Discussion
In this controlled study, patients were all poisoned during the same weather event and over a very short period of time (3 days). They were enrolled and assessed about 7 weeks after the intoxication. In this homogeneous group of patients, we evidenced both cognitive and psychiatric sequelae after CO poisoning.
Performance was significantly lower in patients than in controls in five out of the eight cognitive variables of interest, despite the fact that controls and patients had been rigorously matched. Three of the variables assessed processing speed and executive functions, one working memory and one verbal episodic memory. These results suggest that these patients were suffering from multi-domain cognitive impairment. We are aware of only two studies in which a group of patients was compared to a group of matched controls specifically enrolled for the study.[9,2] Surprisingly, in Deschamps' study no cognitive difference was reported between the two groups but not all the patients underwent cognitive assessment.[9] Significant differences were showed in Chen's study but neuropsychological assessment was only partial and memory function had not been assessed.[2] Other studies investigating cognitive outcome after CO poisoning did not specifically enroll a group of control subjects but reported results that are in accordance with ours.[5,7,14,15] We acknowledge that our study is cross-sectional. Therefore we did not address the delayed neuropsychological impairment issue. The cause of intoxication may be the reason for this apparent difference as previous studies have often included patients who sustained voluntary CO poisoning during suicide attempts, which is a more severe exposure than the involuntary intoxication that happened in our sample.
Psychiatric sequelae such as anxiety and depression have only been reported in a few studies.[8,14] Patients in our sample also reported PTSD after CO poisoning. This is congruent with the patients' complaints about their reviviscences.
It is possible that the recruitment method was a factor of bias. The 42 intoxicated persons who did not enter the study might have had lower cognitive impairment compared to the 38 recruited intoxicated participants. Therefore, the size of the observed effects in our analysis is possibly overestimated. However, we have shown that cognitive complaint was as low in the patient group as it was in the group of controls. We acknowledge that if the recruitment method was not ideal, its influence on the results was probably weak.
BMC Neurol. 2014;14(153) © 2014 BioMed Central, Ltd.
