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MRCME HIV Associated Dementia

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Information about MRCME HIV Associated Dementia
Education

Published on February 29, 2008

Author: Marcell

Source: authorstream.com

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GM Morning Report – HIV Associated Dementia:  GM Morning Report – HIV Associated Dementia Rozina Mithani, PGY2 Monday June 25, 2007 Altered Mental Status in HIV:  Altered Mental Status in HIV Degree of Immunosuppression: > 500: Brain Tumors (benign/malignant) & Mets 200-500: HIV-associated cognitive/motor disorders; w/o focal lesions < 200: Mass lesion i.e. Opportunistic Infx; CNS lymphoma Differential:  Differential Primary: HIV Associate Dementia (HAD) Secondary: Cerbrovascular d/o Neoplasms Nutritional Deficiencies Oportunistic infections: Toxoplasma encephalitis Primary CNS Lymphoma (EBV) PML (JC virus) CMV encephalitis Cryptococcus Tertiary syphilis HIV Associated Dementia - Overview:  HIV Associated Dementia - Overview HIV invades the CNS early Clinical manifestations vary Significant impairment in Daily Activities Clear level of consciousness (vs Delirium) Diagnosis of Exclusion! HIV Associated Dementia:  HIV Associated Dementia Classic Triad of Subcortical Dementia: Memory and Psychomotor speed impairment Depressive Symptoms Movement d/o Presentation:  Presentation Early: Difficulty reading/memory/math Unsteady gait, leg weakness, tremor Affective disturbance Late: Bradyphrenia; Bradykinesis Memory difficulty Saccadic eye movements HAD - staging:  HAD - staging 0: Normal 0.5: Subclinical or Equivocal Minimal or equivocal symptoms Mild (soft) neurological signs No impairment of work or activities of daily living (ADL) Stage 1: Mild Unequivocal intellectual or motor impairment Able to do all but the most demanding work or ADL Stage 2: Moderate Cannot work or perform demanding ADL Capable of self-care Ambulatory, but may need a single prop Stage 3: Severe Major intellectual disability, or Cannot walk unassisted Stage 4: End-Stage Nearly vegetative Pathophysiology:  Pathophysiology Early: basal ganlia & nigrostriatal Late: diffuse; up to 40% loss frontal/temporal neurons Path: White matter changes & demyelinization Microglial nodules Multinucleated giant cells Perivascular infiltrate Infected Monocyte May Inhibit Progenitor cell Proliferation Brain Macrophage Microglial Cell Activation Abnormal Neuronal Pruning Diagnosis:  Diagnosis Risk Factors: Age Viral Load - decreased utility with HAART CD4 Count Low Hct Neuropsychiatric w/u: Impairments in psychomotor speed testing predict development Neuroimaging – helps rule out Metabolic w/u Lumbar Puncture: Mild pleocytosis Elevated protein Cytology (15%) PCR: JC virus, EBV, CMV Treatment:  Treatment HAART Improved surrogate markers of dementia Use drugs with high CSF penetration Psychiatric evaluation Antidepressants Mood elevating agents Symptomatic relief: slowed reactions - psychostimulants i.e. methylphenidate agitated or manic - neuroleptics i.e. risperidone 2.5 X more likely to die if cognitive impairment HAD post-HAART:  HAD post-HAART Incidence declined: 20-30% to 10-15% Prevalence stable – slows progression AIDS-defining diagnosis Higher CD4 counts (200-350) Better: attention/verbal Worse: learning/complex attention

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