Neuro 2.2 Flashcards
How does TIAs look on imaging?
They don’t, fool.
How often do you do the ABCD score?
2, 7, and 90 days after CVA
What do you get points for in the ABCD score?
Age > 60 years (1 point)
BP = 140/90 mmHg at initial evaluation (1 point)
Speech disturbance without weakness (1 point) OR
Unilateral weakness (2 point)
Duration of symptoms of 10-59 minutes (1 point) OR
Duration of symptoms >60 minutes (2 point)
DM mellitus in patient’s history (1 point)
ABCD score where hospital observation is unnecessary
0-3
ABCD score where hospital observation is justified
4-5
ABCD score where hospitalization is worthwhile
6-7
If a TIA is probable, what do you do?
Apply ABCD score, aspirin, refer to TIA clinic
What does ABCD stand for?
age; blood pressure; clinical features of TIA; duration; diabetes
Treatment for patient with TIA and a. fib
anticoagulants
Treatment for patients with TIA and mural thrombus
anticoagulants
All patients with TIA treatment:
ASA
ASA + dipyridamole
Clopidogrel
ASA + clopidogrel
Are anticoagulant drugs recommended in the average patient with a TIA?
No
When do you start OAC in patient with TIA and a.fib?
1 day after acute event
When do you start OAC in patient with mild stroke and a.fib?
3 days after acute event
When do you start OAC in patient with moderate and a.fib?
6 days after acute event
When do you start OAC in patient with severe and a.fib?
16 days after acute event
Mild stroke NIHSS
<8
Moderate stroke NIHSS
8-15
Severe stroke NIHSS
> 16
Recurrent TIAs with identical clinical features are usually caused by
thrombosis or embolism arising from the same site within the cerebral circulation
TIAs that differ in character from event to even suggest ?
recurrent emboli from distant or multiple sites
What’s the most common cause of embolic stroke?
a. fib
Name five causes of embolic stroke?
a. fib; migraine; arterial dissection; temporal arteritis; sickle cell anemia
Name the 5 classic lacunar syndromes
pure motor stroke; pure sensory stroke; ataxic hemiparesis; clumsy hand-dysarthria; sensory-motor
Most common classic lacunar syndrome?
pure motor
Pure motor stroke
hemiparesis affecting the face, arm, and leg to a roughly equal extent, without associated disturbance of sensation, vision, or language- usually located in the contralateral internal capsule or pons
Pure sensory stroke
hemisensory loss, which may be associated with paresthesia, and results from lacunar infarction in the contralateral thalamus
Ataxic hemiparesis
pure motor hemiparesis is combined with ataxia of the hemiparetic side and usually affects the leg predominantly- results from a lesion in the contralateral pons, internal capsule, or subcortical white matter.
Clumsy hand-dysarthria
dysarthria, facial weakness, dysphagia, and mild weakness and clumsiness of the hand on the side of facial involvement
Lacunar strokes occur from?
occlusion of small penetrating arteries
The occlusion of what circulation leads to locked-in syndrome?
basilar artery, vertebral artery
What is vertebrobasilar insufficiency?
poor blood flow to brainstem
Symptoms of vertebrobasilar insufficiency
vertiigo with associated neurologic signs; diplopia; ataxia; dysarthria; weakness/paralysis/numbness; drop attacks; HA
What do you need to rule out in any dizziness work up?
vertebrobasilar insufficiency
Goal standard for vertebrobasilar insufficiency?
Digital subtraction cerebral angiography (DSA)
Two main types of hemorrhagic stroke?
ICH and SAH, both of which can lead to IVH
75% of hemorrhagic strokes are due to?
ICH
Largest risk factor for intracerebral hemorrhage?
HTN
Causes of secondary intracerebral hemorrhage?
trauma, arteriovenous malformation, intracranial aneurysm, intracranial neoplasm, cocaine drug exposure
Define intracerebral stroke:
acute spontaneous bleeding into brain parenchyma
Primary ICH:
results from microscopic small-artery degeneration in the brain, caused by either chronic poorly controlled HTN or amyloid angiopathy
Secondary ICH:
intraparenchymal bleeding from a diagnosable anatomic vascular lesion or coagulopathy
ICH: Plasma that is rich in thrombin and other clotting factors then seeps into the surrounding brain tissue, where it triggers a cascade of secondary brain injury that evolves during days to weeks. This unique form of x causes local brain edema, programmed neuronal and glial apoptotic cell death, and breakdown of the brain-blood barrier
neurohemoinflammation
The most commonly affected structures in ICH are:
basal ganglia and thalamus; lobar regions; brain stem and cerebellum
Cerebral amyloid angiography
non-hypertensive lobar intracerebral hemorrhage in the elderly, is characterized by the deposition of B-amyloid protein in small to medium-sized blood vessels of the brain and leptomeninges
Cerebral amyloid angiography CM
dementia, gait disturbance, complex partial seizures
CM of ICH:
Severe HA, vomiting, BP elevated
Which is more severe ICH or ischemic CVA?
neurologic deficit is frequently more severe in ICH
On an non contrast CT, an acute ICH is?
hyperdense
On an non contrast CT, a subacute ICH is?
isodense
On an non contrast CT, a chronic ICH is?
hypodense
Does an ICH get a hospital stay?
ICU or stroke unit for at least first 24 hours due to high risk of neurologic deterioration
BP goal of ICH?
140 mm HG systolic and MAP of <140 mmHg
In ICH, maintain MAP of <140 mmHg by continuous infusion of?
labetalol or nicardipine
In ICH, for elevated INR reverse with?
Vitamin K and 4F-PCC
In ICH, for heparin reversal?
protamine sulfate
In ICH, for thrombocytopenia or platelet dysfunction?
desmopressin and/or transfuse platelets
Expedited INR reversal for life-saving neurosurgical intervention?
recombinant activated factor VIIa
How to alleviate intracranial pressure?
elevate head of bed to 30 degrees; Mannitol; hyperventilate
Seizure prophylaxis in ICH?
fosphenytoin or phenytoin
When is external ventricular drainage indicated in ICH?
in all stuporous or comatose patients with intraventricular hemorrhage and ventricular enlargement in whom aggressive support is indicated
In ICH, ICP should be below?
20 mmHg
Indications for decompressive posterior fossa surgery in ICH
neurologic deterioration, brainstem compression, and hydrocephalus (cerebellar hemorrhage)
Indications for surgical evacuation for lobar hematomas?
larger than 30 mL and located approximately 1 cm from brain’s surface
Subarachnoid:
caused by rupture of vessels on the brain’s surface, most often due to a congenital aneurysm, and result in diffusion of blood throughout the CSF spaces
Men or Women: subarachnoid?
women
Most common cause of SAH?
trauma
Most common spontaneous cause of SAH?
rupture aneurysms
The thunderclap headache is associated with?
SAH
If you suspect a SAH and it doesn’t show up on a non-contrast CT, what do you do?
lumbar puncture
What will the CSF look like in a SAH LP?
grossly bloody, xanthochromic (yellow-tinged) fluid (present after 12 hours)
Definitive diagnostic procedure to detect intracranial aneurysms and to define their anatomy
angiography
SAH BP goal?
<160 systolic
BP treatment for SAH?
labetalol or nicardipine
Re-bleeding prophylaxis in SAH?
e-aminocaproic acid
Seizure prophylaxis in SAH?
fosphenytoin or phenytoin
vasospasm prophylaxis in SAH?
nimodipine
Cerebral edema treatment in SAH?
mannitol or hypertonic saline
ICP goal in SAH?
<20 mm Hg
How to diagnosis vasospasm in SAH?
transcranial doppler every 1-2 days until the tenth day after SAH; CT angiography and perfusion on day 4-8 after SAH or for neuro worsening
therapy for symptomatic vasospasm in SAH?
place patient in trendelenburg; normal saline; if deficit persists, then raise systolic BP with phenylephrine or norepinephrine
If refractory symptomatic vasospasm in SAH, treatment?
add dobutamine or milrinone
Definitive treatment for the prevention of re-bleeding in SAH?
complete obliteration of a rupture saccular aneurysm by either endovascular coiling or surgical clipping
Procedure that involves packing the rupture aneurysm with platinum coils?
endovascular coil embolization
Endovascular coil embolization is good for aneurysms
<10 mm in diameter
Surgical clipping requires a craniotomy is preferred for?
wide-necked aneurysms
What tool is used to classify SAH?
Hunt-Hess Grading Scale
Hunt-Hess Grading Scale: I
asymptomatic or mild headaches = 5% hospital mortality
Hunt-Hess Grading Scale: II
moderate to severe HA or oculomotor palsy = 5% hospital mortality
Hunt-Hess Grading Scale: III
confused, drowsy, or mild focal signs = 10% hospital mortality
Hunt-Hess Grading Scale: IV
stupor (localizes to pain) = 34% hospital mortality
Hunt-Hess Grading Scale: V
coma (posturing or no motor response to pain) = 52% hospital mortality
Primary intraventricular:
hemorrhage in the ventricular system
primary intraventricular hemorrhage is most common in the?
occipital horns (lateral ventricles)
IVH occurs in x% of the cases of ICH
40%
What volume of bleed is considered lethal?
20 mL
Brain vascular malformations
space-occupying congenital anomalies that can often exist for a lifetime without symptoms
For what is hypertension NOT a risk factor?
brain vascular malformations
CM of an arteriovenous malformation?
most are manifested with intracranial hemorrhage; seizures; or progressive neurologic disability
If someone with an arteriovenous malformation develops seizures, what type would they be?
focal seizures
types of treatment for arteriovenous malformations?
selective embolization of the feeding arteries; surgical resection; radiation-induced thrombosis; stereotactic radiosurgery (small lesions)
Left (dominant) hemisphere:
aphasia, left gaze preference (eyes move toward side of stroke in brain, away from weakness; in a seizure (following a stroke), eyes look away from side of seizure towards weakness); right visual field deficit; right hemiparesis; right hemisensory loss; difficulty reading, writing, or calculating
Right (non-dominant) hemisphere:
neglect = left hemi-inattention (no comprehension of stroke deficit); right gaze preference; left visual field deficit (neglect); left hemiparesis; left hemisensory loss; bluntness to them—loss of ability to calculate what emotions should be; dysarthria; spatial disorientation; fluent speech, verbal; inability to process anything in left field; apraxia (language is intact, but unable to carry out a motor function; apraxia is the loss of ability to plan movements)
subcortical/lacunar:
Unilateral symptoms (face, arm, and leg): pure weakness (hemiparesis), pure sensory loss, weakness AND sensory, clumsy/ataxia/dysmetria (subtle weakness with clumsiness), dysarthria clumsy hand; alert, oriented, following commands; no aphasia
Brainstem infarct symptoms: basilar artery
Hemiparesis (sometimes quadraparesis); crossed sensory signs; diplopia, disconjugate gaze, gaze palsy, nystagmus; vertigo, tinnitus; dysarthria; N/V; hiccups, abnormal respirations; decreased consciousness
Frontal lobe infarct
difficulties with attention, uncontrolled emotional, social, and sexual behavior changes, personality changes, loss of spontaneity, problem-solving difficulties, perseveration, loss of verbal expression, difficulty sequencing, inflexible thinking
Parietal lobe infarct
reading and writing problems; object naming problems; right/left confusion; math difficulties; inability to focus visual attention; problems with eye-hand coordination; lack of awareness of body parts
temporal lobe infarct
difficulty understanding spoken words, disturbance of selective attention, short-term memory loss, change in sexuality, persistent talking, increased aggressive behavior, difficult identifying and categorizing objects, difficulty recognizing faces and visually locating objects
occipital lobe infarct
vision defects (visual field cuts), difficulty visually locating objects, difficulty identifying colors, hallucinations and visual distortions, word blindness, inability to recognize object movement, difficulties reading and writing
cerebellum infarct
decreased breathing capacity; difficulty swallowing food and fluid; problems with balance and movement; dizziness and nausea; vertigo; sleeping difficulties
What tool is used to measure stroke?
NIHSS
NIHSS score greater than or equal to X has a 91% predictive positive value for a central large-vessel stroke
12
NIHSS greater than x indicates a more proximal vessel affected
> 10
Cincinnati Pre-Hospital Stroke Scale
facial droop; arm drift (ten seconds); abnormal speech (“you can’t teach an old dog new tricks”)
If any one of the cincinnati pre-hospital stroke scales is positive, then the probability of a stroke is?
72%
a non-contrast CT scan has high sensitivity for?
detection of hemorrhage
a non-contrast CT scan is insensitive for?
lacunar and posterior fossa strokes
What does a perfusion scan show?
what tissue is already infarcted and what tissue is at risk
A stroke brain volume of X is likely a good outcome
<50 mL
On a CT scan, an ischemic stroke will be?
hypodense
On a CT scan, a bleeding stroke will be?
hyperdense
MRI is sensitive to?
acute ischemia; posterior fossa; small vessel/lacunar strokes
Three tests to assess embolic source of stroke?
TTE; TEE; telemetry
Goal standard echo for stroke?
TEE
family/essential tremor genetics?
AD
patho of family/essential tremor?
microscopic abnormalities of cerebellar Purkinje cells
Patients with essential tremor have a higher risk of developing?
Parkinson disease
what provides transient relief to those with essential tremor?
alcohol
First line treatment of essential tremor?
propranolol; primidone; topiramate
Chorea patho?
cell loss in the caudate nucleus and putamen
Sydenham chorea patho?
immunologic cross-reactivity between the causative group A B-hemolytic streptococcus and the basal ganglia; late component of rheumatic fever
Five causes of chorea?
HD, Wilson, drug toxicity, Addison, HIV
Treatment of chorea in adults?
haloperidol and pimozide
Treatment of chorea in children?
clonazepam, diazepam, clobazam; valproate
drug of choice in Sydenham chorea?
valproate and short term abx
Ballism
extreme form of chorea
Ballism cause?
most often a consequence of an acute cerebral insult such as a stroke (normally one side of body– hemiballism)
Hemiballism cause?
vascular disease in the contralateral subthalamic nucleus
HD patho?
atrophy of the caudate nucleus and to the less degree the putamen and globus pallidus
Symptom onset of HD?
30-55 years
Diagnosis of HD?
CT/MRI; PET; genetic testing
Treatment of HD: movement
reserpine, tetrabenazine, haldol, quetiapine
Treatment of HD: psychosis
olanzapine or risperidone; quetiapine
Dystonia
sustained muscle contractions result in repetitive twisting and sometimes tremulous movements and abnormal postures
Name for twisting neck to one side
torticollis
name for spontaneous, involuntary forced closure of eyelids; difficulty in eye opening; repetitive blinking
blepharosams
name for spasms of the muscles of the mouth
oromandibular dystonia
Slower, sinuous writhing dystonic movements, particularly present in the distal limbs:
athetosis
Dystonia is often made worse by?
activity
First line treatment of dystonia:
focal injections of botulinum
Medications for dystonia:
trihexyphenidyl (anticholinergic), diazepam, tetrabenazine (dopamine depleting), haldol (dopamine blocking
medication treatments for tics
haldol, pimozide, risperidone
CM of Tourette’s
Presence of multiple motor and at least one vocal tic beginning before the age of 21 years (typically between ages 2 and 10 years) and lasting for more than 1 year, waxing and waning symptoms over time (new tics replacing old ones; previous tics sometimes recurring years after they had originally resolved), and the absence of other explanatory medical conditions
treatment for moderate Tourette’s
low-dose clonazepam, clonidine, guanfacine, risperdal, apiprazole, botox
Are motor tics or vocal tics more common as an initial presentation of Tourette’s
motor
involuntary swearing
coprolalia
Myoclonus
Sudden, brief, shock-like, involuntary movements that result from both active muscle contraction (positive myoclonic jerks) and brief inhibition of ongoing muscle activity (negative myoclonic jerks)
Most common myoclonus
asterixis
Myoclonic jerks typically last?
<150 msec
Treatment of myoclonus?
clonazepam, valproic acid, carbamazepine, levetiracetam
Restless leg syndrome inheritance
AD
80% of patients with restless leg syndrome have an associated movement disorder called
nocturnal myoclonus
Treatment of restless leg syndrome
pramipexole, ropinirole, transdermal rotigotine; gabapentin, L dopa
Parkinson disease patho:
due to loss of dopamine in the neostriatum (especially in putamen) secondary to loss of pigmented dopaminergic neurons in the substantia nigra of the midbrain
Four cardinal signs of Parkinson
tremor, rigidity, akinesia, and postural disturbances (TRAP)
Five causes of secondary parkinson?
dementia with lewy bodies, AD, wilson, CJD, MS
AD Parkinson genes
a-synuclein gene mutations, duplications, triplications; LRRK2
AR Parkinson genes
parkin, DJ1, PINK1
what occurs in the substantia nigra of Parkinson
cell loss, gliosis, abnormal deposition of aggregated a-synuclein as Lew bodies and Lew neutrites
What’s the classic symptom of Parkinson’s?
resting tremor
Describe the resting tremor in PD?
4-6 cycles per second; typically with “pill-rolling” character when it involves the hand
Muscle rigidity in PD can be most appreciated ?
slow passive movements
Muscle rigidity in PD can be classified as x when a tremor is superimposed
cogwheel
Muscle rigidity in PD can be classified as x when the tremor is not superimposed
lead pipe
masked facies AKA (in PD)
hypomimia
soft monotonous speech (in PD)
hypophonia
impaired swallowing resulting in drooling ( in PD)
sialorrhea
small handwriting (in PD)
micrographia
postural disturbances in PD
flexed posture in the limbs and trunk (stooped, simian posture), postural instability
Multiple system atrophy: CM
early dysautonomia and bladder dysfunction; cerebellar dysfunction
MSA-P CM
pyramidal tract signs; stimulus-sensitive myoclonus of hands and face
MSA-C CM
extreme forward neck flexion; mottled, cold hands; inspiratory stridor; prominent dysarthria
progressive supranuclear palsy CM
supranuclear vertical ophthalmoplegia; ocular and eyelid disturbances; axial rigidity > limb rigidity; early falls; speech and swallowing disturbances; nuchal extension; cognitive or behavioral changes; progressive nonfluent aphasia; HTN
Corticobasal degeneration CM
apraxia, cortical sensory loss, alien limb phenomenon; pronounced asymmetrical rigidity; limb dystonia; stimulus-sensitive myoclonus; aphasia; cognitive dysfunction
What condition shows a “hot cross bun sign” on MRI
MSA-P
What condition shows a hummingbird sign on midline sagittal view?
progressive supranuclear palsy
What condition shows a morning glory sign on axial view?
progressive supranuclear palsy
Vascular parkinsonism Cm
lower half parkinsonism with gait disturbances predominating
What’s considered lower half parkinsonism?
vascular parkinsonism and normal-pressure hydrocephalus
Parkinson imaging
PET scan
Group A features of Parkinson
resting tremor, bradykinesia, rigidity, asymmetric onset
PD drugs used early on:
anticholinergics; amantadine; MAO-B inhibitors
anticholinergics used in PD
benztropine; trihexyphenidyl
MAO-B inhibitors used in PD
selegiline, rasagiline
drugs used later in PD?
dopamine agonists
what drugs are more helpful in alleviating tremor and rigidity in PD?
muscarinic anticholinergics
MOA for anticholinergic drugs
blockade of NMDA-preferring glutamate and muscarinic cholinergic receptors and stimulation of dopamine release
Amantadine improve?
all motor symptoms of PD; reducing intense fatigue; iatrogenic dyskinesias
Issue with Amantadine?
short lived
Potential first line treatment for PD?
amantadine
Most effective treatment of PD?
levodopa
levodopa is converted in the body to
dopamine
What drug can be given with levodopa to limit the breakdown of levodopa outside the brain?
carbidopa
Carbidopa inhibits?
dopa decarboxylase
Levodopa SE
nausea, vomiting, hypotension, abnormal movements, restlessness, confusion; cardiac arrhythmias
dopamine agonists used in PD
bromocriptine, pramipexole, ropinirole, apomorphine
which two dopamine agonists can be used in early PD?
pramipexole/ropinirole
Pramipexole/ropinirole AE
fatigue, somnolence, nausea, peripheral edema, dyskinesias, confusion, hallucinations, orthostatic hypotension; sleep at inappropriate times; disturbances of impulse control
Apomorphine may help resuce patients with?
advanced PD and severe “off” episodes of akinesia despite optimized oral therapy
Apomorphine AE
severe nausea, vomiting, somnolence, hallucinations, chest pain, hyperhidrosis, dyskinesias may be enhanced
monoamine oxidase B inhibitors used in PD
selegiline and rasagiline
MO and COMT are enzymes that break down?
dopamine
Selegiline MOI
inhibits the metabolic breakdown of dopamine and enhances the antiparkinsonian effect of levodopa and may reduce mild on-off fluctuations in responsiveness
Rasagiline
effective in the initial treatment of early PD; more potent and selective the selegiline
catechol-o-methyltransferase inhibitors used in PD
entacapone, tolcapone
COMT drugs may be used for?
reduce the dose requirements and any response fluctuations to levodopa; more sustained plasma levels of levodopa with improved transport into the blood and across BBB
SE of COMT drugs
diarrhea, confusion, dyskinesias, abnormalities of liver tests
What alternative treatment may be used in PD?
deep brain stimulation
gait disturbances and akinesia may be helped in PD by stimulation of
the pedunculopontine nucleus
