Summary

This document discusses dementia syndrome, encompassing its definition, prevalence, and causes. It explores the clinical course, diagnostic investigations, non-medical treatments, and pharmacological interventions. The text delves into various aspects of dementia management.

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36. Dementia syndrome: definition, prevalence, causes. (L.5.10) Definition: Dementia is a neurocognitive disorder defined by the following: 1. Evidence of substantial cognitive decline from a previous level of performance in one or more domains (complex attention, executive ability, learning...

36. Dementia syndrome: definition, prevalence, causes. (L.5.10) Definition: Dementia is a neurocognitive disorder defined by the following: 1. Evidence of substantial cognitive decline from a previous level of performance in one or more domains (complex attention, executive ability, learning and memory, language, perceptual - motor - visual perception, praxis or social cognition) 2. The cognitive deficits interfere with independence (instrumental activities of daily living). 3. The cognitive deficits do not occur in the context of delirium. 4. The cognitive deficits are not attributable to another mental disorder Prevalence: Age group 60+ yrs prevalence is 5-7% 85+ yrs and older 1 out of 5 has dementia syndrome In Europe - 5 mln In the world appr. 50 mln (2017) Causes of dementia or chronic cognitive impairment: 37. Clinical course of dementia syndrome. (L.5.10) 2 types: 1. Early onset, before 65 yrs of age (rare); 2. Late onset, after 65 yrs of age (more common). Key features: short term memory impairment (later long term memory impaired as well); progressing dependence; worsening motor function; behavioral problems. S m om og e ion in Al heime di ea e There are 3 stages of Alzheimer's disease mild, moderate and severe with cognitive and functional decline stretching over 5 8 years. 1. The initial, mild stage: Usually lasts 2 3 years patients show short-term memory impairment often accompanied by symptoms of anxiety and depression. 2. During the moderate stage: The symptoms appear to abate as neuropsychiatric manifestations such as visual hallucinations, false beliefs and reversal of sleep patterns emerge. 3. Final, severe stage: Motor signs such as motor rigidity and prominent cognitive decline characterize the severe and final stage. Cognitive and functional decline tend to be linear throughout the 3 stages of the disease, whereas caregiver burden peaks with the onset of neuropsychiatric symptoms and declines somewhat during the, when the patient is more sedentary. 38. Investigation if dementia syndrome is suspected. (L.5.10) Evaluation by Neurologist, Psychiatric,Geriatrician 1. Comprehensive physical assessment 2. Lab tests: Peripheral blood count + ESR/ CRP Liver enzymes Renal function (creatinine, potassium) Thyroid gland (US+ check hormones level) According to need EEG, full comprehensive assessment, etc. Glucose Calcium Vitamin B12, folic acid Instrumental investigation: CT various abnormalities found cross sectionally (lateral ventricles, sulci, temporal lobe). Longitudinal assessment of some of these abnormalities might have higher diagnostic accuracy. MRI findings may correlate with degree of dementia. Specific diagnostic features not yet established. Regional cerebral blood flow (CBF) decreased cerebral flow found in AD, but there is significant overlap with normal aging. PET and SPECT temporoparietal deficit; (right) left asymmetry. Diagnostic value of abnormalities still being assessed. 3. Assessment of cognitive functions: Clock drawing test (CDT) Mini- Mental State Examination (MMSE) Blessed dementia scale 4. ADL, IADL 5. Comorbidities 6. Support to family 7. Neuropathology: Amyloid plaques Since the number of plaques increases with age, the number needed for diagnosis of AD is age dependent. Neurofibrillary tangles, amyloid angiopathy Loss of the choline acetyltransferase and acetylcholine in the cerebral cortex in AD. Neuritic plaques in the cerebral cortex (pathognomic microscopic feature), may be reactive astrocytes and microglia at the periphery. 39. Non-medicamental treatment of dementia syndrome. Enabling technologies. (L.5.10) Simplification and familiarization of the patient's environment, Avoid isolation, under stimulation and ensure safety (night lamp, gas cooker and bath monitor). Tools for orientation and support of memory (digital clocks, calendars, day planners, drug carousell, lost items locator, telephone with photos). Physical therapy to reduce restlessness. Occupational and art therapy. Group therapy and family counselling services. GERONTECHNOLOGY 40. Medicamental treatment of various types of dementia. (L.5.10) 1. Cholinergic augmentation therapy It works by increasing cholinergic synaptic transmission by inhibiting acetylcholinesterase in the synaptic cleft, thereby increasing the hydrolysis of acetylcholine released from presynaptic neurons. Drugs in this class differ from one another in the way they inhibit acetylcholinesterase. Treatment with cholinesterase inhibitors can begin at any time after diagnosis, because their efficacy, though limited, is established for patients with mild or moderate disease. 2. N-methyl D-aspartate (NMDA) antagonist: Memantine blocks the toxic effect associated with excess glutamate and regulates glutamate activation and is prescribed to treat symptoms of moderate to severe AD. 5 mg, once a day, available in tablet form. Dosage: increase to 10 mg/day (5 mg twice a day), 15 mg/day (5 mg and 10 mg as separate doses), and 20 mg/day (10 mg twice a day) at a minimum of one-week intervals if well tolerated.. Slowing the progression of Alzheimer’s disease not approved. Alpha-tocopherol (vitamin E), selegiline, propentofylline, Ginkgo biloba, Acetyl- L-Carnitine.

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