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5. HDS Neuro Psych > Behavioral Neurology > Flashcards

Behavioral Neurology Flashcards

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1
Q

Types of Intelligence

A

Used to define age-related neurocognitive changes:

  • Crystalized intelligence
    • Refers to skills, ability and knowledge that is overlearned, well-practiced
    • Examples – vocabulary, general knowledge
  • Fluid intelligence
    • The innate ability to process and deal with new information
    • Examples – executive function, memory, processing speed
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2
Q

Age-Related

Neurocognitive Changes

A

Processing speed starts declining early

Other areas begin to decline ~ age 55

  • Stable Cognitive Areas
    • Autobiographical memory
    • Recall of well-learned information
    • Semantic knowledge (knowledge of meanings)
    • Emotional processing
  • Areas of Improvement
    • Vocabulary
  • Areas of Decline
    • Encoding of new memories
    • Working memory
    • Processing speed
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3
Q

Age-Related

Brain Changes

A
  • Decrease in gray matter volume
    • Primarily dependent on diminishing connections among neurons
    • Partially due to death of neurons
    • Some volume decline starts after age 20
  • Decrease in white matter volume
    • Primarily due to decline in number of axons
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4
Q

Cognition Evaluation

A

Neuropsychological Testing

Objective cognition evaluation

  • Compare vs normative values based on education level and age
  • Evaluates attention, executive function, memory, neurovisual function, language and other aspects of cognition
  • Will determine whether persons cognition is aging normally or abnormally
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5
Q

Cognitive Impairment

Classification

A
  • Impaired cognition established
  • Then classify if:
    • Minor neurocognitive disorder (mild cognitive impairment)
    • Major neurocognitive disorder (dementia)
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6
Q

Mild Cognitive Impairment (MCI)

vs

Dementia

A

Main determinant of dementia vs MCI is whether cognitive deficit(s) interfere with persons abilities to perform their usual activities of daily living and work.

No affect on ADLs ⇒ mild cognitive impairment

Impairment affects ADLs ⇒ dementia

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7
Q

Mild Cognitive Impairment

A
  • MCI could be a:
    • Transitional state between normal and dementia
      • If caused by progressive neurodegenerative condition
    • Temporary condition caused by reversible causes
    • Static condition
      • e.g. in case of cerebrovascular diseases
  • ~ 10% of people with MCI reverse to normal
  • ~ 10% - stay stable and do not progress
  • ↑ Risk for developing dementia, especially AD
    • 10-15% progress to AD annually
    • 80% converted to AD over 6 yr period
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8
Q

Major Neurocognitive Impairment (Dementia)

Differential Diagnosis

A
  • MCI
  • Depression
  • Delirium
  • Reversible causes of cognitive impairment
    • Ex. nutritional deficiencies or metabolic abnl
  • Medications
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9
Q

Depression Mimicking Dementia

A

Depression frequently has associated cognitive complaints.

Suspect that mood disorder may be the cause of cognitive complains when:

  • The pt gives a lot of “I don’t know” answers
  • Mismatch between test results and perception
  • Pt notes more problems than are perceived by family or friends
  • Hx of depression
  • Other symptoms of depression are present: impaired sleep, changes in appetite etc
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10
Q

Distinguishing Delirium

A
  • Usually acute-onset
  • Impaired attention and alertness – reduced or hypervigilant
  • Abnormal sleep pattern
  • Attention, alertness fluctuations
  • Profound disorientation
  • There are metabolic triggers
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11
Q

Cognitive Impairment

Reversible Causes

A
  • Nutrition: vitamin B12, folate deficiency
  • Metabolic: TSH, other endocrine abnormalities
  • Trauma, tumor, other CNS disease
    • SDH, hydrocephalus
  • Infection – syphilis, meningitis, HIV, systemic
  • Anemia
  • Vasculitis
  • Medications
    • Cardiac medications
    • Antidepressants & other psychiatric meds
    • Anti-epileptic drugs (AEDs)
    • Sleep medications
    • Bladder medications
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12
Q

Dementia (Major Neurocognitive Impairment)

Overview

A
  • Acquired condition
  • Involving more than one cognitive domain
  • Severe enough to cause a decline in functioning
  • Alzheimer’s disease is the most common type
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13
Q

Dementia Etiologies

A
  • Vascular Cognitive Impairment
  • Alzheimer’s Disease
  • Dementia with Lewy Bodies
  • Frontotemporal dementia (FTD)
  • Normal Pressure Hydrocephalus
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14
Q

Vascular Cognitive Impairment (VCI)

Characteristics

A
  • Abrupt-onset
  • Stepwise decline
    • Patchy memory loss is usual
    • VCI may know day, but not year
    • More focal cognitive loses, for example naming
    • May improve slightly between episodes
    • Slow mental response
  • Focal neurological symptoms and signs could be present
  • Strokes are seen on imaging studies
  • Hachinski scale: 20-point scale
    • Score > 7 – vascular
    • Score < 4 – degenerative
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15
Q

Alzheimer’s Disease (AD)

Overview

A
  • The most common cause of dementia – about 60% of all the cases
  • Insidious onset, slowly progressive
  • The first sx in typical cases is usually memory loss
  • Behavior problems and neuropsychiatric symptoms are common
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16
Q

Alzheimer’s Disease (AD)

Pathology

A
  • A toxic peptide, beta-amyloid accumulates extracellularly
  • Formed from alternate processing of the amyloid precursor protein
  • Cognitive deficits do not correlate with plaque burden
  • Oligomer is the most likely culprit
    • Attacks on the synapse
    • Disrupts communication between neurons
  • Intraneuronal hyper-P-tau accumulation
  • Associated with neuronal death and development of atrophy and clinical symptoms
17
Q

Alzheimer’s Disease (AD)

Symptoms

A
  • Cognitive symptoms
    • Memory impairment; in almost all cases disease affects memory
    • Orientation
    • Visuospatial function
    • Language
    • Frontal networks
  • Neuropsychiatric
    • Behavioral symptoms – aggression, agitation, restlessness, wandering, delusions, hallucinations, etc

The above affect ADLs

18
Q

Alzheimer’s Disease (AD)

Atypical Signs/Symptoms

A
  • Something other than memory issues as first symptom
  • Presence of movement problems, seizures, or tremor early in disease
  • Anyone under 35
  • Suspected history of stroke
  • History of cancer
  • HIV risk factors
  • Head injury
  • Headache or focal symptoms
19
Q

Alzheimer’s Disease (AD)

Genetics

A
  • Sporadic – not associated with specific mutation, might carry gene variants which increase the risk of developing the disease
    • amyloid is not being cleared well in cases of sporadic disease
  • Genetic – carries specific AD mutations with 100% penetration
    • amyloid is overproduced in these cases
20
Q

Genes associated with AD

A
  • Autosomal dominant / early onset
    • Chromosome 1 – Presenilin 2
    • Chromosome 14 – Presenilin 1
    • Chromosome 21 – APP
  • Susceptibility genes
    • APOE 4 genotype (chromosome 19)
    • Chromosome 12, and other
21
Q

APOE Gene

A
  • APOE E4 allele is a genetic risk factor for developing AD
  • There are 3 human alleles – E2, E3 and E4
  • APOE E3 allele is the most common form
  • E4 allele (10%) increases the risk of developing AD
    • Shifts age of onset from ~75 to late 60’s or early 70’s
  • E2 allele (10%) is protective
22
Q

Alzheimer’s Disease (AD)

Diagnosis

A
  • Clinical assessment
  • Neuropsychological testing
  • Biomarker studies
  • Structural imaging – looking for neurodegeneration
  • Functional imaging – looking for functional changes related to neurodegeneration
  • Identifying amyloid
23
Q

Alzheimer’s Disease (AD)

Biomarker Studies

A
  • Studies evaluating amyloid accumulation
    • Amyloid PET scan
    • CSF A-beta level measurements
  • Studies evaluating neurodegeneration
    • Structural evaluation – MRI, CT
    • Functional evaluation (areas of synaptic dysfunction / loss) – FDG-PET
24
Q

Alzheimer’s Disease (AD)

Treatment

A
  • Cholinergic medications: donepezil, rivastigmine, galantamine
  • NMDA modulators: memantine
  • Disease modifying treatments
    • ↓ Beta-amyloid
    • Preventing accumulation or removing amyloid from the brain
    • Immunotherapy is in development for humans
25
Q

Dementia with Lewy Bodies

A
  • Cognitive impairment with poor attention and relative sparing of memory
  • Fluctuation of cognition
  • Parkinsonism
  • Psychotic symptoms, especially visual hallucinations
  • REM sleep behavior disorder
  • Autonomic instability
26
Q

Frontotemporal Dementia (FTD)

Overview

A
  • Variants: behavioral and language variants (Primary progressive aphasia)
  • Behavioral variant FTD initially presents with:
    • Changes in personality
    • Loss of social decorum
    • Impulsivity
    • Inappropriate behaviors
    • Withdrawal
    • Bizarre behaviors
    • Primarily dysexecutive cognitive syndrome
  • Language variants (Progressive aphasias) initially presents with:
    • Language function disintegration
27
Q

Frontotemporal Dementia (FTD)

Anatomy of Impairment

A

Left frontal: expressive language, depression, frustration

Orbitofrontal: disinhibition

DLPF: executive function

Cingulate gyrus: apathy

Right temporal: bizarre, schizophrenic, facial recognition

Right frontal: irritable, disinhibition, euphoric

Left temporal: semantic impairment

28
Q

Frontotemporal Dementia (FTD)

Genetics

A
  • Tau gene – chromosome 17
  • Progranulin gene – chromosome 17, TDP-43
  • C9orf72 – chromosome 9
  • Many unlinked mutations
29
Q

Normal Pressure Hydrocephalus

A
  • Classical clinical triad:
    • Dementia
    • Urinary incontinence
    • Magnetic (apraxic gait)
  • It can be treatable, and sometimes fully reversible if dx early enough
  • Treatment: drainage of CSF fluid (V-P shunt)
  • Cognitive impairment is the most resistant sx to improve with tx

5. HDS Neuro Psych (46 decks)

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