Different faces of Dementia

1. Different faces of Dementia Neeraj Gupta & Pallavi Dham OPMHS, Glenside

2. Basic Neuroanatomy Dementia overview Differential diagnosis Types of dementia Approach to differentiating Dementias

3. 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.

4. 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 Brain areas and cognition

5. 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

6. 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

7. 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

9. Clinical Presentation in Dementia

10. 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?

11. 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?

12. 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?

13. 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?

14. 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?

15. 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.

16. 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 with schizophrenia

17. http://www.youtube.com/v/9iXPHhfk_7E

21. 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

23. 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 Types of dementias- DSM-IV and ICD 10

24. Alzheimer's Dementia

25. 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

26. 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

27. AD and the Brain • Plaques and Tangles: The Hallmarks of AD • The brains of people with AD have an abundance of two abnormal structures: • 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 An actual AD plaque An actual AD tangle Slide 16

28. AD and the Brain 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 Slide 19

29. AD- Brain areas and cognitive deficits • Initial memory deficits • Global deficits • Impairment in functioning

30. 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

31. AD- course and outcome • Gradual progressive decline • Average survival time -4-6 years • Life expectancy reduced by 50%

32. Vascular Dementia

33. Vascular dementia • Temporal correlation between : • Cognitive decline • Cerebrovascular disease: neurological deficits or vascular damage evident on brain imaging

34. 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

35. 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

36. 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

37. Lewy Body Dementia

38. 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

39. 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

40. Diagnostic criterion- DLB Central 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.

41. 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.

42. Fronto-Temporal Dementia

43. 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

45. 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. 

46. 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

47. 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

48. 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

49. 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

50. 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.