The aim of this study was to provide data on the prognosis and treatment options of headache associated with sexual activity (HSA). Sixty patients diagnosed with HSA between 1996 and 2004 were followed up between 2003 and 2006 at least 12 months after the first interview. The further course of the disease and their contentedness with therapy were requested. On average, the second interview was performed 35.9 months after the first examination. Of the 45 patients who had suffered from single attacks or bouts prior to baseline examination, 37 had no further attacks. Seven patients suffered from at least one further bout with an average duration of 2.1 months. One patient developed a chronic course of the disease after an episodic start. Of the 15 patients with chronic disease at the first examination, seven were in remission and five had ongoing attacks at follow-up. Ten patients received indomethacin for preemptive therapy, with good results in nine patients. Eighteen patients received beta-blockers for prophylaxis, with good results in 15 patients. Episodic HSA occurs in approximately three-quarters and chronic HSA in approximately one-quarter of patients. Even in chronic HAS, the prognosis is favourable, with remission rates of 69% during an observation period of 3 years. For patients with longer-lasting bouts or with chronic HSA, prophylactic treatment with beta-blockers or preemptive therapy with indomethacin are often successful.

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BackgroundPrevious studies have reported white matter (WM) brain alterations in asymptomatic patients with human immunodeficiency virus (HIV).MethodsWe compared diffusion tensor imaging (DTI) derived WM fractional anisotropy (FA) between HIV-patients with and without mild macroscopic brain lesions determined using standard magnetic resonance imaging (MRI). We furthermore investigated whether WM alterations co-occurred with neurocognitive deficits and depression. We performed structural MRI and DTI for 19 patients and 19 age-matched healthy controls. Regionally-specific WM integrity was investigated using voxel-based statistics of whole-brain FA maps and region-of-interest analysis. Each patient underwent laboratory and neuropsychological tests.ResultsStructural MRI revealed no lesions in twelve (HIV-MRN) and unspecific mild macrostructural lesions in seven patients (HIV-MRL). Both analyses revealed widespread FA-alterations in all patients. Patients with HIV-MRL had FA-alterations primarily adjacent to the observed lesions and, whilst reduced in extent, patients with HIV-MRN also exhibited FA-alterations in similar regions. Patients with evidence of depression showed FA-increase in the ventral tegmental area, pallidum and nucleus accumbens in both hemispheres, and patients with evidence of HIV-associated neurocognitive disorder showed widespread FA-reduction.ConclusionThese results show that patients with HIV-MRN have evidence of FA-alterations in similar regions that are lesioned in HIV-MRL patients, suggesting common neuropathological processes. Furthermore, they suggest a biological rather than a reactive origin of depression in HIV-patients.

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.

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.