Delayed Movement Disorders after Carbon Monoxide Poisoning

Abstract

Of 242 patients with carbon monoxide (CO) poisoning examined between 1986 and 1996, delayed movement disorders were diagnosed in 32 (13.2%). There were 15 men and 17 women. Ages at insult ranged from 9 to 69 years (mean 45.3 years). Of the 32 patients with delayed movement disorders, 23 (71.9%) had parkinsonism, 5 dystonia, 3 chorea and 1 myoclonus. All were associated with delayed CO encephalopathy. The median latency between CO poisoning and the onset of movement disorders was 4 weeks for parkinsonism, 51 weeks for dystonia, 4 weeks for chorea and 8 weeks for myoclonus. The latency of dystonia onset after CO poisoning was longer than that of other types of movement disorders. The CT findings in delayed movement disorders after CO poisoning were variable, and there was no correlation between the sites of imaging and the development of movement disorders. Abnormal dyskinesias disappeared within 8 weeks, and patients recovered from parkinsonism within 6 months. In conclusion, delayed movement disorders after CO poisoning are not rare, and usually appear as a part of delayed CO encephalopathy. The prognosis is good.

The Role of MR Imaging in Assessment of Brain Damage from Carbon Monoxide Poisoning: A Review of the Literature

“…31 Parkinsonism is the most commonly seen symptom in patients with CO exposure. 1,32 The possibility that damage to the GP relating to the extrapyramidal tract causes parkinsonism is readily apparent, but parkinsonism can also occur in patients without damage to the GP. Pavese et al 32 hypothesized that lesions in the CWM containing tracts outputting and/or inputting to the basal ganglia might cause parkinsonism in patients without GP damage.…”

“…Surviving patients will display 1 of 3 clinical behavioral types in the chronic phase after CO poisoning: approximately 70% of survivors present with various transient symptoms only in the acute phase; 20% of patients present with symptoms persisting from the acute to the chronic phase; and the remaining 10% exhibit DNS, representing recurrent neuropsychiatric symptoms occurring after an interval of apparent normality (the so-called lucid interval; mean duration, 22 days) after the apparent resolution of acute symptoms. [1][2][3][4][5] Acute conditions including level of consciousness and carboxyhemoglobin concentration have been considered and found to be unhelpful in the prediction of chronic clinical behaviors. 6,7 In particular, predicting whether patients who exhibit resolved acute symptoms have escaped or will experience DNS represents a very important clinical issue.…”

Delayed Onset Parkinsonism in Alcoholic Patient Following ARDS: Alcoholism could be a Risk Factor

“…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 cardiac arrest [1][2][3]10]. In those cases, movement disorders are associated with encephalopathy, which commonly manifest with cognitive dysfunction, mutism or EEG abnormalities.…”

“…The free interval between hypoxia and symptomatology is negatively linked to age, which presumably relates to the quality of the cerebral perfusion or metabolism [10].…”

“…In those cases, movement disorders are associated with encephalopathy, which commonly manifest with cognitive dysfunction, mutism or EEG abnormalities. None of these features were present in our patient.The free interval between hypoxia and symptomatology is negatively linked to age, which presumably relates to the quality of the cerebral perfusion or metabolism [10].Free radicals liberation linked to hypoxy provoke apoptosis and, secondary, clinical manifestations. Toxic effect of chronic alcohol intake on the brain is well known and don't seem to totally subside with abstinence [11].…”