Background: A large proportion of people living with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) suffer from neurocognitive impairment (NCI). The causes of the NCI are multifold in HIV infection although a subset of HIV/AIDS patients are affected by the spectrum syndrome, HIV-associated neurocognitive disorder (HAND). We investigated the Montreal Cognitive Assessment (MoCA) in relation to clinical, demographic and laboratory findings as well as its ability to predict symptomatic HAND (sHAND) among patients with HIV/AIDS. Methods: All subjects were receiving regular HIV care including CD4+ T cell counts, plasma viral load measurements, clinical evaluations and antiretroviral therapy. The diagnosis of sHAND was based upon clinical, neuroimaging, and neuropsychological assessments.Results: Among HIV-1 seropositive subjects (n=125), ethnicity, education and employment were positively correlated with their MoCA scores (p<0.05). In contrast, polypharmacy, central nervous system penetration-effectiveness (CPE) score, antiretroviral drug exposure, substance use and nucleoside/nucleotide reverse transcriptase inhibitor side effects were negatively correlated with MoCA scores (p<0.05). Of note, MoCA scores were not associated with CD4 T cell nadir levels, age, peak viral load, or veterans aging cohort study index. In subjects with or without sHAND, mean MoCA scores differed (sHAND, 22.8±3.51; non-HAND 25.2±2.64) (p<0.05) with a receiver operating characteristic curve showing an area under curve of 0.71 and an optimal MoCA cut-off value of 23.5 when compared to the established diagnostic paradigm. Conclusions: MoCA scores were generally lower in this HIV/AIDS population compared to reported scores in the general population. MoCA performance was associated with multiple clinical variables but displayed limited predictive utility in detecting sHAND.

HIV-1 infection is characterized by multiple neurological syndromes occuring at all stages of infection. HIV-1-associated dementia, however, is the most devastating CNS consequence of AIDS because of its poor prognosis and functional impairment. A clinical triad of progressive cognitive decline, motor dysfunction, and behavioural abnormalities typifies this subcortical dementia which eventually affects 15 to 20% of AIDS patients. Neuroimaging, CSF studies and neuropsychological testing are frequently required in diagnosing HIV-associated dementia, to exclude other conditions including psychiatric illnesses, opportunistic diseases and systemic disorders. The pathogenesis of HIV dementia is uncertain and there is evidence that multiple mechanisms of neurological injury occur. These mechanisms include: the role of neurovirulent strains of HIV; the potential neurotoxicity of HIV gp120, nitric oxide and quinolinic acid; immunologically mediated CNS injury through the action of cytokines and arachidonic acid metabolites; and altered blood-brain barrier permeability. A collective approach involving clinical studies, in vitro assays and animal models will provide greater insight into the pathogenesis and the rational development of therapy for HIV dementia.

We report the clinical and laboratory findings of six Canadian patients with progressive myelopathy associated with HTLV-1 infection. The diagnosis was suspected on clinical grounds and supported by serological studies and positive gene amplification. Only five had emigrated from an area endemic for HTLV-1 infection. Tropical spastic paraparesis should be considered in all patients with myelopathy, even those without standard serological markers of HTLV-1 infection. The pathogenesis of this condition and the serological and molecular biological means by which this diagnosis can be made are reviewed.

We report the pathological and molecular biological findings of human T-cell lymphotropic virus type 1 (HTLV-1) infection of the spinal cord in a patient with a chronic progressive myelopathy. Light microscopy disclosed loss of myelin and axons, thickening of blood vessels and a lymphocytic cell infiltrate in the spinal cord especially at the cervical and thoracic levels. Electron microscopy confirmed the vascuolar appearance seen with light microscopy but virus particles were not observed. The HTLV-1 gag gene could be amplified (by polymerase chain reaction) from cervical spinal cord tissue while not from elsewhere in the neuroaxis. The presence of HTLV-1 geonomic material in spinal cord tissue has not been previously reported.

The human microbiome is comprised of commensal and pathogenic microorganisms, which exert diverse effects in close proximity to the site of intection as well as in remote tissues through immune-mediated mechanisms. Multiple infectious agents have been implicated in the pathogenesis of multiple sclerosis (MS) with variable findings depending on the agent, techniques, and disease phenotype. Herein, the contributions of individual infectious agents to MS and their effects on the immune and nervous systems are reviewed, focusing on herpes viruses, coronaviruses, retroviruses, and synchronic infections. While infectious agents are often assumed to be pathogenic, their effects might also be beneficial to the host in the long-term, depending on age and the type of immunogen/pathogen exposure, as proposed by the hygiene hypothesis. The human microbiome has potential impact on future diagnostic and therapeutic issues in MS.

Over 60,000 Canadians are infected with human immunodeficiency virus (HIV). Greater than 50% of these individuals will develop a neurological disorder despite the availability of highly active antiretroviral therapy. HIV causes nervous system disease at all stages of infection with adverse effects on quality of life, adherence to medications, employment and survival. These disorders include opportunistic infections in addition to distinct HIV-associated neurological syndromes and undesirable treatment-related effects. The latter two groups of disorders are often undiagnosed and untreated in both adolescents and adults. Direct HIV infection of central nervous system causes HIV-associated dementia, which is a progressive subcortical dementia. HIV infection of the peripheral nervous system produces a painful sensory neuropathy termed distal sensory polyneuropathy, which may be exacerbated by several antiretroviral drugs. Other important HIV-induced neurological disorders include vacuolar myelopathy and an increased risk of seizures. Future issues that will confound the presentation and treatment of HIV-induced nervous system disorders include the increasing prevalence of drug-resistant HIV strains, increasing age of HIV-infected patients, hepatitis C virus co-infection and the Immune Reconstitution Inflammatory Syndrome. Herein, we review the clinical presentations, underlying pathogenesis and treatments of this burgeoning group of neurological disorders.

We present the proceedings from a two-day workshop held at Swinburne University on 2005 May 24–25. The workshop participants highlighted current Australian research on both theoretical and observational aspects of galaxy groups. These proceedings include short one-page summaries of a number of the talks presented at the workshop. The talks presented ranged from reconciling N-body simulations with observations, to the Hı content of galaxies in groups and the existence of ‘dark galaxies’. The formation and existence of ultra-compact dwarfs in groups, and a new supergroup in Eridanus were also discussed.