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Biomedical subjects

Harvey Levin

Publications and source records attributed to Harvey Levin.

6 recordsLinked to original sources

Neurobehavioral and quality of life changes associated with growth hormone insufficiency after complicated mild, moderate, or severe traumatic brain injury.

Adult-onset growth hormone deficiency (GHD) has been associated with reduced quality of life (QOL) and neurobehavioral (NB) deficits. This prospective study tested the hypothesis that traumatic brain injury (TBI) patients with GHD or GH insufficiency (GHI) would exhibit greater NB/QOL impairment than patients without GHD/GHI. Complicated mild, moderate, and severe adult TBI patients (GCS score 3-14) had pituitary function and NB/QOL testing performed 6-9 months postinjury. GH-secretory capacity was assessed with a GHRH-arginine stimulation test and GHD and GHI were defined as peak GH<6 or <or=12 ng/mL (5th and 10th percentiles of healthy control subjects, respectively). Of 44 patients (mean age, 32+/-18 years; median GCS, 7), one (2%) was GHD, seven (16%) were GHI, and 36 (82%) were GH-sufficient at 6-9 months post-injury. Mean peak GH was 8.2+/-2.1 ng/mL in the GHD/GHI group versus 45.7+/-29 ng/mL in the GHsufficient group. The two groups were well-matched in injury characteristics, except that one patient with GHD had central hypogonadism treated with testosterone prior to NB/QOL testing. At 6-9 months postinjury, patients with GHD/GHI had higher rates of at least one marker of depression (p<0.01), and reduced QOL (by SF-36 Health Survey) in the domains of limitations due to physical health (p=0.02), energy and fatigue (p=0.05), emotional well-being (p=0.02), pain (p=0.01), and general health (p=0.05). Chronic GHI develops in approximately 18% of patients with complicated mild, moderate, or severe TBI, and is associated with depression and diminished QOL. The impact of GH replacement therapy on NB function and QOL in these TBI patients is being tested in a randomized placebo-controlled trial.

Adolescent↗

Cognitive rehabilitation interventions for executive function: moving from bench to bedside in patients with traumatic brain injury.

Executive function mediated by prefrontally driven distributed networks is frequently impaired by traumatic brain injury (TBI) as a result of diffuse axonal injury and focal lesions. In addition to executive cognitive functions such as planning and working memory, the effects of TBI impact social cognition and motivation processes. To encourage application of cognitive neuroscience methods to studying recovery from TBI, associated reorganization of function, and development of interventions, this article reviews the pathophysiology of TBI, critiques currently employed methods of assessing executive function, and evaluates promising interventions that reflect advances in cognitive neuroscience. Brain imaging to identify neural mechanisms mediating executive dysfunction and response to interventions following TBI is also discussed.

Animals↗

Response inhibition after traumatic brain injury (TBI) in children: impairment and recovery.

Children who experience traumatic brain injury (TBI) often show cognitive impairments postinjury, some of which recover over time. We examined the recovery of motor response inhibition immediately following TBI and over 2 years. We assessed the role of injury severity, age at injury, and lesion characteristics on initial impairment and recovery while considering the role of pre-injury psychiatric disorder. Participants were 136 children with TBI aged 5-16 years. Latency of motor response inhibition was measured with the stop-signal task within 1 month of the injury and again at 3, 6, 12, and 24 months. The performance of the TBI participants at each measurement occasion was standardized with 117 children of similar age, but without injury. Residualized latency scores were calculated. Growth curve analyses showed an initial impairment in response inhibition and improvement over the 2 years following injury. Younger TBI patients were initially more impaired although they exhibited greater recovery of response inhibition than did older TBI patients. Longer duration of coma, but not reactivity of pupils or Glasgow Coma Scale score, predicted initial deficit. Lesion characteristics or pre-injury attention deficit hyperactivity disorder did not predict initial impairment or recovery. Replication with longitudinal testing of a comparison group of children sustaining extracranial injury is necessary to confirm our findings.

Adolescent↗

Phase II clinical trial of moderate hypothermia after severe traumatic brain injury in children.

OBJECTIVE: To determine whether moderate hypothermia (HYPO) (32-33 degrees C) begun in the early period after severe traumatic brain injury (TBI) and maintained for 48 hours is safe compared with normothermia (NORM) (36.5-37.5 degrees C). METHODS: After severe (Glasgow Coma Scale score < or =8) nonpenetrating TBI, 48 children less than 13 years of age admitted within 6 hours of injury were randomized after stratification by age to moderate HYPO (32-33 degrees C) treatment in conjunction with standardized head injury management versus NORM in a multicenter trial. An additional 27 patients were entered into a parallel single-institution trial of excluded patients because of late transfer or consent (delayed in transfer >6 h but within 24 h of admission), unknown time of injury (e.g., child abuse), and adolescence (e.g., aged 13-18 yr). Assessments of safety included mortality, infection, coagulopathy, arrhythmias, and hemorrhage as well as ability to maintain target temperature, mean intracranial pressure (ICP), and percent time of ICP less than 20 mm Hg during the cooling and subsequent rewarming phases. Additionally, assessments of neurocognitive outcomes were obtained at 3 and 6 months of follow-up. RESULTS: Moderate HYPO after severe TBI in children was found to be safe relative to standard management and NORM in children of all ages and in children with delay of initiation of treatment up to 24 hours. Although there was decreased mortality in HYPO in both studies, there was an increased potential for arrhythmias with HYPO, although they were manageable with fluid administration or rewarming. Additionally, there was a reduction in mean ICP during the first 72 hours after injury in both studies, although rebound ICP elevations in HYPO compared with those in NORM were noted for up to 10 to 12 hours after rewarming. Although functional outcome at 3 or 6 months did not differ between treatment groups, functional outcome tended to improve from the 3- to 6-month cognitive assessment in HYPO compared with NORM, although the sample size was too small for any definitive conclusions. CONCLUSION: HYPO is likely a safe therapeutic intervention for children after severe TBI up to 24 hours after injury. Further studies are necessary and warranted to determine its effect on functional outcome and intracranial hypertension.

Adolescent↗

Constraint-induced movement therapy.

Constraint-induced movement therapy improves outcome after chronic stroke, conforms experimental observations of neuronal plasticity, and proves the efficacy of intensive occupational therapy. More acutely instituted constraint-induced movement therapy has both practical and theoretic risks and benefits that deserve further careful evaluation.

Animals↗

The role of injury severity in neurobehavioral outcome 3 months after traumatic brain injury.

OBJECTIVE/BACKGROUND: To assess neurobehavioral outcome using the Neurobehavioral Rating Scale-Revised (NRS-R), an instrument with established specificity and validity in Traumatic Brain Injury (TBI) in a sample including the full spectrum of TBI severity 3 months after injury. METHOD: A cohort group of 102 subjects with mild TBI, 41 with moderate TBI, and 139 with severe TBI, from multiple academic trauma centers, were assessed using the NRS-R and the Glasgow Outcome Scale. RESULTS: Principal components analysis of the NRS-R resulted in a 3-factor model: (1) Cognitive, (2) Emotional, and (3) Hyperarousal. At 3 months, subjects with severe TBI show greater difficulties in cognitive and hyperarousal, but not emotional domains, than those with mild to moderate TBI. More than one third of subjects in all injury severity groups showed evidence of anxiety, depression, irritability, mental fatigability, and memory dysfunction. Scores on the NRS-R were related to outcome on the Glasgow Outcome Scale. CONCLUSIONS: Three months after injury, subjects with severe TBI have more dysfunction in cognitive and behavioral (but not emotional) domains than those with mild-to-moderate TBI. The NRS-R is a useful tool for assessing the full spectrum of neurobehavioral dysfunction at all ranges of TBI severity.

Adult↗