Delayed post-hypoxic encephalopathy is an uncommon but potentially debilitating consequence of hypoxic-ischemic brain injury. This condition is characterized by delayed neurological deterioration days-to-weeks after an initial partial or complete recovery from hypoxic-ischemic brain injury. The course of recovery from this condition is highly variable, ranging from rapid and fatal progression over several weeks to delayed but occasionally complete recovery. There are no reports describing neurorehabilitative, including neuropharmacologic, interventions for persons with persistent neurological and/or neurobehavioural deficits following delayed post-hypoxic encephalopathy. This study describes the case of a 24-year old male who developed delayed post-hypoxic encephalopathy following an unintentional methadone and diazepam overdose and who demonstrated cognitive and neurobehavioural improvements during treatment with amantadine HCl hydrochloride in a single-case, open-label design. A brief review of the literature regarding this condition, its treatment and suggestions for further study are presented.

Psychiatrists are increasingly called upon to care for individuals with cognitive, emotional, and behavioral disturbances after TBI, especially in settings serving military service personnel and Veterans. In both the early and late post-injury periods, cognitive impairments contribute to disability among persons with TBI and are potentially substantial sources of suffering for persons with TBI and their families. In this article, the differential diagnosis, evaluation, and management of posttraumatic cognitive complaints is reviewed. The importance of pre-treatment evaluation as well as consideration of non-cognitive contributors to cognitive problems and functional limitations is emphasized first. The course of recovery after TBI, framed as a progression through posttraumatic encephalopathy, is reviewed next and used to anchor the evaluation and treatment of posttraumatic cognitive impairments in relation to injury severity as well as time post-injury. Finally, pharmacologic and rehabilitative interventions that may facilitate cognitive and functional recovery at each stage of posttraumatic encephalopathy are presented.

Although the O-Log and GOAT perform similarly as measures of PTA severity and duration, PTA assessments using the O-Log offers better prediction of rehabilitation outcomes. Further study of the O-Log as an alternate assessment of PTA is warranted.

The aim of this study was to investigate the impact of a water protocol on the incidence of aspiration pneumonia in persons with cerebrovascular accident and dysphagia admitted to an acute neurologic rehabilitation setting. Retrospective chart review and cohort matching of persons with dysphagia admitted before and after the implementation of a water protocol were carried out. The incidence of aspiration pneumonia was higher in the cohort control group-those patients admitted during the years before the implementation of a water protocol. No persons with dysphagia who received water, even if known aspirators of thin liquids, developed aspiration pneumonia. Our findings support the premise that even in known thin liquid aspirators, offering water does not increase incidence of aspiration pneumonia.