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PubMed1994

HIV-encephalopathy: should we await a catastrophe before screening?

Human Immunodeficiency Virus (HIV)-encephalopathy (formerly AIDS Dementia Complex, or ADC) is characterized by global impairment of intellectual and cognitive functions, personality and behavioral disturbances, decreased memory, inability to concentrate, and apathy. Its motor dysfunction is manifested by impaired speech, gait, and coordination, and by psychomotor retardation. Several scientific reports indicate that ADC may be the earliest, and, at times, the only evidence of human immunodeficiency virus infection, and may present a diagnostic challenge, particularly in the aviation context. Several aviation medicine specialists have pointed out the safety questions raised by this condition when it presents in otherwise asymptomatic individuals. Since October 1985, U.S. military pilots have been tested for the presence of HIV antibody and grounded if found positive. In May 1991, the Executive Council of the Aerospace Medical Association approved a position statement that supports testing of pilots for infection by HIV, and maintains that "individuals confirmed to be infected should be found medically disqualified for flying duties." While bureaucrats delay in resolving HIV mandatory screening, HIV-encephalopathy may be precipitously brought to light, with symptoms involving ocular motor disorders such as dissociated nystagmus, gaze-evoked nystagmus, and impaired saccadic function and smooth pursuit, frequent signs of HIV cerebellar and pontomesencephalic dysfunction.

AIDS Dementia Complex↗
PubMed1989

[High-resolution eye movement recording in the assessment of neurologic complications in HIV-1 infection].

HIV-1 related brain disease gives rise to widespread eye movement abnormalities that include impairment of fixation, saccadic speed and accuracy, antisaccadic generation and smooth pursuit function. Quantitative high resolution recording of eye movements is a valuable, non-invasive technique both for measuring the severity and progression of the AIDS dementia complex and the early detection of neurologic dysfunction in asymptomatic HIV-seropositive subjects or in patients with AIDS. In particular, it may be of use in neurologically at-risk patients requiring antiviral therapy and in monitoring the neurologic responses to such treatment.

AIDS Dementia Complex↗
PubMed1998

Cerebral perfusion scanning in treating AIDS dementia: a pilot study.

UNLABELLED: Acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) is a common effect of the AIDS virus. We studied the regional cerebral blood flow of patients with early ADC and its response to atevirdine mesylate. METHODS: Ten men with early ADC, who had failed or were intolerant to zidovudine or didanosine therapy, were treated with atevirdine mesylate for 12 wk. Cerebral perfusion SPECT using 99mTc-HMPAO was performed at Week 0 and Week 12. SPECT images were analyzed qualitatively and semiquantitatively. RESULTS: The cerebral perfusion abnormalities in early ADC were usually mild and characteristically involved the cortices and periventricular regions bilaterally and symmetrically. Four patients were able to complete the protocol. Three of these patients responded to atevirdine clinically, two of whom showed improvement in their Week 12 SPECT images. The other responder had an essentially unchanged image. The patient who did not respond to atevirdine showed a definite deterioration in cerebral perfusion. CONCLUSION: Cerebral perfusion SPECT is useful in detecting and assessing therapeutic responses in ADC. The preliminary results of atevirdine in treating ADC are promising and need further investigation.

AIDS Dementia Complex↗
PubMed1994

Measurement of CNS HIV burden and its association with neurologic damage.

AIDS dementia complex affects between 20 and 30% of terminally ill AIDS patients. The histopathologic substrate of this clinical syndrome is chronic HIV infection of the nervous system termed HIV encephalitis. We hypothesize that the abundance and length of time that HIV is present in the CNS determines the severity of neurologic damage. We compared three different methods of assessing HIV burden in the CNS. While the assays vary in sensitivity, each provides a quantitative estimate of viral burden that can be compared between laboratories. Assays of provirus were readily divided into two groups, while protein assays showed a wider range. HIV-mediated neurotoxicity might be expected to more closely depend upon productive infection.

AIDS Dementia Complex↗
PubMed1999

Human immunodeficiency virus infection, inducible nitric oxide synthase expression, and microglial activation: pathogenetic relationship to the acquired immunodeficiency syndrome dementia complex.

The regional expression of immune-mediated and neurotoxic events in the human immunodeficiency virus (HIV)-infected brain in relationship to the acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) and brain pathology remains uncertain. The extent of gp41, inducible nitric oxide synthase (iNOS), and HLA-DR expression was examined in the frontal lobe and basal ganglia of 25 patients at varying stages of ADC. The expression of gp41 and iNOS was present predominantly in perivascular cells and most often in the basal ganglia. Staining for gp41 correlated significantly with iNOS in the basal ganglia, whereas the severity of staining for gp41 and iNOS in the basal ganglia and white matter was significantly greater in subjects with moderate to severe dementia compared with those with milder impairment. The degree of macrophage staining in the white matter and basal ganglia also correlated significantly with ADC severity and was more abundant than gp41 or iNOS staining, particularly in the white matter. Logistic regression analysis revealed that staining for iNOS and gp41 increased linearly with ADC severity and was significantly more abundant in the basal ganglia compared with the white matter. Double-immunolabeling studies colocalized iNOS predominantly to macrophage/microglia and to gp41-positive cells. The expression of iNOS and gp41 in the basal ganglia combined with immune activation contributes to the development and progression of the clinical syndrome.

AIDS Dementia Complex↗
PubMed2001

CXCR4 is the primary receptor for feline immunodeficiency virus in astrocytes.

Feline astrocytes were productively infected with the Crandell feline kidney (CrFK) cell-adapted feline immunodeficiency virus (FIV) Petaluma strain in a primary culture. They expressed mRNA of CXCR4, and the FIV infection was blocked by stromal cell-derived factor 1alpha (SDF-1alpha), SDF-1beta, or the bicyclam AMD3100 in a dose-dependent manner. These observations suggest that, like FIV infection in CrFK cells and lymphocytes, the virus uses CXCR4 as a primary receptor for infecting astrocytes and this can be a possible natural model for AIDS dementia complex.

AIDS Dementia Complex↗
PubMed1990

The Neurobehavioral Rating Scale: an interrater reliability study in the HIV seropositive population.

The Neurobehavioral Rating Scale (NRS) has been used in the rapid bedside assessment of closed head-injured and stroke patients in the past and has been found to be highly predictive of long-term outlook. The NRS consists of 27 items in a Likert-type scale and measures cognition and behavioral parameters of brain disease. The NRS was administered to nine human immunodeficiency virus (HIV) positive individuals in a pilot interrater reliability study. Highly significant correlations (r .94 and r .97; p less than .001) were found between interviewers. Content and construct validity had already been established in prior research. To date, no quick, easy assessment tool measuring both cognitive and behavioral manifestations in this population has been widely used. Therefore, it becomes imperative that such a tool be available to nursing staff to aid in monitoring of neurologic deterioration, assist in appropriate placement of acquired immunodeficiency syndrome (AIDS) dementia complex patients and planning of care.

AIDS Dementia Complex↗
PubMed2001

Neurological and developmental effects of HIV and AIDS in children and adolescents.

HIV-related encephalopathy is an important problem in vertically infected children with HIV. Infected infants may manifest early, catastrophic encephalopathy, with loss of brain growth, motor abnormalities, and cognitive dysfunction. Even without evidence of AIDS, infected infants score lower than serorevertors on developmental measures, particularly language acquisition. Children with perinatal or later transfusion-related infection generally are roughly comparable developmentally to their peers until late in their course. Symptoms similar to adult AIDS dementia complex are occasionally seen in adolescents with advanced AIDS, including dementia, bradykinesia, and spasticity. Opportunistic CNS infections such as toxoplasmosis and progressive multifocal leukoencephalopathy are less common in children and adolescents than in adults. Increasing evidence suggests that aggressive antiretroviral treatment may halt or even reverse encephalopathy. Neuroimaging changes may precede or follow clinical manifestations, and include early lenticulostriate vessel echogenicity on cranial ultrasound, calcifying microangiopathy on CT scan, and/or white matter lesions and central atrophy on MRI. Differential diagnosis of neurological dysfunction in an HIV-infected infant includes the effects of maternal substance abuse, other CNS congenital infections, and other causes of early static encephalopathy. Initial entry of HIV into the nervous system occurs very early in infection. The risk of clinical HIV encephalopathy increases with very early age of infection and with high viral loads. Virus is found in microglia and brain derived macrophages, not neurons. The neuronal effect of HIV is probably indirect, with various cytokines implicated. Apoptosis is the presumed mechanism of damage to neurons by HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1999

Characterization of learning and memory deficits in C57BL/6 mice infected with LP-BM5, a murine model of AIDS.

Mice infected with an immunosuppressive murine leukemia virus mixture, LP-BM5 show a profound immunosuppression described as murine acquired immune deficiency syndrome (AIDS). In the present study, we characterized learning and memory deficits in C57BL/6 mice infected with LP-BM5. Spontaneous alternation behavior in a Y-maze and latent learning (spatial attention) in a water-finding test, as well as spatial reference and reversal learning in a water maze test, were significantly impaired in the mice infected with LP-BM5. These deficits appeared in the absence of any motoric and visual impairment as assessed by open-field, rotarod and visual water maze tests. These results suggest that cognitive functions are impaired in the mice infected with LP-BM5. Furthermore, LP-BM5-infected mice may be useful as a model for the AIDS dementia complex.

AIDS Dementia Complex↗
PubMed1990

Quantitative detection of brain aberrations in human immunodeficiency virus type 1-infected individuals by magnetic resonance imaging.

The brains of 65 individuals with antibodies to human immunodeficiency virus type 1 (HIV-1), 20 HIV-1 seronegative homosexual men, and 75 heterosexual controls were examined by a quantitative magnetic resonance imaging technique. A white matter aberration was detected most frequently in patients with AIDS-related complex (ARC) or AIDS, but also in asymptomatic HIV-1 seropositive persons and in HIV-1 seronegative homosexual men, of whom two of three tested were reactive for HIV-1 DNA by polymerase chain reaction. The aberration was not found in the control group. Brain atrophy was mainly confined to patients with ARC or AIDS. The brain lesions correlated with the presence of HIV-1 in cerebrospinal fluid and with elevated levels of beta 2-microglobulin and neopterin. The most pronounced brain aberrations were in patients with AIDS-dementia complex. These findings indicate that brain aberrations may occur in persons in the early stages of HIV-1 infection, although to no greater extent than in HIV-1 seronegative homosexual men. The occurrence of pronounced brain lesions seems to be associated with the presence of an advanced immunodeficiency.

AIDS Dementia Complex↗
PubMed1996

Toxicity of TNF alpha and platelet activating factor for human NT2N neurons: a tissue culture model for human immunodeficiency virus dementia.

A significant proportion of HIV-1 infected individuals develop a symptom complex consisting of dementia and motor deficits termed HIV Dementia (HIVD) or the AIDS Dementia complex (ADC). The pathophysiology of this neurologic complication is unclear, but neuronal injury and death may occur as a direct result of the release of cytokines from HIV-1 infected microglial cells (Everall et al, 1991). To evaluate the utility of a human neuronal cell line, NT2N, for studies of HIV-related neuronal cytotoxicity, we studied cellular viability after exposure to HIV-1 gp120, tumor necrosis factor alpha (TFN alpha), platelet activating factor (PAF), interleukin 1 beta (IL-1 beta), and interferon gamma (IFN gamma), all of which have been implicated in previous publications as having a role in HIVD (Brenneman et al, 1988; Dreyer et al, 1990; Merrill et al, 1992; Gelbard et al, 1993). Neither gp 120 nor the cytokines IL-1 beta and IFN gamma resulted in significant NT2N cell death. However, TNF alpha and PAF were highly neurotoxic in this assay. Pentoxifylline, which inhibits the effects of TNF alpha, had a significant protective effect. This system provides an excellent substrate for the evaluation of neurotoxicity and for the development of pharmacologic agents that may be useful in HIV dementia.

AIDS Dementia Complex↗
PubMed1996

Neurological complications of HIV infection.

Neurological complications of HIV infection cause considerable morbidity and are often associated with high mortality. These complications include not only the more common opportunistic diseases affecting the brain (cerebral toxoplasmosis, primary central nervous system lymphoma, progressive multifocal leucoencephalopathy, and cryptococcal meningitis) but also the AIDS dementia complex, with its characteristic cognitive and motor dysfunction, which is caused by HIV itself. Additionally, the peripheral nervous system is the target of several disorders, including a common painful neuropathy. Because these and other, less common, central and peripheral nervous system complications of HIV can often be specifically treated or effectively palliated, their accurate and timely diagnosis is important.

AIDS Dementia Complex↗
PubMedDate not supplied

[HIV glycoprotein 120: possible etiological agent of AIDS-associated dementia].

The AIDS or HIV associated dementia is a cognitive-motor disease, characterized by a strong deficit of several cognitive processes such as attention, memory, sensory perception, motor control among others. The HIV associated dementia affects 30% of adult to 50% of infant HIV positive subjects. Since neurons are not infected by HIV, its principal target in the brain is microglia. The pathophysiology of this syndrome, therefore, remains to be disclosed. Several hypothesis have been proposed, one of them suggests that opportunistic infections can affect the brain. Another hypothesis suggests that microglia secretes toxic products as a result of HIV infection and those are the ones causing the damage and finally, the hypothesis, suggesting that the brain is damaged as a result of the insult caused by HIV-derived proteins. In vitro studies suggest that the HIVgp120, a viral surface protein, is highly neurotoxic. For example HIVgp120 increases cytoplasmic Ca+2 by two ways: facilitating glutamate neurotransmission increasing Ca+2 conductance, and activating the IP3 pathway, facilitating Ca+2 release from the smooth endoplasmic reticulum. This Ca+2 in turn, activates several internal signaling pathways such as the MAPK pathway. We use an animal model to test the HIVgp120 effect on neurophysiological signals and behavior as well as several pharmacological approaches to prevent the HIVgp120 neurotoxic effects. This review updates with the most recent literature discussing the potential mechanisms implicated in the pathophysiology of the AIDS dementia complex. We, in addition, hope the reader will be able to correlate the clinical symptoms observed in the HIV infected subjects and the HIVgp120-induced behavioral changes observed in animal models. Likewise, we discuss the new drugs we are testing, in order to offer a new pharmacological treatment to the patient.

AIDS Dementia Complex↗
PubMed1993

Characterizing the neuropsychological functioning of persons with human immunodeficiency virus infection, Part I. Acquired immunodeficiency syndrome dementia complex: a review.

The findings of studies that use psychoneuroimmunological frameworks can help nurses evaluate and treat patients' psychological and physical responses to infection with the human immunodeficiency virus (HIV). One response to HIV infection, acquired immunodeficiency syndrome (AIDS) dementia complex (ADC), may occur at any stage of the infection and is particularly distressing to both patients and nurses. In Part I of this series, current research pertinent to ADC is reviewed. In Part II, we describe an approach used to characterize the neuropsychological functioning of persons at different stages of HIV infection.

AIDS Dementia Complex↗
PubMed2000

Seizures in patients with human immunodeficiency virus infection.

OBJECTIVE: To study the significance of new onset seizure in patient with human immunodeficiency virus (HIV) infection. METHODS: Patients infected with HIV with the new onset seizure were enrolled in the study. Seizure type was classified. Adequate work up was done to search for a cause of their initial seizure. All patients were administered antiepileptic drugs in addition those detected to have treatable opportunistic infection were treated for the same. RESULTS: A total of 455 patients of HIV infection were admitted to this centre during study period, of these twenty three patients had new onset seizures. Seizures were generalized tonic-clonic in fifteen patients (65.21%), partial motor in six patients (26.08%) and partial motor with secondary generalization in two patients (8.69%). Recurrence of seizures was observed in 69.56% patients. Identified causes included cerebral toxoplasmosis in seven patients (30.43%), cryptococcal meningitis in four (17.39%), tuberculoma in three (13.04%), AIDS dementia complex in one (4.34%) and progressive multifocal leucoencephalopathy in one (4.34%). In seven patients (30.43%) seizures were not associated with any identifiable cause. Phenytoin was used for control of seizures and no side effects to the drug were noted during the brief period of follow up. CONCLUSION: Majority of patients with HIV infection and new onset seizures have secondary brain lesion as the cause of seizure. High rate of seizure recurrence mandates therapy of solitary seizure in patients with HIV infection.

AIDS Dementia Complex↗
PubMed1994

Myelin degrading activity in the CSF of HIV-1-infected patients with neurological diseases.

Degradation of purified myelin basic protein (MBP) was studied by SDS gel electrophoresis after addition of CSF samples obtained from HIV-1-infected patients. An increase in MBP degradation was detected in patients with neurological complications, such as AIDS dementia complex (ADC) or progressive multifocal leukoencephalopathy (PML), when compared with patients with no neurological symptoms (NA) or with other neurological opportunistic infections (OI). In the ADC and PML patients, in addition to CSF proteolytic activity, an increase in CSF-MBP levels and presence of white matter lesions were also observed by neuroimaging (MRI). In other opportunistic infections of the brain, MBP levels but not anti-MBP proteolytic activity increased. Results suggest the involvement of proteases in the virus-induced demyelination.

AIDS Dementia Complex↗
PubMed1989

Acquired immune deficiency syndrome in childhood. Neurological aspects.

Central nervous system (CNS) involvement is very frequently observed in pediatric AIDS. Clinical manifestations include encephalopathy, cognitive deficits, acquired microcephaly, neurological signs, myelopathy, and peripheral neuropathy. Neurological complications can be related to opportunistic viral infections such as encephalitis, atypical aseptic meningitis, progressive multifocal leukoencephalopathy, and myelitis. Nonviral syndromes include: toxoplasmosis, cryptococcal meningitis, candidiasis, Mycobacterium tuberculosis meningitis, and Mycobacterium avium subacute encephalitis. Bacterial infections, tumors, cerebrovascular complications, and peripheral neuropathies are not frequently observed in pediatric AIDS. The most severe complications of HIV infection is encephalopathy resulting from HIV infection of brain tissue. Direct HIV invasion of the CNS has been demonstrated. Clinical features of HIV encephalopathy are classified into three categories: (1) normal neurological findings; (2) static encephalopathy; and (3) progressive encephalopathy. AIDS dementia complex can be differentiated from the predominance of behavioral and cognitive disabilities.

AIDS Dementia Complex↗
PubMed1991

The immune system is a key factor in the etiology of psychosocial disease.

The immune system is proposed as the key to understanding the etiology and treatment of psychosocial disease. There is a dense communication network between the immune system and the central nervous system (CNS). Immune cell cytokines, via direct action on the CNS, induce fever, alter sleep, pain perception and pituitary hormone release and reduce appetite and activity in animals. Interleukin-2 and interferon given to humans result in global behavioral and cognitive pathology. Activation of the immune system by pathogens produces global cognitive and behavioral pathology also. Recently, controlled trials have demonstrated that diet can cause psychosocial disease, presumably by an immune mechanism. Immune system abnormalities have been identified in manic-depressive psychosis, schizophrenia and alcoholism. Lithium carbonate is not only prophylactic for all three of these diseases, but it also powerfully stimulates the immune system. This is proposed as the mechanism of lithium's therapeutic effect. The antipsychotics, haloperidol and the phenothiazines, affect the immune system also. The rapid development of AIDS dementia complex can be explained by the remarkable influence the immune system has on the CNS.

AIDS Dementia Complex↗