Dementia



velez college; Department of occupational therapyDementiaNeurologic Disorders: Diseases of CNSSerohijos,Christine Marie M.10/1/2012DEMENTIA a progressive impairment of cognitive functions occurring in clear consciousness (i.e., in the absence of delirium)an acquired deterioration in cognitive abilities that impairs the successful performance of activities of daily living.Affects > 4 million AmericansMemory is the most common cognitive ability lost with dementia; 10% of persons >70 and 20–40% of individuals >85 have clinically identifiable memory loss. Other mental faculties are also affected in dementia. These include:language, visuospatial ability, calculation,judgment, problem solving Neuropsychiatric and social deficits also develop in many dementia syndromes resulting in:depression,withdrawal,hallucinations, delusions,agitation,insomnia,disinhibition The disorder can be progressive or static and unchanging or fluctuating from day to day, or permanent or reversible. PathoPhysiology of Dementia: disruption of cerebral neuronal circuits;the quantity of neuronal loss and the location of affected regions are factors that combine to cause the specific disorderBehavior and mood are modulated by noradrenergic, serotonergic, and dopaminergic pathways, while acetylcholine seems to be particularly important for memory. Therefore, the loss of cholinergic neurons in Alzheimer’s disease (AD) may underlie the memory impairment while in patients with non-AD dementias, the loss of serotonergic and glutaminergic neurons causes primarily behavioral symptoms, leaving memory relatively spared.Neurotrophins represent a pharmacologic pathway toward slowing or reversing the effects of AD.Patterns of Neuronal Degeneration AD begins in the entorhinal cortex, spreads to the hippocampus, and then moves to posterior temporal and parietal neocortex, eventually causing a relatively diffuse degeneration throughout the cerebral cortex.Multi-infarct dementia is associated with focal damage in a random patchwork of cortical regions Diffuse white matter damage may disrupt intracerebral connections and cause dementia syndromes similar to those associated with leukodystrophies, multiple sclerosis, and Binswanger’s disease.The effect that these patterns of cortical degeneration have on disease symptomatology is clear: AD primarily presents as memory loss and is often associated with aphasia or other disturbances of language. In contrast, patients with frontal lobe or subcortical dementias such as frontotemporal dementia (FTD) or Huntington’s disease (HD) are less likely to begin with memory problems and more likely to have difficulties with attention, judgment, awareness, and behavior. The dorsolateral prefrontal cortex has connections with dorsolateral caudate, globus pallidus, and thalamus. Lesions of these pathways result in poor organization and planning, decreased cognitive flexibility, and impaired judgment.The lateral orbital frontal cortex connects with the ventromedial caudate, globus pallidus, and thalamus. Lesions of these connections cause irritability, impulsiveness, and distractibility.The anterior cingulate cortex connects with the nucleus accumbens, globus pallidus, and thalamus. Interruption of these connections produces apathy and poverty of speech or even akinetic mutism. Causes of DEMENTIA: Global impairment of intellect is the essential feature, manifested as difficulty with memory, attention, thinking, and comprehension. Most common type of dementia is Dementia of the Alzheimer's type followed by Vascular Dementia followed by Dementia associated with PD. Dementia of Alzheimer’s type increases in prevalence with increasing age and 60% common in males. Vascular Dementia is caused by Cerebrovascular Disease. Most common in persons between the ages of 60 and 70 and is more common in men than in women.Other Causes of Dementia:Head trauma, alcohol-related dementias, and various movement disorder-related dementias, such as Huntington's disease and Parkinson's disease. The three most common potentially reversible diagnoses were: Depression HydrocephalusAlcohol dependence Benign forgetfulness of the elderly is the subtle cumulative decline in episodic memory is a natural part of aging. Benign means that it is not so progressive or serious that it impairs reasonably successful and productive daily functioning Mild Cognitive Impairment is a cognitive problem that has begun to subtly interfere with daily activities. A sizeable proportion of persons with MCI will progress to frank dementia, usually caused by AD. The major degenerative dementias include AD, FTD and related disorders, DLB, HD, and prion disorders including Creutzfeldt-Jakob disease (CJD). These disorders are all associated with the abnormal aggregation of a specific protein: Aβ42 in AD, tau or TDP-43 in FTD, α-synuclein in DLB, polyglutamine repeats in HD, and prions in CJD. Approach to Patient:History:The major degenerative dementias can usually be distinguished by the initial symptoms; neuropsychological, neuropsychiatric, and neurologic findings; and neuroimaging features.The history should concentrate on the onset, duration, and tempo of progression of the dementia.An acute or subacute onset of confusion may represent delirium and should trigger the search for intoxication, infection, or metabolic derangement.An elderly person with slowly progressive memory loss over several years is likely to suffer from AD.A change in personality, disinhibition, and gain of weight or food obsession suggests FTD, not AD. FTD is also suggested by the finding of apathy, loss of executive function, or progressive abnormalities in speech, or by a relative sparing of memory or spatial abilities.The diagnosis of DLB is suggested by the early presence of visual hallucinations; parkinsonism; delirium; REM sleep disorder (the merging of dreamstates into wakefulness); or Capgras’ syndrome, the delusion that a familiar person has been replaced by an impostor.A history of sudden stroke with irregular stepwise progression suggests multi-infarct dementia. Multi-infarct dementia is also commonly seen in the setting of hypertension, atrial fibrillation, peripheral vascular disease, and diabetes.Physical and Neurologic Examination:A thorough general and neurologic examination is essential to document dementia, look for other signs of nervous system involvement, and search for clues suggesting a systemic disease that might be responsible for the cognitive disorder.Please see table 365-4 below to see the clinical differentiation of major dementias.Cognitive and Neuropsychological Examination:Brief screening tools such as the mini-mental state examination (MMSE) help to confirm the presence of cognitive impairment and to follow the progression of dementia. The MMSE, an easily administered 30-point test of cognitive function, contains tests of orientation, working memory (e.g., spell world backwards), episodic memory (orientation and recall), language comprehension, naming, and copying.When the etiology for the dementia syndrome remains in doubt, a specially tailored evaluation should be performed that includes tasks of working and episodic memory, frontal executive function, language, and visuospatial and perceptual abilities.A functional assessment should also be performed. The physician should determine the day-to-day impact of the disorder on the patient’s memory, community affairs, hobbies, judgment, dressing, and eating. Knowledge of the patient’s day-to-day function will help the clinician and the family to organize a therapeutic approach.Neuropsychiatric assessment is important for diagnosis, prognosis, and treatment.Laboratory Tests:The choice of laboratory tests in the evaluation of dementia is complex.Neuroimaging studies will identify primary and secondary neoplasms, locate areas of infarction, diagnose subdural hematomas, and suggest NPH or diffuse white matter disease.Lumbar puncture need not be done routinely in the evaluation of dementia, but it is indicated if CNS infection is a serious consideration. Cerebrospinal fluid (CSF) levels of tau protein and Aβ42 amyloid show differing patterns with the various dementias; however, the sensitivity and specificity of these measures are not sufficiently high to warrant routine measurement.Formal psychometric testing, though not necessary in every patient with dementia, helps to document the severity of dementia, suggest psychogenic causes, and provide a semiquantitative method for following the disease course.EEG is rarely helpful except to suggest CJD (repetitive bursts of diffuse high voltage sharp waves) or an underlying nonconvulsive seizure disorder (epileptiform discharges).Brain biopsy (including meninges) is not advised except to diagnose vasculitis, potentially treatable neoplasms, unusual infections, or systemic disorders such as vasculitis or sarcoid, or in young persons where the diagnosis is uncertain.Angiography should be considered when cerebral vasculitis is a possible cause of the dementia.Clinical Features:Clinicians should note patients' complaints about intellectual impairment and forgetfulness as well as evidence of patients' evasion, denial, or rationalization aimed at concealing cognitive deficits. Patients' appearance and behavior should be observed. Memory impairment is typically an early and prominent feature in dementia.Dementia affects the cortex exhibiting such symptoms. Changes in the personality of a person with dementia are especially disturbing for their families. Hallucinations, delusions and physical aggression and other forms of violence are common in demented patients who also have psychotic symptoms.Patients with dementia also may exhibit pathological laughter or crying that is, extremes of emotions with no apparent provocation.Pseudobulbar palsy, dysarthria, and dysphagia are also more common in vascular dementia than in other dementing conditions.SUNDOWNER SYNDROME characterized by drowsiness, confusion, ataxia, and accidental falls. It occurs in older people who are overly sedated and in patients with dementia who react adversely to even a small dose of a psychoactive drug. ................
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