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Results for “Neurologic Recovery”

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At least 181 records · Page 10Linked to original sources
PubMed2002

Recombinant human erythropoietin counteracts secondary injury and markedly enhances neurological recovery from experimental spinal cord trauma.

Erythropoietin (EPO) functions as a tissue-protective cytokine in addition to its crucial hormonal role in red cell production. In the brain, for example, EPO and its receptor are locally produced, are modulated by metabolic stressors, and provide neuroprotective and antiinflammatory functions. We have previously shown that recombinant human EPO (rhEPO) administered within the systemic circulation enters the brain and is neuroprotective. At present, it is unknown whether rhEPO can also improve recovery after traumatic injury of the spinal cord. To evaluate whether rhEPO improves functional outcome if administered after cord injury, two rodent models were evaluated. First, a moderate compression of 0.6 N was produced by application of an aneurysm clip at level T3 for 1 min. RhEPO (1,000 units per kg of body weight i.p.) administered immediately after release of compression was associated with partial recovery of motor function within 12 h after injury, which was nearly complete by 28 days. In contrast, saline-treated animals exhibited only poor recovery. In the second model used, rhEPO administration (5,000 units per kg of body weight i.p. given once 1 h after injury) also produced a superior recovery of function compared with saline-treated controls after a contusion of 1 N at level T9. In this model of more severe spinal cord injury, secondary inflammation was also markedly attenuated by rhEPO administration and associated with reduced cavitation within the cord. These observations suggest that rhEPO provides early recovery of function, especially after spinal cord compression, as well as longer-latency neuroprotective, antiinflammatory and antiapoptotic functions.

Animals↗
PubMedDate not supplied

Neurologic recovery following injuries to the cervical spinal cord and nerve roots.

From this literature, we have made the following conclusions: (1) Complete cord lesions do not recover cord functional motor control. (2) Complete lesions recover one nerve root level of function at the fracture site. (3) Partial lesions recover partially. (4) The less the injury, the greater the recovery. (5) Brown-Sequard lesions recover more than central cord syndromes, which recover more than anterior cord syndromes. (6) Reduction of dislocated facets facilitates nerve root recovery. (7) Better documentation of specific pathology and recovery rates are necessary to determine the surgical benefits in complete lesions, incomplete lesions, and nerve root recovery.

Humans↗
PubMedDate not supplied

Neurologic recovery after penetrating craniocerebral war injury.

From June 1, 1991, until December 31, 1992, 116 patients with penetrating craniocerebral war injuries inflicted at the east Slavonian front were treated at the Osijek University Hospital. There were 26 (22.4%) gunshot wounds and 90 (77.6%) wounds inflicted by explosive devices and projectiles. Four years after the injury, a study of the survivors' condition was carried out. No difference was recorded in the survival rate between the patients with gunshot wounds compared with explosive wounds. Rehabilitation produced good results in the survivors, in the prevention of both acute and chronic complications and permanent damage. Older age, lower Glasgow Coma Scale, and level of consciousness were found to be prognostic indicators of outcome.

Adolescent↗
PubMed1990

Ischemic reperfusion injury in rabbit spinal cord: protective effect of superoxide dismutase on neurological recovery and spinal infarction.

The potential role of superoxide dismutase (SOD), a specific superoxide anion radical scavenger, in treating spinal cord ischemia was investigated in rabbits subjected to aortic occlusion for 20 min. SOD treatment, targeted to the early reperfusion period, reduced both motor dysfunction and incidence of spinal infarcts at 7 days after ischemia. Present results suggest that oxygen-derived free radicals play a role in the pathogenesis of infarcts developing in the spinal cord after ischemia and reperfusion injuries.

Animals↗
PubMed2006

Seizures during stroke thrombolysis heralding dramatic neurologic recovery.

Seizures during thrombolytic therapy for ischemic stroke have not previously been described as a favorable prognostic sign. We report three patients with severe stroke (NIH Stroke Scale [NIHSS] score 15 to 20) who experienced a seizure during tissue plasminogen activator (tPA) infusion. While initially raising alarm about possible hemorrhage, the seizures heralded dramatic recovery (an immediate 15-point NIHSS score improvement after tPA; NIHSS score 0 or 1 at 24 hours). We propose that the seizures during thrombolysis may indicate cortical reperfusion and/or hyperperfusion due to early recanalization of an acutely occluded intracranial artery.

Adult↗
PubMed1985

Opiate antagonist WIN44,441-3 stereospecifically improves neurologic recovery after ischemic spinal injury.

In the unanesthetized rabbit, temporary aortic occlusion results in predictable patterns of spinal cord injury. We use this "spinal stroke" model to assess the potential role of opiate antagonists in treating CNS ischemia. WIN44,441-3 (WIN(-], an opiate antagonist with enhanced activity at the kappa-receptor, reduced motor dysfunction after ischemic spinal cord injury. The effect was stereospecific and dose-related; beneficial actions were seen at doses as low as 40 micrograms/kg. Opiate receptor antagonists may be therapeutically useful in ischemic CNS injury, and the beneficial actions of these compounds may be at the kappa-receptor site.

Animals↗
PubMed2006

Delayed transplantation of adult neural precursor cells promotes remyelination and functional neurological recovery after spinal cord injury.

Spinal cord injury (SCI) results in loss of oligodendrocytes demyelination of surviving axons and severe functional impairment. Spontaneous remyelination is limited. Thus, cell replacement therapy is an attractive approach for myelin repair. In this study, we transplanted adult brain-derived neural precursor cells (NPCs) isolated from yellow fluorescent protein-expressing transgenic mice into the injured spinal cord of adult rats at 2 and 8 weeks after injury, which represents the subacute and chronic phases of SCI. A combination of growth factors, the anti-inflammatory drug minocycline, and cyclosporine A immunosuppression was used to enhance the survival of transplanted adult NPCs. Our results show the presence of a substantial number of surviving NPCs in the injured spinal cord up to 10 weeks after transplantation at the subacute stage of SCI. In contrast, cell survival was poor after transplantation into chronic lesions. After subacute transplantation, grafted cells migrated >5 mm rostrally and caudally. The surviving NPCs integrated principally along white-matter tracts and displayed close contact with the host axons and glial cells. Approximately 50% of grafted cells formed either oligodendroglial precursor cells or mature oligodendrocytes. NPC-derived oligodendrocytes expressed myelin basic protein and ensheathed the axons. We also observed that injured rats receiving NPC transplants had improved functional recovery as assessed by the Basso, Beattie, and Bresnahan Locomotor Rating Scale and grid-walk and footprint analyses. Our data provide strong evidence in support of the feasibility of adult NPCs for cell-based remyelination after SCI.

Animals↗
PubMed1999

Group II metabotropic glutamate receptor activation attenuates traumatic neuronal injury and improves neurological recovery after traumatic brain injury.

We examined the effects of modulating group II metabotropic glutamate receptors (mGluRs) on traumatic neuronal injury using both in vitro and in vivo models. Treatment with various selective group II mGluR agonists significantly decreased lactate dehydrogenase release, a marker of cell death, after traumatic injury to rat neuronal-glial cultures; injury-induced increases in cyclic AMP and glutamate levels were also significantly reduced by a group II agonist. The neuroprotective effects of group II agonists were markedly attenuated by coadministration of a group II antagonist or a membrane-permeable cyclic AMP analog and were additive to those provided by an N-methyl-D-aspartate receptor antagonist or a selective group I mGluR antagonist. Administration of a group II mGluR agonist 30 min after lateral fluid percussion-induced brain injury in rats significantly improved subsequent behavioral recovery as compared with vehicle-treated controls. Together these studies indicate that group II mGluR agonists protect against traumatic neuronal injury by attenuating glutamate release and cAMP levels and suggest a potential role for these agents in the treatment of clinical neurotrauma.

Animals↗
PubMed1998

Neurological recovery following posterior decompression of spinal secondaries.

This is a retrospective study comprising 45 patients who underwent decompressive laminectomy due to secondary malignancy in the spine. There were 31 males and 14 females. Two of them had no weakness, one was treated for radicular pain and the other for severe intractable back pain. Forty-three patients presented with weakness of the limb of which six patients were able to walk unaided, four with an aid, twenty four were unable to walk of which eleven of them were completely paralysed. Nineteen of the patients had urinary incontinence. Out of 10 patients in Frankel's D, 3 of them regained almost normal power post operatively and were able to walk without any aids at the time of discharge. There were 6 patients in Frankel's C and 2 improved. Of 17 patients in Frankel's B, 6 of them improved and were able to walk with walking aids. Only one out of ten patient from Frankel's A had showed an improvement. A total of three patients deteriorated post operatively and all of them presented with multiple level involvement. There was no change in the post operative status of the two patients who did not have weakness. Overall only 27% of the patient showed improvement following decompressive laminectomy.

Adolescent↗