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Dementia- recent updates
1. Dementia is defined as a progressive impairment of cognitive functions occurring in clear consciousness. The most common causes are Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, and vascular dementia. 2. Neuroimaging and neuropathological findings help characterize different dementias. Alzheimer's disease shows hippocampal and temporal lobe atrophy on MRI and beta-amyloid plaques and neurofibrillary tangles microscopically. Frontotemporal dementia presents with frontal and anterior temporal lobe atrophy. 3. Treatment involves pharmacological interventions like cholinesterase inhibitors and memantine for Alzheimer's, as well as non-pharmacological approaches like cognitive stimulation, environmental modifications, and
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Dementia- recent updates
- 1. Dr. Santanu Ghosh,MD Assistant Professor, Department of Psychiatry Tripura medical College
- 2. What is dementia?? Dementiais defined as a progressive impairment of cognitive functions occurring in clear consciousness (that is, in the absence of delirium)
- 3. HISTORY 1 2 3 Dementia= Dementatus Meaning out of one's mind Celsus First used the term dementia Oribasius, first attempts to describe an etiology beyond old age
- 4. Epidemiology >65 years >85 years (OutpatientPopulation) >85 years (General Population Chronic Care Facilities By 2050 5% 15 - 20 % 20 -40 % 50% • 14 million :Alzheimer's disease • >18 million people with dementia Prevalence
- 5. Etiologies of Dementia Degenerative Alzheimer'sdisease Frontotemporal degeneration Parkinson's diseaseLewy body deposition Progressive supranuclear palsy Idiopathic cerebral ferrocalcinosis
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- 7. Persistent hemodialysis Heavy metals Irradiation CarbonMonoxide Anticholinergic Drugs Drugs & toxins Alcohol Etiology cont….
- 8. Etiology cont…. Cognitive decline in schizophrenia Pseudodementia ofdepression Psychiatric
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- 11. Infarction (single ormultiple or strategic lacunar) Binswanger's disease (subcortical arteriosclerotic encephalopathy) Hemodynamic insufficiency (e.g., hypoperfusion or hypoxia) Cardiac,Cardiac, vascular &vascular & anoxiaanoxia Etiology cont….
- 12. Neuropathology of dementia Denselypacked microfibrils found in cytoplasm of dead neuron Consists of paired helical filaments of abnormally phosphorylated tau protein Primarily affects hippocampal pyramidal neurons and consists of group of intra-cytoplasmic vacuoles about 5 µm in diameter congaing small granule Neurofibrillary Tangle Senile Plaques Granulovacuolar Degeneration Extracellular deposits of 42 – amino acid amyloid β peptide derived from amyloid precursor protein Grossly: Cortical atrophy particularly involving anterior frontal & temporo-parietal area
- 13. Neuropathology of dementiacont.. 1= Congophilic angiopathy consisting of amyloid deposit in the wall of small arteries 2= Generalized loss of neuronal dendrites 3= Loss of choloinergic neurons nucleus basalis of Meynert 4= Loss of noradrenergic neurons in locus coeruleus, loss of serotonergic neurons of the dorsal raphe nucleus
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- 15. Neurotransmitters in Dementia SerotoninDopamine Glutamine Acetyl Choline
- 17. Types of dementiaand BPSD Aspontinity, aggression, wandering Incontinence, Paranoid symptoms Alzheimer Disease
- 18. Types of dementiaand BPSD cont.. • Visual hallucination • Auditory hallucination • Persecutory delusion • Anxiety • Depression • Agitation • Insomnia Lewy BodyLewy Body DementiaDementia • Changes of character & social behavior • Sexual misadventure • Overeating • Tendency to touch Pick’sPick’s DementiaDementia • Anxiety • Depression • Labile mood • Judgment and insight remains intact for long time VascularVascular DementiaDementia
- 20. Assessment Other medical conditions Behavioral problems, psychoticsymptoms, or depression Mini Mental status Examination • Severe : 0-10 • Moderate : 11-17 • Mild : 18-23 • Normal : 24-30 Daily function •Feeding •Bathing •dressing, • Mobility • Manage finances and medications
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- 23. Alzheimr’s Disease (AD) •Is the most common cause of dementia. • > 90% sporadic , age usually >65yrs. • <10% familial, age usually <60 yrs. • Clinically: Initially normal- develops ‘Mild Cognitive Impairment’ – goes on to develop AD. • Pathology: AD is characterized by senile plaques, neurofibrillary tangles, decreased synaptic density, neuron loss and cerebral atrophy.
- 24. sMRI- Alzehimer’s Disease Assessmentof cerebral atrophy of hemisphere particularly posterior temporal and parietal lobes & specific anatomic areas like hippocampus and medial temporal lobe 1. Visual ranking system: Mild / moderate / severe. 2. Quantitative measurement : Linear / area / volumetric*. Measurements must be adjusted for age, gender and head size and then referenced to an appropriate control population.
- 25. Among these measurementsof hippocampus was most sensitive marker of pathology of AD early in disease. Normal ALZHEIMER’S DISEASE
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- 27. MR Perfusion studyin Alzheimer’s disease A characteristic bilateral temporoparietal decrease in blood flow is noted.
- 28. STRUCTURAL ANALYSIS Amygdala Hippocampus Rest ofcortex PET: Reduced uptake of glucose in temporal lobe. SPECT/MR perfusion Reduced perfusion MR SPECTROSCOPY: -Decrease in NAA. -Increase in myoinositol. Alzheimer’s disease
- 29. 2. DEMENTIA WITHLEWY BODIES
- 30. • It ischaracterized by presence of lewy bodies in the cortical neurons on histology. • It is 2nd / 3rd most common cause of dementia in elderly. • To date, no MRI features have been identified that to characterize DLB. • “THE ABSENCE OF SIGNIFICANT MEDIAL TEMPORAL LOBE ATROPHY” in a elderly demented patient suggests DLB etiology rather than AD etiology.
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- 32. • Age ofonset: 50-65 yrs. • Genetically linked to chromosome 3 and 17 • FTD is a term used to describe a family of neurodegenerative disorders characterized by degeneration of frontal and temporal lobes. • The three most common HISTOLOGICALLY classified(Not radiological) FTD syndromes are Pick's disease. Frontal-lobe degeneration & FTD with amyotrophic lateral sclerosis.
- 33. MRI features ofFTD • MR features: Severe sharply localized atrophy- bilaterally symmetric- “knife-blade atrophy.” Hyperintense signal in the cortex and underlying white matter of the affected areas. • Areas involved: frontal lobe, anterior temporal lobes, extra pyramidal nuclei especially the caudate nucleus, insular cortex & anterior corpus callosum. • Areas spared: Posterior two thirds of the superior temporal gyrus, occipital lobes, parietal lobes & perirolandic region • These MR findings in an appropriate clinical setting may support the diagnosis of FTD.
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- 36. 4. DEMENTIA OFVASCULAR ETIOLOGY
- 37. • Dementia dueto chronic cerebrovascular disease is 2nd / 3rd most common cause of dementia in elderly(AD and dementia with Lewy bodies). • Three main forms are recognized: Multi infarct dementia. Sub cortical vascular dementia/ Binswanger’s disease Cerebral amyloid angiopathy.
- 39. SPECT-Vascular Dementia • 99mTc-HMPAO SPECTof the brain in vascular dementia shows multiple patchy perfusion defects.
- 40. 5. NORMAL PRESSUREHYDROCEPHALUS
- 41. • TRIAD: Dementia+ gait disturbance + Urinary incontinence. • AGE: usually after 60 yrs. • Theories: Impaired extraventricluar CSF absorption due to prior subarachnoid hemorrhage / meningitis. Decrease white matter tensile strength due to deep white matter infarction / ischemic changes. • Three primary MR findings have been described in NPH: Enlargement of the ventricular system out of proportion to the subarachnoid space A prominent periventricular halo and A prominent CSF flow void in the cerebral aqueduct.
- 43. MRS- Dementia • NAAloss is consistently seen in Alzheimer's disease. • NAA loss is also seen in Parkinson’s disease & Huntington’s disease. • Significantly elevated myoinositol in grey matter of Alzheimer's disease.
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- 46. Cognitive enhancer Rivastigmine Donepezil Galantamine Mamentine Piracetam 4. Neurotonic Dose:400-800 mg/day 5. NMDA -receptor antagonist Dose: 5 mg OD - 10 mg BD 1. Acetyl Cholinesterase inhibitor Dose: 1.5 mg BD to 6 mg BD 2. Acetyl Cholinesterase inhibitor Dose: 5mg - 10 mg daily 3. Acetyl Cholinesterase inhibitor Dose4 mg BD - 12 mg BD
- 47. Guidelines for prescribingcholinesterase inhibitors A. Prescription only for patients- a) Fulfilling criteria for probable AD b) Duration of illness being more than 6 months c) MMSE score more than 10 (i.E., Mild or moderately severe dementia) B. Three phase evaluation of response- a) Early (2 weeks) for assessing tolerance and side effects, b) Later (3 months) for cognitive state, c) Continued (6 months) for disease state C. Stop treatment- a) If early evaluation shows poor tolerance or compliance b) If deterioration continues at pre-treatment rate after 3-6 months of treatment c) If even after reaching maintenance dose accelerating deterioration continues
- 48. Anti-amyloid therapy Vaccines toprevent amyloid plaque formation : Under experimental stage Secretase Inhibitor Fibrilogenesis inhibitor e.g. cliniquinol Cholesterine Newer drugs
- 49. Other drugs Quetiapine is safest Valproateis preferable Sertraline is preferable Non benzodiazepines are preferable Sedatives Antidepressants Mood stabilisers Antipsychotics
- 50. Non-pharmacological Intervention I. Environmentalmodifications 1 2 3 Enhanced Environment Simulated home environment with appropriate visual auditory and olfactory stimuli which may decrease the chance of trespassing, exit seeking and other agitation behaviors Reduced Stimulation Environment Camouflaged doors, neutral colors and pictures on walls, no televisions, radios, stereo players or ringing telephones, added with a consistent daily routine, and slow and soft speech for communication Natural Environment Mimic natural surroundings consisting of recorded songs of birds, babbling brooks or small animals, together with large bright picture
- 51. Environment Calm, non-taxing environments, goodlighting, prominent placement of frequently required objects Soft wall colours, non-skid flooring contrast between the wall and floor, handrails are useful Clear and repetitive instructions, visual direction to different rooms through colour lines and pictures decrease confusion without frequent change of furniture minimum change of caregivers or staff. Environmental modifications contd..
- 52. II. Social interactions ““simulatedpresence therapy,”simulated presence therapy,”““simulated presence therapy,”simulated presence therapy,” Audio or videos containing a relative’s portion of interaction is played, and pauses are given that allow the patient to respond to the relative’s questions. Displaying photos and names of family and friends in the patient’s living area is helpful. LanguagePet therapyInteraction Non-pharmacological Intervention cont. One to one interaction for 30 min per day for 10 days to be effective in decreasing verbally disruptive behaviour. Interaction in the mother tongue and regular intensive interaction help in reality orientation. Spending time with pets or having a pet at home (pet therapy) decreases agitation and verbal aggression
- 53. III. Minimize theimpact of sensory deficits Provide favourite foods Devices Patience Rapport Food Slow and repetitive explanations reduce confusion and agitation. Massage and touch, aromatherapy Minimize the impact of sensory deficits Corrective eyeglasses and hearing aids decrease risk of disorientation Non-pharmacological Intervention cont.
- 54. IV. Medical andnursing interventions Music Therapy Proper food Sleep Hygiene Light Therapy Frequent outing Pain Management Personal Hygiene Non-pharmacological Intervention cont.
- 55. Title in here Reinforcements & Extinction Stimuluscontrol Spiritual & religious activities
- 56. VI. Cognitive activities MindgameMind game Crossword Puzzles Chess Su-doku
- 57. CARE NACSP ADL CalmingAggressive Reactions In Elderly Nursing Assistant Communication Skill Program Abilities-focused program of morning care, and training on activities of daily living (ADL) Nonpharmacological Intervention cont.