Successful operative management of an upper lumbar spinal canal stenosis resulting in multilevel lower nerve root radiculopathy.

Lumbar stenosis is a common disorder, usually characterized clinically by neurogenic claudication with or without lumbar/sacral radiculopathy corresponding to the level of stenosis. We present a case of lumbar stenosis manifesting as a multilevel radiculopathy inferior to the nerve roots at the level of the stenosis. A 55-year-old gentleman presented with bilateral lower extremity pain with neurogenic claudication in an L5/S1 distribution (posterior thigh, calf, into the foot) concomitant with dorsiflexion and plantarflexion weakness. Imaging revealed grade I spondylolisthesis of L3 on L4 with severe spinal canal stenosis at L3-L4, mild left L4-L5 disc herniation, no stenosis at L5-S1, and no instability. EMG revealed active and chronic L5 and S1 radiculopathy. The patient underwent bilateral L3-L4 hemilaminotomy with left L4-L5 microdiscectomy for treatment of his L3-L4 stenosis. Postoperatively, he exhibited significant improvement in dorsiflexion and plantarflexion. The L5-S1 level was not involved in the operative decompression. Patients with radiculopathy and normal imaging at the level corresponding to the radiculopathy should not be ruled out for operative intervention should they have imaging evidence of lumbar stenosis superior to the expected affected level.

Factors affecting survival in 267 consecutive patients undergoing surgery for spinal metastasis from renal cell carcinoma.

OBJECT: Renal cell carcinoma (RCC) frequently metastasizes to the spine, and the prognosis can be quite variable. Surgical removal of the tumor with spinal reconstruction has been a mainstay of palliative treatment. The ability to predict prognosis is valuable when determining the role and magnitude of surgical intervention in cancer patients. To better identify factors affecting survival in patients undergoing surgery for spinal metastasis from RCC, the authors undertook a retrospective analysis of a large patient cohort at a tertiary care cancer center. METHODS: Relevant clinical data on a consecutive series of patients who had undergone surgery for spinal metastasis of RCC between 1993 and 2007 at The University of Texas MD Anderson Cancer Center were retrospectively reviewed. Demographic data, histopathological grade of primary tumor, timing of spinal surgery relative to diagnosis, treatment history prior to surgery, neurological status, and systemic disease burden were analyzed to determine the impact of these factors on survival outcome. RESULTS: The authors identified 267 patients who met the study criteria. Five-year overall survival (OS) after spine tumor resection was 7.8%, with a median OS of 11.3 months (95% CI 9.5-13.0 months). Patients with Fuhrman Grade 4 RCC had a median OS of 6.1 months (95% CI 3.5-8.7 months), which was significantly lower than the 14.3 months (95% CI 9.1-19.4 months) observed in patients with Fuhrman Grade 3 or less RCC (p < 0.001). Patients with preoperative neurological deficits had a median survival of 5.9 months (95% CI 4.1-7.7 months), which was significantly lower than the 13.5 months (95% CI 10.4-16.6 months) observed in patients with a normal neurological examination (p < 0.001). Patients whose spine was the only site of metastasis had a median OS of 19 months (95% CI 9.8-28.2 months) after surgery, significantly longer than the 9.7 months (95% CI 8.1-11.3 months) observed in patients with additional extraspinal metastasis sites (p < 0.001). Patients with nonprogressing extraspinal metastasis (no metastasis, stable, or concurrent) had a median survival of 20.6 months (95% CI 15.1-26.1 months), compared with 5.6 months (95% CI 4.4-6.8 months) in patients with progressing metastasis (p < 0.001). CONCLUSIONS: The authors identified several factors influencing survival after spine surgery for metastatic spinal RCC, including grade of the original nephrectomy specimen, activity of the systemic disease, and neurological status at the time of surgery. These clinical features may help to identify patients who may benefit from aggressive surgical intervention.

Aquaporin-1-mediated cerebral edema following traumatic brain injury: effects of acidosis and corticosteroid administration.

OBJECT: Dysregulation of water homeostasis induces cerebral edema. Edema is a major cause of morbidity and mortality following traumatic brain injury (TBI). Aquaporin-1 (AQP-1), a water channel found in the brain, can function as a transporter for CO2 across the cellular membrane. Additionally, AQP-1's promoter contains a glucocorticoid response element. Thus, AQP-1 may be involved with edema-related brain injury and might be modulated by external conditions such as the pH and the presence of steroids. In this study, the authors investigated the hypotheses that: 1) AQP-1 participates in brain water homeostasis following TBI; 2) secondary injury (for example, acidosis) alters the expression of AQP-1 and exacerbates cerebral edema; and 3) corticosteroids augment brain AQP-1 expression and differentially affect cerebral edema under nonacidotic and acidotic conditions. METHODS: Anesthetized Sprague-Dawley rats were subjected to moderate to severe TBI (2.5-3.5 atm) or surgery without injury, and they were randomized to receive a 3-mg/kg bolus of intravenous dexamethasone within 10 minutes after injury or surgery, a 3-mg/kg bolus of dexamethasone followed by 1-mg/kg maintenance doses every 8 hours for 24 hours, or saline boluses at similar time intervals. A second group of animals was subjected to respiratory acidosis with target arterial blood pH 6.8-7.2 for 1 hour following the surgery or injury. To evaluate selective blockage of AQP-1, some animals received a single intraperitoneal dose of HgCl2 (0.3-30.0 mmol/L) within 30 minutes of injury or surgery. At 4 or 24 hours postinjury, animals were killed and their brains were harvested for mRNA, protein, or water content analyses. RESULTS: The authors demonstrated elevated cerebral edema levels at 4 and 24 hours following TBI. Dexamethasone administration within 1 hour of TBI attenuated the cerebral edema under nonacidotic conditions but worsened it under acidotic conditions. Selective blockage of AQP-1 channels with HgCl2 attenuated the edematous effects of corticosteroids and acidosis. Reverse transcriptase polymerase chain reaction and immunohistochemical analyses demonstrated a paucity of AQP-1 in the cerebral cortices of the uninjured animals. In contrast, AQP-1 mRNA and protein levels were higher in the cerebral cortices of animals that sustained a TBI. CONCLUSIONS: These findings implicate an important, modifiable role for AQP-1 in water homeostasis within the CNS following TBI.

Awake craniotomy for brain tumors near eloquent cortex: correlation of intraoperative cortical mapping with neurological outcomes in 309 consecutive patients.

OBJECTIVE: Intraoperative localization of cortical areas for motor and language function has been advocated to minimize postoperative neurological deficits. We report herein the results of a retrospective study of cortical mapping and subsequent clinical outcomes in a large series of patients. METHODS: Patients with intracerebral tumors near and/or within eloquent cortices (n = 309) were clinically evaluated before surgery, immediately after, and 1 month and 3 months after surgery. Craniotomy was tailored to encompass tumor plus adjacent areas presumed to contain eloquent cortex. Intraoperative cortical stimulation for language, motor, and/or sensory function was performed in all patients to safely maximize surgical resection. RESULTS: A gross total resection (> or =95%) was obtained in 64%, and a resection of 85% or more was obtained in 77% of the procedures. Eloquent areas were identified in 65% of cases, and in that group, worsened neurological deficits were observed in 21% of patients, whereas only 9% with negative mapping sustained such deficits (P < 0.01). Intraoperative neurological deficits occurred in 64 patients (21%); of these, 25 (39%) experienced worsened neurological outcome at 1 month, whereas only 27 of 245 patients (11%) without intraoperative changes had such outcomes (P < 0.001). At 1 month, 83% overall showed improved or stable neurological status, whereas 17% had new or worse deficits; however, at 3 months, 7% of patients had a persistent neurological deficit. Extent of resection less than 95% also predicted worsening of neurological status (P < 0.025). CONCLUSION: Negative mapping of eloquent areas provides a safe margin for surgical resection with a low incidence of neurological deficits. However, identification of eloquent areas not only failed to eliminate but rather increased the risk of postoperative deficits, likely indicating close proximity of functional cortex to tumor.