[Update HIV and neurology]. / Update HIV und Neurologie.

With modern antiretroviral drug regimens, HIV-infected people are living longer and HIV has transformed into a chronic illness. The review summarizes pathophysiological as well as clinical aspects of a chronic infection from a neurological point of view including neurocognitive impairment, depression, neuropathies and myopathies. It also draws attention to comorbidities such as syphilis and hepatitis C. They are of particular neurological interest because of the interaction of the pathogens.

Intrathecal viral replication and cerebral deficits in different stages of human immunodeficiency virus disease.

The objectives of this study is to clarify whether there are phases critical for the infection of the central nervous system (CNS) as defined by active viral replication in the cerebrospinal fluid (CSF) in human immunodeficiency virus (HIV) infection. One hundred and nine HIV-1-positive homo- and bisexual patients in early and late disease stages with or without highly active antiretroviral therapy (HAART) were included in the cross-sectional, diagnostic (phase I) multicenter study. No patients had any overt neurological deficits; all underwent venous and lumbar puncture as well as neuropsychological testing. In untreated early-stage patients, cerebrospinal fluid (CSF) viral load correlated with inflammatory parameters, but not significantly with neuropsychological abnormalities. CSF viral load and inflammatory reactions were suppressed in HAART-treated early-stage patients. In HAART-treated late-stage patients, there was a weak correlation between CSF viral load and CSF cell count as well as a moderate correlation with immune activation markers and with distinct cerebral deficits independent of CSF viral load. Seventeen of the 109 patients had higher CSF than plasma viral loads and marked inflammatory reactions and immune activation. In patients with greater plasma than CSF viral loads, the factors contributing to cerebral deficits still need to be identified. The results suggest not only that there is an early "set point" for CSF/central nervous system (CNS) infection, but also that there is a subgroup of patients in whom intrathecal viral replication correlates with cerebral deficits. Lumbar puncture should be performed in all positive patients to identify members of this subgroup and to ascertain what characteristic factors they have in common in order to improve therapy.

Treatment of cluster headache attacks with less than 6 mg subcutaneous sumatriptan.

BACKGROUND: Subcutaneous (SQ) sumatriptan 6 mg is effective in the treatment of acute cluster headache attacks. However, patients sometimes benefit from a dose less than 6 mg. OBJECTIVE: Therefore, we designed a prospective open study to evaluate how many patients benefit from a dose less than 6 mg SQ sumatriptan. METHODS: We enrolled 81 consecutive patients with cluster headache and recorded their use of SQ sumatriptan and oxygen. Patients regularly using SQ sumatriptan 6 mg were advised to treat attacks with doses less than 6 mg and with oxygen. Efficacy and side effects of the different treatment options (6 mg, 3 mg, 2 mg, and oxygen) were evaluated. RESULTS: As a result, 74% of the patients using SQ sumatriptan 3 mg showed efficacy and 89% reported efficacy after 2 mg. Seventy-nine percent reported side effects after the use of SQ sumatriptan 6 mg (29% severe side effects). After the use of 2 mg SQ sumatriptan, only 50% of the patients reported side effects, none of these were classified as severe. Patients' preference was 41% for 6 mg sumatriptan, 28% for doses less than 6 mg, and 31% for oxygen. CONCLUSIONS: We conclude that sumatriptan in doses less than 6 mg can be effective in the acute treatment of cluster headache attacks. We suggest that patients should have experience in their individual efficacy of sumatriptan doses less than 6 mg.