Patients infected with the human immunodeficiency virus (HIV) appear t
o have a high risk of ischaemic cerebral events. We observed two cases
of cerebral infarction in patients with acquired immune deficiency sy
ndrome (AIDS). In the first case, a 38-year-old homosexual with no car
diovascular risk other than smoking presented with rapidly progressive
hemiparesia. Brain CT-scan visualized two infarcts in the territory o
f the right sylvian artery and the arteriography an occlusion of the i
nternal carotid artery, In the second, a 37-year-old homosexual, hospi
talization was required for a left-sided pure sensitive epilepsy seizu
re. There was no cardiovascular risk other than smoking. Magnetic reso
nance imaging showed parietal ischaemia and thrombus in the left atriu
m without atrial hypertrophy was seen at transoesophageal echocardiogr
aphy. In both cases, there was no evidence of endocarditis, dissection
of the neck vessels or disseminated intravascular coagulation nor of
associated viral or bacterial infectious complication of AIDS. Angiogr
aphic findings eliminated cerebral vascularitis. Among the perturbed h
aemostasis factors previously reported in HIV+ patients, we observed f
ree proteins S deficiency (68 and 43%) and heparin cofactor II deficie
ncy (54 and 40%), Serum albumin was 33 and 32 g/l respectively. Outcom
e was favourable in both cases with anticoagulant therapy. These coagu
lation anomalies would not appear sufficient to explain cerebral infar
ction. Other mechanisms including immune complexed deposition, direct
HIV toxicity for endothelial cells or the effect of cytokines on smoot
h muscles fibres and fibroblasts are probably more important causal fa
ctors.