A case of delayed vascular parkinsonism resulting from an hypoxic insult is reported in a alcoholic patient. Hypoxic events are more frequent in alcoholic patients probably through a mechanism of increased lung vulnerability. When present, hypoxia has more severe neurological consequences in this population, occurring in a context of diminished cerebral blood flow. Alcoholism could be a risk factor for the occurrence of delayed onset parkinsonism following ARDS.Keywords: Vascular Parkinsonism, ARDS, alcohol, apoptosis, delayed symptoms.
CASE REPORTWe report a 40-days delayed onset case of vascular parkinsonism resulting from an hypoxic insult (acute respiratory distress syndrome, ARDS). Parkinsonism following cerebral anoxia has been widely documented [1][2][3][4]. Our patient was alcoholic and this condition could have been a predisposing factor to his neurological outcome.A 52 year-old man was admitted in coma following a medication suicide attempt with benzodiazepines. His psychiatric history included social phobia, long-term severe alcohol dependence, in remission for two months, and tobacco dependence.Cardio-respiratory status was normal on admission. He went out of coma several hours later but had to be put on artificial ventilation due to acute pulmonary failure. Pulmonary failure was attributed to false deglutition and to inhalation pneumonia. He was extubated on day 10 and left the unit on day 12, without any clinically apparent cognitive or motor deficits. Cardiac monitoring had been normal all along.From day 45 on, the following neurological signs appeared progressively over 2 weeks, then remained stable: dysarthria, postural instability including unsteady gait, bradykinesia and reduced automatic movements. There was no tremor. Muscle tone was slightly increased with lower extremity predominance. There was no cogwheel phenomenon. Cognitive functions did not seem to be altered. Sphincter control remained intact. Electroencephalogram was normal. Brain magnetic resonance imaging showed moderate cerebellar atrophy, a common finding in heavy alcoholics [5] as well as patchy increase signal in the cortex (with a predominance in the temporal lobes), in the periventricular white matter and in the pons on T2-weighted sequences but no abnormal signal in the basal ganglia.*Address correspondence to this author at the Psychiatric Institute, CHU Brugmann, Place Van Gehuchten 4, 1020 Brussels, Belgium; Tel: 3224772705; Fax: 3224772162; E-mail: ckornrei@ulb.ac.beThe patient was treated with levodopa and physical therapy. Slight clinical improvement was noted after 3 weeks. Six months after that episode, the patient still showed difficulties to walk and a rigidity.This patient met the diagnostic criteria for vascular parkinsonism [6-9], i.e. co-existence of the clinical features described above and of cardio-vascular risk factors (obesity, tobaco consumption, sedentarity). Delayed-onset movement disorders are quite common after hypoxic or anoxic events such as carbon monoxyde poisonning, hypoglycemia and ca...
