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Introduction: A marker predictive of hematoma expansion in the central nervous system could aid the selection of patients for hemostatic or surgical treatment., Case Report: Here, we present a 83-year-old patient with acute spinal subdural hematoma with paraparesis progressing to paraplegia. A contrast extravasation within the intraspinal hematoma was visualized on spinal MR indicating active bleeding (spinal spot sign). A second acquisition of contrast-enhanced MR images showed progression of contrast extravasation helping to different active bleeding from spinal arteriovenous malformations/fistula., Conclusions: A "spinal spot sign" may be important for treatment decisions, notably in patients with incomplete neurological deficits at the time of imaging.

Introduction: Both sarcopenia and spinal cord injury (SCI) are characterized by the loss of skeletal muscle mass and function. Despite obvious similarities in atrophy between both models, differences in muscle fiber size and satellite cell content may exist on a muscle fiber type-specific level., Methods: In the present study, we compared skeletal muscle fiber characteristics between wheelchair-dependent young males with SCI (n = 8, 32 ± 4 yr), healthy elderly males (n = 8, 75 ± 2 yr), and young controls (n = 8, 31 ± 3 yr). Muscle biopsies were collected to determine skeletal muscle fiber type composition, fiber size, and satellite cell content., Results: Severe atrophy and a shift toward approximately 90% Type II muscle fibers were observed in muscle obtained from males with SCI. Muscle fiber size was substantially smaller in both the SCI (Types I and II fibers) and elderly subjects (Type II fibers) when compared with the controls. Satellite cell content was substantially lower in the wheelchair-dependent SCI subjects in both the Types I and II muscle fibers (0.049 ± 0.019 and 0.050 ± 0.005 satellite cells per fiber, respectively) when compared with the young controls (0.104 ± 0.011 and 0.117 ± 0.009 satellite cells per fiber, respectively). In the elderly, the number of satellite cells was lower in the Type II muscle fibers only (0.042 ± 0.005 vs 0.117 ± 0.009 satellite cells per fiber in the elderly vs young controls, respectively)., Conclusion: This is the first study to show that muscle fiber atrophy as observed with SCI (Types I and II fibers) and aging (Type II fibers) is accompanied by a muscle fiber type-specific reduction in satellite cell content in humans.

Study Design: A case report., Objective: To report an unusual neurologic complication caused by traumatic disc herniation through atypical posterior Schmorl's node (SN) opening into the spinal canal in lumbar Scheuermann's disease., Summary of Background Data: Neurologic complications in Scheuermann's disease are rare and disc hernia has been reported as one of the causes of neural compression. However, there has been no report on acutely progressing paraplegia caused by traumatic disc herniation through an atypical posterior SN opening into the spinal canal in lumbar Scheuermann's disease., Methods: A clinical and radiologic review of such a case of traumatic disc herniation through an atypical posterior SN that resulted in acutely progressing paraplegia in Scheuermann's disease was performed., Results: The patient presented with severe back pain after a fall, without any neurologic abnormalities. Computed tomographic scan revealed lumbar Scheuermann's disease, acute compression fracture of T12, and a large posterior SN with "trough-like" indentation of the lower endplate of T12 opening into the spinal canal. Abruptly progressing paraplegia occurred in less than 24 hours after the first visit and the magnetic resonance imaging revealed severe spinal cord compression by large disc extrusion with superior migration at T12-L1 through the atypical posterior SN at the lower endplate of T12. The patient underwent posterior decompression and discectomy at T12-L1 through transfacet pedicle-sparing approach. Postoperatively, the patient showed immediate improvement in the sensory deficit on L1 dermatome and the perianal area and motor function of the hip flexors to grade 2 without further neurologic improvement, at 2-year follow-up., Conclusion: The case report highlights the clinical significance of the atypical posterior SN that could be a channel for large disc extrusion after a traumatic event in Scheuermann's disease and the clinical importance of surgeon's close attention to the possibility of abruptly progressing neurologic compromise in this situation.

Background and Purpose: Delayed paraplegia remains a devastating complication after ischemic spinal cord injury associated with aortic surgery and trauma. Although apoptosis has been implicated in the pathogenesis of delayed neurodegeneration, mechanisms responsible for the delayed paraplegia remain incompletely understood. The aim of this study was to elucidate the role of apoptosis in delayed motor neuron degeneration after spinal cord ischemia., Methods: Mice were subjected to spinal cord ischemia induced by occlusion of the aortic arch and left subclavian artery for 5 or 9 minutes. Motor function in the hind limb was evaluated up to 72 hours after spinal cord ischemia. Histological studies were performed to detect caspase-3 activation, glial activation, and motor neuron survival in the serial spinal cord sections. To investigate the impact of caspase-3 activation on spinal cord ischemia, outcome of the spinal cord ischemia was examined in mice deficient for caspase-3., Results: In wild-type mice, 9 minutes of spinal cord ischemia caused immediate paraplegia, whereas 5 minutes of ischemia caused delayed paraplegia. Delayed paraplegia after 5 minutes of spinal cord ischemia was associated with histological evidence of caspase-3 activation, reactive astrogliosis, microglial activation, and motor neuron loss starting at approximately 24 to 48 hours after spinal cord ischemia. Caspase-3 deficiency prevented delayed paraplegia and motor neuron loss after 5 minutes of spinal cord ischemia, but not immediate paraplegia after 9 minutes of ischemia., Conclusions: The present results suggest that caspase-3 activation is required for delayed paraplegia and motor neuron degeneration after spinal cord ischemia.

We describe a previously unreported combination of lumbar flexion-distraction ligamentous disruption and incomplete thoracic spinal cord injury in a 2-year-old boy. Magnetic resonance imaging of the thoracolumbar spine showed hemorrhagic cord contusion at the T11-T12 level. Plain radiographs showed mild kyphosis of the L3-L4 segment. Fluoroscopy showed pathological motion at L3-L4 in flexion indicating a ligamentous injury. The lumbar spine was surgically stabilized and at 1-year follow-up, a remarkable neurological recovery was noted. We believe that physicians managing children with multiple trauma injuries should be aware of this rare type of injury that might be underdiagnosed.

Study Design: Report of a traumatic posterior lumbosacral spondyloptosis in a 6-year-old., Objectives: To describe this type of fracture-dislocation in children. To evaluate a possible trauma mechanism. To evaluate specific characteristics of this type of lesion in children., Summary of Background Data: Fractures of the lumbar spine in children are rare. They are without exception caused by high-energy trauma. Fracture-dislocations mostly occur in the anterior direction. There are several reports of traumatic retrolisthesis in adults. To our knowledge, this is the first report of a retrolisthesis at the lumbosacral junction in a child., Methods: While sitting, a 6-year-old boy was hit by a truck. He presented with a flaccid paraparesis below L3. Radiologic investigations showed a posterior spondyloptosis at L5-S1. He was treated by open reduction with a pediatric posterior spinal instrumentation and posterolateral grafting., Results: After 1 year, the patient showed good radiologic fracture reduction and graft incorporation. There was no pain in the lumbar area. There was still a complete neurologic deficit beneath the L3 level, with loss of bladder and anal sphincter function. The patient was entered into a children's rehabilitation program 5 weeks after surgery and is continuously improving his overall functional level., Conclusion: Traumatic retrolisthesis of the lumbosacral spine is extremely rare, especially in children. We believe shear force while sitting is the key traumatic factor. We believe a simple posterior fusion with posterolateral grafting is sufficient to stabilize the spine in children. Extensive soft tissue damage causes an elevated risk of infection. Because of root avulsion, the level of paralysis can be several levels higher than the level of dislocation.

Study Design: Case report of a patient with transient paraplegia and spine instability because of sarcoidosis of 2 vertebral bodies., Objectives: To report a rare case of vertebral sarcoidosis accompanied by transient neurologic symptoms and spine instability, and to discuss the diagnostic and therapeutic management., Summary of Background Data: Vertebral sarcoidosis is a rare condition, and only a few case reports exist in the literature. In most cases, treatment with steroids improves associated neurologic symptoms. Operative intervention is necessary in cases with spinal instability because of progressive vertebral destruction and impending or progressive neurologic deterioration., Methods: After steroids therapy and subsequent neurologic improvement, operative treatment by a 2-stage posterior stabilization followed by anterior vertebrectomy and fusion was given to a patient with 2-level vertebral sarcoidosis and residual spine instability., Results: After steroids therapy, the patient had a complete neurologic recovery; satisfactory spinal stability was achieved after surgery., Conclusion: In the absence of any spinal instability, neurologic symptoms associated with vertebral sarcoidosis respond satisfactorily to nonoperative treatment with steroids. Progressive neurologic deterioration or spinal instability caused by bone destruction requires operative intervention. Steroids therapy provided neurologic improvement, posterior stabilization combined with anterior vertebrectomy and fusion provided spine stability for the patient in this report.

We describe a newly diagnosed HIV-infected child, without prior history of AIDS-defining disease, who presented with Burkitt lymphoma-related cauda equina syndrome that rapidly progressed to a flaccid paraplegia. Diagnosis was confirmed on biopsy and magnetic resonance imaging of the spine showed multiple epidural masses with involvement of several vertebral bodies, cord edema and compression of the cord and cauda equina. The child's immune status was relatively preserved and Epstein-Barr serology proved negative. Chemotherapy (LMB 89 modified protocol) was initiated immediately after histopathologic confirmation, together with highly active antiretroviral therapy. A follow-up magnetic resonance imaging 6 weeks later showed segmental cord atrophy at the site of previous edema despite complete resolution of all the epidural masses. Unfortunately, the child's neurologic state did not improve beyond the recovery of sphincter control and lower limb sensation. The patient is the first reported case of Burkitt lymphoma-related spinal cord compression as an initial AIDS-defining illness, in a 10-year-old child. The outcome of the case highlights the importance of early diagnosis and prompt treatment of this aggressive tumor to avoid permanent neurologic deficits.

Background: Bone marrow stromal cells (BMSC) transplantation offers promise in the treatment of chronic paraplegia in rodents. Here, we report the effect of this cell therapy in adult pigs suffering chronic paraplegia., Methods: Three months after spinal cord injury, autologous BMSC in autologous plasma was injected into lesion zone and adjacent subarachnoid space in seven paraplegic pigs. On the contrary, three paraplegic pigs only received autologous plasma. Functional outcome was measured weekly until the end of the follow-up, 3 months later., Results: Our present study showed progressive functional recovery in transplanted pigs. At this time, intramedullary posttraumatic cavities were filled by a neoformed tissue containing several axons, together with BMSC that expressed neuronal or glial markers. Furthermore, in the treated animals, electrophysiological studies showed recovery of the previously abolished somatosensory-evoked potentials., Conclusions: These findings confirm previous observations in rodents and support the possible utility of BMSC transplantation in humans suffering chronic paraplegia.

Objective: Severe global ischemia often results in severe damage to the central nervous system of survivors. Hind-limb paralysis is a common deficit caused by global ischemia. Until recently, most studies of global ischemia of the central nervous system have examined either the brain or spinal cord, but not both. Spinal cord damage specifically after global ischemia has not been studied in detail. Because the exact nature of the neuronal damage to the spinal cord and the differences in neuronal damage between the brain and spinal cord after global ischemia are poorly understood, we developed a new global ischemia model in the rat and specifically studied spinal cord damage after global ischemia. Further, we compared the different forms of neuronal damage between the brain and spinal cord after global ischemia., Design: Randomized, controlled study using three different global ischemia models in the rat., Setting: University research laboratory., Subjects: Male, adult Sprague-Dawley rats (300 g)., Interventions: Animals were divided into three experimental groups, group A (n = 6, survived for 7 days), 12 mins of hemorrhagic shock; group B (n = 6, survived for 7 days), 5 mins of cardiac arrest; or group C (n = 6, each for 6 hrs, 12 hrs, 1 day, 3 days, and 7 days), 7 mins of hemorrhagic shock and 5 mins of cardiac arrest. Motor deficit of the hind limbs was studied 6 hrs to 7 days after resuscitation. Also, nonoperated animals (n = 6) were used as the control. Histologic analysis (hematoxylin and eosin, Fluoro-Jade B, terminal deoxynucleotidyl transferase- mediated dUTP end-labeling [TUNEL], Klüver-Barrera) and ultrastructural analysis using electron microscopy were performed on samples from the CA1 region of the hippocampus and lumbar spinal cord. Demyelination of the white matter of the lumbar spinal cord was analyzed semiquantitatively using Scion Image software., Main Results: No paraplegic animals were observed in either group A or B. All group C animals showed severe hind-limb paralysis. Severe neuronal damage was found in the CA1 region of the hippocampus in all groups, and the state of delayed neuronal cell death was similar among the three groups. Neuronal damage in the lumbar spinal cord was detected only in group C animals, mainly in the dorsal horn and intermediate gray matter. Demyelination was prominent in the ventral and ventrolateral white matter in group C. A significant difference was observed between control and group C rats with Scion Image software. Ultrastructural analysis revealed extensive necrotic cell death in the intermediate gray matter in the lumbar spinal cord in group C rats., Conclusion: The combination in the global ischemia model (i.e., hemorrhagic shock followed by cardiac arrest) caused severe neuronal damage in the central nervous system. Thereby, hind-limb paralysis after global ischemia might result from spinal cord damage. These results suggest that therapeutic strategies for preventing spinal cord injury are necessary when treating patients with severe global ischemia.

Objective: To develop and evaluate a clinical Spastic Paraplegia Rating Scale (SPRS) to measure disease severity and progression., Methods: A 13-item scale was designed to rate functional impairment occurring in pure forms of spastic paraplegia (SP). Additional symptoms constituting a complicated form of SP are recorded in an inventory. Two independent patient cohorts were evaluated in a two-step validation procedure., Results: Application of SPRS requires less than 15 minutes and does not require any special equipment, so it is suitable for an outpatient setting. Interrater agreement of SPRS was high (intraclass correlation coefficient = 0.99). Reliability was further supported by high internal consistency (Cronbach alpha = 0.91). SPRS values were almost normally distributed without apparent floor or ceiling effect. Construct validity was shown by high correlation of SPRS to Barthel Index and the International Cooperative Ataxia Rating Scale (convergent validity) and low correlation to Mini-Mental Status Examination (discriminant validity)., Conclusion: The Spastic Paraplegia Rating Scale is a reliable and valid measure of disease severity.

Sinus histiocytosis with massive lymphadenopathy is a benign lymphoproliferative disorder growing in frequency as awareness of the disease increases. Also known as Rosai-Dorfman disease, it typically presents as painless cervical lymphadenopathy with fever and malaise. A review of the literature reveals approximately 400 cases of extranodal involvement and approximately 44 cases of central nervous system involvement. Less than 10 of the reported central nervous system tumors have presented as an epidural spinal cord tumor. The authors describe the case of a 29-year-old woman with progressive paraplegia and leg pain. Magnetic resonance imaging of the thoracic spine revealed a tumor mass from T5 to T9. The tumor was resected, and the spinal column was stabilized with pedicle screw fixation and fusion. Postoperative treatment was initiated with radiation and physical rehabilitation. The following is a case report with literature review of the entity.

We report a case of permanent paraplegia in an 81-yr-old patient who had thoracic epidural catheterization performed under general anesthesia for abdominal surgery. The epidural needle was introduced at the T9-10 interspace, and 3 passes were made to locate the epidural space with the loss-of-resistance-to-air technique. During the postoperative epidural pump infusion, the patient was unaware of the progressive motor and sensory impairment. Sensory loss below T11 and paraplegia with no movement of either lower extremity were identified 8 h after surgery. Magnetic resonance imaging demonstrated an intramedullary split-like lesion extending from T4 to T12 and an intramedullary air bubble at T9. Spinal cord injury caused by an intracord catheterization with subsequent local anesthetic injection was diagnosed. Little improvement was noted after large-dose IV methylprednisolone for initial treatment and subsequent rehabilitation for 6 mo. The possible causes of the delayed detection of the neurologic deficits and the timing of performing epidural anesthesia are discussed.

Thirteen patients with Schistosoma mansoni myelopathy are reported. Neurologic syndromes included acute areflexic flaccid paraplegia (three), thoracic myelopathy with hyperreflexia and Babinski sign (six), and a cauda equina syndrome (four). Inflammatory granulomas and a schistosome worm in a leptomeningeal vein of the spinal cord were observed in the one patient coming to necropsy.

Previous reports showed the therapeutic effect of transplants of bone marrow stromal cells (BMSC) after incomplete traumatic spinal cord lesions. We studied the effect of this form of therapy in chronically paraplegic Wistar rats due to severe spinal cord injury (SCI). Rats were subjected to weight-drop impact causing paraplegia, and BMSC or phosphate buffered saline (PBS) was injected into spinal cord 3 months after injury. Functional outcome was measured using the Basso-Beattie-Bresnehan score until sacrifice of the animals, 4 weeks after transplantation. At this time, samples of spinal cord tissue were studied histologically. The results showed a clear and progressive functional recovery of the animals treated with BMSC transplantation, compared to controls. Grafted BMSC survived into spinal cord tissue, forming cell bridges within the traumatic centromedullary cavity. In this tissue, cells expressing neuronal and astroglial markers can be seen, together with a marked ependymal proliferation, showing nestin-positivity. These findings suggest the utility of BMSC transplantation in chronically established paraplegia., (Copyright 2004 Lippincott Williams and Wilkins)

PS1 mutations are associated with classic Alzheimer's disease (AD); however, some families develop AD and spastic paraplegia (SP) with brain pathology characterized by Abeta cotton wool plaques. The authors report a variant AD family with the E280Q PS1 mutation. The fact that the same PS1 mutation can be found in patients with either variant or classic AD argues in favor of the presence of a genetic modifier. The authors have excluded that this modifier effect originates from coding sequence variations in three SP genes or from a second mutation in the other AD genes.

Implications: Our case report describes the electrophysiological features associated with the development of a spinal epidural hematoma during surgery of the lumbar spine. It stresses the importance of the evaluation of nonsurgical factors, which can potentially affect intraoperative evoked potentials; in this case, epidural local anesthetic or epidural hematoma.

Unlabelled: In the present study, we sought to elucidate the temporal profile of the reaction of microglia, astrocytes, and macrophages in the progression of delayed onset motor dysfunction after spinal cord ischemia (15 min) in rabbits. At 2, 4, 8, 12, 24, and 48 h after reperfusion (9 animals in each), hind limb motor function was assessed, and the lumbar spinal cord was histologically examined. Delayed motor dysfunction was observed in most animals at 48 h after ischemia, which could be predicted by a poor recovery of segmental spinal cord evoked potentials at 15 min of reperfusion. In the gray matter of the lumbar spinal cord, both microglia and astrocytes were activated early (2 h) after reperfusion. Microglia were diffusely activated and engulfed motor neurons irrespective of the recovery of segmental spinal cord evoked potentials. In contrast, early astrocytic activation was confined to the area where neurons started to show degeneration. Macrophages were first detected at 8 h after reperfusion and mainly surrounded the infarction area later. Although the precise roles of the activation of microglia, astrocytes, and macrophages are to be further determined, the results indicate that understanding functional changes of astrocytes may be important in the mechanism of delayed onset motor dysfunction including paraplegia., Implications: Microglia and macrophages play a role in removing tissue debris after transient spinal cord ischemia. Disturbance of astrocytic defense mechanism, breakdown of the blood-spinal cord barrier, or both seemed to be involved in the development of delayed motor dysfunction.

Heterotopic ossification is a benign, ectopic bone growth that develops in muscle and other soft tissue. The exact cause is poorly understood, but it is a rarely serious complication of soft tissue trauma. Its most common form, myositis ossifications traumatica, occurs as a secondary complication of direct muscle injury. However, other forms are less common and can result from specific pathologic conditions, such as spinal cord trauma and metabolic disorders. In patients who have had spinal cord injury and subsequent paraplegia, heterotopic ossification often results in ankylosis of the hip and a loss in range of motion. Ectopic ossification occurs below the injury site, and, although the specific muscle groups can vary, it usually involves those for which the origin and insertion involve the anterior pelvis and proximal femur. In dried bone, heterotopic ossification can appear as a smooth, irregularly shaped benign tumor of mature bone, extending from the surface but not invading the cortical bone. These tumors range in size from a few millimeters to several centimeters. Because heterotopic ossification is often associated with specific types of injuries, it has a unique anthropological use in forensic cases.

Study Design: Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI., Objectives: To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia., Summary of Background Data: Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury., Methods: The study group comprised 18 cases of spinal cord compression (17 due to fracture dislocation of the vertebral column and 1 iatrogenic compression from Harrington rods) and two normal control. All the cords were examined according to a standard protocol, and at least 10 segmental levels were immunostained using a monoclonal antibody to amyloid precursor protein and immunopositive AI was semiquantitated using a grading system to provide the axonal injury severity score (AISS). The focal injury at the site of cord compression (haemorrhage, haemorrhagic necrosis, ischaemic necrosis) was also semiquantitated to provide the focal injury area score (FIAS). AI occurring around the site of focal compression (focal axonal injury severity score or FAISS) was distinguished from AI distant to the focal injury (nonfocal axonal injury severity score or NFAISS)., Results: All 18 cases showed widespread amyloid precursor protein immunoreactive axonal injury and the AISS ranged from 28 to 60%. In all cases, the FAISS was greater than the NFAISS and there was a statistically significant relationship between the AISS and the FIAS., Conclusion: Acute spinal cord compression of sufficient severity to produce permanent paralysis causes widespread axonal damage that is maximal at the site of compression but also present throughout the length of the cord in segments far distant from the site of the focal injury.

Objective: To determine whether a previously identified posterior reorganization of the cortical motor network after spinal cord injury (SCI) is correlated with prognosis and outcome., Methods: We applied the techniques of high-resolution EEG and dipole source analysis to record and map the motor potentials (MPs) of the movement-related cortical potentials in 44 patients after SCI. Twenty normal controls were also tested. Results were analyzed using a distance metric to compare MP locations. EEG was coregistered with individual specific MR images and a boundary element model created for dipole source analysis., Results: MPs with finger movements were mapped to a posterior location in 20 of 24 tetraplegics compared with normal controls. Two patients, one studied 4 and one 6 weeks after injury, initially had posterior MPs that, on serial testing, moved to an anterior position with recovery. Dipole source localization of the MP generators confirmed these results. Nine of 20 paraplegics had a posterior MP location with actual or attempted toe movements. All 5 patients who could move their toes had posterior MPs. The MP was posterior in 4 of the 15 paralyzed patients. This is a significant difference in proportions. The only patient with paraparesis whose testing was repeated had an MP that moved to an anterior position with recovery., Conclusions: Posterior reorganization has a significant relationship to prognosis in paraplegia and is reversed in some SCI patients who recover function. Posterior reorganization may result from a preferential survival of axons that originate in somatosensory cortex and contribute to the corticospinal tract. These preliminary results should be verified by a larger prospective study.

We evaluated the pattern of osteoporosis after spinal cord injury, determined the time-frame of the changes, and elucidated the relationship among parathyroid hormone levels, biochemical markers of bone formation, and the pattern of bone mass loss. We included 176 subjects with spinal cord injury and 62 subjects without spinal cord injury as controls in the study. Bone mineral density of the spine and the proximal femur was measured. The participants' age, level of injury, and length of time since injury were compared with the nonspinal cord-injured controls and with each other. Serum levels of calcium, calcitonin, biochemical markers of bone formation, and parathyroid hormone were determined. Our results revealed that bone mineral density of the proximal femur declined and reached fracture threshold at one to five years after injury. The decline was detected at 12 months after injury in all age groups. Spinal bone mineral density neither declined significantly nor reached fracture threshold. Parathyroid hormone levels declined before the end of the first year postinjury and increased at one to nine years postinjury in the 20- to 39-year age group. The increase correlated with the initial decline of bone mineral density of the proximal femur. Our studies in spinal cord-injured subjects revealed a pattern of osteoporosis similar to age and parathyroid dysfunction-related osteoporosis. No other correlation was detected between indexes of bone metabolism and bone mineral density measurements.

Background and Purpose: In a porcine model of thoracic aortic cross-clamping (AoXC), we compared the incidence and severity of paraplegia with two surgical techniques: left atrial-femoral artery (LA-FA) bypass (BP group; n = 9) and clamp/repair (CR group; n = 8). The descending thoracic aorta was clamped near its origin and distal to the third intercostal artery for 30 minutes. The intervening three intercostal arteries were ligated and divided., Methods: All animals received methohexital anesthesia and were hyperventilated to a Paco2 of 28 to 32 mm Hg. Animals in the CR group received mannitol, and after AoXC, proximal hypertension was controlled with phlebotomy. In the BP group, proximal hypertension was controlled with LA-FA bypass using a centrifugal pump (Biomedicus 520C). Proximal mean arterial pressure, distal mean arterial pressure, central venous pressure, and cerebrospinal fluid pressure were measured; radioactive microspheres were injected at baseline, at AoXC + 5 minutes, at AoXC + 20 minutes, at AoXC off + 5 minutes, and after resuscitation. Neurological function was assessed at 24 hours. The animals were killed, and the spinal cord was removed to determine spinal cord blood flow. Histological cross sections of the lumbar spinal cord were stained with cresyl violet/acid fuchsin and then examined with light microscopy to determine the ratio of altered to total spinal cord neurons., Results: Fifteen animals survived (one death in each group) and were assessed neurologically at 24 hours after AoXC. Despite better distal perfusion and lumbar spinal cord blood flow in the BP group, during AoXC, and at AoXC off + 5 minutes, there was no significant difference in the severity of spinal cord ischemic injury between groups as assessed neurologically by Tarlov score (P = .90, Mann-Whitney U test). As well, the ratio of altered to total lumbar spinal cord neurons did not differ between groups (P = .24)., Conclusions: In this chronic porcine model, distal circulatory support with LA-FA bypass afforded better distal perfusion and improved lumbar spinal cord blood flow but did not influence the severity of spinal cord ischemic injury when compared with a clamp/repair technique.

Background and Purpose: We used a rat model of reversible spinal ischemia to assess the effect of spinal cord temperature on the development of neurological and histopathologic changes after 20 minutes of reversible aortic occlusion. Spinal cord blood flow and CO2 reactivity was tested by using laser Doppler before and 60 minutes after ischemia., Methods: In halothane (1%)-anesthetized rats, the spinal cord temperature as assessed by using thermocouple in the paraspinal muscles was lowered to 34 degrees, 31 degrees, or 27 degrees C. After ischemia, spinal cord temperature was raised to 37 degrees C for the next 30 minutes. Animals were maintained in this normothermic condition for 8 hours, after which motor and sensory function were assessed. All animals were then anesthetized and perfused with 10% formalin for light microscopic analysis of spinal cords., Results: In normothermic animals, 20 minutes of ischemia resulted in a loss of CO2 reactivity and hind limb paraplegia with an attendant allodynia that persisted for the 8 hours of reperfusion. Even mild (34 degrees C) hypothermia resulted in significant improvement of neurological function compared with the normothermic group. In paraplegic animals, lumbosacral interneuronal pools localized primarily in laminae III through VII displayed heavy argyrophilic neurons and areas of localized necrosis. In moderate and deep hypothermic animals preservation of CO2 responsivity and complete recovery of neurological function were seen with no detectable histopathologic changes., Conclusions: These results show that a slight decrease in spinal cord temperature in the peri-ischemic period provides significant protection as measured by histopathology and neurological function.

Spinal cord injury disrupts micturition reflexes, which produces morbidity. The contribution of endogenous opioid systems to urinary retention were assessed in chronic spinal cats by administering the opioid receptor antagonist, naloxone (5-500 micrograms kg-1, i.p.), to unanesthetized paraplegic cats while monitoring lower urinary tract function and observing hind limb reflexes. While naloxone had no overt effect in acute spinal cats, in chronic spinal cats naloxone induced the release of large volumes of urine and produced marked hind limb hyper-reflexia. Prominent tachyphylaxis and tolerance to the effects of naloxone were evident. Immunohistochemical studies indicated a marked increase in leucine enkephalin and dynorphin in sacral spinal neurons. Together, these data indicate hyperactivity of the endogenous spinal opioid system following recovery from spinal cord injury and, furthermore, suggest that the spinal neural circuitry may become 'dependent' upon elevated levels of endogenous opioid peptides.

The electrophysiological, neurological, and neuropathological correlates of the spinal cord ischemia induced by the aortic cross-clamping of cats were studied with the goal of developing the reliable evoked spinal cord potentials (ESCPs) for the monitoring of spinal cord ischemia. The five types of ESCPs were elicited as follows; descending ESCPs recorded from the L2 and L5 vertebral levels, vertex motor evoked potential from the L2 vertebral level, ascending ESCP from the T1 vertebral level, and segmental ESCP after sciatic nerve stimulation. The late negative waves of both descending ESCP from L5 and segmental ESCP were susceptible to ischemia. The descending ESCP from L5 was not influenced by peripheral nerve ischemia or reflected ischemia in the whole spinal cord. Therefore, the late negative wave of the descending ESCP from L5 served as the most reliable index for spinal cord ischemia. When aortic clamping was continued for > or = 30 min after the disappearance of the late negative wave of descending ESCP from L5, the amplitude recovery of this wave decreased to 25%, resulting in paraplegia. Histologically, the posterior horn of the gray matter in the lumbar enlargement was the most vulnerable to ischemia.

Magnetic resonance imaging (MRI) has been used widely in the diagnosis of acute spinal cord injuries. The association between MRI findings and histologic changes, however, remains unclear. Using a rabbit spinal cord injury model, the authors compared the MRI and histologic abnormalities as they evolved over the first post-trauma month. Bleeding in the gray matter, visualized as a low-intensity area on T1-weighted views and high-intensity area on T2-weighted views, observed immediately after injury, disappeared within the first week. Edema, appearing 6 hours after the initial injury and seen as a high-intensity T2-weighted MRI image, became maximal 1 week later and gradually decreased thereafter. Also appearing 1 week later, were necrotic changes in the gray matter, corresponding to low signals on T1-weighted studies but high signals on T2-weighted studies. MRI therefore helped differentiate hemorrhage and necrosis, presumably irreversible lesions, from the more reversible findings related to edema.

Background and Purpose: We compared the incidence and severity of paraplegia following thoracic aortic cross-clamping in dogs for two anesthetic regimens. Animals were randomly assigned to receive methohexital (group M; n = 9) or isoflurane (group I; n = 9). We expected a better neurological outcome in animals administered methohexital because of superior neuronal protection and greater spinal cord perfusion pressure (mean arterial pressure below the cross-clamp site minus mean cerebrospinal fluid pressure)., Methods: After surgical preparation and a 30-minute stabilization period, dogs in group M received 14 +/- 6 mg.kg-1 i.v. methohexital to induce an isoelectric electroencephalogram followed by a continuous infusion of methohexital at 20 mg.kg-1 x h-1. Dogs in group I received 1.4 +/- 0.2% end-tidal isoflurane (1 minimum alveolar concentration). The thoracic aorta was then occluded 2.5 cm distal to the left subclavian artery for 30 minutes and then released. Hemodynamics and cerebrospinal fluid pressure were measured at (1) baseline, (2) 2 minutes after aortic cross-clamping, (3) 20 minutes after aortic cross-clamping, (4) 5 minutes after aortic unclamping, and (5) 30 minutes after resuscitation. At 24 hours a neurological assessment was performed. After the clinical assessment the dogs were killed and the spinal cord removed immediately for histopathologic study., Results: There were no differences in nasopharyngeal temperature, PaCO2, pH, or hemoglobin at any time between groups. With cross-clamping, the spinal cord perfusion pressure decreased precipitously. However, there was no difference in spinal cord perfusion pressure between groups at any time (P = .5555). The neurological outcome, assessed at 24 hours after thoracic aortic cross-clamping by a veterinarian unaware of the anesthetic protocol, was not different between groups (P > .5, two-tailed Mann-Whitney rank-sums test). When anesthetized with methohexital 5 of 9 dogs were paraplegic; with isoflurane 7 of 9 dogs were paraplegic. By Spearman's rank test, a strong inverse correlation between the Tarlov score and the ratio of dead to total lumbar anterior spinal cord neurons was seen (Spearman's correlation coefficient = -.8358; P = .0001)., Conclusions: We conclude that no advantage was offered by the choice of anesthesia to neurological outcome after 30 minutes of thoracic aortic cross-clamping in this canine model.

To clarify the cause of delayed-onset paraplegia, the authors evaluated the neurologic outcome after temporary (10 to 30 minutes) spinal cord ischemia in the awake rabbit. Loss of motor function occurred in less than 2 minutes in all animals. Restoration of flow within 16 minutes always resulted in full return of function, whereas with occlusion times of greater than 27 minutes all animals remained paralyzed. After temporary occlusion of 20 to 21 minutes, however, 71% of animals returned to normal neurologic function but developed delayed-onset paraplegia 14 to 48 hours later. This appears to be a reliable method for the creation of a model of delayed-onset paraplegia in the awake animal, and will facilitate more detailed studies of the pathophysiology of ischemia-induced paraplegia.

The body composition and anthropometric characteristics of male paraplegic athletes (PARA, N = 22) were contrasted to an able-bodied ectomorphic (N = 22) and mesomorphic (N = 31) comparison group of moderately and highly trained male subjects. The validity of 12 body composition [density (Db)] prediction equations reported in the literature, 4 generalized, were determined (tested) on this special group of athletes (PARA). On the whole, the prediction equations over-predicted Db in PARA by 0.0039 to 0.0166 g X cm-3 (under-predicted relative fat by 1.8 to 7.4%). Five diameter, 11 circumference, and 7 skinfold measures were used in a SAS-STEPWISE multiple regression procedure with hydrostatically determined Db to develop several suitable Db prediction equations for the paraplegic athlete. Diameters were poor predictors (r = 0.60, SEE = 0.0164), while skinfolds, circumferences, or a combination of measures were acceptable, with the combined equation being best (r = 0.95, SEE = 0.0064). The findings of this study suggest that even generalized equations do not adequately predict Db in PARA and that paraplegic specific equations are presently best suited for predicting Db in paraplegic athletes. The results further indicate that although these equations meet many of the criteria of Lohman, the SEE and total error values are unusually high and make prediction of body composition using anthropometry in a heterogeneous group of PARA athletes slightly unreliable.

The distribution of pressure points in 16 patients with paraplegia, nine with ulcers, and six who were ulcer free were compared with the distribution in 15 normal individuals using an instrument capable of simultaneously measuring multiple pressure points under the buttocks and thighs. The nine patients with ischial and sacral decubiti showed redistribution of their sitting pressures posteriorly, asymmetrical loading of the ischiae, and higher than normal pressures under the sacrococcygeum. These abnormal pressures were associated with unbalanced scoliosis, pelvic obliquity, and the loss of physiological lordosis following a spinal fusion. We defined four criteria of risk for decubitus ulceration.