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Bariş Yaşar, Serkan Şimşek, Uygur Er, Kazim Yiğitkanli, Emel Ekşioğlu, Tibet Altuğ, Deniz Belen, Zafer H. Kars and Murad Bavbek

Object

This study was designed to evaluate the efficacy of decompressive surgery for degenerative lumbar spinal stenosis (LSS) on a functional and clinical basis.

Methods

A prospective analysis and follow-up of 125 consecutive patients with degenerative LSS between 2000 and 2006 were performed. All patients underwent surgery for lumbar stenosis. Functional evaluations of the patients were performed using a treadmill, the visual analog scale, and the Oswestry Disability Questionnaire (ODQ). These parameters were recorded before surgery and the 3rd month and 1st and 2nd years after treatment. The first symptom time (FST), maximal walking duration (MWD), and thecal sac cross-sectional area (CSA) before and after surgery were also recorded. Statistical relations between variables were calculated.

Results

As patient ages increased, the CSA of the thecal sac decreased. Decompressive surgery reached the target according to the difference between the preoperative and postoperative thecal sac CSA. A correlation between the CSA of the thecal sac and FST, and between the CSA of the thecal sac and MWD could not be established. There was a significant correlation between the FST and MWD, and a negative correlation could be established between the MWD and the ODQ score. Surgery led to significant decreases in the ODQ score. Maximal improvement was observed in the 3rd month after decompressive surgery.

Conclusions

The treatment for LSS should be decided using functional criteria; radiological criteria may not correlate with the severity of the disease. Improvements following lumbar decompression surgery continued within 1 year of treatment according to the ODQ and did not change significantly thereafter.

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Mehmet Sorar, Hakan Seçkin, Cem Hatipoglu, Isil Irem Budakoglu, Kazim Yigitkanli, Murad Bavbek and H. Zafer Kars

Object

A variety of factors may affect the neurological improvement in patients with cervical compression myelopathy (CCM) after surgery. The aim of this study was to report and discuss the prognostic factors in a group of patients with insufficient decompression of the spinal canal.

Methods

A prospective follow up and analysis of 20 consecutive patients with CCM treated between 2000 and 2002 was performed. All patients were surgically treated via an anterior approach, either by anterior cervical discectomy and fusion with instrumentation or by cervical corpectomy and fusion with instrumentation. The surgical results were examined using the modified Japanese Orthopaedic Asssociation disability scale, with reference to the findings of magnetic resonance imaging, computed tomography, and radiography. Seventeen patients (85%) experienced a 50% or more recovery rate as calculated using the Hirabayashi formula during the follow-up period (mean 32.5 months), despite a persistently narrow spinal canal and permanent or increased intramedullary high-intensity signal after surgery.

Conclusions

Results of the study showed that patients with CCM benefited from anterior cervical discectomy and fusion with instrumentation or cervical corpectomy and fusion with instrumentation procedures despite insufficient decompression of the spinal canal. Fusion of the affected level(s) might be the reason for the acquired high recovery rates. The authors also conclude that the neurological improvement is not correlated with the reversal of or decrease in the intramedullary high-intensity signal change after surgery.

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Nur Altinörs, Murad Bavbek, Hakan H. Caner and Bülent Erdoğan

Object. Hydatidosis is both a medical and an economic problem in Turkey. The aim of this study was to analyze central nervous system (CNS) involvement in this disease, the related problems the disease causes, and its diagnostic and therapeutic aspects.

Methods. The authors conducted an extensive literature survey of the subject, in which papers published by Turkish authors in international and domestic journals were carefully analyzed. In addition, the authors conducted a cooperative study in which data were gathered from 47 neurosurgery departments across the country. The purpose was to determine the current status of the disease in Turkey; thus, each unit was questioned about their experience over the past 5 years.

Contrary to common belief, the incidence of hydatidosis has not decreased significantly in Turkey. However, computerized tomography and magnetic resonance imaging have tremendously increased diagnostic specificity. Incidences of morbidity and mortality have improved over time, according to the results of the cooperative study, although these changes are not statistically significant. This may be attributed to experience that has been gained and to more frequent use of chemotherapy, as reflected by the cooperative study data. The two statistically significant findings of that study were expanded use of chemotherapy in the management of hydatidosis, and a higher rate of extraneural involvement in the disease. The cooperative study revealed that chemotherapy was being used more often and that there was a wider range of indications for this treatment than previously reported. The higher rate of extraneural involvement was predictable because lesions in the CNS are typically secondary in this disease. With regard to the studies' findings on cases of spinal hydatid cysts, the authors found that administration of chemotherapeutic drugs was the only statistically significant parameter (t = 3.78, p < 0.05), with the rate of chemotherapy higher in the cooperative study.

Conclusions. Morbidity, mortality, and recurrence rates of hydatidosis uncovered by the cooperative study and the literature survey were not statistically significant.

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Richard S. Polin, Murad Bavbek, Mark E. Shaffrey, Kevin Billups, Christopher A. Bogaev, Neal F. Kassell and Kevin S. Lee

Object. The goal of this study was to explore whether the levels of soluble adhesion molecules were elevated in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). This association was suggested by the known inflammatory response in vasospasm and the role of vascular adhesion molecules in regulating leukocytic adhesion to, and migration across, vascular endothelium.

Methods. A prospective analysis was performed on CSF samples obtained in 17 patients who had suffered a recent aneurysmal SAH and in 16 control patients by using quantitative enzyme-linked immunosorbent assays for E-selectin, intercellular adhesion molecule—1 (ICAM—1), vascular adhesion molecule—1 (VCAM-1), and L-selectin.

Levels of soluble forms of E-selectin (p = 0.0013), ICAM-1 (p = 0.0001), and VCAM-1 (p = 0.048) were found to be elevated in the CSF of patients after SAH compared with levels in the CSF of normal controls, patients with unruptured aneurysms, and patients tested months after SAH occurred. In addition, individual patients tested at the time of their initial ictus demonstrated a fall in adhesion molecule levels over time. Levels of E-selectin (p = 0.044) were highest in patients who later developed moderate or severe vasospasm.

Conclusions. Adhesion molecules are known to be involved in white cell adherence to the endothelium and subsequent diapedesis and migration in which a role in initiation of tissue damage is postulated. The authors have demonstrated the elevation of three adhesion molecules, with severely elevated levels of E-selectin seen in patients who later develop vasospasm. A correlation with a role of vascular adhesion molecules in the pathogenesis of cerebral vasospasm is suggested.

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Tomikatsu Toyoda, Aij-Lie Kwan, Murad Bavbek, Neal F. Kassell, John E. Wanebo and Kevin S. Lee

Object. Monophosphoryl lipid A (MPL) and diphosphoryl lipid (DPL) are derivatives of the lipopolysaccharide (endotoxin) of Salmonella minnesota strain R595. Monophosphoryl lipid A is relatively nontoxic and can stimulate the natural defense or immune system. Diphosphoryl lipid is relatively toxic; however, at higher concentrations, it can also stimulate an immune response. The purpose of the present study was to determine the effects of these endotoxin analogs on cerebral vasospasm after the onset of subarachnoid hemorrhage (SAH) in rabbits.

Methods. Intrathecal administration of MPL or DPL (5 µg/kg) was performed immediately before and 24 hours after induction of SAH in New Zealand White rabbits. Forty-eight hours after induction of SAH, the animals were killed by perfusion fixation for morphometric analyses of vessels or perfused with saline and assayed for superoxide dismutase (SOD) activity. Additional rabbits were administered MPL or DPL and killed 24 hours later for assessment of SOD activity; no SAH was induced in these animals.

Experimental SAH elicited spasm of the basilar arteries in each group. Vasospasm was markedly attenuated in animals treated with MPL (p < 0.01 compared with vehicle-treated animals), but not in animals treated with DPL. A substantial reduction in SOD activity in the basilar artery accompanied the vasospasm; this loss of activity was significantly blocked by treatment with MPL, but not DPL. In animals that were not subjected to experimental SAH, MPL elicited a significant increase in SOD activity over basal levels, whereas DPL was ineffective.

Conclusions. These data provide evidence of a marked protective effect of the endotoxin analog MPL against vasospasm. Although the mechanism(s) responsible for the protective effect of MPL remains to be verified, an enhancement of basal antioxidant activity and an inhibition of SAH-induced loss of this activity are attractive candidates. An MPL-based therapy could represent a useful addition to current therapies for SAH-induced cerebral injury.

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Aij-Lie Kwan, Murad Bavbek, Arco Y. Jeng, Wieslawa Maniara, Tomikatsu Toyoda, Rodney W. Lappe, Neal F. Kassell and Kevin S. Lee

✓ Delayed cerebral ischemia due to cerebral vasospasm is a major cause of morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). Increasing evidence implicates the potent vasoconstrictor peptide endothelin (ET) in the pathophysiology of cerebral vasospasm. In the present study the authors examined the therapeutic value of blocking the production of ET-1 by inhibiting the conversion of its relatively inactive precursor, Big ET-1, to a physiologically active form. An inhibitor of ET-converting enzyme (ECE), CGS 26303, was injected intravenously after inducing SAH in New Zealand white rabbits. Injections of CGS 26303 were initiated either 1 hour after SAH (prevention protocol) or 24 hours after SAH (reversal protocol). One of three concentrations (3, 10, or 30 mg/kg) of CGS 26303 was injected twice daily, and all animals were killed by perfusion fixation 48 hours after SAH occurred. Basilar arteries were removed and sectioned, and their cross-sectional areas were measured in a blind manner by using computer-assisted videomicroscopy.

Treatment with CGS 26303 attenuated arterial narrowing after SAH in both the prevention and reversal protocols. The protective effect of CGS 26303 achieved statistical significance at all dosages in the prevention protocol and at 30 mg/kg in the reversal protocol. These findings demonstrate that inhibiting the conversion of Big ET-1 to ET-1 via intravenous administration of an ECE inhibitor can be an effective strategy for limiting angiographic vasospasm after SAH. Moreover, the results demonstrate that treatment with the ECE inhibitor is capable of reducing vasospasm even when initiated after the process of arterial narrowing has begun. Finally, the results provide further support for the role of ET in the establishment of cerebral vasospasm. The ECE inhibitor CGS 26303 thus represents a promising therapeutic agent for the treatment of cerebral vasospasm following aneurysmal SAH.

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Kevin S. Lee and Murad Bavbek