Duret hemorrhages in diencephalic herniation
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shearing and traction on the basilar perforators and compression of their intramedullary portions
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usual forst sign of tentorial (uncal) herniation
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ipsilateral CNIII palsy
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result of upward cerebellar hemorrhage
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vermis can ascend rostral to tentorium cerebelli , compressing the midbrain and may compress the cerebral aqueduct
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nature of 20/30/40 rule
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vital capacity < 20 mL/kg, max inspiratory pressure - 30 cm H2O, max expiratory pressure 40 cm H2O
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antibody associated with miller-fisher variant of GBS
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Anti-GQ1b ganglioside
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2 variant forms of guillain-barre syndrome
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Miller-fisher and pharyngeal-cervical-brachial variants
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side effects of IviG
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aseptic meningitis, ARF, anaphylaxis, pseudohyponatremia
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lab abnormalities with plasma exchange
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hypocalcemia, thrombocytopenia, hypokalemia
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contraindications to plasma exchange
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septic shock, recent MI, marked dysautonomia, active bleeding
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usual course with GBS
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most patients plateau at 2 weeks and improve over months, most have a good outcome
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imaging modality for patients with acute spinal cord compression who cannot undergo MRI
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CT myelography
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general etiology of subdural hematoma
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trauma causing tearing of bridging veins traversing subdural space
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surgical indications for SAH
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symptomatic, blood more than 1 cm
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lab studies needed for SAH
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PT, INR, CBC, PTT
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usual etiology of epidural hematoma
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blunt skull trauma and injury to the middle meningeal artery (less common, venous sinus)
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most common location of epidural hematoma
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laterally over the cerebral hemisphere (temporal or temporoparietal)
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side of CNIII palsy with epidural hematoma
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ipsilateral (due to Kernohan's notch)
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% of patients with spinal cord injury who have more than 1 spinal cord segment involved
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20.00%
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% of neonates with bw less than 1500 g who have IVH
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20-40%
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usual timecourse of IVH in neonates
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in 1st 24 h, 90% within 1st 72 h postpartum
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efficacy of daily LP for IVH
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reduces immediately harmful effects of hemorrhage but doesn't have much effect on long-term stuff.
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% of kids with IVH for whom progession to hydrocephalus stops and sometimes resolves spontaneously
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50.00%
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neurologic disease for which hyperemesis gravidarum is a risk factor
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Wernicke's encephalopathy
