Prognosis and recovery in ischaemic and traumatic spinal cord injury: clinical and electrophysiological evaluation.
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OBJECTIVES: To compare prognostic factors and functional recovery between paraplegic patients with either ischaemic (28 patients) or traumatic (39 patients) spinal cord injury (SCI). METHODS: On admission to the spinal injury centre and 6 months later the patients underwent clinical (following the guidelines set down by the American Spinal Injury Association) and electrophysiological (tibial and pudendal somatosensory evoked potentials) examinations in parallel. The degree of ambulatory capacity was assessed after discharge from the rehabilitation programme or at least 6 months after trauma. RESULTS: At the acute stage of either ischaemic or traumatic SCI similar motor and sensory deficits and pathological SSEP recordings were present. Both patient groups recovered to similar degrees with respect to motor, sensory, and ambulatory capacity. The clinical examination in both patient groups was the most sensitive prognostic factor of functional recovery irrespective of the aetiology of the SCI. In the ischaemic patients only the tibial SSEP whereas in the traumatic patients both the pudendal and tibial SSEP were of value in predicting recovery. CONCLUSIONS: Although the two patient groups are pathophysiologically different, the severity and extent of neurological deficits and rate of recovery are quite similar. In both ischaemic and traumatic SCI clinical and electrophysiological examinations are of prognostic value for the functional recovery. (+info)
Comparison of transcranial motor evoked potentials and somatosensory evoked potentials during thoracoabdominal aortic aneurysm repair.
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OBJECTIVE: To compare transcranial motor evoked potentials (tc-MEPs) and somatosensory evoked potentials (SSEPs) as indicators of spinal cord function during thoracoabdominal aortic aneurysm repair. SUMMARY BACKGROUND DATA: Somatosensory evoked potentials reflect conduction in dorsal columns. tc-MEPs represent anterior horn motor neuron function. This is the first study to compare the techniques directly during thoracoabdominal aortic aneurysm repair. METHODS: In 38 patients, thoracoabdominal aortic aneurysm repair (type I, n = 10, type II, n = 14, type III, n = 6, type IV, n = 8) was performed using left heart bypass and segmental artery reimplantation. tc-MEP amplitudes <25% and SSEP amplitudes <50% and/or latencies >110% were considered indicators of cord ischemia. The authors compared the response of both methods to interventions and correlated the responses at the end of surgery to neurologic outcomes. RESULTS: Ischemic tc-MEP changes occurred in 18/38 patients and could be restored by segmental artery reperfusion (n = 12) or by increasing blood pressure (n = 6). Significant SSEP changes accompanied these tc-MEP events in only 5/18 patients, with a delay of 2 to 34 minutes. SSEPs recovered in only two patients. In another 11 patients, SSEP amplitudes fell progressively to <50% of control without parallel tc-MEP changes or association with cross-clamp events or pressure decreases. At the end of the procedure, tc-MEP amplitudes were 84 +/- 46% of control. In contrast, SSEP amplitudes were <50% of control in 15 patients (39%). No paraplegia occurred. CONCLUSION: In all patients, tc-MEP events could be corrected by applying protective strategies. No patient awoke paraplegic. SSEPs showed delayed ischemia detection and a high rate of false-positive results. (+info)
Cyclin D1 and Cdk4 protein induction in motor neurons after transient spinal cord ischemia in rabbits.
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BACKGROUND AND PURPOSE: The mechanism of spinal cord injury has been thought to be related to the vulnerability of spinal motor neuron cells against ischemia. However, the mechanisms of such vulnerability are not fully understood. We hypothesized that spinal motor neurons might be lost by programmed cell death and investigated a possible mechanism of neuronal death by detection of double-strand breaks in genomic DNA and immunohistochemical analysis for cyclin D1 and cyclin-dependent kinases (Cdk) 4. METHODS: We used a rabbit spinal cord ischemia model with a balloon catheter. Spinal cord was removed at 8 hours and 1, 2, and 7 days after 15 minutes of transient ischemia, and histological changes were studied with hematoxylin-eosin staining. In situ terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL), DNA fragment with gel electrophoresis, Western blot analysis for cyclin D1 and Cdk4, and temporal profiles of cyclin D1 and Cdk4 immunoreactivity were investigated. RESULTS: Most motor neurons were preserved until 2 days but were selectively lost at 7 days of reperfusion. Immunocytochemistry showed positive TUNEL selectively at 2 days of reperfusion in spinal motor neuron nuclei. Typical ladders of oligonucleosomal DNA fragments were detected at 2 days of reperfusion. Immunoreactivity of cyclin D1 and Cdk4 proteins was induced selectively at 8 hours in motor neuron nuclei, which eventually died. CONCLUSIONS: These results indicate that induction of cyclin D1 and Cdk4 may be implicated in programmed cell death change after transient spinal cord ischemia in rabbits. (+info)
Spinal cord ischemia. Development of a model in the mouse.
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BACKGROUND AND PURPOSE: Spinal cord ischemia with resulting paraplegia is a devastating complication of thoracoabdominal aortic surgery. Experimental models of spinal cord ischemia have been developed in primate, dog, pig, rabbit, and rat with variable reproducibility, but none has been developed in mouse. Because genetically engineered mice have become important to examine the impact of specific genes in ischemic pathophysiology, we sought to develop a reproducible mouse model of spinal cord ischemia. METHODS: C57BL/6NCrlBR mice were subjected to cross-clamping of the aortic arch, left subclavian artery, and internal mammary artery for 9 minutes (group A; n=8) or 11 minutes (group B; n=29) followed by reperfusion for 24 or 48 hours. Mean distal arterial blood pressure (left femoral artery) and lumbar (L1) spinal cord blood flow (laser-Doppler flowmetry) were measured for the duration of the procedure. The arterial blood supply of the spinal cord was visualized by intravascular perfusion of carbon black ink. We evaluated motor function in the hind limbs at 0, 1, 3, 6, and 24 hours after reperfusion using a rating scale of 0 (normal function) to 6 (total absence of movement). Spinal cord histopathology was evaluated after 24 and 48 hours of reperfusion by Luxol fast blue-hematoxylin and eosin. RESULTS: The vascular anatomy of the mouse and human spinal cord appeared similar in that blood was supplied by 1 anterior and 2 posterior spinal arteries and heterosegmental radicular arteries. During combined occlusion of aortic arch and left subclavian artery, mean distal arterial blood pressure dropped to 10+/-5 mm Hg, and spinal cord blood flow at the L1 level decreased to 27+/-7% of baseline. All animals recovered from anesthesia with acute paraplegia. Animals in the 9-minute group (group A) showed steady recovery of hind limb function over the ensuing 24 hours, whereas the majority (80%) in the 11-minute group (group B) remained paralyzed with maximum deficit throughout the postoperative period. Mortality was 0% and 21% in groups A and B, respectively. Maximal ischemic damage was observed at the lower thoracic and higher lumbar spinal levels in both groups. In group A (9 minutes), tissue damage was mild, affecting predominantly dorsal horns and intermediate gray matter, whereas ventral horns were minimally involved. All mice in group B (11 minutes) showed extensive gray matter lesions particularly involving dorsal horns and intermediate areas; in ventral horns, >50% of motor neurons died. White matter lesions were present in the most severely damaged cords only. CONCLUSIONS: Spinal cord ischemia caused by aortic arch plus left subclavian artery cross-clamping provides a mouse model useful for the study of spinal cord injury and of potential relevance to the complications following thoracoabdominal aortic surgery in humans. (+info)
Reversal of twice-delayed neurologic deficits with cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a national database collection.
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Delayed neurologic deficits are an uncommon yet devastating complication of thoracoabdominal aortic aneurysm repair. The mechanisms involved in the development of delayed spinal cord ischemia remain ill defined. We report a case of complete reversal of delayed neurologic deficits with postoperative cerebrospinal fluid (CSF) drainage. After a thoracoabdominal aneurysm extent I repair, the patient experienced delayed paraplegia at 6 hours and again at 34 hours after the operation, with elevated CSF pressure (>10 mm Hg) on both occasions. Prompt CSF decompression completely reversed the neurologic deficits within hours after onset. The findings in this case further support the role of CSF drainage in spinal cord protection for patients who undergo thoracoabdominal aneurysm repair and make a plea for a national database collection. (+info)
Surgical repair of aneurysms involving the suprarenal, visceral, and lower thoracic aortic segments: early results and late outcome.
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OBJECTIVE: The purpose of this study is to review our experience with surgical repair of lower thoracoabdominal and suprarenal aortic aneurysms to determine early and late survival rates and identify factors influencing morbidity and survival among these patients. MATERIALS: From 1989 through 1998, 165 consecutive patients underwent repair of 108 thoracoabdominal (55 group III and 53 group IV) and 57 suprarenal aneurysms. The study group consisted of 109 men and 56 women with a mean age of 70 years (median, 70 years; range, 29-89 years). Mean aneurysm diameter was 6.9 cm (median, 6.5 cm; range, 4-12 cm). There were 125 aneurysms (76%) repaired electively; 40 repairs (24%) were nonelective. The cause of 12 aneurysms (7%) was chronic aortic dissection; the remaining 153 (93%) were degenerative aneurysms. RESULTS: The early postoperative (30-day) mortality rates were 7% (9/125) for elective and 23% (9/40) for nonelective operations (P =.016). For both elective and urgent procedures, early mortality was 1.8% (1/57) for suprarenal aneurysm repair, 11% (6/53) for group IV thoracoabdominal aneurysms, and 20% (11/55) for group III thoracoabdominal aneurysms (P =.013, suprarenal vs group III). Spinal cord ischemia occurred after 6% (10/165) of aneurysm repairs (4% paraplegia, 2% paraparesis). None of the 57 suprarenal aneurysm repairs were complicated by spinal cord ischemia, whereas it occurred in 2% (1/53) of group IV thoracoabdominal aneurysms and 16% (9/55) of group III thoracoabdominal aneurysms (P =.001, suprarenal vs group III; P =. 016, group IV vs group III). Three (25%) of the 12 patients with dissection developed spinal cord ischemia; this compared with seven (5%) of 153 patients with degenerative aneurysms (P =.027). The cumulative 3-year survival rate for the entire series was 71% (95% CI, 64%-79%), and 5-year survival was 50% (95% CI, 40%-60%). CONCLUSIONS: Aneurysms involving the suprarenal, visceral, and lower thoracic aorta may be repaired with acceptable perioperative mortality and late survival rates. The risk of spinal cord ischemia is increased for patients with aortic dissection and may be stratified according to the proximal extent of the aneurysm. (+info)
Spinal cord infarction and tetraplegia--rare complications of meningococcal meningitis.
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A previously healthy 25-yr-old female developed flaccid areflexic tetraplegia, with intact cranial nerve function, 36 h after the diagnosis of bacterial meningitis. Polymerase chain reaction studies of cerebrospinal fluid and blood were positive for Neisseria meningitidis, serogroup B. Magnetic resonance of the cervicothoracic spine revealed increased signal intensity and expansion in the lower medulla, upper cervical cord and cerebellar tonsils. Neurosurgical consultation recommended hyperventilation, dexamethasone and regular mannitol therapy rather than decompressive intervention. The clinical course over the following 12 days was complicated by the development of progressive central nervous and multisystem organ failure with disseminated intravascular coagulopathy. Autopsy revealed cerebral oedema with cystic infarction extending from the medulla to the upper cervical cord and cerebellar tonsils. Flaccid areflexic tetraplegia with spinal cord infarction has not been reported following bacterial infection in an adult. The clinical implications would suggest complete central nervous system evaluation of patients recovering from meningococcal meningitis, since spinal cord lesions, although uncommon, do occur. In those very rare situations where a patient develops significant peripheral neurological deficits, urgent magnetic resonance imaging is warranted, to rule out an infective focus or an underlying anatomical anomaly. (+info)
Epidural cooling for spinal cord protection during thoracoabdominal aneurysm repair: A five-year experience.
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PURPOSE: We developed and applied a method for providing regional spinal cord hypothermia with epidural cooling (EC) during thoracoabdominal aneurysm (TAA) repair. Preliminary results indicated significant reduction in spinal cord ischemic complications (SCI), compared with historical controls, and a 5-year experience with EC was reviewed. METHODS: From July 1993 to September 1998, 170 patients with thoracic aneurysms (n = 14; 8.2%) or TAAs (types I and II, n = 83 [49%]; type III, n = 66 [39%]; type IV, n = 7 [4.1%]) were treated with EC. An earlier aneurysm resection was noted in 44% of patients, an emergent operation was noted in 20% of patients, and an aortic dissection was noted in 16% of patients. The EC was successful (mean cerebrospinal fluid [CSF] temperature at cross-clamp, 26.4 +/- 3 degrees C) in 97% of cases, with all 170 patients included in an intention-to-treat analysis. The operation was performed with a clamp/sew technique (98% patients) and selective (T(9) to L(1) region) reimplantation of intercostal vessels. Clinical and EC variables were examined for association with operative mortality and SCI by means of the Fischer exact test, and those variables with a P value less than.1 were included in multivariate logistic regression analysis. RESULTS: The operative mortality rate was 9.5% and was weakly associated (P =.07) with SCI; postoperative cardiac complications (odds ratio [OR], 35. 3; 95% CI, 5.3 to 233; P <.001) and renal failure (OR, 32.2; 95% CI, 6.6 to 157; P <.001) were the only independent predictors of postoperative death. SCI of any severity occurred in 7% of cases (type I/II, 10 of 83 [12%]; all other types, 2 of 87 [2.3%]), versus a predicted (Acher model) incidence of 18.5% for this cohort (P =. 003). Half the deficits were minor, with good functional recovery, and devastating paraplegia occurred in three patients (2.0%). Independent correlates of SCI included types I and II TAA (OR, 8.0; 95% CI, 1.4 to 46.3; P =.021), nonelective operation (OR, 8.3, 95% CI, 1.8 to 37.7; P =.006), oversewn T(9) to L(2) intercostal vessels (OR, 6.1; 95% CI, 1.3 to 28.8; P =.023), and postoperative renal failure (OR, 23.6; 95% CI, 4.4 to 126; P <.001). These same clinical variables of nonelective operations (OR, 7.7; 95% CI, 1.4 to 41.4; P =.017), oversewn T(9) to L(2) intercostal arteries (OR, 9.7; 95% CI, 1.5 to 61.2; P =.016), and postoperative renal failure (OR, 20.8; 95% CI, 3.0 to 142.1; P =.002) were independent predictors of SCI in the subgroup analysis of high-risk patients, ie, patients with type I/II TAA. CONCLUSION: EC has been effective in reducing immediate, devastating, total paraplegia after TAA repair. A strategy that combines the neuroprotective effect of regional cord hypothermia, avoiding the sacrifice of potential spinal cord blood supply, and postoperative adjuncts (eg, avoidance of hypotension, CSF drainage) appears necessary to minimize SCI after TAA repair. (+info)