Different faces of Dementia
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Transcript of Different faces of Dementia
Different faces of Dementia
Neeraj Gupta & Pallavi DhamOPMHS, Glenside
> Basic Neuroanatomy> Dementia overview> Differential diagnosis> Types of dementia> Approach to differentiating
Dementias
What is Cognition?
> The term cognition (Latin: cognoscere, "to know", "to conceptualize" or "to recognize") refers to a faculty for the processing of information, applying knowledge, and changing preferences.
> These processes include attention, memory, producing and understanding language, solving problems, and making decisions, higher order motor and sensory functions.
Brain areas and cognition
Cortex> Frontal Lobe- executive
functions, speech, movement
> Parietal Lobe- associated with movement, perception of stimuli, orientation, recognition,
> Occipital Lobe- associated with visual processing
> Temporal Lobe- associated with perception and recognition of auditory stimuli, memory, and speech
Subcortical areas> Limbic system
(amygdala, hippocampus, Thalamus, hypothalamus and pituitary): Emotions, memories
> Basal ganglia, Cerebellum: movement and coordination
> Brain stem: vital functions
All parts are interconnected. Impairment in one area can influence another
What is dementia?
> Dementia (taken from Latin, originally meaning "madness", from de- "without" + ment, the root of mens "mind")
> Differentiated from “madness” by Emil Kraepelin
> Diagnosis made on clinical observations
DSM IV TR definition of Dementia
> The essential feature of a dementia is the development of multiple cognitive deficits that include memory impairment and at least one of the following cognitive disturbances:• aphasia, apraxia, agnosia, or a disturbance in
executive functioning.
> The cognitive deficits must be sufficiently severe to cause impairment in occupational or social functioning and must represent a decline from a previously higher level of functioning
Metabolic
Endocrine
Infection
Drugs &Toxins
Tumour
Trauma
Other neurological
Miscellaneous
Vascular
Neuro-degenerative
Dementia
Clinical Presentation in Dementia
Symptoms of Dementia
> Memory impairment • refers to the inability to learn new information
or to recall previously learned information. Does he have difficulty remembering recent
conversations? Is he frequently repetitive? Is he aware of current events? Does he misplace or lose things? Does he forget to turn off the stove?
Cognitive impairment contd
> Aphasia, or language impairment• Does he have difficulty finding correct word?• Is it sometimes difficult for others to
understand him?• Does he have difficulty remembering names? • Does he have difficulty maintaining or initiating
conversations?
Cognitive impairment contd
> Apraxia, or • impaired ability to carry out motor activities
despite intact motor function Does he have difficulty using familiar objects? Does he have difficulty performing simple tasks
at home? Does he have trouble performing previously
acquired skills (i.e., knitting, woodworking)? Is there any difficulty in dressing, bathing, or
feeding?
Cognitive impairment contd
> Agnosia• failure to recognize or identify objects despite
intact sensory function, Does he have difficulty recognizing people,
objects or places? Does he lack insight into his own impairment?
Cognitive impairment contd
> Impairment in executive functioning • refers to disturbances in planning, organizing,
sequencing, and abstracting. > Does he have difficulty relating to
newspapers or television?
> Is he still able to manage finances, the checkbook, medications or taxes?
> Does he or she show problems in judgment or problem solving?
> Does he have difficulty remembering short lists for shopping?
> Does he need assistance with ADL’s?
Neuropsychiatric symptoms
• Not required for the diagnosis of dementia. • Commonly co-occur with dementia• Often the cause of greatest caregiver distress.• Neuropsychiatric Inventory (NPI) evaluates 12
neuropsychiatric disturbances: Delusions, hallucinations, agitation,
dysphoria, anxiety, apathy, irritability, euphoria, disinhibition, aberrant motor behavior, night-time behavior disturbance, and appetite and eating abnormalities.
PSYCHOSIS OF ALZHEIMER'S DISEASE COMPARES WITH SCHIZOPHRENIA IN THE
ELDERLY
Psychosis of AD Schizophrenia
• Bizarre or complex delusions Rare Frequent• Misidentifications of caregivers Frequent Rare• Common form of hallucinations Visual Auditory• Schneiderian first-rank Rare Frequent• Active suicidal ideation Rare Frequent• Past history of psychosis Rare Frequent• Eventual remission of Frequent Uncommon
psychosis• Need for long-term treatment Uncommon Very common
with antipsychotics• Mean optimal daily dose of 15–25% of that in a 40–60% of that• antipsychotics young adult with in a young
schizophrenia adult withschizophrenia
http://www.youtube.com/v/9iXPHhfk_7E
Normal ageing MCI Dementia
Some cognitive decline expected for the age/education
Cognitive decline, more than expected for age/education
Definite cognitive decline
Subjective complaint with little objective findings
Objective deficits
Objective deficits
Little impairment in functioning
Little impairment in functioning
Impaired functioning
Is it Delirium , Dementia or Depression?
Delirium Dementia
Onset Rapid (hours/days); rapid decrease in MMSE score.
Slow (months, years); slow decline of 2 to 3 MMSE points over a period of years.
Symptoms Fluctuate over the course of the day.
Relatively stable.
Duration Days to weeks. Years.
Orientation Disorientation and disturbed thinking are intermittent.
Persistent disorientation.
Level of consciousness
Fluctuates, with inability to concentrate.
Alert, stable.
Sleep/wake cycle
Sleep/wake cycle may be reversed.
Sleep may be fragmented.
Depression
Subacute onset- weeks to months, pseudodementia
Persistent and pervasive
Weeks to months
Oriented
Alert, stable
Early morning awakening
Types of dementia
Response to
treatmentEtiology
Cognitive Profile
ReversibleIrreversible
AlzheimersOther
medical conditions
Cortical SubcorticalVascular
Reversible dementias
Irreversible Dementias
> Infection: HIV, syphilis, encephalitis
> Tumours> Trauma: SDH> Toxins: heavy metal,
alcohol, cancer chemotherapy
> Metabolic: B12,thiamine, Niacin deficiency
> Endocrine: thyroid, diabetes
> Normal pressure hydrocephalus
> Sub classified based on pathology and areas of the brain effected
> Alzheimer's Dementia> Vascular dementia> Lewy body dementia> Fronto-temporal
dementias> Traumatic brain injury> Mixed etiology> Others
•Correcting the underlying reversible cause may improve dementia
Characteristics Cortical D Subcortical D
Language Aphasia -early Late
Memory Recall & recognition Recall>recognition
Attention impaired impaired
Visuospatial impaired impaired
calculation early late
Executive function Proportionate to other deficits Disproportionate
Speed of cognition fine Slowed
personality unconcerned apathetic
mood euthymic depressed
speech articulate dysarthric
posture upright Bowed/extended
coordination preserved impaired
Adventitious movements absent Tremor, chorea, tics
Types of dementias- DSM-IV and ICD 10
DSM IV> Alzheimers dementia> Vascular dementia> Due to general
medical conditions: HIV, picks, brain injury, tumours,etc
> Substance induced persisting dementia
> Due to multiple etiologies
ICD 10> Alzheimers D> Vascular D> Dementia in other
diseases: Picks, Creutzfeldt jacob, huntingtons disease, parkinsons disease, HIV, others
Alzheimer's Dementia
Prevalence-
accounts for up to 90% of the dementia cases. 2/3 have concomitant pathologies prevalence increases exponentially every 5
years Sex differences- females>males
Aetiology
> Exaggeration of normal aging process> Genetic
• Amyloid precursor protein (APP), • Presenilin-1 (PS-1),.• Presenilin-2 (PS-2),.• Apolipoprotein E-e4 (APOE4), • Other risk factors: Lifestyle and heart health
Plaques and Tangles: The Hallmarks of AD
The brains of people with AD have an abundance of two abnormal structures:
An actual AD plaque An actual AD tangle
• beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells
• neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell
AD and the Brain
Slide 16
The Changing Brain in Alzheimer’s Disease
No one knows what causes AD to begin, but we do know a lot about what happens in the brain once AD takes hold.
Pet Scan of Normal Brain
Pet Scan of Alzheimer’s Disease Brain
AD and the Brain
Slide 19
AD- Brain areas and cognitive deficits
> Initial memory deficits
> Global deficits> Impairment in
functioning
AD- BPSD
> Anosognosia- unaware of the illness/impact
> Passivity-apathy -70%, 2years prior to the diagnosis
> Psychosis-later on> Depression, anxiety, catastrophic
reactions> Aggression> Sun downing
AD- course and outcome
> Gradual progressive decline> Average survival time -4-6 years > Life expectancy reduced by 50%
Vascular Dementia
Vascular dementia
> Temporal correlation between :• Cognitive decline• Cerebrovascular disease: neurological
deficits or vascular damage evident on brain imaging
VD:
> Account for about 17% of all dementias> Males> Females> Overall prevalence is increasing with
ageing population> Risk factors: hypertension, diabetes,
hypercholesterolemia, obesity, smoking, cardiovascular disorders
VD- types
> Subcortical ischemia- frontal lobe and basal ganglia: executive dysfunction, slowed processing
> Multi-infarct: disjointed deficits> Strategic infarcts: areas related to
cognition> Mixed alzheimers and VD
Course and prognosis
> Step ladder pattern of cognitive decline> Shorter life expectancy compared to
Alzheimer's. Yet it is variable and depends on the age and underlying risks
Lewy Body Dementia
Dementia Lewy Body (DLB)
> Recognised as the second most common type of neurodegenerative dementias after Alzheimer's Disease
> Lewy bodies- protein deposits in neurons and glia
DLB- clinical presentation
> Shares features of Alzheimer's and Parkinson's disease
> Cognitive deficits: visuospatial, executive, memory-benefits from cueing
> Parkinson's features :bradykinesia, tremor, rigidity, autonomic instability
> Additional features: detailed visual hallucinations, fluctuations, day time drowsiness
> Depression and anxiety
Diagnostic criterion- DLBCentral feature> Progressive dementia - deficits in attention and executive function are typical.
Prominent memory impairment may not be evident in the early stages. Core features: > Fluctuating cognition with pronounced variations in attention and alertness. > Recurrent complex visual hallucinations, typically well formed and detailed. > Spontaneous features of parkinsonism. Suggestive features:> REM sleep behavior disorder (RBD), which can appear years before the onset of
dementia and parkinsonism. > Severe sensitivity to neuroleptics occurs in up to 50% of LBD patients who take
them. > Low dopamine transporter uptake in the brain's basal ganglia as seen on SPECT
and PET imaging scans. (These scans are not yet available outside of research settings.)
Supportive features: > Repeated falls and syncope (fainting). > Transient, unexplained loss of consciousness. > Autonomic dysfunction. > Hallucinations of other modalities. > Visuospatial abnormalities. > Other psychiatric disturbances.
> A clinical diagnosis of LBD can be probable or possible based on different symptom combinations. • A probable LBD diagnosis requires either:
Dementia plus two or more core features, or Dementia plus one core feature and one or
more suggestive features.
• A possible LBD diagnosis requires: Dementia plus one core feature, or Dementia plus one or more suggestive features.
Fronto-Temporal Dementia
Fronto-temporal Dementia (FTD)
> Occurs most commonly in the 50’s (less than 65 years)
> Most common form of pre-senile dementia
> Frontal and temporal lobe atrophy> 1/3 to ½- genetic aetiology> Nature of the pathological changes vary-
pick body/ vacuolisation
FTD- clinical presentation
> Changes in behaviour: • impulsive, apathetic, socially disinhibited, lack
of empathy, judgement or insight, hypersexual, neglect, compulsive behaviours
> Problems with language: • including difficulty making or understanding
speech, often in conjunction with the behavioural type’s symptoms.
Dementia due to prion disease
> Rapidly progressive neurodegerative disorder
> Abnormal protein called prion> Sporadic, inherited or exposure to
infected material> Rapidly progressive decline, ataxia,
myoclonic jerks
Dementia due to brain damage- other causes
> Head trauma- direct damage and increased predisposition to further degeneration
> Huntingtons disease: familial,hyperkinesia, dementia
> Parkinsons disease> Wilson’s disease> Leukodystrophies> Idiopathic basal ganglia calcification> Dementia due to mixed causation
Evaluation of Dementia
> A thorough history• An assessment of each cognitive domain• Behavioral and neuropsychiatric symptoms• Degree of socio-occupational impairment
> A physical and neurological examination> Mental status examination> Bedside or detailed cognitive testing> Investigations
ASSESSMENT
• Common tools to assist include:
• ADL (activities of daily living) and IADL (instrumental activities of daily living) checklists.
• Cognitive screens (MMSE, RUDAS, KICA – for Indigenous clients).
• Clock drawing test.
• Animal naming (1 Minute).
• Informal tests of frontal lobe functioning
IMPACT ON FAMILY AND CAREGIVERS• Caregivers are at high risk for developing
psychological distress.
• The rates of depression and anxiety are increased compared with the general population.
• Anger and resentment are emotions commonly felt by caregivers.
• Reduced physical and mental health.
MODEL OF EFFECTS OF DEMENTIA ON CAREGIVERS
MANAGEMENT
• Consider both non-pharmacological and pharmacological management strategies.
• Base management on a detailed assessment of specific symptoms and contributing medical, psychological or environmental factors.
• Treat underlying medical causes such as infection, delirium, pain.
• Cease medications that are unnecessary, change medications that may aggravate the specific symptoms.
• Address environmental factors such as under or over stimulation.
Role of medication
> Controversial> Consent> Safety- side effects, stroke, cardiac, Lewy
Body Dementia
SUPPORT AVAILABLE
• Ideally it is best to assist the client to live as independently as possible in familiar surroundings, such as at home, whilst they can be managed with community support.
• Home and Community Care (HACC).
• Department Veteran Affairs (DVA).
• Community Aged Care Package (CACP).
• Extended Aged Care at Home (EACH).
• Extended Aged Care at Home-Dementia (EACH-D).
• Also consider psychosocial rehabilitation, Rapid Intensive Brokerage Service (RIBS) or Transition Care Package (TCP) (needs to be in or avoid hospital for RIBS and in hospital for TCP).
Conclusion
> DEMENTIA is a • Complex neuropsychiatric illness• Multiple etiologies• Varied clinical manifestations• Requires detailed evaluation• Multidisciplinary management