EXPORT CITATION

Chapter-14 Dementia

BOOK TITLE: Neurology

Author
1. Kenkre Rajendra B
ISBN
9788184489477
DOI
10.5005/jp/books/11181_14
Edition
1/e
Publishing Year
2010
Pages
28
Author Affiliations
1. Goa, India
Chapter keywords

Abstract

Basic clinical features, cognitive impairment, deterioration of previously acquired intellectual abilities which interfere with social and occupational function. Apraxia, aphasia, agnosia, personality changes, depression, apathy, hallucinations, delusions, poor visuospatial abilities. Alzeihmers disease, rising prevalence and incidence over the age of 60. Familial in 5 to 10% of cases. Genetic factors commonly present, mutation chromosome 2, presinilin I and presinilin II may be affected genes in early onset dementia. Late onset AD chromosome 19, Apo E4 gene may be involved. Pathology extensive neuronal loss. Loss of cholinergic neurons of nucleus Basalis of meynert and substantiainominata. Intraneuronal neurofibrillary tangles, entorhinal cortex, limbic cortex and cortex. Amyloid plaques extracellular diffuse synaptic alterations. Granulovacuolar degeneration. Dementia with lewy bodies defecit of frontal, subcortical abilities decreased visuospatial skills memory deficits, Parkinsonian features poor response to L-Dopa REM Sleep disorder, syncope, depression pathology Lewy bodies present: Antigenic components include presynaptic protein and alpha-synuclein NF Protein, seen in temporal lobe also in frontal cortex, cingulate gyrus entorhinal cortex and amygdala. Multiinfarct dementia most commonly form of vascular dementia, patients older than 50, episodic focal deficits, include, hemiparesis ataxia, dysarthria, diplopia and dysphasia. Associated medical problems include diabetes, intermittent claudication, myocardial infarction and generalized vascular disease. The lesions may occur in basal ganglia internal capsule or subcortical white matter. The leasians may be bilateral MRI evaluation infarction in multiple cortical areas. T2 weighted lesions around ventricles periventricular white matter lesions prominent on T2 weighted images. Ventricular enlargement. Numerous microscopic infarcts in the cortex cause cortical granular atrophy HIV and dementia. Clinical features: forgetfulness, poor concentration ataxia, paraparesis, CSF protein elevated > 50 mg% lymphocytes increased. MRI gray and white matter atrophy. Microglia and cellular reservoirs of virus. Neurosyphilis may occur 20 years after infection memory loss apathy dysphasia, seizures, trombone tongue, tremor Argyl Robertson pupil, brainstem strokes CSF elevated protein IgG IgM raised inacute infection few cells, slight increase in proteins. Cysticercosis is also cause of dementia and the onset may be with seizures raised intracranial pressure, hydrocephalus and later stage if untreated chronic dementia. Cysts are found in cortex, ventricles, meninges, cerebellum. Dementia following repeated white matter trauma is seen in boxers, football players soccer players. It is subcortical dementia. In the early stage, dysphasia dysarthria may be the feature and later pseudo bulbar palsy ,ataxia and parkinsonian features may manifest. It may be diffuse brain damage and diffuse axonal injury with ischemic brain damage. This form of diffuse axonal injury may manifest as focal lesion of corpus callosum and there may be focal lesions in the quadrants of the brainstem, loss of Purkinje cells and cortical neuronal loss is seen .MRI evaluation global atrophy ventricular dilatation and lesions of the corpus callosum.

© 2019 Jaypee Brothers Medical Publishers (P) LTD.   |   All Rights Reserved