Active clinical trials for "Brain Injuries"

The purpose of this study is to examine the effects of exercise on recovery after traumatic brain injury. Investigators will determine if exercise enhances rehabilitation by increasing substances (proteins) that can facilitate recovery.

This study is a prospective multicenter randomized controlled trial from Asian countries to compare the effect and safety of right median nerve stimulation versus traditional treatment for comatose patients at the early stage following traumatic brain injury.

This clinical trial evaluates the safety and diagnostic performance of a newly developed combined catheter that will be implanted into the brain of patients with severe brain injury for short time (up to 28 days) monitoring of the electric activity and the metabolism of brain tissue at risk. Ten patients will be monitored with the new device and seven patients will be monitored by intracerebral probes according to standard treatment.

Traumatic brain injury (TBI) is a devastating disease with high morbidity and mortality. Although not fully proved, it is commonly accepted that the morbidity and mortality and proportional to the extent of intracranial bleeds (i.e. - larger hemorrhages cause more injury than smaller ones). Aspirin is a commonly used antiaggregate drug that interferes with the clotting system. The antiaggregate effect may be neutralized by administration of platelets. Thus, potentially, patients receiving Aspirin and undergoing TBI, are at a higher risk for increasing an intracranial bleed. In this prospective study, the investigators randomize patients receiving aspirin that have a traumatic intracranial bleed to two groups, one - that will receive platelets, and the other that will not receive platelets. The primary end point of the study is to evaluate the effect of platelet administration of the enlargement of traumatic intracranial bleeds, and try and evaluate any clinical outcome differences between the two groups.

The hypothesis is that brain injury patients have alterations of the respiratory system related to intraabdominal pressure. Furthermore application of moderate levels of PEEP may improve respiratory function in these patients.

Current standard of care prior to determination of brain death in subjects with suspected anoxic brain injury is to exclude complicating medical conditions that may confound clinical assessment (such as severe electrolyte, acid base, endocrine or circulatory disturbance), achieve normothermia and normal systolic blood pressure over 100 mmHg (with or without vasopressor use), exclude the presence of neuromuscular blocking agents (with the presence of a train of 4 twitches with maximal ulnar nerve stimulation) as well as to exclude the presence of CNS depressant drug effects. At the present time the latter is done by history, drug screen and allowing enough time for paralytic and sedative drugs to be metabolized and cleared from the body. Clearance is calculated by using 5 times the drug's half-life assuming normal hepatic and renal functions. Half-life can also be prolonged in subjects who have been treated with induced hypothermia. Literature search revealed articles with general guidelines and approaches to brain death, but none addressed pharmacological reversal of sedative drugs

The aim is to evaluate the study design, procedure and measurements in a randomised controlled pilot study.

The aim of the study is to investigate the effectiveness of motor and cognitive virtual environment rehabilitation on upper limb function in sub-acute patients after an acquired brain injury.

This randomized study aims at comparing between the effects of amantadine, citcholine and its combinations on arousal and behavioral consequences in early phase of moderate Traumatic Brain injury (TBI).

The investigators propose that immune effector cell-associated neurotoxicity syndrome (ICANS) is predicated upon the early loss of blood brain barrier (BBB) integrity with subsequent monocyte infiltration leading to cross-activation of native glial cells. Glial overstimulation leads to neuroinflammation, synaptic dysfunction, and ultimately neuronal injury.