Sparing of spatial mental imagery in patients with hippocampal lesions.

In four experiments, we explored the capacity for spatial mental imagery in patients with hippocampal lesions, using tasks that minimized the role of learning and memory. On all four tasks, patients with hippocampal lesions performed as well as controls. Nonetheless, in separate tests, the patients were impaired at remembering the materials that had been used to assess mental imagery. The findings suggest that the hippocampus is not needed for constructing many forms of spatial imagery but is needed for the formation of long-term memory. In future studies of the neural organization of spatial mental imagery, it will be important to separate the contribution of spatial processing from the contribution of learning and memory.

Apolipoprotein E genotype and response of carbon monoxide poisoning to hyperbaric oxygen treatment.

RATIONALE: Hyperbaric oxygen (HBO2) reduced the incidence of cognitive sequelae 6 weeks after carbon monoxide (CO) poisoning compared with normobaric oxygen (NBO2). The apolipoprotein (APOE) epsilon4 allele predicts unfavorable neurologic outcome after brain injury and stroke. OBJECTIVES: To assess the effects of the epsilon4 allele on 6-week cognitive sequelae after CO poisoning. METHODS: We tested APOE genotypes in 86 of 152 CO-poisoned patients from our randomized trial. Logistic regression was used to control for risk factors while testing for effects with the epsilon4 allele or interactions with epsilon4 and treatment on 6-week and 6- and 12-month cognitive sequelae. MEASUREMENTS AND MAIN RESULTS: We enrolled 86 patients: 44 received HBO2 and 42 NBO2 therapy. A total of 31 (36%) patients had at least one epsilon4 allele. Six-week cognitive sequelae rates for patients treated with HBO2 and NBO2, respectively: epsilon4 allele absent, 11% (3/27) and 43% (12/28); epsilon4 allele present, 35% (6/17) and 29% (4/14). The epsilon4 allele was not associated with 6-week cognitive sequelae, 27% (15/55) without and 32% (10/31) with the epsilon4 allele (P = 0.323). The interaction between the epsilon4 allele and treatment was significantly associated with 6-week cognitive sequelae (P = 0.048). The interaction between the epsilon4 allele and treatment was not associated with 6- and 12-month cognitive sequelae. CONCLUSIONS: HBO2 therapy reduces cognitive sequelae after CO poisoning in the absence of the epsilon4 allele. Because apolipoprotein genotype is unknown at the time of poisoning, we recommend that patients with acute CO poisoning receive HBO2.

Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen.

RATIONALE: Carbon monoxide poisoning is common and causes cognitive sequelae. Hyperbaric oxygen (HBO(2)) reduces cognitive sequelae incidence, but which patients may benefit from HBO(2) is unclear. OBJECTIVES: Risk factor determination for 6-wk cognitive sequelae from CO poisoning and risk modification with HBO(2). METHODS: Patients were from a randomized controlled trial, enrolling acutely CO-poisoned patients more than 15 years of age. Patients eligible but not enrolled in the randomized trial, and not receiving HBO(2), were followed during the study interval. In patients not receiving HBO(2), we performed univariate analyses including risk factors identified by randomized trial subgroup analyses. A multivariable analysis was performed using univariate results with and without HBO(2). MEASUREMENTS AND MAIN RESULTS: In 163 patients not receiving HBO(2), 68 (42%) manifested sequelae. Risk factors for sequelae from subgroup analyses were loss of consciousness, age of 36 years or more, and carboxyhemoglobin levels greater than or equal to 25%. By univariate analyses, risks for sequelae were age of 36 years or more (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.3-4.9; P = 0.005), and exposure intervals greater than or equal to 24 hours (OR, 2.4; 95% CI, 1.2-4.8; P = 0.019). Including 75 patients receiving HBO(2), cognitive sequelae was reduced in patients age of 36 years or more (OR, 0.3; 95% CI, 0.2-0.6; P < 0.001). Exposure intervals greater than or equal to 24 hours are an independent risk factor for sequelae (OR, 2.0; 95% CI, 1.0-3.8; P = 0.046). CONCLUSIONS: HBO(2) oxygen is indicated for patients with acute CO poisoning who are 36 years or older or have exposure intervals greater than or equal to 24 hours. In addition, subgroup analyses support that patients with loss of consciousness or higher carboxyhemoglobin levels warrant HBO(2).

Affective outcome following carbon monoxide poisoning: a prospective longitudinal study.

OBJECTIVE: To longitudinally assess the prevalence of depression and anxiety following carbon monoxide (CO) poisoning and to assess the contributions of mode of poisoning (accidental versus suicide attempt), cognitive sequelae, and oxygen dose (hyperbaric oxygen versus normobaric oxygen) to depression and anxiety. BACKGROUND: CO is the most common cause of poisoning in the United States and may result in neuropathologic changes and cognitive and neurologic sequelae, yet little is known regarding affective outcomes. METHOD: We prospectively assessed affect in 127 CO-poisoned patients. Self-report inventories of depression and anxiety were administered at 6 weeks and at 6 and 12 months post CO poisoning. The primary outcome was prevalence of depression and anxiety at 6 weeks. To determine the effect of mode of poisoning, cognitive sequelae, and oxygen dose, odds ratio estimates were calculated at all three times using logistic regression. RESULTS: Depression and anxiety were present in 45% of patients at 6 weeks, 44% at 6 months, and 43% at 12 months. Patients with suicide attempt and cognitive sequelae had higher prevalence of depression and anxiety at 6 weeks. At 12 months, there were no differences in depression or anxiety regardless of mode of poisoning, presence of cognitive sequelae, or oxygen dose. CONCLUSIONS: CO poisoning results in significant depression and anxiety that persist to at least 12 months. Patients with cognitive sequelae and suicide attempt had a higher rate of depression and anxiety at 6 weeks but not at 12 months. Clinicians need to be aware of affective morbidity following CO poisoning and remain vigilant about CO prevention.

Carbon Monoxide Research Group, LDS Hospital, Utah in reply to Scheinkestel et al. and Emerson: the role of hyperbaric oxygen in carbon monoxide poisoning.

UNLABELLED: This comprehensive response was invited by the Editor of Emergency Medicine Australasia to allow our Group from Salt Lake City, Utah to review the two articles 'Where to now with carbon monoxide poisoning?' by Scheinkestel et al. and the accompanying COMMENTARY: 'The dilemma of managing carbon monoxide poisoning' by Emerson published in the April issue of Emergency Medicine Australasia.

Hyperbaric oxygen for acute carbon monoxide poisoning.

BACKGROUND: Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. METHODS: We randomly assigned patients with symptomatic acute carbon monoxide poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. RESULTS: The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in each group. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.007), even after adjustment for cerebellar dysfunction and for stratification variables (adjusted odds ratio, 0.45 [95 percent confidence interval, 0.22 to 0.92]; P=0.03). The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio, 5.71 [95 percent confidence interval, 1.69 to 19.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.03). Cognitive sequelae were less frequent in the hyperbaric-oxygen group at 12 months, according to the intention-to-treat analysis (P=0.04). CONCLUSIONS: Three hyperbaric-oxygen treatments within a 24-hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning.