Articles: brain-injuries.
-
To determine whether proton MRS (1H-MRS) neurochemical measurements predict neuropsychological outcome of patients with traumatic brain injury (TBI). ⋯ 1H-MRS provides a rapid, noninvasive tool to assess the extent of diffuse injury after head trauma, a component of injury that may be the most critical factor in evaluating resultant neuropsychological dysfunction. 1H-MRS can be added to conventional MR examinations with minimal additional time, and may prove useful in assessing injury severity, guiding patient care, and predicting patient outcome.
-
Kathy Cook won the $750 first prize in CMAJ's 7th Annual Amy Chouinard Memorial Essay Contest. The deadline for entries to the contest, which is designed to stimulate interest in medical writing among journalism students, is June 1. Entries should be forwarded to the news and features editor. In her winning essay, Cook explores the frustrations and quality-of-life issues that arise in a chronic care institution that is trying to operate in the midst of serious funding cuts.
-
Journal of neurotrauma · Apr 1999
Case ReportsCitalopram treatment of traumatic brain damage in a 6-year-old boy.
Traumatic brain damage may cause acute emotional symptoms such as uncontrolled crying, apathy, and sleep problems. Rehabilitation may be less effective in patients afflicted by these symptoms. Citalopram, a selective serotonin reuptake inhibitor (SSRI), has a documented immediate and dramatic effect on pathological crying in stroke patients. The present case history of a 6-year-old boy with a traumatic right-sided hemorrhage in the basal ganglia indicates that early SSRI treatment has a dramatic effect on pathological crying and in addition may have a concomitant beneficial effect on motor paresis, sleep disturbance, and neurobehavioral problems.
-
J. Cereb. Blood Flow Metab. · Apr 1999
An intrathecal bolus of cyclosporin A before injury preserves mitochondrial integrity and attenuates axonal disruption in traumatic brain injury.
Traumatic brain injury evokes multiple axonal pathologies that contribute to the ultimate disconnection of injured axons. In severe traumatic brain injury, the axolemma is perturbed focally, presumably allowing for the influx of Ca2+ and initiation of Ca2+ -sensitive, proaxotomy processes. Mitochondria in foci of axolemmal failure may act as Ca2+ sinks that sequester Ca2+ to preserve low cytoplasmic calcium concentrations. ⋯ Further, this mitochondrial protection translated into axonal protection in a second group of injured rats, whose brains were reacted with antibodies against amyloid precursor protein, a known marker of injured axons. Pretreatment with CsA significantly reduced the number of axons undergoing delayed axotomy, as evidenced by a decrease in the density of amyloid precursor protein-immunoreactive axons. Collectively, these studies demonstrate that CsA protects both mitochondria and the related axonal shaft, suggesting that this agent may be of therapeutic use in traumatic brain injury.