Dementia Flashcards
Dementia
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.
Alzheimer’s Disease
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
AD Stage 4
Early Alzheimer’s Disease Diagnosis
Multiple facets of memory impairment – typically difficulty recalling short-term memories; problems with new learning
AD Stages 1 & 2
effects of normal aging (everyday forgetfulness)
AD Stage 3
mild cognitive impairment
AD Stages 5-7
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
AD Neuropathology:
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
AD Neuropathological changes:
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
AD Neuropsychological changes:
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
AD Language Impairments
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
AD Visuo-spatial relationships
May be impaired early
See over time
Difficulty navigating while traveling
May appear disoriented
AD Motor abilities
relatively intact until late stages
May see restlessness- early on
Immobile- late stage
AD Medical management:
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
Pick’s Disease
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
PD Clinical presentation:
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
PD Neuropathology:
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
PD Neuropsychological changes:
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
PD Medical treatment:
No cure
Personality changes managed pharmacologically
Train caregivers to assist with daily living needs
Parkinson’s
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
Parkinson’s Clinical presentation:
Deficits in: Memory Executive functions Personality Motor movements Balance Dementia Depression
Parkinson’s Neuropathology:
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
Parkinson’s Neuropsychological changes:
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
Parkinson’s Hallmark
Motor abilities: Rigidity Bradykinesia Cogwheeling- jerky, ridged movements of limbs Resting tremors Intention tremors Balance and postural changes Shuffling gait
Parkinson’s Medical treatment
Drug treatments to either
Decrease excitatory neurotransmitters
Increase dopamine levels (Levodopa)
Drug treatments have side effects
Huntington’s
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
HD
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
HD Neuropsychological changes:
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
HD Deficits
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
AIDS
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
AIDS Neuropathology:
Cerebral atrophy
Frontal
Parietal
Temporal
Enlarge ventricles
Inflamed brain tissue
Multinucleated giant cells
Small inflammatory noodles found in white matter and subcortical nuclei
AIDS Neuropsychological changes:
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
Vascular Dementia –Multi-Infarct Dementia
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
Vascular Dementia Neuropathology:
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
Vascular Dementia Deficits
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
Infectious Dementia –Creutzfeldt-Jakob’s Disease
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
CJD Clinical presentation:
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
CJD Neuropathology:
Diffuse or focal brain atrophy Enlarged ventricles Neuronal degeneration or death Gliosis Spongiform (holes in the brain)
CJD Neuropsychological changes:
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
Magnetic Resonance Imaging (MRI)
Uses powerful magnetic fields
Examines brain structures-static
Role of SLP in Dementia
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
