Cerebral Infarction after Toluene Inhalation

Inhalation of organic solvents has long been known to cause central nervous system damage [1]. In the past two decades, toluene and n-hexane have replaced benzene as the major organic constituents of these industrial compounds. Pure toluene inhalation and glue sniffing have become common practice and neurologic damage in association with prolonged daily toluene inhalation has been reported frequently [2]. We report the case of a 37-year-old woman with no previous history of known vascular risk factors or drug abuse accidentally exposed to a mixed inhalation of solvents and glue (Gomafer®, containing 45% toluene, probably more than 2,000 ppm of this compound in the air inhaled) while working in a leather manufacturing company. Immediately after the incident she noted slight lightheadedness and had an episode of unconsciousness. On examination she was disoriented regarding time, place and persons. She had a mild impairment of memory and concentration. Furthermore, she presented pathological emotionality (inappropriate euphoria) without signs of frontal lobe release but no clear neuropsychiatric pattern could be derived from psychological testing. There was a dense right hemiparesis and gait apraxia. Muscle stretch reflexes were increased on the right with bilateral plantar normal responses. No other neurologic abnormalities were seen. Computed tomography on the day of admission to hospital showed a left frontal infarction. A cranial MRI and cerebral and neck vessel angiography performed 2 days after admission showed an occlusion of the left middle cerebral artery and confirmed the left frontal infarction (fig. 1, 2). Other investigations including full blood count, platelets, packed cell volume, plasma viscosity, erythrocyte sedimentation rate, lupus anticoagulant, biochemical profile and fasting lipids were unremarkable. Screening tests for antinuclear antibodies, rheumatoid factor, homocystinuria and syphilis were negative and there was neither an increase in acute phase reactants nor any suggestion of disseminated intravascular coagulation. Cerebrospinal fluid examination was unremarkable. Electrocardiogram and radiographs of the chest were all within normal limits. There was no evidence supporting a transient hypercoagulability of blood (antithrombin III, protein C, protein S, APC resistance, factor V of Leyden). Transthoracic and transesophageal echocardiographies showed normal heart valves and no evidence of mural thrombosis. Extracranial and transcranial Doppler ultrasound findings were unremarkable. Cerebral and cerebellar damage has been documented in cases of inhalant abusers [2]. Cerebral infarction with other forms of drug Fig. 1. Axial T2-weighted MRI scan obtained 48 h after the accident shows acute left prefrontal cerebral artery infarction.