Dementia Flashcards

1
Q

Dementia

A

Acquired disorders – progressive cognitive decline

Individual has to have:

Memory impairment + 1 other cognitive domain
Examples: language, visuo-spatial skills, abstract thinking, or judgement

Significant loss in functional abilities
Examples: social, vocational, daily living, etc.

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2
Q

Alzheimer’s Disease

A

Cortical Dementia

Clinical presentation:
Slow onset with ~ 10 year progression to death

Global Deterioration Scale (Ferris, de Leon, & Crook, 1982)
7-point rating scale of cognitive and functional capacity

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3
Q

AD Stage 4

A

Early Alzheimer’s Disease Diagnosis

Multiple facets of memory impairment – typically difficulty recalling short-term memories; problems with new learning

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4
Q

AD Stages 1 & 2

A

effects of normal aging (everyday forgetfulness)

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5
Q

AD Stage 3

A

mild cognitive impairment

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6
Q

AD Stages 5-7

A

Advanced Stages of Alzheimer’s

Memory and other cognitive functions progressively decline

Changes in personality and emotional regulation

No longer live independently

Bed ridden- primitive reflexes return

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7
Q

AD Neuropathology:

A

Diffuse brain atrophy (the brain shrinks)
~20% reduction in weight compared to normal controls

Temporal, frontal, & parietal lobes

Ventricles enlarge
Begins in hippocampus & entorhinal cortex

Impacts connections between these areas, the amygdala and neocortex

Vulnerable regions of neocortex 
Temporal lobe
Frontal lobe
Parietal lobe
Associations between these lobes
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8
Q

AD Neuropathological changes:

A

Senile plaques:
Round with beta-amyloid core; found outside the neuron
Abnormal amounts or structures of beta-amyloid

Neurofibrillary tangles:
Found inside the neuron
Tangles of abnormally decomposed tau protein

Neuronal and synaptic loss

Reduction in neurotransmitters
Including: acetylcholine & serotonin

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9
Q

AD Neuropsychological changes:

A

Memory – difficulty recalling current or recent information
Difficulty with learning new information
Remote memory is impaired over time
Procedural memory remains intact until late stages

Executive dysfunction- difficulty setting and achieving goals
Reduced attention
Difficulty problem solving
Difficulty with reasoning

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10
Q

AD Language Impairments

A

Naming/word finding problems

Semantic paraphasias

Difficulty comprehending complex sentences
multiple step directions

Eventually problems with simple sentences
Discourse errors
Maintaining topic
Producing a variety of sentences
Difficulty with abstract language
jargon

Difficulty with reading and writing

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11
Q

AD Visuo-spatial relationships

A

May be impaired early
See over time
Difficulty navigating while traveling
May appear disoriented

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12
Q

AD Motor abilities

A

relatively intact until late stages
May see restlessness- early on
Immobile- late stage

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13
Q

AD Medical management:

A

No cure

Drug treatments
Modulating neurotransmitters- to improve cognitive functioning
Neuroleptics- treat behavioral symptoms
Tacrine-to improve memory
Inhibits a chemical that prevents the breakdown acetylcholine

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14
Q

Pick’s Disease

A

Restricted brain atrophy
Cortical Dementia

Temporal and frontal lobes
Atrophy may be symmetrical or asymmetrical

Rare disease with onset typically in 40’s

Cause unknown

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15
Q

PD Clinical presentation:

A
Early changes in personality
Poor social skills
Emotional blunting (no emotions)
Disinhibition
Poor insight and judgement
Language disorder
Naming problems and empty speech seen early, then gets worse
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16
Q

PD Neuropathology:

A

Atrophy of the temporal and/or frontal lobe(s)

Pick bodies
Dense structures found inside cortical cells – occurs in ~ ¼ of cases
Do not occur in normal age and not found in other diseases

Pick cells
Inflated or enlarged neurons – occurs in ~ ½ of cases

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17
Q

PD Neuropsychological changes:

A

Memory- deficits occur in later stages of the disease

Language-
Early difficulties include naming and empty speech

Mid-late difficulties include aphasia and mutism

Visuo-spatial – impaired late

Motor abilities- impaired late
Tremor, rigidity, and slow movements
Muscle weakness

18
Q

PD Medical treatment:

A

No cure

Personality changes managed pharmacologically

Train caregivers to assist with daily living needs

19
Q

Parkinson’s

A

Subcortical Neurodegenerative disorder that affects the extrapyramidal system

Gradual onset of symptoms

Typically seen in older individuals

Symptoms include:
Tremors
Rigidity
Posture and balance problems
Masked-like face
Eventual dementia
20
Q

Parkinson’s Clinical presentation:

A
Deficits in:
Memory
Executive functions
Personality
Motor movements
Balance
Dementia
Depression
21
Q

Parkinson’s Neuropathology:

A

Loss of dopamine in substantia nigra and other brain structures

Lewy body inclusions- found in substantia nigra neurons and other brain structures
Outer region is loosely packed neurofilaments and inner region is tightly packed

22
Q

Parkinson’s Neuropsychological changes:

A
Memory- procedural and spontaneous recall impaired
Language- hypokinetic dysarthria (impaired respiration, phonation, articulation, and resonance)
Harsh vocal quality
Reduced syllabic stress
Monoloudness
Imprecise consonants
Increased rate of speech
Palilalia- stuttering-like repetitions
Also see flat affect

Visuo-spatial- impaired to some degree

23
Q

Parkinson’s Hallmark

A
Motor abilities:
Rigidity
Bradykinesia
Cogwheeling- jerky, ridged movements of limbs
Resting tremors
Intention tremors
Balance and postural changes
Shuffling gait
24
Q

Parkinson’s Medical treatment

A

Drug treatments to either
Decrease excitatory neurotransmitters
Increase dopamine levels (Levodopa)
Drug treatments have side effects

25
Q

Huntington’s

A

Subcortical Inherited progressive disease

A child of a parent with the disease has a 50% of developing it

Onset in adulthood but can be adolescences or elderly

Duration approximately ~14 years

Associated with changes in personality, memory motor and intellectual functioning

Psychological issues include:
Depression
Mania
Delusional thoughts
Paranoia
26
Q

HD

A

Clinical presentation:
Initial symptoms are chorea and behavioral changes

Movements affect face, trunk, and limb muscles

Neuropathology:
Loss of neurons in the caudate nucleus, projects to the globus pallidus, and substantia nigra
Atrophy of frontal lobe over time
Some reductions in neurotransmitters

27
Q

HD Neuropsychological changes:

A

Memory- difficulty encoding and retrieving information

Language- 
Reduced verbal fluency
Word finding difficulties and paraphasias
Hyperkentic dysarthria
Harsh vocal quality/excessive loudness
Prolonged phonemes or pauses
Monopitch
Hypernasality
Imprecise consonants
Involuntary inspiration/ex
28
Q

HD Deficits

A

Visuo-spatial- some deficits observed

Motor abilities- problems with voluntary and involuntary muscle movements

Involuntary- chorea, dystonia, athetosis, motor restlessness, and myoclonus

Medical treatments:
No cure
Pharmacological treatments

29
Q

AIDS

A

Subcortical Neurological disorder associated with the AIDS virus

The AIDS virus is complex and has a variable course
Lots of things can go wrong

Clinical presentation:
“Probable dementia” if 2 or more issues are present
Attention, processing speed, reasoning skills, visuo-spatial, memory, learning, speech and language

Must also have:
Motor impairment, change in social or emotional behavior, alterations in consciousness, or psychiatric disorder

30
Q

AIDS Neuropathology:

A

Cerebral atrophy
Frontal
Parietal
Temporal

Enlarge ventricles

Inflamed brain tissue

Multinucleated giant cells

Small inflammatory noodles found in white matter and subcortical nuclei

31
Q

AIDS Neuropsychological changes:

A

Memory-may or may not be impaired and may be impaired early
R
educed processing speed

Language- ataxic dysarthria

Visuo-spatial- not impaired

Motor abilities- motor learning issues

Medical treatments:
Pharmacological

32
Q

Vascular Dementia –Multi-Infarct Dementia

A

Multiple small infarcts in a person with hypertension

Clinical presentation:
Occurs abruptly and shows stepwise deterioration

Can show fluctuations-alternating improvement and deterioration

Case history of hypertension and/or stroke

Deficits will depend on areas of brain damaged

33
Q

Vascular Dementia Neuropathology:

A

Multiple infarcts in both cortical and subcortical areas

Combination of distribution and the number of lesions that determine severity

Neuropsychological changes:

Memory- problems with recent memory
Patient is aware and doesn’t deny problems

Language-If lesion is in language areas will have deficits
If lesion is small deficits may be transient
If in white matter may impact speech

34
Q

Vascular Dementia Deficits

A

Visuo-spatial- may be impacted if lesions is in parietal lobe

Motor abilities- depends on location of lesion

Medical treatments:
Underlying pathology can be treated

Rehabilitation services for speech, cognitive, and motor impairments

35
Q

Infectious Dementia –Creutzfeldt-Jakob’s Disease

A

Transmissible disease that results in a spongiform encephalopathy

Rare disease, how it’s transmitted is unknown

Appears not to be easily transmissible
Genetic
Can be transmitted to other species

Typically seen in individuals ages 60 and older
Documented in a patient as young as 16

36
Q

CJD Clinical presentation:

A

Patient complains of changes in eating in sleeping

Weight loss and feeling anxious
Three initial neurological presentations in 1/3 of cases

Mental deterioration
Confusion
Changes in behavior

Ataxia and tremor reported in 1/3 of cases

Another 1/3 of cases report a combination

37
Q

CJD Neuropathology:

A
Diffuse or focal brain atrophy
Enlarged ventricles
Neuronal degeneration or death
Gliosis
Spongiform (holes in the brain)
38
Q

CJD Neuropsychological changes:

A

Memory- hallmark of disorder
Impaired recent memory early
Impaired long-term memory over time

Language- may present with aphasia
Poor verbal fluency
Mutism may occur over time

Visuo-spatial- impaired and visual disturbances

Motor abilities-
Dysarthria early in disease
Dysphagia
Dystonia
Gate issues
Tremors
Rigidity
39
Q

Magnetic Resonance Imaging (MRI)

A

Uses powerful magnetic fields

Examines brain structures-static

40
Q

Role of SLP in Dementia

A

Diagnosis & treat communication problems

Need to consider diseases are progressive; get worse over time

Can have short-term success

Differential diagnosis
Aphasia
Cognitive-communication
Motor speech
Resonance, respiration, phonation, and articulation
Treatment focus may include: 
Maintain communication strengths
Compensatory strategies
Direct treatment (when appropriate)
Support networks/group therapy
Caregiver training