Behavior, Cortical Function and Dementia Flashcards

1
Q

Memory = ability to LEARN and THEN RECALL information after different periods of time

What are the following types of memories and how can we test?

Immediate memory:

Recent/short-term memory:

Remote/long-term memory:

A

Memory = ability to LEARN and THEN RECALL information after different periods of time

Immediate memory: misnomer, pertains to the pre-requisite state of attentiveness req for learnign something; pt should be ALERT and AWAKE enough to immediately repeat / recite a sequence of 5 numbers spoken outloud. (careful w/pt that are sleepy, sedated with meds, systemic illness inhibiting cortical fxn, or affecting RAS)

Recent/short-term memory: ability to recall info a_fter several minutes of retention_. Pt would be give 3 items to repeat out loud and instructed to recall them 5 minutes later on command.

Remote/long-term memory: ability to recall past events, hours, weeks or even eyars. Hard to test because examiner would have to also know these past details

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2
Q

Apraxia is the inability to….

What are examples of types of apraxia and where the lesion would be?

A

Apraxia = inability to conceptualize and perform a skilled, learned, motor act on command

prefrontal lesions –> gait apraxia = inability to walk on command

Posterior lesions, esp parietal lobe –> construction apraxia (can’t draw a house or copy a simple drawing), dressing apraxia

*Although pt cannot perform task on command, the person may be able to sponatenously carry out these actions as there should be no exisiting significant or severe impairments of sensation, strength, comprehension or attention to prevent performance of the task

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3
Q

Agnosia =

likely due to lesion @:

A

Agnosia = is the impaired recognition of perceived stimuli caused by lesions of sensory association cortex; object not identified by one sensory modality often recognized by a different stimuli or characteristics.

Likely due to lesion @ sensory association cortex

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4
Q

Focal cerebral syndrome:

Prefrontal or fronta lobe syndrome

Patients are (5)…..

Behaviorly, they act….

Their executive function are _____ with

What apraxia may be present?

What signs may be noted on exam?

A

Prefrontal or fronta lobe syndrome

Patients are listless, apathetic and unconcerned with poor hygiene and incontinence

The exhibit poor judgement, impolite outburts/rude/imappropriate sexual behavior

Executive functions are impiared, poor planning and performance of multistep or novel task, lack creative thinking and creativity, limited attention and motor perservation

Gait apraxia may be present

Signs:

Gegenhalten / paratonia : increased limb tone / resistence felt as the examier moves the patient limbs more rapidly.

Frontal lobe release signs : previously normal signs are now abnormal, “duck lips” to touching lips, palmar and plantar graps with touch “latching onto” examiner

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5
Q

Focal Cerebral Syndromes:

Syndromes of temporal lobes =

what can be caused by lesions ot the temporal lobes?

A

bilateral hippocampal lesion –> amnesia

bilateral auditory cortex lesions –> cortical deafness

Kluver-Bucy syndrome

unilateral lesion of the sup-post dominnat temporal lobes –> Wernicke’s aphasia

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6
Q

Focal Cerebral Syndromes:

What deficits could be seen with parietal lobe syndromes?

A

lesions of the NON-dominant parietal lobe cause impairment of spatial relationships between the body and its surroundings

Anosognosia -pt is unaware of his/her hemiparesis, which in its extreme form consists of a “denial” of that half of hte body or hemispatial neglect.

can produce asterognosis, agraphesthesia, extinction on double simultaneous stimulation

Lesions to the supramarginal or angular gyrus of the dominant parietal loe –> Gerstmann’s Syndrome, consists of agraphia, right-left disorientation, dyscalculia (difficult with calculations) and finger agnosia (inabilty to identify one’s fingers).

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7
Q

Focal Cerebral Syndromes:

Occipital Lobe Syndromes

A

Occipital lobe syndromes - may invovle enough bilateral visual cortex to produce cortical blindness, which is sometimes accompanied by a denial or unawareness of visual loss, Anton’s syndrome

Bilateral temporo-occipital lesions may produce visual agnosia, a subtype of which is prosopagnosia (inability to recognize previously known faces)

Dominant temporo-occipital lobe lesion –> color anomia, inability to name colors

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8
Q

Alzheimer’s Disease:

Pathogenesis

A

Alzheimer’s Disease: most common type of dementia in the US

Pathogen: Degenerative disease, neurons gradually destroyed by metabolic changes. Most are sporadic, increasing prevalence with age, some rare familial forms exist. Initially, there are changes in the medial temporal lobes and hippocampi –> excessive accumulation of the protein B-amyloid in the for of extracellular amyloid or senile cortical plauqes (hallmakr of AD), unknown trigger –> B-amyloid deposition –> INTRANEURONAL NEUROFIBRILLARY TRANGLES, consisiting of microtubule-associated tau protein

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9
Q

AD:

Increased risks…

A

INC risk: age, trisomy 21, familial types w/ gene mutations affecting B-APP.

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10
Q

AD: symptoms

A

SX: earliest sign is memory loss, followed by cognitive decline

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11
Q

AD: Diagnosis

What lobes in the brain would be important for us to focus our exam on? temporal and parietal cortex

A

formerly a clinical diagnosis “of exclusion” and confirmed only at postmortem examination of the brain

W/out cerebral infarctions, CT or MRI brain scans show only age-related atrophy in AD pateints

PET or SPECT may show hypoperfusion of temporal and parietal cortex, reflecting the underlying hypometabolism in these areas of AD

*PET scan utilizing Pittsburgn Compound B (PIB), which selectively binds to B-amyloid, apparently show the typical AD uptake in the prefrontal, temporal and sensory association cortex, sparing the occipital and primary sensorimotor cortex.

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12
Q

AD: Treatment

A

No curative treatment for AD

Course can be SLOWED by enhancing the cholinergic system with central ACH inhibitors such as donepezil, rivastigmine or galantamine

Memantine can be added or used in place of AChE-I

NMDA antagonist (opposes the excitatory effects of glutmate in CNS)

Sedatives** and **antipsychotic meds may also be needed to control agitation and behavioral symptoms in AD patients

**IMPORTANT to provide support and time off for caregivers

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13
Q

Delirium:

_____ confusional state; global, extensive cognitive impairment, abnormal behavior and cortical dysfunction occur when:….

TIME lapse:

SX: fluctuating levels of ______ and _______ activity, with alternating from ___ to ____.

Prominent findings:

Causes

A

Delirium:

ACUTE confusional state; global, extensive cognitive impairment, abnormal behavior and cortical dysfunction occur when: SEVERAL LOBES OF THE CEREBRAL HEMISPHERES ARE SIMULTANEOUSLY OR PROGRESSIVELY AFFECTED. If it occurs over a short period of hours to days = acute confusional state / delirium

SX: fluctuating levels of ATTENTION and MOTOR activity, with alternating from overly-excitable agitation and often purposeless hyperactivity (as in high on drugs) to periods of obtundation and stupor

Prominent findings: tremulousness, asterixis, myoclonus, ataxia, dysarthia

Causes: multiple causes, brain can be involved (viral-encephalitis or post-ictal state after seizure) or indirectly involved (systemic ilness like kidney failure, metabolic abnormalities, the effects of medications or illict drugs)

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14
Q

Dementia is a general term for a _________ of cortical function which usually evolves _____ abruptly over a ____ period of time (…) and _____ daily function of a patient

How does dementia differ from mental retardation or learning disorders?

SX:

DX.:

Evaluations:

A

Dementia is a general term for a DIFFUSE IMPAIRMENT of cortical function which usually evolves LESS abruptly over a LONGER period of time MONTHS TO YEARS and IMPEDES daily function of a patient

Dementia VS Mental Retardation/Learning Disabilities: this is a loss of PREVIOUSLY acquired mental/intellecutal abilities, differing from other disorders where such abilities were never attained

SX: #1 Memory loss, changes in judgement and intellect

aphasia, apraxia and agnosia can be found; personality changes, and behavior –> as dementia progresses, and pt gets disoriented to time and place/fails to recognize family and friends, unable to perform basic tasks

DX.: relies heavily on the observaiton of family and friends since the pt may deny / be unaware of any cognitive trouble

Evaluations: evaluation for dementia should include standard cognitive testing such as: Mini-Mental State Examination (MMSE), or more detailed neuropsychological profile.

A brain scan, such as MRI, served to determine if dementia is caused by chronic subdural hematomas, brain tumors or abscesses, multiple infarctions or hemorrhages or normal pressure hydrocephalus.

Lumbar puncture (chornic meningitis?), HIV (younger pt),

CBC, chemistry profile, vitamib B12 level and thyroid fxn

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