Exam 6 Flashcards

1
Q

Q2. A 50-year-old man with atrial fibrillation suddenly becomes “confused.” He is alert and attentive. His speech is fluent but paraphasic, and he has difficulty following commands. Where is this likely localized and what other neurological abnormalities might be expected?

A

Sudden onset indicates vascular etiology.

Patient confused with low comprehension indicates Wernicke aphasia. This involves the posterior temporal lobe of the dominant hemisphere,

apraxia and acalculia may also be present.

The visual field fibers pass through this region and ischemia may cause right homonymous hemianopsia.

Therefore, patients with Wernicke aphasia may also have right homonymous hemianopsia but no hemiparesis/ hemianesthesia.

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2
Q

When is it best to use demographically adjusted versus population based norms?

When are regression norms and age base norms appropriate?

A

TBD

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3
Q

What does the research tell us about TBI history and AD, PD, ALS, and CTE?

A

Around 5% of all dementia cases may be attributable to TBI, assuming a conservative 1.5 times increase in relative risk for dementia postinjury.

The relative risk of AD after TBI has been estimated in a large meta-analysis to be increased by about 1.5 times,5 similar to earlier estimates.

PD risk is increased after single TBI

The risk of amyotrophic lateral sclerosis (ALS) has been reported to be modestly increased after single TBI

No recent meta-analysis describes the relationship between TBI and frontotemporal dementia (FTD)

Although CTE has distinctive neuropathological features, no consensus clinical diagnostic criteria currently exist. Hence, the prevalence of the condition is unknown.

The lack of a distinct clinical phenotype associated with neuropathologically proven cases of CTE makes it particularly difficult to disentangle the direct effects of TBI from those due to progressive neurode- generation with cross-sectional studies.

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4
Q

Name some common neuronal migrational disorders and accompanying symptoms.

A

Neuronal migration disorders (NMDs) are a group of birth defects caused by the abnormal migration of neurons (nerve cells) in the developing brain and nervous system. In the developing brain, nerve cells migrate or move from their place of origin to the place where they will remain for life. When this process goes wrong, neurons do not end up where they belong. This can result in structurally abnormal or missing areas of the brain in the cerebral hemispheres, cerebellum, brainstem, or hippocampus.

Some Types are:
Agenesis of the corpus callosum
Agenesis of the cranial nerves
Agyria- (no gyrus) a congenital disorder where the cerebral cortex lacks gyrations, or convolutions
Lissencephaly- severe and rare brain malformations. smooth brain.
Microgyria- gyri too small
Micropolygyria- abnormal number of small folds, or gyri
Neuronal heterotopias (including band heterotopia)
Pachygyria
Polymicrogyria
Porencephaly
Schizencephaly

Symptoms vary but often feature:

Poor muscle tone and motor function
Seizures
Developmental delays
Impaired cognitive development / lower IQ
Failure to grow and thrive
Difficulties with feeding
Swelling in the extremities
A small head

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5
Q

Discuss dementia risk and anticholinergic medication

A

Medications with anticholinergic activity are used widely by older adults for diverse conditions, such as overactive bladder, seasonal allergies, and depression

Some anticholinergics achieve the intended therapeutic outcome by blocking the effect of acetylcholine at the muscarinic receptor within specific organ systems (eg, antispasmodics for the gastrointestinal tract, antimuscarinics for the bladder, and antiparkinsonians)

Higher cumulative anticholinergic use is associated with an increased risk for dementia

a person taking an anticholinergic, such as oxybutynin chloride, 5 mg/d, or doxepin hydrochloride, 10 mg/d, for more than 3 years would have a greater risk for dementia

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6
Q

Discuss chronic statin use and cognitive functioning

A

The answer here is vauge- generally that it MAY or MAY Not.

Extensive and prolonged use of statins may affect cognitive functions in healthy subjects and dementia patients (from a survey).

Statins improve reaction time in the old age group, whereas it reduces functional working memory in the younger age group.

Randomized controlled trials and well-conducted observational studies of baseline statin use and subsequent cognition over several years of follow-up do not support a causal preventative effect of late-life statin use on cognitive decline or dementia.

statins given to elderly at risk of vascular disease have no effect in preventing AD or dementia.

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7
Q

True/False
Anticholerergics block ACH in the brain

A

True
Anticholenergics act to reduce ACH

So, anticholinergics in dementia is BAD

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8
Q

Multifocal Leukoencephalopathy

A

a disease of the white matter of the brain, caused by a virus infection (polyomavirus JC) that targets cells that make myelin

AKA Progressive Miltifocal leukoenceph. (PML)

MRI findings: bilateral, asymmetric, usually with no mass effect.
HIV patients with CD4<100 are at risk for this
Most die in 2 years (progressive)

Treatment: nothing direct- need to treat immune system. Control viral load, control AIDS virus, stem cell replacement, vaccines..

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9
Q

True/False
Presence of small vessel ischemic disease with dementia means the dx must be vascular dementia or mixed

A

False

Alzheimers can have small vessel ischemic disease on imaging, and not be given a dx of Mixed or Vascular dementia instead.

small vessel disease is not enough to say vascular dementia

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10
Q

True/False
Teleneuropsychology means remote administration of cognitive tests

Q17

A

False

Teleneuropsychology is the integration of technology instruments into NPSY; remote administration is a subset of teleneuropsych.

Remote assessment has shown: more reliable scoring, greater precision in stimulus presentation, broader access to services

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11
Q

Some facts about posterior fossa syndrome
Q23

A

AKA cerebellar mutism
Can onset after tumor surgery (cerebellum damaged)
25% medulloblastoma removal will get PFA

reduced speech / mutism / poor muscle control to speak / slowed speech
hypotonia
irritability / lability
ataxia / reduced muscle control

Higher risk if tumor is in bilateral cerebellum, large, affects the brain stem.

Speech can return in days to months

Other Cog SX: slow, inattentive, forgetful, issues with executive skills

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12
Q

Define dysmetria

A

difficulty reaching for an item or pointing to an item

misjudging the length needed when reaching, relates to trouble judging scales or distances

A type of ataxia

Looks like understooting/overshooting

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13
Q

Difference between photon beam
& proton beam radiation

A

Photon Beam: X or gamma rays.
Beams pass into and behind the tumor (“exit dose”), which is worse because it affects more tissue. It is worse radiation exposure.

Proton (+) Beam: Proton particles.
Much less damage. Beam is more controllable and targeted. Not associated with exit dose.

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14
Q

Difference between memantine
& donepezil

Q28

A

Memantine (Namenda): approved for Alz but not LB
NMDA agonist - blocks glutamate
In Alz+LB, there is too much glutamate

Donepezil (Aricept): better for Lewy Body
Increases acetylcholine (stops the enzyme that breaks it down)

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15
Q

Lewy Bodies are made up of what

A

misfolded alpha synuclein + ubiquitin + other things.

Those clumps can cause too much glutamate formation, clumps interfere with dopamine + ACH
This can cause cells to die

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16
Q

Risk is higher for agranulocytosis with
First or Second Gen antipsychotics?

A

Second Generation

Risk is highest with clozapine (2nd gen med)

17
Q

Risk is higher for extrapyramidal SFX with
First or Second Gen antipsychotics?

A

First generation.

Extrapyramidal symptoms (EPS) are a group of movement disorders that can be a side effect of antipsychotic drugs.

They can include:

Akathisia: Motor restlessness, anxiety, and an inability to sit still

Parkinsonian symptoms: Mask-like face, tremors, shuffling gait, and hypersalivation

Acute dystonias: Torticollis (neck muscle spasm), opisthotonos (rigidity of back muscles), and oculogyric crisis (rolling back of eyes)

Tardive dyskinesia: Tongue protrusion, puffing of the cheeks, and puckering of the mouth

18
Q

Where is the cavernous sinus

A

The cavernous sinus is located in the skull base, beneath the brain, and behind each eye socket

19
Q

Name some SLE lupus symptoms

A

Symptoms can come and go, with periods of increased symptoms called flares. Flares can range from mild to severe, and new symptoms may appear at any time.

Fatigue: The most common symptom, which can affect a person’s physical and mental health

Joint pain and swelling: Often affects the fingers, hands, wrists, and knees

Skin rash: A butterfly-shaped rash that appears on the cheeks and bridge of the nose in about half of people with SLE

A fever with no other cause

Can cause dry, coarse hair that breaks off easily

Mouth sores:

Sensitivity to sunlight

Chest pain: Can occur when taking a deep breath, and can be caused by pleuritis, pleural effusion, or pericarditis

Swollen lymph nodes:

Raynaud phenomenon: Fingers or toes turn blue or white or feel numb due to cold and stress

Swelling in legs or around eyes:

Headache and dizziness:

Confusion and memory problems:

20
Q

Name some SLE lupus cognitive problems

A

Lupus fog
50%+ Pts have cognitive problems
(20% with severe dysfunction)

Domains: many / generalized

Causes: inflammation, sleep loss, fatigue, stroke

21
Q

Difference between MS and SLE cognitive problems

A

MS: more slowly worsen over time
MS attacks nervous system, more common in women

SLE: cognitive issues worse during a flare and then some recovery. Can cause personality changes which is not hallmark of MS.
SLE: attacks many more tissues in body, more common in women, can cause seizure/stroke which are rare in MS.

22
Q

Q36

A