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Results for “Spinal Injuries”

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At least 433 records · Page 24Linked to original sources
PubMed2003

Calpain inhibitor prevented apoptosis and maintained transcription of proteolipid protein and myelin basic protein genes in rat spinal cord injury.

Spinal cord injury (SCI) is associated with progressive neurodegeneration and dysfunction. Multiple cellular and molecular mechanisms are involved in this pathogenesis. In particular, the activation of proteases following trauma can cause apoptosis in the spinal cord. Calpain, a calcium-dependent cysteine protease, plays a major role in apoptosis following trauma. We identified apoptosis and decrease in transcription of the genes for proteolipid protein (PLP) and myelin basic protein (MBP) in five 1-cm long spinal cord segments (S1, distant rostral; S2, near rostral; S3, lesion; S4, near caudal; and S5, distant caudal) 24 h after induction of SCI (40 g.cm force) in rats by weight-drop method. Sham rats underwent laminectomy and did not receive injury. Internucleosomal DNA fragmentation occurred prominently in the lesion (S3), moderately in near segments (S2 and S4), and slightly in distant segments (S1 and S5) of injured rats, indicating the occurrence of apoptosis in the lesion and penumbra. Levels of transcription of PLP and MBP were reduced highly in the lesion and moderately in near segments, suggesting that apoptotic loss of cells impaired biosynthesis of two important structural components of myelin. Immediate administration of the calpain inhibitor E-64-d (1 mg/kg) to injured rats prevented apoptosis and restored transcription of these genes, indicating the therapeutic efficacy of calpain inhibitor for treatment of SCI.

Animals↗
PubMed2005

Changes in electrophysiological properties and sodium channel Nav1.3 expression in thalamic neurons after spinal cord injury.

Spinal cord contusion injury (SCI) is known to induce pain-related behaviour, as well as hyperresponsiveness in lumbar dorsal horn nociceptive neurons associated with the aberrant expression of Na(v)1.3, a rapidly repriming voltage-gated sodium channel. Many of these second-order dorsal horn neurons project to third-order neurons in the ventrobasal complex of the thalamus. In this study we hypothesized that, following SCI, neurons in the thalamus undergo electrophysiological changes linked to aberrant expression of Na(v)1.3. Adult male Sprague-Dawley rats underwent contusion SCI at the T9 thoracic level. Four weeks post-SCI, Na(v)1.3 protein was upregulated within thalamic neurons in ventroposterior lateral (VPL) and ventroposterior medial nuclei, where extracellular unit recordings revealed increased spontaneous discharge, afterdischarge, hyperresponsiveness to innocuous and noxious peripheral stimuli, and expansion of peripheral receptive fields. Altered electrophysiological properties of VPL neurons persisted after interruption of ascending spinal barrage by spinal cord transection above the level of the injury. Lumbar intrathecal administration of specific antisense oligodeoxynucleotides generated against Na(v)1.3 caused a significant reduction in Na(v)1.3 expression in thalamic neurons and reversed electrophysiological alterations. These results show, for the first time, a change in sodium channel expression within neurons in the thalamus after injury to the spinal cord, and suggest that these changes contribute to altered processing of somatosensory information after SCI.

Action Potentials↗
PubMed1986

Changes in TRH immunoreactivity in spinal cord after experimental spinal injury.

Concentrations of immunoreactive TRH (TRH-ir) in rat spinal cord were examined after traumatic injury. TRH-ir was significantly increased at the injury site (thoracic region) and rostral areas (cervical region), and significantly decreased below the injury site. Changes were delayed and time-dependent. Since TRH may serve as an excitatory neurotransmitter within the spinal cord, these changes may contribute to the functional alterations observed after spinal injury.

Animals↗
PubMed1984

Surgical management of thoracolumbar spinal injuries. General principles and controversial considerations.

Based on a review of the literature and experience with over 100 surgically treated thoracolumbar spinal injuries, the following information summarizes present knowledge of the subject. Reduction and internal fixation of the injured spine allows early mobilization of all patients, regardless of neurologic deficit, while protecting the neurologic structures from further injury and enhancing their recovery. The ability of the posterior ligamentous complex and the anterior bony column to withstand physiologic loads must be assessed by the history, physical examination, and radiography; then the injured structures should be protected from load or their function replaced by an appropriate surgical implant. Maximum neurologic recovery can be expected with prompt and complete decompression by reduction of the deformity, restoration of the spinal canal, and rigid internal fixation. The internal fixation system selected must provide compression for posterior injuries and distraction for anterior injuries, resist bending in combined injuries, and always restore normal spine shape. The rod-long, fuse-short technique provides the advantages of a more accurate reduction and a more secure fixation, and the minimum length of the fused region results in a more normal spine. The advantages of prompt and rigid but temporary internal fixation justify the risks both short- and long-term.

Adult↗
PubMedDate not supplied

Spinal injuries in children: role of MR.

PURPOSE: To define the clinical and prognostic role of MR in a pediatric population with spinal cord injury. METHODS: Fifteen children underwent MR 12 hours to 2 months postinjury using decoupled surface coils and ventilator support as needed. MR was correlated retrospectively with clinical, CT, and radiographic findings. RESULTS: On MR, of seven children with spinal cord neurologic deficits, four had hemorrhagic contusions, one had nonhemorrhagic contusion, one had extensive infarction, and one revealed a normal cord. All had persistent deficits on hospital discharge. Eight without cord neurologic deficit revealed no cord lesions on MR; this group included two with epidural hematoma, four with ligamentous disruption, and two with bone compression. CONCLUSIONS: Children may have extensive cord contusion and/or infarction with minor, remote, or no fracture dislocation. Because both hemorrhagic and nonhemorrhagic cord lesions found on MR were associated with significant, persistent cord deficits, the authors conclude that MR provides a practical tool for diagnosis/prognosis in children with acute/subacute spinal injury.

Adolescent↗
PubMed1998

Heart rate variability is altered following spinal cord injury.

Spinal cord injury (SCI) patients are known to suffer from autonomic failure as a result of their injury. The magnitude of the dysautonomia resulting from such an injury is difficult to predict or characterize and, in varying degree, it impedes the recovery of physiological homeostasis. This study is intended to investigate the effectiveness of heart rate variability (HRV) analysis as a method of quantifying and characterizing autonomic function in patients with traumatic spinal myelopathy. HRV analysis was carried out in 13 male SCI patients (six tetraplegic, seven paraplegic) and 13 age-matched, able-bodied controls. Twenty-four hour ambulatory and sleep ECG tracings were obtained. Time domain, amplitude, and power spectral analyses were used to study HRV and autonomic function. Both tetraplegic (20+/-12 ms, mean+/-SD) and paraplegic (22+/-8 ms) subjects demonstrated significant loss of low frequency 24-hour HRV compared to able-bodied controls (36+/-14 ms, p < 0.05) and during sleep. This was interpreted as being consistent with predominantly sympathetic denervation uninfluenced by degree of physical activity. There were no significant differences between groups in parasympathetically mediated high frequency HRV. We conclude that HRV analysis is capable of distinguishing between SCI or able-bodied humans and among tetraplegic and paraplegic patients. Patterns of altered HRV may be useful in more completely characterizing or stratifying changes in physiology associated with injury level and may have diagnostic, prognostic, or therapeutic significance.

Adult↗
PubMed2003

Synaptic pathways to phrenic motoneurons are enhanced by chronic intermittent hypoxia after cervical spinal cord injury.

Spinal hemisection at C2 reveals caudal synaptic pathways that cross the spinal midline (crossed phrenic pathways) and can restore inspiratory activity in ipsilateral phrenic motoneurons. Intermittent hypoxia induces plasticity in the cervical spinal cord, resulting in enhanced inspiratory phrenic motor output. We hypothesized that chronic intermittent hypoxia (CIH) (alternating 11% O(2) and air; 5 min periods; 12 hr per night; 7 nights) would strengthen crossed phrenic pathways. Experiments were performed on anesthetized, vagotomized, paralyzed, ventilated, and spinally injured (C2 hemisection) rats that were exposed to either normoxia or CIH before acute injury (preconditioning) or after chronic injury (postconditioning). Spontaneous inspiratory bursts or compound action potentials evoked via stimulation of the ventrolateral funiculus (contralateral to injury) were recorded in both phrenic nerves. Spontaneous or evoked activity in crossed phrenic pathways were minimal or absent in all acutely injured rats regardless of preconditioning. In rats postconditioned with normoxia, crossed phrenic inspiratory bursts were observed occasionally during baseline conditions and always during chemoreceptor stimulation (hypoxia and hypercapnia). However, CIH postconditioned rats had substantially larger crossed phrenic inspiratory bursts during baseline, hypoxia, and hypercapnia (all p < 0.05 vs normoxic group). Short-latency (0.7 msec) evoked crossed phrenic potentials were also enhanced by CIH conditioning in chronically injured rats (p < 0.05). We conclude that CIH induced spinal cord plasticity-enhanced phrenic motor output. This plasticity required preconditions established by chronic spinal injury.

Animals↗
PubMed2001

Changes in metabotropic glutamate receptor expression following spinal cord injury.

Spinal cord injury (SCI) initiates biochemical events that lead to an increase in extracellular excitatory amino acid concentrations, resulting in glutamate receptor-mediated excitotoxic events. These receptors include the three groups of metabotropic glutamate receptors (mGluRs). Group I mGluR activation can initiate a number of intracellular pathways that increase neuronal excitability. Group II and III mGluRs may function as autoreceptors to modulate neurotransmission. Thus, all three groups may contribute to the mechanisms of central sensitization and chronic central pain. To begin evaluating mGluRs in SCI, we quantified the changes in mGluR expression after SCI in control (naive), sham, and impact injured adult male Sprague-Dawley rats (200-250 g). SCI was produced at spinal segment T10 with a New York University impactor (12.5-mm drop, 10-g rod of 2-mm diameter). Expression levels were determined by Western blot and immunohistochemistry analyses at the epicenter of injury, as well as segments rostral and caudal. The group I subtype mGluR1 was increased over control levels in segments rostral and caudal by postsurgical day (PSD) 7 and remained elevated through PSD 60. The group I subtype mGluR5 was unchanged in all segments rostral and caudal to the injury at every time point measured. Group II mGluRs were decreased compared to control levels from PSD 7 through PSD 60 in all segments. These results suggest that different subtypes of mGluRs have different spatial and temporal expression patterns following SCI. The expression changes in mGluRs parallel the development of mechanical allodynia and thermal hyperalgesia following SCI; therefore, understanding the expression of mGluRs after SCI may give insight into mechanisms underlying the development of chronic central pain.

Animals↗
PubMed1992

Clinical predictors of unstable cervical spinal injury in multiply injured patients.

All victims of major blunt trauma have been said to be at risk of cervical spinal injury. In a prospective study of 410 such patients at our institution, we identified 13 patients (6.12 per cent) with unstable cervical spines. Loss or defect of consciousness following injury (regardless of duration), neurological deficit consistent with cervical cord or nerve root injury and neck tenderness were significantly predictive of an unstable cervical spine. Immediate radiographic investigation of the cervical spine is mandatory in such patients, but may not be required in patients without these signs.

Adolescent↗