Limiting progressive hippocampal metabolic abnormalities after smoke inhalation injury

Abstract

A 46-year-old man had a smoke inhalation injury. Within 1 month, he developed neuropsychiatric problems including toxic encephalopathy, cognitive disorder, depression symptoms and personality change. From 3 to 14 years after the toxic inhalation injury, the patient received treatment with sertraline and methylphenidate. The ¹⁸F-fluorodeoxyglucose positron emission tomography scan at 3 years after injury showed deterioration of glucose metabolism in the hippocampus and orbital frontal region; at 14 years after injury, the hippocampus had no significant change but the orbital frontal region had deterioration of glucose metabolism. It was hypothesised that sertraline may have provided selective hippocampal neuroprotection. Further study is justified to evaluate sertraline as a possible neuroprotective agent after smoke inhalation injury.

Background

Toxic inhalation is common. There are >23 000 injuries and 5000–10 000 deaths in the USA annually caused by smoke inhalation.¹ People may be exposed to toxins from inhaled synthetic chemicals that may compromise intracellular neuronal metabolism.¹

In a previous report, abnormalities in glucose metabolism were noted in several brain regions in a patient who had a smoke inhalation injury.² Further discussion of this case was performed at a grand rounds presentation, and it was hypothesised that sertraline may have provided selective hippocampal neuroprotection. The purpose of the present report was to describe the additional evaluation of this case and encourage other physicians to evaluate brain pathology and attempt to prevent regional brain deterioration after smoke inhalation injury.

Case presentation

As previously reported, a 46-year-old man had a smoke inhalation injury that caused chronic pulmonary illness, several hospitalisations for pneumonia, and obstructive sleep apnoea.² The pulmonary condition necessitated daily treatment with oral corticosteroids. The patient also developed neuropsychiatric problems including toxic encephalopathy, cognitive disorder, depression symptoms and personality change within 1 month after toxic smoke inhalation injury.

The patient previously held leadership positions at work and at two non-profit national organisations. Within 3 years after the smoke inhalation injury, he resigned from the non-profit organisations because of impaired memory and concentration. During the next 11 years, he had no further deterioration of memory or concentration.

Investigations

Quantitative comparison of ¹⁸F-fluorodeoxyglucose positron emission tomography scans made at 3 and 14 years after injury showed significant differences in improvement or deterioration of glucose metabolism in different regions of the brain.² Quantitative analysis of regional glucose metabolism between 3 and 14 years after the smoke inhalation injury did not support an association between regional brain connections. Within 3 years after injury, the hippocampus and orbital frontal region had significant deterioration of glucose metabolism; at 14 years after injury, the hippocampus had no significant change but the orbital frontal region had deterioration of glucose metabolism on the ¹⁸F-fluorodeoxyglucose positron emission tomography scan compared with the scan at 3 years.

Treatment

From 3 to 14 years after the toxic inhalation injury, the patient received treatment with sertraline and methylphenidate. He also received valproic acid for 22 months, beginning at 3 years after the injury, but this was changed to topiramate because of weight gain.

Outcome and follow-up

The ¹⁸F-fluorodeoxyglucose positron emission tomography scan made at 14 years after smoke inhalation injury showed that some areas of the brain improved and other areas deteriorated. The hippocampal abnormalities were unchanged on scans from 3 to 14 years after injury.

Discussion

Smoke inhalation injury can produce neuropsychiatric changes, including depression, personality change and cognitive disorder. Alterations in brain glucose metabolism after smoke inhalation injury may be shown on ¹⁸F-fluorodeoxyglucose positron emission tomography scans.³ Literature review showed no other published cases of quantitative evaluation of long-term improvement or deterioration of brain metabolism on ¹⁸F-fluorodeoxyglucose positron emission tomography scans.

The differences in the scans at 3 and 14 years after injury may be explained by regional differences in vascularity, myelination and sensitivity to neurotoxins and exogenous steroids.²

This case was discussed at Psychiatry Grand Rounds at Cooper Medical School of Rowan University, including a videotaped interview of the patient. Although deterioration of the hippocampus was expected from 3 to 14 years after injury, no hippocampal deterioration was noted on the ¹⁸F-fluorodeoxyglucose positron emission tomography scans. It was hypothesised that sertraline may have provided selective hippocampal neuroprotection. Further study is justified to evaluate sertraline as a possible neuroprotective agent after smoke inhalation injury.

Learning points.

• Toxic smoke inhalation may impair brain tissue morphology and function acutely and chronically.

• The hippocampus may facilitate memory, concentration and affect regulation.

• Further study is justified to evaluate sertraline as a neuroprotective agent for the hippocampus after toxic smoke inhalation injury.