1. Simultagnosia: inability to integrate a visual scene or picture 2. Ocular apraxia: inability to stabilize eye movements 3. Optic ataxia: misreaching under visual guidance

RITE Exam Flashcards by David Rendon

Balint Sydrome: where is the lesion

Bilateral occipitoparietal lobes

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Balint syndome triad

Simultagnosia: inability to integrate a visual scene or picture
Ocular apraxia: inability to stabilize eye movements
Optic ataxia: misreaching under visual guidance

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Side effect of DA AGO used to treat PD

Compulsive behavior

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Alzheimers, DLB or FTD: which would you see hypometabolism of bilateral parietal and precuneus regions

Alzheimers: you see CORTICAL atophy of the parietal and temporal lobes

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Alzheimers, DLB or FTD: which would you see hypometabolism of bilateral parieto-occipital lobes?

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Alzheimers, DLB or FTD: which would you see hypometabolism of bilateral frontotemporal lobes

FTD

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Anton syndrome: localize and what does it cause

Bilateral medial occipital lobes, cortical blindness without recognizing loss of vision (a form of anosoagnosia)

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Cardinal manifestations of dementia with Lewy bodies (DLB)

Dementia (attention, executive, visuospatial domains)
SYMMETRIC parkinsons signs without resting tremor
Visual hallucinations
Dysautonomia
REM sleep behavior disorder
Fluctuating course: mixed periods of confusion and lucidity
EPS sx with even small amounts of antipsychotics

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Wisconsin Card Sort Test (WCST), which challenges a patient to change cognitive sets without warning, is particularly sensitive to _____ damage

frontal

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Lecanemab is directed against ______________ seen in Alzheimer disease. The drug acts by… removes amyloid from the brain through passive immunization and significantly reduces fibrillar amyloid burden as measured by amyloid PET.

beta-amyloid protein plaques
removes amyloid from the brain through passive immunization

ecanemab significantly slowed disease progression as measured by CDR-SB by 27% at 18 months. There was 31% lower risk of converting to the next stage of disease as measured by global CDR.

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______ is another protein that is deposited as neurofibrillary tangles in Alzheimer disease.

Tau

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Alpha- synuclein is seen in what dementia

DLB (dementia with lewy body)

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What is a common finding on imaging in Huntingtons disease?

Bilateral caudate atropgy

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Imaging, CSF findings for CJD

Hyperintensity of BG, thalamus, cortex (cortical ribboning): Sen 87%, Spec 82%
CSF: elevated 14-3-3 (sens 72%, spec 46%), total tau, neuron specific enolase

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How do you confirm diagnosis of CJD

Real-time quaking-induced conversion (RT-QuIC) assays of CSF

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What is the least sensitive test for CJD diagnosis (HINT: its an EEG finding)

periodic sharp waves

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Typical CSF biomarker for patient with Alzheimers

Low amyloid beta-42
Elevated total tau
Elevated phosphorylated tau

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Most structural lesions associated with development of obsessive- compulsive behavior involve what…

frontal lobe and/or frontal cortex-basal ganglia network connections

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_______ connections are associated with risky behaviors induced by emotional stimuli.

Insular cortex-amygdala connections are associated with risky behaviors induced by emotional stimuli.

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In right-handed individuals, the ______ in the ______ lobe
is the most common region associated with acalculia (inability to do math).

L angular gyrus in the parietal lobe

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Gerstmann Syndrome: What is it and localize

Dominant parietal lobe (angular gyrus)
Agraphia + acalculia + finger agnosia + R/L confusion

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What finding do you see with PSP on MRI

Hummingbird/Penguin sign: Atrophy of midbrain without atrophy of pons

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What does the stroop test test (ppl are presented with colors written in other colors than the ones spelled out)?

Executive function: you have to inhibit unwanted or inappropriate responses

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What is the Trail Making Test test (first part of MOCA where you connect numbers and letters in order)

Task switching (mental flexability), visual attention

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Lesion that causes Kluver-Busey Syndrome

Bilateral temporal lobes (amygdala), hippocampus is also affected

PAtient is walking through woods, see something in their peripheral vision and assume its a snake -> startles. This can occur in what disease? What are features of this disease

Kluver Busey: 1. Impulsive reactions to external stimuli (hypermetamorphisis) - easy to startle 2. Hyperorality 3. Hypersexuality 4. Visual agnosia 5. Anterograde amnesia

Causes of Kluver Busey Syndrome

HSV encephalitis, alzheimers, FTD, TBI,

Classes of Alz meds

1. Acetylcholinesterase inhibitors (increases ACh) 2. NMDA Ant

Acetylcholinesterase inhibitors in Alzheimers & SE

Donepazil, Galantamine, Rivastigmine - Symptomatic bradycardia (use in caution in people with AV block, SSS, bradycardia)

NMDA-R ANT for Alzheimers

Memantine

Can't read but can spell and write

Alexia w/o agraphia: L visual cortex + splenium of corpus callosum

Friedreich ataxia- a disorder associated with reduced expression of _________ (a small mitochondrial protein) due to ______. _______ is encoded by the ____ gene on chromosome ___.

Frataxan due to GAA triplet repeats Frataxan is encoded by FXN gene on Chr 9.

What is Friedriches ataxia? Genetics

AR Starts in 2nd decade of life -> progressive ataxia. 10-15 years later patient is unable to walk. Also associated with PN, diabetes, skeletal abnormalities (pes clavus)

Vertex waves are seen in sleep stage _ K complex and sleep spindles are seen in stage _

1 2

CNS manifestations of acute liver failure include encephalopathy, asterixis, seizures, intracranial hypertension, and coma. Due to liver failure, there is decreased intrahepatic metabolism of ammonia to urea, with concomitant elevation of ___________. You can also see what on MRI with hepatic encephalopathy

- Glutamine -> sequestered in cells -> increases osmolarity and brain edema - diffuse atrophy + T1 hyperintensity in BG

Delayed cerebral ischemia caused by cerebral vasospasm is a serious complication of subarachnoid hemorrhage (SAH), typically occurring between _______ after hemorrhage, peaking at days ____

occurs between 4-14, peaking at days 5-7.

AICA stroke: localize, sx

- Lateral pons - Ataxia, vertigo, ipsilateral CN 7 or 8 (facial droop or hearing loss)

Foster Kennedy Syndrome: what is it caused by and what sx

1. Caused by a space occupying mass (like a meningioma in frontal lobe) 2. Contralateral papilledema (from compression) due to increased ICP, anosmia, ipsilateral optic nerve atrophy

Pseudo-foster Kennedy syndrome

Optic nerve atrophy and CL papilledema, without signs of increased ICP (no N/V, HA) usually due to NAION in ppl > 50 with RF

Repeat expansions on what Chromosome link FTD with ALS

Chromome 9

delusional midentification disorder (belief that somone you know is an imposter) is called what?

Capgras syndrome

HIV associated dementia (HAND) is cortical/subcortical/both. What do you see on MRI

SUBCORTICAL? Confluent subcortical T2 hyperintensities

Sumatriptan MOA

5HT-1B AGO

Anti LGI1 encephalitis sx

Memory problems Faciobrachial dystonic seizures MRI: T2 FLAIR hyperintensities in temporal lobes

Concussion: LOC (length if any), posturing, recovery at 3 months

No LOC, no posturing, 100%

Cerebral contusion: LOC (length if any), posturing, recovery at 3 months

LOC <6hrs, no posturing, 95%

Mild diffuse axonal injury: LOC (length if any), posturing, recovery at 3 months

6-24 hours, rare, 63%

Moderate diffuse axonal injury: LOC (length if any), posturing, recovery at 3 months

>24 hrs - days of LOC, occasional, 38%

Severe DAI: LOC (length if any), posturing, recovery at 3 months

days - weeks, yes, 15%

_____ period paralysis is the MC period paralysis, but still rare. Triggers? How often does it happen and how long does it last?

Hypokalemic. - Triggers: heavy exercise, too much carbs or not eating enough, cold or stress. - Once qweeks or months, lasts hrs - days.

Hyperkalemic period paralysis. Frequency and how long does it last?

Several times a day (HYPER), lasting minutes to hours

Myotonic discharges are seen in ______ periodic paralysis, not the other one

Hyperkalemic

Genetics for Hypo/hyperkalemic PP. and what can be used to prevent attacks

AD, hypokalemic (CAI, K-sparing diuretics), hyperkalemix (CAI, thiazides)

Syringomyelia - what does it present as, wht is it assx with

Expansion of the central canal - Affects spinothalamic pathway (pain and temperature) in a cape like pattern - Can sometiems cause a Horner syndrome - Assx with chiari malformation

What is apraxia. Lesion

inability for perform a previously learned task - Dominant side

Sturge Weber Syndrome

1. Seizures 2. Developmental Delay 3. Port wine stain in V1/2 distrubution. On the same side, you will see cerebral atrophy and calcification due to vascular steal from leptomeningeal hemangioma

How to taper Benzo

Decrease by 25% every 2 weeks

What does a normal cold caloric test look like?

If brainstem is intact: - Cold water: slow deviation to the same side, followed by a fast nystagmus in the opposite direction

What is anosodiaphoria? Where is the lesion?

- you are aware of your neurologic deficit, you just dont really care. - R Frontal lesion - You may also expect a gaze preference due to frontal eye fields q

What are lewy bodies

accumulation of alpha-synuclein

What diseases are your alpha synucleinopathies? You will see lewybodies in?

1. Parkinsons 2. LBD 3. MDA

Hyperphosphorylated 4R tau accumulates in what

corticobasal degeneration

TDP 43 acculates in

ALS FTD

EMG findings in MG

Slow RNS (2-3Hz) cause a 10% decrease in amplitude

What is an EMG finding suggestive of CTS?

A combined sensory index of 1.0ms or more

Anti-Ta (Ma2) is associated with what? What cancer is it assx with?

limbic encephalitis (also vertical opthamoparesis) and somnolence, testicular cancer

What travels through the inguinal canal?

Ilioinguinal N. External spermatic N

Charles Bonnet syndrome (CBS) is a condition that causes people with_______ to experience __________

severe vision issues, visual hallucinations

__________ is a disorder that makes it difficult to perform gestures or use tools on command. Lesion?

Ideomotor apraxia (IMA) L sided lesions (dominant lobe)

Autonomic dysreflexia can be caused by lesios where in the spine?

Above T6

What causes autonomic dysreflexia?

You get exagerrated sympathetic responses to noxious stimuli (constipation, urinary retention, pain, sacral ulcers) BELOW the level of injury causes diffuse vasoconstriction and HJTN below the level of the lesion. Above the level, baroreceptor in the carotid sinus/aortic arch respond to HTN through CN 9 -> nucleus ambiguous -> strong vagal outflow (CN X), bradycardia and vasodilation above the level of injury (flushing, sweating, miosis)

_____________ are brief (lasting up to 30 minutes) motor, somatosensory, visual, or language deficits (+ or - symptoms) that can occur in patients with (CAA) and are predictive future ICH. Therefore, it is important to differentiate from TIA and avoid use of antiplatelet drugs. The mechanism may be blood products that trigger cortical spreading depression or depolarization.

Amyloid spells

Cerebral amyloid angiopathy (CAA) - PAthophysiology? - Age? - Findings on MRI - Treatment?

- B-amyloid is deposited in vessels -> weakening -> increased risk of bleeding - >80 - Cortical microhemorrhages - Tx: only tx is BP control

Adrenoleukodystrophy (ALD) is a progressive neurologic disorder caused by.. - Gene The disorder has three clinical presentations:

very-long chain fatty acids are not oxidized -> causing them to build-up. - X-Linked; ABCD1 geene - a slowly progressive myelo- neuropathy (adrenomyeloneuropathy) - a rapidly progressive leukodystrophy (cerebral ALD), - primary adrenal insufficiency

What does a kid with X-linked ADL look like? MRI?

2-10YO, behavior issues, school issue as a kid - T2 hyperintesity symmetrical involvement of splenium of CC