Behavior, Cortical Function, and Dementia

Question 1

Lesions in what three areas can lead to amnesia?

Answer 1

Thalamus, hippocampus and the mammillary bodies.

Question 2

Why does a thiamine deficiency lead to amnesia in Wernicke- Korsakoff syndrome?

Answer 2

Bilateral thalamic and mammillary body lesions

Question 3

Name three etiologies of bilateral hippocampal lesions

Answer 3

Anoxia (sensitive to O2 deprivation)
Herpes simplex encephalitis
Early alzheimer’s disease

Question 4

What is transient global amnesia?

Answer 4

Inability to learn new things (anterograde amnesia) that goes away after a little bit

Question 5

Define apraxia

Answer 5

Inability to conceptualize and perform a skilled, learned act on command

“Cannot open the brain file to execute a task”..yet the act could occur spontaneously at another time

Question 6

A lesion in what lobe causes constructional and dressing apraxia?

Answer 6

Parietal lobe

Question 7

What is gait apraxia?

Answer 7

Feet glued to floor. Unable to walk

Question 8

Define agnosia

Answer 8

Impaired recognition (gnosis) of perceived stimuli caused by lesions in sensory association cortex;

Question 9

Name a few features of Frontal (prefrontal) lobe syndrome

Answer 9

Think of phineas gage (rail road spike dude)

• Disinhibition: lack of concern, poor judgement
• Slowed, distractible motor and mental function
• Gait apraxia
• Gegenhalten or paratonia (resistance to more rapid passive movements of the limb)

Question 10

What is Kluver-Bucy syndrome?

Answer 10

bilateral lesions in the temporal lobe

hyperphagia, hypersexuality, hyperorality, visual agnosia, and docility

Question 11

What is the difference between in clinical symptoms seen in lesions of the dominant vs non-dominant parietal lobe?

Answer 11

Nondominant parietal lesions—impairment of spatial relationships between the body and its surroundings
* anosognosia—unawareness of hemiparesis, or worse, denial of that half of the body (hemispatial neglect)

Dominant parietal lesion (supramarginal or angular gyrus) Gerstmann’s syndrome (agraphia, R-L disorientation, dyscalculia, finger agnosia

Question 12

What are the clinical features of an acute confusional state (delirium)?

Answer 12

fluctuating attention, level of consciousness, motor activity
subsequently impaired memory, language, thinking
mood changes or hallucinations
tremulousness, tremor, asterixis, myoclonus, ataxia, dysarthria

Question 13

What are the clinical features of dementia?

Answer 13

general term for diffuse impairment of acquired cortical function, progressing over months to years, and impeding daily activities of the patient

memory (often first deficit noted)
intellect (relative to patient’s educational level)
orientation, judgment, language, personality, and behavior

Question 14

Is dementia treatable?

Answer 14

There are many causes of dementia that are treatable. (infections, drug/alcohol abuse, chronic subdural hematomas, nutritional deficiencies etc..)

Treat the underlying problem

Some of the causes are irreversible

Question 15

How do you evaluate for dementia clinically?

Answer 15

Detailed history, observations of family, caregivers
Observe any neurological signs suggestive of a focal lesion (infarction, tumor)
Neuropsychological testing
MRI (or CT) brain scan
“Basic” blood work emphasizing treatable causes
CBC, chemistry profile, vitamin B12 level, thyroid functions
Specific blood (e.g., HIV antigen) and cerebrospinal fluid tests (e.g., chronic meningitis) where appropriate

Question 16

WHat are the initial presenting features of Alzheimer’s?

Answer 16

Initial problems with memory

Question 17

What are later symptoms of alzheimer’s disease?

Answer 17

Impaired judgement, personality changes, incontinence, terminal bed-bound state

Question 18

What composes the senile plaques seen in alzheimer’s?

Answer 18

beta-amyloid

Question 19

What is the intraneuronal depositions in alzheimers disease?

Answer 19

Neurofibrillary tangles composed of hyperphosphorylated tau protein

AD is considered a tauopathy

Question 20

How do we diagnose AD clinically?

Answer 20

AD is a diagnosis of exclusion. The only definitive diagnosis is that of beta-amyloid plaques and neurofibrillary tangles at autopsy

Question 21

What are the available treatments for alzheimer’s disease?

Answer 21

No curative treatments exist
Deterioration can be slowed with acetylcholinesterase inhibitors (Donepezil, rivastigmine, galantamine)
Memantine is added later on in the course of the disease

Question 22

IN addition to treating the progression of AD, what other medications are given to AD patients?

Answer 22

Sedatives and antipsychotics for agitation, hallucination and insomnia