Biomedical subjects

Douglas I Katz

Publications and source records attributed to Douglas I Katz.

5 recordsLinked to original sources

PubMed2006

Guidelines for the pharmacologic treatment of neurobehavioral sequelae of traumatic brain injury.

There is currently a lack of evidence-based guidelines to guide the pharmacological treatment of neurobehavioral problems that commonly occur after traumatic brain injury (TBI). It was our objective to review the current literature on the pharmacological treatment of neurobehavioral problems after traumatic brain injury in three key areas: aggression, cognitive disorders, and affective disorders/anxiety/ psychosis. Three panels of leading researchers in the field of brain injury were formed to review the current literature on pharmacological treatment for TBI sequelae in the topic areas of affective/anxiety/ psychotic disorders, cognitive disorders, and aggression. A comprehensive Medline literature search was performed by each group to establish the groups of pertinent articles. Additional articles were obtained from bibliography searches of the primary articles. Group members then independently reviewed the articles and established a consensus rating. Despite reviewing a significant number of studies on drug treatment of neurobehavioral sequelae after TBI, the quality of evidence did not support any treatment standards and few guidelines due to a number of recurrent methodological problems. Guidelines were established for the use of methylphenidate in the treatment of deficits in attention and speed of information processing, as well as for the use of beta-blockers for the treatment of aggression following TBI. Options were recommended in the treatment of depression, bipolar disorder/mania, psychosis, aggression, general cognitive functions, and deficits in attention, speed of processing, and memory after TBI. The evidence-based guidelines and options established by this working group may help to guide the pharmacological treatment of the person experiencing neurobehavioral sequelae following TBI. There is a clear need for well-designed randomized controlled trials in the treatment of these common problems after TBI in order to establish definitive treatment standards for this patient population.

Aggression↗

PubMed2006

Neuroprotection and stroke rehabilitation: modulation and enhancement of recovery.

Recent advances in research are modifying our view of recovery after nervous system damage. New findings are changing previously held concepts and providing promising avenues for treatment of patients after stroke. This review discusses mechanisms of neuronal injury after brain ischemia and the attempts to study neuroprotection options based on such mechanisms. It also considers measures available at present to improve outcome after stroke and presents new areas of research, particularly stimulation techniques, neurogenesis and trophic factors to enhance recovery. In order to improve outcomes, medications that may be detrimental to recovery should be avoided, while symptomatic therapy of problems such as depression, pain syndromes and spasticity may contribute to better results. Continued surveillance and early treatment of complications associated with acute stroke, along with supportive care remain the mainstay of treatment for stroke patients in the recovery phase. Present research on limiting brain damage and improving recovery and plasticity enhance the prospects for better clinical treatments to improve recovery after stroke.

Brain Damage, Chronic↗

PubMed2005

Multiple frontal systems controlling response speed.

This study evaluated a model of attention that postulates several distinct component processes, each mediated by specific neural systems in the human frontal lobes. A series of reaction time (RT) tests (simple, choice, and prepare) examined the hypothesis that different attentional processes are related to distinct regions within the frontal lobes. These tests were given to 38 patients with frontal lesions and 38 age-matched control subjects. Lesions were localized both by general regions (superior medial, inferior medial, left and right lateral) and by individual architectonic areas. Lesions in the superior medial (SM) frontal lobes, particularly involving areas 24 and 32 on the right, were associated with slow RT in all tests and with failure to decrease RT after a warning signal. Lesions in the right lateral (RL) frontal lobe, centred in area 9/46v, prevented the decrease in RT with increasing foreperiod that was seen in normal subjects and in patients with lesions elsewhere in the frontal lobes. The ability to energize a response for rapid RT, either generally or specifically following a warning stimulus, is sensitive to lesions of the right SM. Monitoring of stimulus occurrence and response behaviour in order to enhance the speed of response to upcoming stimuli is sensitive to RL lesions.

Adult↗

PubMed2004

Recovery of ambulation after traumatic brain injury.

OBJECTIVES: To identify variables that are predictive of independent ambulation after traumatic brain injury (TBI) and to define the time course of recovery. DESIGN: Retrospective review of consecutive admissions of patients with severe TBI over a 32-month period. SETTING: Brain injury unit in an acute, inpatient rehabilitation hospital. PARTICIPANTS: Of 264 patients screened, 116 met criteria that included the ability to participate in motor and functional evaluation on admission to acute rehabilitation, and the absence of other neurologic disorders or fractures that affect one's ability to ambulate. INTERVENTION: Inpatient rehabilitation on a specialized TBI unit by an interdisciplinary team.Main outcome measures Recovery of independent ambulation and time to recover independent ambulation. RESULTS: Of eligible patients, 73.3% achieved independent ambulation by latest follow-up (up to 5.1 mo). Patients who achieved independent ambulation were significantly younger (P<.05), had better gait scores on admission (P<.05), and tended to be less severely injured-based on duration of posttraumatic amnesia (PTA; P=.058)-than those who did not ambulate independently. There were no differences in recovery based on neuropathologic profile. Mean time to independent ambulation +/- standard deviation was 5.7+/-4.3 weeks; of those achieving independent ambulation, 82.4% did so by 2 months and 94.1% by 3 months. If not independent by 3 months postinjury, patients had a 13.9% chance of recovery. Multivariate regression analysis generated prediction models for time to independent ambulation, using admission FIM instrument scores and age (38% of variance); initial gait score, loss of consciousness, and age (40% of variance); or initial gait score and PTA (58% of variance), when restricted to just those patients with diffuse axonal injury. CONCLUSIONS: Most patients with severe TBI achieved independent ambulation; the vast majority did so within 3 months postinjury. Functional measures, injury severity measures, and age can help guide prognosis and expectations for time to recover.

Activities of Daily Living↗

PubMedDate not supplied

Update of neuropathology and neurological recovery after traumatic brain injury.

This review focuses on the potential for traumatic brain injury to evoke both focal and diffuse changes within the brain parenchyma, while considering the cellular constituents involved and the subcellular perturbations that contribute to their dysfunction. New insight is provided on the pathobiology of traumatically induced cell body injury and diffuse axonal damage. The consequences of axonal damage in terms of subsequent deafferentation and any potential retrograde cell death and atrophy are addressed. The regional and global metabolic sequelae are also considered. This detailed presentation of the neuropathological consequences of traumatic brain injury is used to set the stage for better appreciating the neurological recovery occurring after traumatic injury. Although the pathological and clinical effects of focal and diffuse damage are usually intermingled, the different clinical manifestations of recovery patterns associated with focal versus diffuse injuries are presented. The recognizable patterns of recovery, involving unconsciousness, posttraumatic confusion/amnesia, and postconfusional restoration, that typically occur across the full spectrum of diffuse injury are described, recognizing that the patient's long-term recovery may involve more idiosyncratic combinations of dysfunction. The review highlights the relationship of focal lesions to localizing syndromes that may be embedded in the evolving natural history of diffuse pathology. It is noted that injuries with primarily focal pathology do not necessarily follow a comparable pattern of recovery with distinct phases. Potential linkages of these recovery patterns to the known neuropathological sequelae of injury and various reparative mechanisms are considered and it is proposed that potential biological markers and newer imaging technologies will better define these linkages.

Brain Injuries↗