Neurologic Disorders Flashcards
1
Q
stroke syndromes;
- motor/sensory = upper body, facial droop
- visual = eyes deviate TOWARDS lesion
- other = receptive or expressive aphasia
A
MCA (anterior circulation)
2
Q
stroke syndromes;
- motor/sensory = lower body
- visual = n/a
- other = urinary incontinence, personality change
A
ACA (anterior circulation)
3
Q
stroke syndromes;
- motor/sensory = n/a
- visual = CONTRAlateral homonymous hemianopsia
- other = visual hallucinations
A
PCA (posterior circulation)
4
Q
stroke syndromes;
- motor/sensory = contralateral hemiplegia
- visual = IPSilateral CN 3 palsy (“down and out”), ipsilateral Horner’s syndrome
- other = mild contralateral gait disturbance
A
Weber’s (posterior circulation)
5
Q
stroke syndromes;
- motor/sensory = contralateral hemiplegia
- visual = IPSilateral CN 3 palsy (“down and out”), ipsilateral Horner’s syndrome
- other = severe contralateral gait disturbance
A
Benedikt’s (posterior circulation)
6
Q
stroke syndromes;
- motor/sensory = IPSilateral FACIAL sensory loss (CN 5), CONTRAlateral BODY sensory loss
- visual = ipsilateral Horner’s syndrome
- other = vertigo, ataxia, dysarthria, dysphagia
A
PICA (Wallenberg’s) (posterior circulation)
7
Q
in a patient w/ a previous stroke, what are the 2 most likely processes if there’s an abrupt worsening of symptoms?
A
- new stroke
- seizure from the stroke scar
8
Q
in acute ischemic stroke, the eyes tend to move in which direction?
A
TOWARD the stroke lesion
9
Q
in seizures, the eyes tend to move in which direction?
A
AWAY from the focus of the seizure
10
Q
which neurological condition could lead to the eyes deviating TOWARDS the seizure focus?
A
Todd’s paralysis
11
Q
what is the dosing for tPA for acute ischemic stroke?
A
0.9 mg/kg (up to a total dose of 90 mg) IV; divided into 10% bolus followed by 90% of the remaining dose infused over 60 minutes
12
Q
what are the 2 important points to d/w a patient about tPA for stroke?
A
- doesn’t change mortality, but increases likelihood of recovery to independence
- hemorrhage risk is slightly higher in patients who get tPA (< 7%) than those who don’t
13
Q
contraindications for tPA in acute ischemic stroke
A
- recent major surgery
- AC w/ INR > 1.7
- thrombocytopenia
- recent stroke or head trauma w/i 3 months
- GIB w/i 3 weeks
- uncontrollable HTN before administration
- h/o intracranial hemorrhage
14
Q
contraindications for tPA in acute ischemic stroke
A
- recent major surgery
- AC w/ INR > 1.7
- thrombocytopenia
- recent stroke or head trauma w/i 3 months
- GIB w/i 3 weeks
- uncontrollable HTN before administration
- h/o intracranial hemorrhage
15
Q
how to calculate NIH stroke scale
A
- level of consciousness
- ask month and age
- can blink eyes and squeeze hands
- horizontal EOM
- visual fields
- facial palsy
- UE motor drift
- LE motor drift
- limb ataxia
- sensation
- language/aphasia
- dysarthria
- extinction/inattention
16
Q
NIH stroke scale score range
A
0 to 42
17
Q
time window for tPA administration for acute ischemic stroke
A
w/i 3-4.5 hours from LSW
18
Q
SAH diagnosis
A
- acute-onset severe headache
- neck stiffness
- noncontrast CT scan
19
Q
when is LP done to diagnose SAH?
A
if CTH is negative but high clinical suspicion based on patient history
20
Q
most important early consideration in a patient diagnosed w/ SAH
A
identifying a vascular abnormality that could rebleed
21
Q
in a patient w/ SAH and a cerebral angiogram negative for aneurysm, what other imaging study should be performed?
A
MRI of the spine to check for spinal AVMs
22
Q
spinal AVMs can lead to neurological disability in what 2 ways?
A
- bleeding causing damage to the spinal cord or brainstem
- venous HTN from arterialization of the spinal draining veins which leads to spinal infarction
23
Q
what intervention has the best evidence of improving outcome in severe traumatic brain injury (TBI)?
A
prevention of hypotension
24
Q
what are some triggers of enzymatic dysfunction of urea cycle metabolism leading to hyperammonemia?
A
- infection
- severe exercise
- seizures
- dietary protein loading
- TPN
- drugs (abx, valproate, anti-TB meds)
25
what is the most common inborn error of metabolism affecting the urea cycle?
ornithine transcarbamylase deficiency
26
- evidence of cirrhosis at an early age
- Kayser-Fleisher rings
- disrupted copper metabolism leading to cirrhosis and neurologic injury
Wilson's disease
27
what AED can cause decompensation in patients w/ urea cycle enzymatic dysfunction and CI?
valproate
28
medication and dose that is MOST successful at both stopping convulsions in the first 20 minutes and preventing the recurrence of status epilepticus?
lorazepam 0.1 mg/kg iv
29
what paralytic is contraindicated in patients w/ chronic hemiplegia or chronically bed-bound patients and why?
- succinylcholine
- potential for massive hyperkalemia and arrhythmias
30
depolarizing paralytic agents
succinylcholine
31
- fast-acting
- nondepolarizing paralytic
- relatively long half-life; approximately 45 minutes
rocuronium
32
what is a common feature in the first 72 hours in patients w/ ICH, and is more frequent in patients w/ ICH who have intraventricular extension?
fever
33
what is the cause of fever in approximately half of the patients in the neurological ICU?
noninfectious
34
what lab test might assist in the diagnosis of infection and deescalation or discontinuation of abx w/ suspected infection, especially PNA?
procalcitonin, however, brain injury is a/w elevated procalcitonin levels which may complicate its application
35
autoimmune paraneoplastic syndrome often lead to what?
- severe encephalopathy
- seizures
- eventually death
36
the most common precipitating illness for autoimmune paraneoplastic syndrome is
small cell lung cancer (SCLC)
37
benign ovarian and testicular teratomas are a/w what syndrome?
anti-NMDA receptor encephalitis syndrome
38
opsoclonus-myoclonus is most commonly a/w
SCLC in older patients
39
retinal blindness is typically a/w
breast cancer
40
Lambert-Eaton myasthenic syndrome (LEMS) is often a/w
SCLC but can be a/w breast cancer and lymphosarcoma
41
anti-NMDA receptor encephalitis syndrome is a unique paraneoplastic syndrome for what reasons?
- atypical presentation
- initially manifest w/ paranoia and psychosis followed by progressive encephalopathy and seizures until 1 of 3 things happens:
- patient is treated
- syndrome resolves spontaneously
- patient succumbs
- most commonly seen in young adults
- majority of patients are found to have nonmalignant disease
42
treatment for all paraneoplastic syndromes
- plasmapheresis or IVIG
- followed by suppression of immune response w/ immunomodulatory medications
43
what is the most common neurological syndrome found in the critical care setting?
delirium
44
delirium, by definition, is what type of encephalopathy?
- not a/w an identifiable cause, and
- is a diagnosis of exclusion
45
what are patient-inherent factors that are significant risk factors for delirium?
- age
- dementia
- previous episodes of delirium
46
what are extrinsic risk factors for delirium?
- lack of sleep-wake cycle regulation
- medications (including γ-aminobutyric acid agonists such as benzodiazepines)
- immobility
47
delirium is defined as
- confusion
- waxing and waning course
- periods of agitation or withdrawal
48
clinical trials and quality initiatives have attempted to address preventing delirium in susceptible patients w/ what interventions?
- early mobility
- sleep hygiene
- activities
- limiting benzodiazepines
- limiting sleep-disrupting interventions
- are only marginally successful
49
what pharmacological interventions have been shown to improve patients w/ delirium?
none
50
treatment for delirium w/ agitation
behavior control
51
treatment for delirium w/ withdrawal
??? (few interventions tested)
52
what does the term "completed stroke" mean?
- old term that shouldn't really be used anymore
- usually signifies a focal neurological disability that came on abruptly and has become stabilized; 18-24 hours if the lesion is in the carotid system, and up to 72 hours if in vertebral-basilar system
- others use the term to mean that all the deficit that is to occur has already accrued
- others have used the term to imply that all the deficit possible in a given vascular territory is already present
53
based on the DAWN and DIFUSE-3 trials, if a patient has a LVO in the IC or MCA, and little evidence of a "completed stroke," patients outside the 3 and 4.5 hour windows for tPa should be evaluated for what?
mechanical thrombectomy
54
how are stroke patients evaluated for thrombectomy?
proprietary software (RAPID) that calculates the percentage of the entire affected vessel occlusion field that is involved BUT not yet infarcted (brain at risk)
55
in both the DAWN and DIFUSE-3 trials, both MR and CT angiography were accepted, and required LVO for enrollment; patients need to have what on CT perfusion scan or MR diffusion scan before thrombectomy?
significant mismatch between occluded vessel territory and brain infarction
56
the INTERACT 2 trial found what regarding patients w/ ICH w/ ventricular extension?
target SBP < 140 mm Hg was a/w lower rate of hematoma expansion and modestly improved neurologic outcomes, but no improvement in the primary outcome of combined mortality and major disability
57
the ATACH 2 trial demonstrated what regarding patients w/ ICH w/ ventricular extension?
no improvement in neurologic outcome w/ more aggressive treatment of SBP < 120 mm Hg, but a/w 2x worsening renal function
58
what did the PATCH trial demonstrate regarding patient on an antiplatelet medication that p/w supratentorial ICH?
- platelet transfusion did not improve neurological outcomes at 3 months
- higher odds of death or dependency in platelet transfusion group
59
ICH w/ intraventricular blood is a/w a high mortality rate and severe disability d/t what mechanisms?
- excitatory neurotoxicity
- acute hydrocephalus
60
in the CLEAR III trial, intraventricular alteplase or saline administered through a previously inserted EVD in patients w/ ICH and ventricular blood w/ 3rd or 4th ventricle obstruction showed what?
no improvement in survival
61
autoimmune syndrome that attacks the myelin covering the neurons of the peripheral nervous system
Guillain-Barré syndrome (GBS)
62
Guillain-Barré syndrome (GBS) is often preceded by what?
- prodromal viral infection, or
- prodromal Campylobacter infection
63
what are the 2 variants of Guillain-Barré syndrome (GBS)?
- AXONAL variant that manifests w/ a similar progression as a typical demyelinating disease
- Miller Fisher variant is a/w early CRANIAL nerve dysfunction and respiratory failure
64
which variant of Guillain-Barré syndrome (GBS) is more amenable to treatment?
the demyelinating syndrome
65
how does the axonal variant w/ demyelinating disease typically present?
- ascending paralysis
- sensory loss
- affects the most distal nerve territories first then progresses more proximally
66
in the worst cases, Guillain-Barré syndrome (GBS) can lead to
complete paralysis, including all of the cranial nerves
67
what are the typical treatments for Guillain-Barré syndrome (GBS)?
- IVIG
- plasmapheresis
68
what happens when you treat Guillain-Barré syndrome (GBS)?
typically stops progression of damage, but recovery is limited by the speed at which nerves can remyelinate or grow depending on the mechanism
69
in the axonal variant of Guillain-Barré syndrome (GBS), how long can recovery take?
can be as long as 2-4 years; the time it takes to regrow peripheral nerves
70
mortality in Guillain-Barré syndrome (GBS) is almost entirely d/t medical complications a/w severe paralysis; what is one complication that is directly related to the disease?
autonomic insufficiency
71
in severe cases of Guillain-Barré syndrome (GBS), the autonomic nerves can be denervated (particularly but not exclusively in patients w/ the axonal variant); this manifests how clinically?
- hypotension
- bradycardia
- hypothermia
- constipation
72
in Guillain-Barré syndrome (GBS), the presence of dysautonomia has what effect on mortality?
3x motality
73
what are the most likely causes of death in patients w/ Guillain-Barré syndrome (GBS)?
- arrhythmias
- profound hypotension
- infections
74
what treatments may be used for hypotension d/t dysautonomia from Guillain-Barré syndrome (GBS)?
- mineralocorticoid = fludrocortisone
- α-agonist = midodrine
75
if nerve dysfunction from Guillain-Barré syndrome (GBS) is severe enough to functionally denervate the heart, what medication will not help w/ bradycardia?
atropine
76
some patients w/ Guillain-Barré syndrome (GBS) develop a forme fruste of autonomic denervation that leads to what?
wild shifts in BP and HR as autonomic nerves intermittently respond to stimuli
77
in patients w/ aneurysmal SAH and AMS most likely d/t hyponatremia, what is the next best step?
hypertonic saline
78
in patients w/ hyponatremia in the period of delayed cerebral ischemia (DCI or vasospasm), even in patients thought to have SIADH, what should be avoided and why?
- fluid restriction
- worsens outcomes
79
should albumin infusion be given in patients w/ delayed cerebral ischemia (DCI or vasospasm)?
no, no clear evidence of benefit
80
patients w/ aneurysmal SAH classically p/w
- headache
- LOC
- stroke symptoms
81
what 2 grading systems are used to stratify patients w/ SAH?
- Hunt/Hess grade
- modified Fisher scale
82
the Hunt/Hess grades predicts what?
outcome after SAH
83
the modified Fisher scale predicts what and how?
uses the amount of hemorrhage and the presence of intraventricular blood to predict which patients will develop DCI (vasospasm)
84
management of SAH after securing the aneurysm
largely reactive
85
what is the ddx of AMS in a patient w/ SAH after securing the aneurysm?
- rebleeding from the aneurysm (less likely after successful coiling)
- hydrocephalus
- seizures
- fever
- meningitis (for patients w/ an EVD or who have surgical clipping)
- hyponatremia
- DCI (vasospasm)
86
DCI (vasospasm) after SAH can lead to stroke or long-term cognitive deficits and usually occurs w/i what timeline?
5 to 14 days after hemorrhage
87
in a patient w/ SAH, does successful vasodilation of arteries in spasm improve outcomes?
no, suggesting spasm isn't the only mechanism of damage
88
what is known to lead to stroke in the setting of DCI (vasospasm)?
volume depletion
89
what is the only therapy that treats hyponatremia from both cerebral salt wasting and SIADH in the setting of post-SAH?
hypertonic saline solutions
90
what is the most severe consequence of cerebral edema after brain injury?
brain herniation
91
in large ischemic strokes that occupy > 50% of the territory of a hemisphere, herniation in the first 48-72 hours is likely d/t what?
cerebral edema in the damaged brain
92
why does cerebral edema lead to herniation syndromes?
the calvarium is a fixed structure that limits the amount of volume that can be accomodated (Monro-Kellie principle)
93
there is only room in the calvarium for what compartments?
- brain
- blood
- CSF
94
treatments to alleviate herniation syndromes have the goal of decreasing ≥ 1 compartments; what 2 treatments are used to decrease blood flow to the brain?
- induced hyperventilation --> alkalosis --> alkalization of CSF --> smooth muscle contraction and vasoconstriction by neurovascular unit modulation (brain control of blood vessels)
- systemic cooling --> decreases metabolic demand of the brain --> decreases blood flow (through the neurovascular unit)
95
can hyperventilation lead to brain ischemia and how?
- yes, it's a potential side effect
- blood flow by this mechanism is not paired to decreased metabolism
96
when is ischemia d/t hyperventilation most commonly seen?
when PCO2 levels are < 20 mm Hg
97
can systemic cooling lead to brain ischemia?
no, because metabolic demand drives blood flow
98
how do mannitol and hypertonic saline act to reduce cerebral edema?
increases tonicity of blood --> drives water from the lower tonic environment of the brain to the blood --> excess volume can then be transported out of the brain
99
can brain water removal w/ mannitol or hypertonic saline cause ischemia?
no, does not impair O2 delivery
100
what is the only treatment used acutely to decrease CSF in a patient w/ cerebral edema?
EVD or lumbar drain
101
can ischemia occur in a patient w/ cerebral edema that has an EVD or lumbar drain?
no, they do not impede blood flow or substrate delivery
102
what is the pathophysiology of SDH?
rupture of bridging veins that traverse the subdural space as they drain the cerebral and/or cerebellar cortex to veins in the skull; as people get older and their brains atrophy, the length of the bridging veins increases and are more prone to damage
103
what is the most common cause of SDH?
mild trauma w/ or w/o coagulopathy
104
can spontaneous SDH occur in patients w/ coagulopathies?
yes, w/ warfarin being the most common
105
because SDH is a venous bleeding syndrome, the collection of blood can occur over what time period?
weeks
106
symptoms from SDH occur because of 3 separate processes; what are they?
- blood in the subdural space can irritate the brain leading to cognitive decline and delirium
- as the blood collection occupies more space, it compresses adjacent brain regions leading to focal neurologic symptoms
- SDH can lead to seizures
107
the presentation of subdural blood on CT scan changes over time; what are these changes?
- initially, bright (because of [Ca++] in blood collection)
- transition period, from bright to dark, isodense w/ brain parenchyma
- over time, hypodense as blood degrades (same density as CSF)
108
treatment of small SDH w/o significant mass effect
conservatively w/o surgery
109
treatment of larger SDH and more symptomatic hemorrhages
surgery
- if fresh clot that forms a solid rind = open neurosurgery
- if chronic SDH which liquifies = burr hole and catheter-based drainage
110
treatment for symptomatic SDH w/ large mass effect
surgery
111
patients w/ severe traumatic brain injury (defined as GCS of ≤ 8) should receive what ppx?
phenytoin x 7 days posttrauma to reduce the incidence of early posttraumatic seizures
112
what is a/w worse neurologic outcomes at 3 and 6 months and why?
- prophylactic hyperventilation
- hyperventilation-induced reduction in brain blood flow worsening cerebral ischemic injury
113
in patients w/ severe TBI and elevated ICP, what intervention is a/w worse neurologic outcome at 6 months?
cooling to 32°C to 35°C
114
the CRASH trial showed what in patients w/ severe TBI?
- risk of death at 2 weeks was higher in the methylprednisolone group
- risk of death and death or severe severe disability at 6 months was higher in the methylprednisolone group
115
what are some myths regarding critically ill patients in a coma in the ICU?
- patients in coma do not sense anything in
the environment; some patients likely have
no environmental awareness, but predicting
which patients is not reliably possible
- patients in a coma remember events from
the time when they are unconscious; most
patients w/ altered consciousness claim not
to remember anything of their ICU stay; there
are very few cases of patients under sedation
or anesthesia who are awake and aware of
what is going on around them, but this is rare
and relegated to patients w/o brain injury
- patients in a coma proceed to brain death;
not all patients in a coma proceed to brain
death
116
what is the most common cause of poor responsiveness in the ICU?
oversedation
117
what 2 syndromes are occasionally confused w/ coma?
- locked-in state
- catatonia
118
locked-in state is characterized as
- patient is fully awake and aware
- cannot respond to environment d/t dysfunction of ventral brainstem (not the reticular activating system but the motor output of the brainstem)
119
typically, how can patients w/ locked-in state show that they can follow commands?
eye movement (often upward gaze)
120
catatonia is characterized as
- patients are unable to respond to the environment
- might have abnormal postures
- oscillates w/ other behaviors
121
what is one of the most common methods for assessing delirium in the ICU in conscious patients?
Confusion Assessment Method ICU (CAM-ICU) test
122
the CAM-ICU test cannot be performed on which patients?
unconscious patients
123
the MIND-USA trial showed what regarding
all patients w/ delirium?
neither haloperidol nor ziprasidone was
better than placebo for the treatment of
delirium in the ICU
124
multiple studies of dexmedetomidine vs benzodiazepines have suggested what for patients in the ICU?
- possibility of briefer duration of MV
- no improvement in cognitive impairment or survival
125
studies of daily awakening trials have suggested what for patients in the ICU?
improve duration of MV and survival
126
do daily awakening trials lead to increased incidence of airway injury or unplanned extubation?
no
127
if no CIs, what is the time cutoff for tPa in a patient that p/w ischemic stroke?
- 4.5 hours
- 3 hours if > 80 yoa
128
intracytoplasmic protein that can abnormally aggregate in various cells in the CNS
α-synuclein
129
clinical entity resulting from accumulation of α-synuclein in the substantia nigra and striatonigral tract
Parkinson's disease
130
clinical entity resulting from diffuse accumulation of α-synuclein at onset
dementia w/ Lewy bodies
131
what clinical entities fall w/i the spectrum of multiple system atrophy (MSA) as a result of deposition of α-synuclein?
- olivopontocerebellar atrophy
- striatonigral degeneration
- Shy-Drager syndrome
132
the clinical spectrum of disease caused by accumulation of α-synuclein includes
- hypokinetic movement d/o's
- dementia
- dysautonomia
133
- classically reported in elderly patients
- elevated BP
- hyperthermia
apathetic thyrotoxicosis
134
- chromaffin cells of the sympathetic nervous system in the urinary bladder
- micturition syncope from release of catecholamines by bladder contraction
pheochromocytoma in the urinary bladder
135
in patients w/ pheochromocytoma, what are the 2 ways that can result in loss of vasoconstriction leading to postural or orthostatic hypotension?
- desensitization to norepinephrine
- loss of blood vessel norepinephrine receptors
136
how does hyperthermia occur in patients w/ pheochromocytoma?
- peripheral vasoconstriction
- excess production of IL-1
137
recent studies have demonstrated that bedside US assessment of the diaphragm in patients undergoing MV can provide what valuable pronostic information?
patients w/ either thickening or thinning of the diaphragm over the first week of MV have longer weaning times, longer ICU stays, and more complications of MV
138
in one study of serial measurements of diaphragm thickness over the first week of MV, which patients had significantly longer weaning periods, longer ICU stays, and more complications of MV, including need for tracheostomy?
patients w/ either a 10% increase OR decrease in diaphragm thickness
139
thinning of the diaphragm in a MV patient suggests what?
marked reduction in diaphragm activation (signaled by atrophy and thinning)
140
thickening of the diaphragm in a MV patient suggests what?
excessive loading of the diaphragm (d/t inadequate ventilatory support or dyssynchrony w/ the ventilator and signaled by diaphragm injury, edema, and thickening)
141
what are the mechanisms proposed for diaphragm injury?
- overassistance
- underassistance
- eccentric contraction
- excessive end-expiratory shortening
142
what 2 entities should be carefully considered in MV patients regarding diaphragmatic injury?
- critical illness-associated diaphragm weakness
- ventilator-induced diaphragm dysfunction
143
how can fat embolism syndrome occur?
- long-bone fracture
- orthopedic surgery
- sickle cell crisis
- cosmetic surgery that involves withdrawal or injection of fat
144
fat embolism syndrome is a/w
- direct endothelial injury
- microvascular occlusion
- systemic inflammatory changes
145
clinically, fat embolism syndrome manifests w/
- hypotension
- neurological dysfunction
- rash
146
what happens in severe cases of fat embolism syndrome?
pulmonary vascular resistance increases, which may lead to right ventricular cardiogenic shock
147
in most cases of fat embolism syndrome, what will the CTH show?
nothing
148
in most cases of fat embolism syndrome, what will the CTH show?
nothing
149
neurological dysfunction is commonly seen in fat embolism syndrome, but what about coma?
rarely a/w coma
150
in a patient w/ fat embolism syndrome that has disproportionate encephalopathy w/ coma, what should be further evaluated?
nonconvulsive status epilepticus w/ EEG
151
can hemodialysis remove bone marrow particles in a patient w/ fat embolism syndrome?
no
152
q23
