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PubMed1987

Prostaglandin derivative PGBx improves neurologic recovery after ischemic spinal injury.

Neurological dysfunction resulting from an ischemic insult in the central nervous system (CNS) is believed to be an indirect outcome of impaired energy production. Recent studies suggest that prostaglandin Bx (PGBx), an oligomer of PGB1 and 15-keto-PGB1, may be beneficial in protecting mitochondrial function after ischemic insults by preventing uncoupling of oxidative phosphorylation. In the present study, PGBx had a significant influence on neurological outcome after ischemic injury in the rabbit spinal cord. These findings suggest that PGBx may be beneficial in the treatment of CNS ischemic injuries.

Animals↗
PubMed1981

Opiate antagonist improves neurologic recovery after spinal injury.

The opiate antagonist naloxone has been used to treat cats subjected to cervical spinal trauma. In contrast to saline-treated controls, naloxone treatment significantly improved the hypotension observed after cervical spinal injury. More critically, naloxone therapy significantly improved neurologic recovery. These findings implicate endorphins in the pathophysiology of spinal cord injury and indicate that narcotic antagonists may have a therapeutic role in this condition.

Animals↗
PubMed2000

Neurological recovery from closed head injury is impaired in diabetic rats.

Diabetes mellitus is a metabolic disorder associated with central nervous system impairments. Recent studies implicate oxidative stress mediated by reactive oxygen species (ROS) in the pathogenesis of diabetic complications. ROS have been shown to play role in the pathophysiology of brain injury. In the present study, closed head injury (CHI) was induced in diabetic rats to test the hypothesis that chronic oxidative stress exacerbates brain damage following CHI. Neurological recovery, edema, levels of low molecular weight antioxidants (LMWA), and markers of lipid peroxidation were determined at different intervals after injury. Diabetic rats (4 weeks after induction with streptozotocin) were subjected to CHI. Brain edema (percent water) and clinical status (neurological severity score) were assessed during 7 days. Brain LMWA were determined using cyclic voltammetry (CV) and HPLC-EC. In addition, conjugated dienes and thiobarbituric acid reactive substances (TBARS) were measured. Diabetic-CHI rats exhibited a lower rate of recovery and greater and more sustained edema (p < 0.01), as compared with the controls. At all times diabetic rats had higher levels of TBARS and conjugated dienes and lower concentrations of LMWA, and of vitamins C and E, suggesting chronic oxidative stress. At 5 min of CHI, the amounts of LMWA in control-CHI brains decreased (approximately 50%, p < 0.01) and returned to normal by 48 h and 7 days. In the diabetic-CHI brain only one class of LMWA slightly declined but remained low for 7 days. The present results support the hypothesis that diabetic rats are under chronic oxidative stress, and suffer greater neurological dysfunction, associated with further lipid peroxidation following CHI.

Animals↗
PubMed2004

Ischemic preconditioning does not improve neurological recovery after spinal cord compression injury in the rat.

Ischemic preconditioning (IPC) has been defined as the endogenous cellular protective mechanism evoked by brief ischemic periods. IPC renders the tissue of the central nervous system more resistant to subsequent lethal ischemic insults, and similar protective effect of IPC has been observed after experimental traumatic brain injury. Spinal cord trauma differs from cerebral trauma in that the secondary processes are damaging mostly the white matter. In the present study, we have tested the hypothesis that a transient non-lethal ischemic insult would improve outcomes after subsequent traumatic spinal cord injury (SCI). In the IPC group, 5-min spinal cord ischemia has been induced by aortic occlusion combined with hypotension. Forty-eight hours after IPC, moderate spinal cord injury has been induced by epidural balloon inflation at T8 level. Control group underwent identical surgical procedures without ischemia followed by SCI after 48 h. During the 4-week survival, locomotor performance of all rats was repeatedly tested and evaluated according to BBB scale. After 4 weeks, the animals were perfusion-fixed for histopathology, and morphometric analyses were performed in order to quantify the extent of the spinal cord lesion. All animals were completely paraplegic after SCI, and showed partial neurological recovery during their survival period. No significant differences were detected either in neurological scores or in morphometric measurements after 4 weeks' survival. These results indicate that in contrary to cerebral trauma, IPC does not improve the outcome after SCI.

Animals↗
PubMed1998

Delayed treatment with aminoguanidine decreases focal cerebral ischemic damage and enhances neurologic recovery in rats.

Delayed treatment with aminoguanidine (AG), a relatively selective inhibitor of inducible nitric oxide synthase, ameliorates brain damage produced by occlusion of the rat's middle cerebral artery (MCA). We investigated whether the protection exerted by AG is dose-dependent and whether it is associated with improved neurologic outcome. We also studied the effect of the timing of administration of AG relative to the induction of cerebral ischemia. Halothane-anesthetized spontaneously hypertensive rats underwent permanent MCA occlusion distal to the lenticulostriate branches. Neurologic deficits were assessed daily by the postural reflex test and beam balance test. Infarct volume was determined in thionin- stained sections 96 hours after ischemia and values corrected for swelling. Treatment with AG (intraperitoneally, twice daily), starting 24 hours after MCA occlusion, decreased neocortical infarct volume in comparison to vehicle-treated rats. After correction for swelling, the decrease was 8 +/- 12% at 50 mg/kg (n = 8; P > .05; analysis of variance), 25 +/- 13% at 100 mg/kg (n = 7; P < .05), 30 +/- 16% at 200 mg/kg (n = 7; P < .05) and 32 +/- 9% at 400 mg/kg (n = 5; P < .05). Twenty-four hours after induction of ischemia neurologic deficits scores did not differ between treated and untreated rats (P > .05). However, from 48 to 96 hours after ischemia, neurologic deficits improved significantly in rats treated with AG (100 to 400 mg/kg) compared to rats in which vehicle was administered (P < .05). The decrease in neocortical infarct volume was greatest when AG (100 mg/ kg; twice daily) was administered 12 (26 +/- 17%; n = 9) or 24 hours (25 +/- 13, n = 7) after MCA occlusion. The findings show that AG decreases ischemic brain damage dose-dependently and improves neurologic recovery. Delayed treatment with AG may be a therapeutic strategy to selectively target the evolution of ischemic damage that occurs in the post-ischemic period.

Animals↗
PubMed2005

Prolonged refractory status epilepticus following acute traumatic brain injury: a case report of excellent neurological recovery.

INTRODUCTION: Refractory status epilepticus (RSE) secondary to traumatic brain injury (TBI) may be under-recognized and is associated with significant morbidity and mortality. METHODS: This case report describes a 20 year old previously healthy woman who suffered a severe TBI as a result of a motor vehicle collision and subsequently developed RSE. Pharmacological coma, physiological support and continuous electroencephalography (cEEG) were undertaken. RESULTS: Following 25 days of pharmacological coma, electrographic and clinical seizures subsided and the patient has made an excellent cognitive recovery. CONCLUSION: With early identification, aggressive physiological support, appropriate monitoring, including cEEG, and an adequate length of treatment, young trauma patients with no previous seizure history and limited structural damage to the brain can have excellent neurological recovery from prolonged RSE.

Adult↗
PubMed1994

Neurological recovery after cranioplasty.

A patient who sustained a gunshot wound to the head was successfully treated with acute neurosurgical intervention. Six months after the injury, cranioplasty was used to repair a large skull defect. After cranioplasty, the patient developed significant improvement in motor function in his left upper extremity, which had been plegic after his injury. Although the mechanism of neurological recovery after cranioplasty is controversial, the occurrence of such improvement may be a sufficient indication for cranioplasty in certain patients.

Adult↗
PubMed2005

Neurological recovery after decompressive craniectomy for massive ischemic stroke.

INTRODUCTION: Decompressive craniectomy has demonstrated efficacy in reducing morbidity and mortality in critically ill patients with massive hemispheric cerebral infarction. However, little is known about the patterns of functional recovery that exist in patients after decompressive craniectomy, and controversy still exists as to whether craniotomy and infarct resection ("strokectomy") are appropriate alternatives to decompression alone. We therefore used functional magnetic resonance imaging (f-MRI) to assess the extent and location of functional recovery in patients after decompressive craniectomy for massive ischemic stroke. METHODS: f-MRI was obtained in three patients with massive nondominant cerebral infarction who had undergone decompressive craniectomy for severe cerebral edema 13 to 26 months previously. Brain activation was triggered by hand-gripping or foot- movement tasks. Imaging results were combined with periodic clinical follow-up to determine the extent of neurological recovery. RESULTS: Activation of the contralateral hemisphere was seen in the sensorimotor cortex, premotor, and supplementary motor areas. Lesser activation patterns were seen in equivalent regions of the infarcted hemisphere. Peri-infarct activation foci were seen in two of the three patients, but no activation occurred within the area of infarction as defined by the initial stroke seen on diffusion-weighted MRI. All three patients demonstrated some corresponding neurological improvement. CONCLUSION: After massive hemispheric cerebral infarction requiring decompressive craniectomy, patients may experience functional recovery as a result of activation in both the infarcted and contralateral hemispheres. The evidence of functional recovery in peri-infarct regions suggests that decompression alone may be preferable to strokectomy where the risk of damage to adjacent nonischemic brain may be greater.

Adult↗
PubMedDate not supplied

Glucocorticoid treatment does not improve neurological recovery following cardiac arrest. Brain Resuscitation Clinical Trial I Study Group.

Glucocorticoids are commonly given to patients with global brain ischemia, although their efficacy has not been proved. The database of the Brain Resuscitation Clinical Trial I, a multi-institutional study designed to evaluate the effect of thiopental sodium therapy on neurological outcome following brain ischemia, was used for a retrospective review of the effects of glucocorticoid treatment on neurological outcome after global brain ischemia. This study included 262 initially comatose cardiac arrest survivors who made no purposeful response to pain after restoration of spontaneous circulation. The standard treatment protocol left glucocorticoid therapy to the discretion of the hospital investigators. This resulted in four patient groups that received either no, low, medium, or high doses of glucocorticoids in the first 8 hours after arrest. Neurological outcome was scored using a modification of the Glasgow Cerebral Performance Category Scale. None of the steroid regimens statistically improved mean group survival rate or neurological recovery rate over that observed in the group that did not receive steroids. The routine clinical practice of administrating glucocorticoids after global brain ischemia may be associated with serious complications and is not justified.

Aged↗
PubMed1988

Post-ischemic neurologic recovery and cerebral blood flow using a compression model of complete "bloodless" cerebral ischemia in dogs.

Complete "bloodless" cerebral ischemia was produced in 14 dogs by increasing intracranial pressure above systolic blood pressure (compression ischemia) for 10 min after the onset of an isoelectric EEG. Six dogs were observed for 48 h post-ischemia to assess neurologic recovery, and in 6 other dogs, acute post-ischemic cerebral blood flow was determined for 2 h. In 2 additional dogs, pre-ischemic and intra-ischemic cerebral blood volume (CBV) was measured using 111In-labeled red blood cells. Compression ischemia resulted in 2 of 6 dogs that were normal at 48 h post-ischemia, 3 dogs had moderate cerebral injury, and 1 dog died. These results were similar to results from previous studies in our laboratory in which complete "stagnant" cerebral ischemia of a comparable duration was produced in dogs using aortic and caval cross-clamping. Restoration of cerebral perfusion pressure following compression ischemia was accompanied by an initial phase of cerebral hyperemia followed by a delayed period of hypoperfusion similar to that observed following stagnant ischemia. The CBV studies in 2 dogs revealed that compression ischemia decreased CBV to 12% and 14% of pre-ischemic control values, respectively. The authors conclude, contrary to previous reports, that compression ischemia, although producing near bloodless ischemia, does not improve the brain's tolerance to ischemia.

Animals↗
PubMed2002

Psychosocial outcomes at three and nine months after good neurological recovery from aneurysmal subarachnoid haemorrhage: predictors and prognosis.

OBJECTIVES: To investigate (1) the prevalence of various aspects of cognitive and psychosocial dysfunction, including post-traumatic stress symptoms, over nine months after subarachnoid haemorrhage (SAH); (2) whether SAH is preceded by increased life stress; (3) to what extent adverse outcomes may be predicted from preillness life stress, early neurological impairment, age, and sex; and (4) relations between emotional and functional outcomes. METHODS: 52 patients with good neurological recovery after surgery for SAH were each matched for age, sex, and occupation with a healthy control participant. SAH patients were assessed three and nine months postdischarge on measures of cognitive functioning, mood, and social functioning. Objective stressors and subjective life change during the preceding year were rated retrospectively. Controls completed measures of mood and social functioning once only. RESULTS: Compared with controls, SAH patients showed increased mood disturbance, subtle cognitive impairment, and abnormally low independence and participation on measures of social functioning. 60% showed clinically significant post-traumatic stress symptomatology (intrusive thoughts or avoidance of reminders) at three months and 30% at nine months. Independence in activities of daily living was greatly reduced in half to a third of the sample at both three and nine months. Productive employment was below the 10th percentile of the control group for 75% of patients at three months and for 56% at nine months; this outcome could not be predicted from selected demographic, premorbid, or clinical variables but dependence on others for organisational activities was predicted by impaired prose recall. Mood at nine months was strongly predicted by prior mental health problems, poor physical health, dysphasia, and impaired prose recall at three months. There was no evidence of an abnormally high level of stressful life events in the year before SAH, although patients rated their subjective level of stress in this period slightly more highly than did the control participants. CONCLUSIONS: These findings highlight the need for structured support and treatment after surgery for SAH to reduce persisting mood disturbance and increase independence and participation.

Adult↗
PubMed2004

Relevance of transient ischemic attack to early neurological recovery after nonlacunar ischemic stroke.

BACKGROUND: We hypothesized that previous transient ischemic attack (TIA) had a favorable effect on early outcome after acute nonlacunar ischemic stroke. METHODS: Data of 1,753 consecutive patients with ischemic stroke collected from a prospective hospital-based stroke registry were studied. A comparison was made of the groups with and without previous TIA. Favorable outcome included spontaneous neurological recovery or grades 0-2 of the modified Rankin scale at hospital discharge. RESULTS: Previous TIA occurred in 55 (11.5%) of 484 patients with lacunar stroke and in 166 (13.1%) of 1,269 patients with nonlacunar stroke. The percentage of nonlacunar ischemic stroke patients with favorable outcome was 21.7% in those with a history of TIA compared to 15% without TIA (p < 0.03). In the lacunar stroke group, differences were not significant. In the multivariate analysis, TIA was an independent predictor of spontaneous in-hospital recovery. CONCLUSIONS: Prior TIA was associated with a favorable outcome in nonlacunar ischemic stroke, suggesting a neuroprotective effect of TIA possibly by inducing a phenomenon of ischemic tolerance allowing better recovery from a subsequent ischemic stroke.

Activities of Daily Living↗
PubMed1989

The natural history of neurological recovery in patients with traumatic tetraplegia.

During the years 1965 to 1986 the Rehabilitation Institute in Konstancin, Poland provided treatment for about 1400 patients admitted to hospital within the first hours or days after injury to the cervical spinal cord. This communication presents an analysis of 122 patients with tetraplegia, with absent sensation or only slight deep sensation preserved on admission. The patients showed considerable neurological recovery of the paralysed muscles. The analysis includes the age of patients, the level and degree of spinal cord injury, the mechanism of spinal injury, the time interval from injury to the return of sensation, voluntary movements and bladder automatism functions, as well as the ability to walk.

Adult↗
PubMed1996

Spontaneous neurological recovery after stroke and the fate of the ischemic penumbra.

We prospectively tested the hypothesis that early recovery after ischemic stroke depends on the ultimate survival of functionally impaired, critically ischemic (i.e., "penumbral") tissue. From a series of 26 consecutive patients studied with positron emission tomography within 18 hours of first-ever stroke in the middle cerebral artery territory, all 11 survivors to the 2-month end point who exhibited increased oxygen extraction fraction were declared eligible. The positron emission tomographic images were compared to ultimate infarction defined by computed tomography performed during the chronic stage. The penumbra (operationally defined by increased oxygen extraction fraction and divided outcome despite uniformly reduced cerebral blood flow) was individually detected in 10 of the 11 patients; cerebral blood flow ranged from 7 to 17 ml/100 gm x min, consistent with that found in monkey studies. The volume of the penumbra that escaped infarction was highly correlated with neurological recovery (p < 0.04 to p < 0.0001, depending on the scale used). This longitudinal study is the first to characterize the penumbra in humans and to document one mechanism strongly influencing recovery; the surviving penumbra may offer opportunities for secondary perifocal neuronal reorganization. Therapeutic measures to prevent infarction of the penumbra (up to 16 hours in this series) may have reduced residual neurological impairment. Mapping the extent of the penumbra, according to prospective criteria, may allow one to predict each patient's potential for recovery, and to select the most appropriate candidates for therapeutic trials.

Aged↗
PubMed1991

Rehabilitation in spinal cord disorders. 2. Anatomy, pathogenesis, and research for neurologic recovery.

This self-directed learning module highlights advances in this topic area. It is part of the chapter on rehabilitation in spinal cord disorders in the Self-Directed Medical Knowledge Program Study Guide for practitioners and trainees in physical medicine and rehabilitation. This article contains learning objectives on the anatomy of the spine and spinal cord, pathogenesis of spinal cord trauma, mechanisms of spinal fractures and dislocations, causes of nontraumatic spinal cord disorders, and research on neurologic recovery. Advances that are covered in this section include various experimental animal models for producing spinal cord injury and new approaches to limit damage in acute injury and to promote recovery in chronic injury.

Animals↗
PubMed1988

Pretreatment with alpha tocopherol enhances neurologic recovery after experimental spinal cord compression injury.

Lipid hydrolysis with subsequent production of eicosanoids and lipid peroxidation are two of the earliest potentially pathochemical events induced in spinal cord tissue by mechanical trauma. Although these membrane lipid disturbances are thought to contribute to the paralysis that occur subsequent to spinal cord injury, such a correlation has not been demonstrated directly. Consequently, the purpose of this study was to test the capacity of alpha tocopherol, the major lipid antioxidant in cellular membranes and a compound that limits the injury-induced lipid hydrolysis and peroxidation in spinal cord tissue, to promote functional recovery in a static loading model of spinal cord injury. After laminectomy, the L2 spinal cord of cats was compressed with 180 g for 5 min. For 5 days before injury and for 5 days postinjury, treated cats received orally 1000 IUD-alpha tocopherol acetate daily. Control cats were similarly injured but untreated. All cats were blindly evaluated weekly for 4 weeks for their neurologic recovery based on an 11 point behavioral scale that assessed walking, running, and stair climbing. By the second postinjury week, alpha tocopherol-pretreated cats demonstrated significantly better recovery than untreated controls. By 4 weeks, treated cats had recovered 72% of their preinjury function as compared with 20% for untreated controls, i.e., a 3.5-fold difference. These results strongly suggest that lipid peroxidation and/or hydrolysis is primarily involved in the genesis of posttraumatic paralysis and that alpha tocopherol exerts its protection of injured spinal cord tissue, at least in part, by its antioxidant and/or antilipolytic activity.

Animals↗
PubMed1984

Improved neurologic recovery and survival after early defibrillation.

Eighty-seven patients who had out-of-hospital cardiac arrests received defibrillating shocks delivered by minimally trained first responders before the arrival of paramedics in a city with short emergency response times. Their outcomes were compared with those of 370 other victims who received only basic life support by first responders until paramedics arrived. Survival was improved by early defibrillation in cases in which there was a delay in initiating cardiopulmonary resuscitation and in which paramedic response times exceeded 9 min; there was 62% survival after early defibrillation by first responders and 27% if first responders provided only basic life support (p less than .02). Neurologic recovery was also improved after early defibrillation. Eighteen of 46 resuscitated patients (39%) receiving early defibrillation were awake at 24 hr compared with 49 of 204 patients (24%) who received only basic life support while awaiting paramedics (p less than .02). Incorporating defibrillation as part of basic life support can reduce both mortality and morbidity from cardiac arrest, even in cities with established, rapidly responding emergency care systems.

Allied Health Personnel↗