Dementia
28
-
Upload
dhavalshah4424 -
Category
Documents
-
view
1.639 -
download
13
Transcript of Dementia
Progressive deterioration of intellect, behavior and personality as a consequence of diffuse disease of the brain hemispheres, maximally affecting the cerebral cortex and hippocampus Symptom of disease rather than a single disease entity Caused by at least 80 different diseases, many reversibleSignificantly impaired intellectual functioning that interferes with normal activities and relationshipsPseudodementia: When Depression mimics the initial phases of dementia
Affects 10% of individuals over 65Accounting for 40% of long-term psychiatric in-patients over the age of 65 years. The prevalence in persons aged between 50 and 70 years is about 1% and in those approaching 90 years reaches 50%An annual incidence rate is 190/100 000 personsNearly 1.5 million people living with dementia in India
The rate of progression depends upon the underlying cause.
• The duration of history helps establish the cause of dementia: Alzheimer‘s disease is slowly progressive over years, whereas encephalitis may be rapid over weeks. Dementia due to cerebrovascular disease appears to occur ’stroke by stroke‘
Alzheimer‘s disease (~60% of all dementias) Cerebrovascular (multiinfarct state, subcortical small vessel, amyloid angiopathy,…) (~20%) Neurodegenerative (DLB, Pick‘s disease, Huntington‘s chorea, Parkinson‘s disease)Infectious (Creutzfeld-Jakob disease, HIV infection, progressive multifocal leucoencephalopathy)Normal pressure hydrocephalus TREATABLE!Nutritional (thiamine deficiency in alcoholics!, B12 deficiency, folate deficiency)Metabolic (hepatic disease, thyroid d., parathyroid d., Cushing‘s syndrome)Chronic inflammatory (MS, …)Trauma (head injury, ’Punch drunk‘ syndrome)Tumour (e.g. subfrontal meningioma)
The commonest cause of dementiaThe disorder rarely occurs under the age of 45 yearsThe incidence increases with ageThe cause of AD is not knownUp to 30% of cases are familial (the loci were found on chromosome 21 and 19)Pathology – the presence of senile plaques and neurofibrillary tangles in the brainDiagnosis of AD may be established during life by early memory failure, slow progression and exclusion of other causes
CT scanning aids diagnosis by excluding multiple infarction or a mass lesion.MRI shows bilateral temporal lobe atrophy.SPECT usually shows temporoparietal hypoperfusion.
- Acetylcholinesterase inhibitors (Donepezil , Rivastigmine, Galantamine have been shown to enhance cognitive performance in early disease. Memantine is approved for moderate disease. However they do not cure!
- Treat concurrent depression, anxiety and sleep disorders- Neuroleptic use may be required for behavioral disturbance- Mangement of AD requires careful advice and counseling of the
patient and family and shared care involving the family, caregivers, GPs, hospital specialist, and community psychiatric services
- Long-term residential care is ofte required- THESE AGENTS DO NOT SLOW THE RATE OF DECLINE
2nd most common cause of dementiaCaused by atherosclerosis, or "hardening of the arteries," in the brain Deposits of fats, dead cells, and other debris form on the inside of arteries, partially (or completely) blocking blood flowThese blockages cause multiple strokes, or interruptions of blood flow, to the brain This type of dementia is sometimes called multi-infarct dementia
13
This is an overdiagnosed condition which accounts for less than 10% of cases of dementia MID is caused by multiple strokes - SILENT STROKESDementia occurs ’stroke by stroke‘, with progressive focal loss of functionClinical features of stroke profile – hypertension, diabetes, etc. – are present. More often in malesDiagnosis is obtained from the history and confirmed by CT or MRI scan:(the presence of multiple areas of infarction)Treatment: Maintain adequate blood pressure control, anti-platelet aggregants (aspirin).
13
This progressive condition accounts for 5% of all dementiasUsually sporadic, it more commonly affect women between 40 and 60 yearsPersonality and behaviour are initially more affected than memoryFrontal lobe dysfunction predominates with apathy, lack of initiative and personality changesCT or MRI scans show frontal (and/or temporal) atrophy, often asymmetricalSPECT reveal anterior hypoperfusion, EEG is usually normalThe disorder is characterized pathologically by argyrophylic inclusion bodies within the cytoplasm of cells of the frontotemporal cortexThere is no treatment, death occuring within 2-3 years of the onset
This condition is one of a group of disorders characterized by asymmetrical cortical degenerationDominant hemisphere perisylvian atrophy is associated with loss of language, which, after many years, becomes a more widespread dementiaPathologically non-specific cell loss, Pick’s pathology or spongiform changes are describedMRI and SPECT confirm focal changes
Second most common dementia in autopsy studiesCaused by abnormal microscopic deposits of protein, called Lewy bodies, which destroy nerve cellsLewy bodies cause symptoms typical of Parkinson disease, such as tremor and muscle rigidity, as well as dementia similar to that of Alzheimer diseaseProgressive cognitive decline, combined with three additional defining features: (1) pronounced “fluctuations” in alertness and attention; (2) recurrent visual hallucinations, and (3) parkinsonian motor symptoms, such as rigidity and the loss of spontaneous movement DLB usually occurs sporadically, in people with no known family history of the disease. However, rare familial cases have occasionally been reportedNon-familial2:1 male:female ratioLewy body dementia is not reversible and has no known cure
= term applied to the triad of:1. Dementia2. Gait disturbance3. Urinary incontinenceoccuring in conjunction with hydrocephalus and normal CSF pressure.
Two types: - NPH with a preceding cause (SAH, meningitis, trauma,
radiation-induced).- NPH with no known preceding cause – idiopathic (50%).
Aetiology is unclear. It is presumed that at some preceding period, impedence to normal SCF flow
causes raised intraventricular pressure and ventricular dilatation. Compensatory mechanisms permit a reduction in CSF pressure yet the ventricular dilatation persists and causes symptoms.
19
Diagnosis is based on clinical picture plus CT scan/MRI evidence of ventricular enlargement.
NPH must be differentiated from pts whose ventricular enlargement is merely the result of shrinkage of the surrounding brain, e.g. AD. These pts do not respond to CSF shunting, whereas a proportion of NPH pts (but not all) show a definitive improvement with ventriculo-peritoneal shunting.
19
Approximately two-thirds of persons with AIDS develop dementia, mostly due to AIDS dementia complexIn some patients HIV is found in the CNS at postmortem. In others an immune mechanism or an unidentified pathogen is blamedDementia is initially of a "subcortical " typeCT - atrophy; MRI - increased T2 signal from white matterTreatment with Zidovudine (AZT) halts and partially revers neuropsychological deficit
Reduction of intellectual function is common after severe head injury Chronic subdural haematoma can also present as progressive dementia, especially in the elderlyPunch-drunk encephalopathy (dementia pugilistica) is the cumulative result of repeated cerebral trauma It occurs in both amateur and professional boxers and it manifests by dysarthria, ataxia and expy signs associated with ’subcortical‘ dementia. There is no treatment for this progressive syndrome
Dementia rarely may be due to intracranial tumour, especially when tumours occur in certain anatomical sitesMental or behavioral changes occur in 50-70% of all brain tumours as distinct from dementia which is associated with frontal lobe tumours, III ventricle tumours and corpus callosum tumoursTumor can press on structures such as the hypothalamus or pituitary gland, which control hormone secretionThey can also press directly on brain cells, damaging themCognitive impairment also occurs as a non metastatic complication of systemic malignancyTreating the tumor, either medically or surgically, can reverse the symptoms in some cases
23
American Psychiatric Association (APA) has established 2 criteria for the diagnosis of dementia:
erosion of recent and remote memoryImpairment of one or more of the following functions
Language Misuse of words or inability to remember and use words correctly (i.e., aphasia)
Motor activity Unable to perform motor activities even though physical ability remains intact (i.e., apraxia)
Recognition Unable to recognize objects, even though sensory function is intact (i.e., agnosia)
Executive function
Unable to plan, organize, think abstractly
23
Intake of vegetarian diet rich in beta-carotene and vit. E and CDiet low in saturated animal fat and stopping smoking can reduce the risk for stroke and other cardiovascular disorders that may lead to dementiaLifestyle habits that can reduce the risk for head injuryAvoiding substance abuse and addictionSafer sex practices can help prevent HIV and syphilis infection, reducing the risk for AIDS dementia complex and neurosyphilis dementiaPrompt medical attention at the first sign of illness
The American College of Physicians and the American Academy of Family Physicians have published a clinical practice guideline on pharmacologic therapies for dementia based on a review of 59 randomized trials of 5 FDA-approved drugs (donepezil, galantamine, rivastigmine, tacrine, and memantine) in more than 16,000 patients The guideline recommends the following:
Base decisions about starting a cholinesterase inhibitor on individualized assessments.
Base the choice of pharmacologic agent on tolerability, adverse effects, ease of use, and cost
Further research on effectiveness of the medications alone and in combination for clinical outcomes is required
Current Pharmacologic Treatment of Dementia: A Clinical Practice Guideline from the American College of Physicians and the American Academy of Family Physicians ; Ann Intern Med. 2008;148:370-378
Studies That Reported the Proportion of Patients Who Achieved a Clinically Significant Change on 2 Domains of Dementia
Qaseem A et al. Ann Intern Med 2008;148:370-378
©2008 by American College of Physicians
