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An association between cerebrovascular disease (causing transient neurological deficit, transient ischaemic attacks, or cerebral infarction) and advanced HIV disease or AIDS is recognised.1-3 There is also one report of ischaemic stroke as the first manifestation of HIV infection.4 We report a patient with primary HIV-1 infection who presented with a transient neurological deficit. A previously healthy 33 year old right handed male homosexual presented as an emergency with sudden onset of right sided weakness, dysarthria, and dysphasia. He had been unwell for 10 days with fever, pharyngitis, malaise, myalgia, transient non-pruritic macular rash on the upper chest, and transient paraesthesiae affecting the hands. On admission to hospital the neurological features were improving but mild weakness of the right lower limb and expressive dysphasia were present. The neurological deficit resolved completely within 24 hours. Fever (>39°C), a petechial enanthem on the hard palate, and cervical lymphadenopathy were also noted. There were no features of endocarditis or meningeal irritation. Atypical lymphocytes were present in a blood film with normal full blood count. The erythrocyte sedimentation rate was raised at 45 mm/h; serum C reactive protein concentration was 14 mg/l (normal <10 mg/l). A chest radiograph,, echocardiogram, cerebral MRI, urinalysis, blood and urine bacterial cultures, and serological tests for syphilis were negative. An examination of CSF showed a lymphocytic pleocytosis (70 lymphocytes/mm3) and increased CSF protein (1.62 g/l; normal <0.45 g/l); HIV RNA gag and pol sequences were detected in the CSF by polymerase chain reaction. Antibody studies indicated recent HIV-1 seroconversion, with rising anti-HIV IgG (enzyme linked immunosorbent assay (ELISA)) and falling anti-HIV IgM (ELISA). Serology for Epstein-Barr virus, cytomegalovirus, and toxoplasma was negative. Serum anticardiolipin antibodies were detected at a low concentration (18 GPL U/ml, normal <10 U/ml); lupus anticoagulant was not detected. Fever and leg pains persisted for three weeks. He was treated with zidovudine, lamivudine, saquinavir, and low dose aspirin, and made a complete symptomatic recovery within one month. No explanation other than HIV infection was identified to account for the neurological features, which were assumed to have an ischaemic cause. Antiviral triple therapy was continued for six months.The most common neurological manifestations of primary HIV infection are lymphocytic meningitis, reversible acute encephalitis, and peripheral mononeuritis; these have previously been found to be associated with accelerated progression of HIV disease. Focal neurological events would seem to occur rarely during primary HIV illness but they may be underreported; we were unable to identify other reports of transient neurological deficit in this setting. In patients with advanced HIV disease, transient neurological deficit, and cerebrovascular events including cerebral infarction may be associated with non-bacterial endocarditis, CNS infections (including Cryptococcus andtoxoplasma), and CNS tumours, but they may also occur in the absence of an identifiable underlying cause.1-3 In these patients the mechanism for transient neurological deficit and cerebrovascular events in HIV disease is unknown; anticardiolipin antibodies, which may predispose to cerebrovascular disorders,5 were detected in 70% of patients with HIV-related transient neurological deficits in a controlled study.2 In our patient, the cause of the transient neurological deficit is unknown; the possibilities include localised ischaemia caused by vascular obstruction or spasm, or a focal inflammatory lesion developing at the time of seroconversion. The preponderance of transient neurological deficit in late stage HIV disease and its occurrence during primary infection in our patient suggest a possible association with high HIV viral load. Primary HIV infection should be considered in at risk patients presenting with unexplained focal neurological symptoms.
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