Delayed Neurological Syndrome Following Carbon Monoxide Poisoning

It was a beautiful Spring day and S.Y. was living his dream. He was working on a ranch, tending to the livestock, as he had done for the past 25 years. Each and every day, S.Y. was working hard to create a better life for his family. Then life drastically changed.

S.Y. was found unresponsive in his trailer by his co-workers. A gas powered space heater had malfunctioned, causing toxic carbon monoxide to be released into the air. It was not known how long S.Y. had been exposed to the toxic fumes before paramedics arrived. Carbon monoxide deprives cells in the body and brain of oxygen by combining with the oxygen carrying hemoglobin of the blood to form carboxyhemoglobin. This reaction prevents oxygen from binding to hemoglobin, thus leading to anoxia (lack of oxygen).

Paramedics placed S.Y. on 100% oxygen and took him to the local emergency room for further treatment. While in the ER, a CT scan was done which showed damage to the cerebellum, consistent with carbon monoxide poisoning. S.Y.’s blood level of carbon monoxide was 28%. Hyperbaric oxygen treatment (HBOT) is the only proven therapy for acute carbon monoxide poisoning. HBOT is able to accelerate the elimination of carbon monoxide. Unfortunately, the local ER where S.Y. was transported did not have HBOT available; thus S.Y. was airlifted to an academic medical center where he could receive this treatment.

Approximately two weeks after being exposed to toxic levels of carbon monoxide, S.Y. was responsive, able to ambulate without assistive devices, and no longer in any acute distress. He was alert and oriented to person, place and year but still exhibited confusion regarding what happened to him. Although S.Y. was making progress, he was not able to care for himself or return to work. S.Y. was admitted to Centre for Neuro Skills (CNS) for inpatient, postacute brain injury rehabilitation to improve his functional abilities. S.Y. received up to 6 hours of treatment Monday through Friday, including physical therapy, occupational therapy, speech therapy, and counseling. Residential treatment programs were provided in the mornings, evenings and weekends when S.J. was not at the clinic setting.

Upon admission to Centre for Neuro Skills, S.Y. was intermittently confused, complained of difficulty sleeping, had significant memory deficits, slowed thinking and flattened emotions. S.Y. had difficulty picking up his feet when walking and had postural instability.

After two months of treatment, S.Y. had made improvements in all areas of functioning. It seemed as though S.Y. had recovered from the majority of his deficits caused by carbon monoxide poisoning. Of the patients who survive carbon monoxide poisoning, 3% will develop delayed neurological syndrome. This syndrome is characterized by a period of pseudo-recovery which ranges from 2-40 days, followed by rapid deterioration. Symptoms of delayed neurological syndrome include memory disturbances, disorientation, hallucinations, apathy, emotional lability, gait abnormalities, urinary incontinence, personality changes, and anxiety.

Unfortunately, approximately 45 days after prolonged exposure to carbon monoxide, S.Y. began to experience a shuffling gait, increased confusion, decreased memory, and urinary incontinence. He went from being able to independently perform many of his activities of daily living to being dependent on others for assistance. S.Y.’s shuffling gait became so severe that he could no longer walk and required a wheelchair for mobility. Repeat neuroimaging scans were performed, but revealed no findings that would explain S.Y.’s sudden decline in functioning.

Since delayed neurological syndrome following carbon monoxide poisoning is rare, there are few, if any, proven treatments to reverse its effects. The multi-disciplinary team at Centre for Neuro Skills reviewed S.Y.’s case, consulted with other healthcare professionals and added Mirapex (a medication that has been used to treat gait disturbances in Parkinson’s disease), melatonin to assist with disrupted sleep and Vitamin E (an antioxidant) to the treatment protocol. Within a month, S.Y. was no longer experiencing symptoms of delayed neurological syndrome. S.Y. was back to ambulating independently, demonstrated improved memory, and urinary incontinence was no longer an issue. S.Y. was now able to enjoy community outings with other patients.

Delayed neurological symptoms following carbon monoxide poisoning are a rare occurrence but may be reversed with combination therapy including HBOT, antioxidants, dopaminergic medications and intense inpatient rehabilitation.