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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Involvement of the central nervous system (CNS) is common in patients with advanced disease due to human immunodeficiency virus (HIV). Symptoms range from lethargy and apathy to coma, incoordination and ataxia to hemiparesis, loss of memory to severe dementia, and focal to major motor seizures. Involvement may be closely associated with HIV infection per se, as in the AIDS dementia complex, but is frequently caused by opportunistic pathogens such as Toxoplasma gondii and Cryptococcus neoformans or malignancies such as primary lymphoma of the CNS. The clinical presentations of attendant and direct CNS involvement are remarkably non-specific and overlapping, yet a correct diagnosis is critical to successful intervention. Toxoplasmic encephalitis is one of the most common and most treatable causes of AIDS-associated pathology of the CNS. A great deal has been learned in the last 10 years about its unique presentation in the HIV-infected patient with advanced disease. Drs. Benjamin J. Luft of the State University of New York at Stony Brook and Jack S. Remington of the Stanford University School of Medicine and Palo Alto Medical Foundation's Research Institute have studied T. gondii for many years and are two of the leading experts in the field. This commentary comprises an update of their initial review (J Infect Dis 1988;157:1-6) and a presentation of the current approaches to diagnosing and managing toxoplasmic encephalitis in HIV-infected patients.
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PMID:Toxoplasmic encephalitis in AIDS. 152 Jul 57

The acquired immunodeficiency syndrome (AIDS) dementia complex is a frequent and devastating complication of infection with human immunodeficiency virus-type 1 (HIV-1). Features of the AIDS dementia complex include decreased memory, the inability to concentrate, apathy, and psychomotor retardation. Typical neuropathologic findings include gliosis, focal necrosis of neurons, perivascular inflammation, formation of microglial nodules, multinucleated giant cells, and demyelination. That HIV-1 is the direct cause of this neurologic syndrome is strongly supported by the available evidence. In addition, several studies have identified the monocyte-macrophage as the predominant cell type in the brain infected with HIV-1. However, the mechanisms by which the infected monocytes-macrophages mediate neurologic dysfunction and destruction have not been elucidated.
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PMID:The acquired immunodeficiency syndrome (AIDS) dementia complex. 254 29

HIV encephalopathy, which is probably primarily caused by human immunodeficiency virus, is the most common neurological disorder in HIV-infected patients and is more frequent than opportunistic diseases of the central nervous system. It is characterized most often by slowly progressing cognitive impairment, psychomotoric slowing and increasing apathy. The syndrome is found almost exclusively in the late stages of HIV infection; its frequency in patients with full-blown AIDS is estimated as being between 40 and 70%. Although numerous studies have demonstrated alterations in the electrophysiological parameters, cerebral perfusion and cerebrospinal fluid in many asymptomatic patients, there are no reliable parameters that can predict the risk of developing HIV encephalopathy. Also, there is no sufficient correlation between the extent of the frequent but mostly subtle neuropathological changes and the clinical degree of the severity of the encephalopathy. The mechanisms causing cerebral injury are poorly understood. Recent studies indicate that the indirect effects of HIV infection of the brain are the most important pathogenetic factors. In particular, certain viral proteins and cytokines produced by infected macrophages or activated microglia seem to induce neuronal dysfunction and finally loss of nerve cells.
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PMID:[HIV encephalopathy--clinical aspects, neuropathology and pathogenesis]. 845 Aug 99

The human immunodeficiency virus (HIV)-associated dementia complex is characterized by difficulties in concentration and memory followed by apathy, social withdrawal and motor dysfunction. Decreased serum vitamin B12 levels occur in up to 20% of patients with acquired immune deficiency syndrome (AIDS) and may adversely contribute to the haematologic and neurologic dysfunction which is frequently attributed to the human immunodeficiency virus. We describe a patient with AIDS who presented with an apparent advanced AIDS dementia complex. There was an associated low serum vitamin B12 resulting from malabsorption due to low gastric intrinsic factor secretion. Following treatment with vitamin B12 the symptoms resolved over a 2-month period. We believe that the AIDS dementia complex represented a reversible adverse synergistic interaction between the human immunodeficiency virus and vitamin B12 deficiency.
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PMID:Reversal of apparent AIDS dementia complex following treatment with vitamin B12. 850 20

The pathogenesis of human immunodeficiency virus-associated motor and cognitive disorders is poorly understood. In this context both a protective and a harmful role of the immune system has been discussed. This question was addressed in the present study by correlating the occurrence of neurologic disease in simian immunodeficiency virus (SIV)-infected macaques with disease progression and the humoral and cellular intrathecal antiviral immune response. Overt neurologic signs consisting of ataxia and apathy were observed at a much higher frequency in rapid progressor animals (6 of 12) than in slow progressors (1 of 7). Whereas slow progressors mounted a strong antiviral antibody (Ab) response as evidenced by enzyme-linked immunosorbent and immunospot assays, neither virus-specific Ab titers nor Ab-secreting cells could be found in the cerebrospinal fluid (CSF) or brain parenchyma of rapid progressors. Similarly, increased infiltration of CD8(+) T cells and cytotoxic T lymphocytes specific for viral antigens were detected only in the CSF of slow progressors. The finding that neurologic signs develop frequently in SIV-infected macaques in the absence of an antiviral immune response demonstrates that the immune system does not contribute to the development of motor disorders in these animals. Moreover, the lower incidence of neurologic symptoms in slow progressors with a strong intrathecal immune response suggests a protective role of the virus-specific immunity in immunodeficiency virus-induced central nervous system disease.
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PMID:Protective role of the virus-specific immune response for development of severe neurologic signs in simian immunodeficiency virus-infected macaques. 981 31

Prominent apathy and/or irritability are frequently observed among individuals infected with the human immunodeficiency virus (HIV). Although these symptoms often occur as part of a mood disorder, compelling evidence suggests that they may occur independently of depression in neurologic disease/disorder. The current study examined the prevalence of both apathy and irritability among a sample of HIV-infected individuals and explored the degree to which these neuropsychiatric (NP) phenomena were associated with performance on neuro-cognitive measures thought to be sensitive to the potential CNS effects of HIV-1. Clinician-administered rating scales assessing apathy and irritability were administered to 65 HIV-seropositive (HIV+) and 21 HIV-seronegative (HIV-) participants who also completed a dual-task reaction time paradigm and the Stroop task. NP disturbance was significantly more prevalent among HIV+ participants compared with HIV- controls and was associated with specific neuro-cognitive deficits suggestive of executive dysfunction. Relative to both HIV- controls and to neuro-psychiatrically intact HIV+ participants, those HIV+ individuals with evidence of prominent apathy and/or irritability showed deficits in dual-task, but not single-task, performance and on the interference condition of the Stroop. Unexpectedly, NP disturbance did not show a robust relationship with HIV disease stage. These results suggest that the presence of prominent apathy and/or irritability among HIV+ individuals may signify greater HIV-associated CNS involvement. In HIV/AIDS, the disruption of frontal-subcortical circuits may be a common mechanism causing both executive dysfunction and NP disturbance.
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PMID:Neuropsychiatric disturbance is associated with executive dysfunction in HIV-1 infection. 1157 99

Needle sharing contributes to the spread of the human immunodeficiency virus and other health concerns and remains a persistent problem among injection drug users. We determined whether needle sharing may be related to the discounting of the value of delayed outcomes. Outpatients in treatment for heroin dependence indicated preference for immediate versus delayed hypothetical monetary and heroin outcomes in a titration procedure that determined indifference points at various delays. The degree to which the delayed outcomes lost value was estimated with a nonlinear decay model. Participants who agreed to share a needle in a scenario (N=15) discounted delayed money more steeply than did the nonsharing group (N=17). Both groups discounted delayed heroin more steeply than delayed money. Persistent needle sharing may be related to the relative inability of delayed outcomes to impact current behavior. Training to mitigate the effect of delay on outcome value may offer reductions in needle sharing and drug abuse.
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PMID:Needle sharing in opioid-dependent outpatients: psychological processes underlying risk. 1105 60

The clinical features of human immunodeficiency virus (HIV) dementia exhibit the hallmarks of a subcortical dementia. These features include psychomotor slowing, apathy, bradykinesia and altered posture and gait similar to those observed in advanced Parkinson's disease. The dementia has the hallmarks attributed to subcortical dementia. The exquisite sensitivity of many of these patients to dopamine receptor blockade suggested a profound and, perhaps, selective abnormality of striatal dopaminergic systems. Additional investigations, electrophysiological, pathological, virological, metabolic and radiological studies, indicate that the basal ganglia are a major target of HIV infection. In this review, we describe the evidence for involvement of basal ganglia and, in particular, the dopaminergic systems, in HIV dementia. We also suggest novel therapeutic strategies that may be beneficial in the treatment of this disorder.
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PMID:HIV dementia: the role of the basal ganglia and dopaminergic systems. 1110 99

A great number of human immunodeficiency virus (HIV)-infected patients develop a central nervous system disorder, commonly called HIV dementia or AIDS dementia complex (ADC). HIV dementia is independent of opportunistic infections and is due to the virus itself. Symptoms include psychomotor slowing, apathy and motor disorders similar to the bradykinesia and postural and gait abnormalities observed in late Parkinson's disease. Consequently, HIV has been discussed during the last few years as an additional cause for parkinsonism, and parkinsonian syndromes as manifestations of HIV dementia. Moreover, the early phase of HIV infection gains increasing interest because of studies which report subtle neurological symptoms at this stage. Accordingly, we found in SIV-infected monkeys that dopamine is reduced by 44% within as few as two months of infection, indicating that changes during early infection must be thoroughly evaluated. In this short review, we discuss alterations in the nigrostriatal dopaminergic system during early and late immunodeficiency virus infection and the common clinical and biochemical features shared by HIV dementia and Parkinson's disease.
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PMID:Parkinsonism in HIV dementia. 1211 66

Apathy is a prominent neuropsychiatric symptom associated with human immunodeficiency virus (HIV). The increased frequency of apathy in this population may reflect the direct involvement of the virus on the central nervous system (CNS), but the severity of apathy has not been shown to consistently relate to markers of disease activity or other neuropsychiatric complications of the virus. We examined the relationship between ratings of apathy and performance on measures of cognitive function and immune system status in a sample of HIV-infected patients. Apathy was significantly elevated among HIV-infected individuals compared to healthy comparison subjects. Apathy was significantly related to performance on measures of learning efficiency and a measure of cognitive flexibility. Ratings of apathy did not relate to CD4 cell count, but they were associated with disease duration. In addition, ratings of depression were independent of ratings of apathy. These findings suggest that apathy does not co-vary with a proxy measure of active disease status, but apathy does relate to several measures of cognitive dysfunction in patients with HIV. As such, the increased prevalence of apathy among HIV-infected adults may reflect HIV-associated neurologic dysfunction.
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PMID:Apathy correlates with cognitive function but not CD4 status in patients with human immunodeficiency virus. 1574 91


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