ABSTRACT
OBJECTIVES: Delayed neuropsychiatric syndrome (DNS) is characterized by mental impairment, motor dysfunction, dementia, or psychosis that develops between a few days and weeks after acute carbon monoxide (CO) poisoning. One possible mechanism responsible for CO-mediated encephalopathy involves oxidative stress, such as lipid peroxidation, caused by the cellular uptake of CO and which leads to an inflammatory cascade. There is no current effective treatment for DNS. We applied 8-40 sessions of hyperbaric oxygen therapy (HBO2) to patients with DNS and evaluated its effectiveness. METHODS: After admission, all patients were administered piracetam or bromocriptine, or both, and received HBO2. Neuropsychiatric tests included EEG, mini-mental status examination (MMSE), brain MRI, event-related potential (ERP), and brain perfusion scan (brain SPECT). Results of these tests were compared before and after HBO2, and the clinical features were monitored during this period. RESULTS: The symptoms of DNS for all patients improved significantly after HBOT. Although white matter changes remained evident in the brain MRI scans, other examinations such as EEG, MMSE, ERP, and 99mTc-ECD brain SPECT were nearly normal after HBOT. CONCLUSION: Our results suggest that HBO2 decreases the severity of impairment in patients with DNS. Although a large randomized trial is required to address the efficacy of this therapy, therapeutic application of HBO2 may be recommended in patients with DNS after CO poisoning.
Subject(s)
Carbon Monoxide Poisoning/therapy , Hyperbaric Oxygenation , Mental Disorders/therapy , Movement Disorders/therapy , Adult , Carbon Monoxide Poisoning/complications , Carbon Monoxide Poisoning/diagnosis , Dementia/etiology , Dementia/therapy , Female , Humans , Magnetic Resonance Imaging , Male , Mental Disorders/diagnosis , Mental Disorders/etiology , Middle Aged , Movement Disorders/etiology , Psychotic Disorders/etiology , Psychotic Disorders/therapy , SyndromeABSTRACT
The antiinflammatory activity of Terminalia catappa leaves ethanolic extract was studied using 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear edema in acute and chronic models. A bioassay-oriented fractionation procedure showed that the activity concentrates in the chloroform fraction. Ursolic acid (1) and 2alpha,3beta,23-trihydroxyurs-12-en-28-oic acid (2), isolated from the chloroform fraction, exhibited strong antiinflammatory activities. The results suggest that the triterpenic acids 1 and 2 are responsible for the antiinflammatory activity of T. catappa leaves.