Abstract Metastatic Iesions involving the spine may cause vertebral body collapse, resulting in either spinal instabiIity or neural compression or both. Pathological fracture and instability involving the Iower thoracic and Iumber Ievels may be adequately reduced and stabilized by decompressive Iaminectomy with Harrington rod+sleeve application. We recently had an opportunity to treat such a patient- Details of this case are described and the pertinent Iiterature is reviewed. Özet Vertabrayı tutan metastatik lezyonlar spinal instabilite veya nöral bası ya da her ikisi ile sonuçlanan patoIojik kompresyon kırıklarına sebep olabilirler. Bu kompresyon ve instabilite, alt dorsal ve Iomber düzeylerdeyse dekompressif Iaminektomi ile birlikte Harrington rod+sleeve yöntemi uygulanarak tatmin edici şekilde düzeltilerek stabilizasyon sağlanabilir. Bu yazımızda kliniğimizde tedavi ettiğimiz böyle bir hasta bildirilmiş ve ilgiIi Iiteratür tartışılmıştır.

Greater clinical understanding of the pivotal role of apoptosis in spinal cord injury (SCI) has led to new and innovative apoptosis-based therapies for patients with an SCI. Tauroursodeoxycholic acid (TUDCA) is a biliary acid with antiapoptotic properties. To our knowledge, this is the first study in the English language to evaluate the therapeutic efficacy of TUDCA in an experimental model of SCI. Thirty rats were randomized into three groups (sham-operated, trauma only, and trauma plus TUDCA treatment) of 10 each. In groups 2 and 3, spinal cord trauma was produced at the T8-T10 level via the Allen weight drop technique. Rats in group 3 were treated with TUDCA (200 mg/kg intraperitoneal) 1 min after trauma. The rats were killed either 24 h or 5 days after injury. The neuroprotective effect of TUDCA on injured spinal cord tissue and the effects of that agent on the recovery of hind-limb function were assessed. The efficacy of treatment was evaluated with histopathologic examination and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) analysis. Histopathologic characteristics were analyzed by comparison of hematoxylin-and-eosin stained specimens. Neurologic evaluations were performed 24 h, 3 days, and 5 days after trauma. Hind-limb function was assessed with the inclined plane technique of Rivlin and Tator and the modified version of Tarlov's grading scale. Twenty-four hours after injury, there was a significantly higher number of apoptotic cells in the lesioned spinal cord group than in the sham-operated control group. Treatment of the rats with TUDCA significantly reduced the number of apoptotic cells (4.52+/-0.30 vs. 2.31+/-0.24 in group 2) and the degree of tissue injury. Histopathologic examination showed that group 3 rats had better spinal cord architecture compared with group 2 rats. Five days after injury, the mean inclined plane angles in groups 1, 2, and 3 were 65.50 degrees +/- 2.09, 42.00 degrees +/- 2.74, and 53.50 degrees +/- 1.36. Motor grading of the rats revealed a similar trend. These differences were statistically significant (p<0.05). The mechanism of neuroprotection in the treated rats, although not yet elucidated, may be related to the marked antiapoptotic properties of TUDCA. A therapeutic strategy using TUDCA may eventually lead to effective treatment of SCI without toxic effects in humans.

We investigated the therapeutic efficacy of Ac-DMQD-CHO, a caspase-3 inhibitor, and functional recovery in spinal cord injury in a rat model. Thirty rats were randomized into three groups of 10 each. In groups 2 and 3, spinal cord trauma was produced in the thoracic region. Group 3 rats were treated with Ac-DMQD-CHO. Treatment responses were evaluated based on histopathological and TUNEL staining findings at 24 h and 5 days post-injury. Neurologic performance was assessed during and following treatment. Twenty-four hours after injury, light microscopy examination revealed diffuse hemorrhagic necrosis, edema, vascular thrombi, and polymorphonuclear leukocyte infiltration in group 2 and 3 rats, but cavitation and demyelinization were less prominent in group 3. At this time point, treatment of the rats with Ac-DMQD-CHO significantly reduced the number of apoptotic cells. Traumatic injury to the spinal cord causes apoptosis and administration of Ac-DMQD-CHO decreases apoptosis and improves functional outcome.

Background: Cerebral vasospasin remains a major cause of morbidity and mortality in patients with SAH. Although many pharmacologic agents and chemicals have been used to prevent and treat CV, the pathogenesis of that condition has not been established. We investigated the efficacy of resveratrol, a stilbene polyphenol and tyrosine kinase inhibitor that occurs naturally in grapes and red wine, in a murine basilar artery vasospasm model.Methods: Forty-two Wistar albino rats were used in this study. The rats were divided into 3 groups of 14 animals each: the sham-operated control group (group 1), the vasospasm group (group 2), and the treatment group (group 3). In groups 2 and 3, autologous blood (0.3 mL) was injected into the cisterna magna. After that injection, the rats in group 3 received an intravenous injection of resveratrol (10 mg/kg) for 72 hours. The evaluation of the response to both the injection of autologous blood and treatment was based on biochemical markers in tissue and serum and on light microscopic findings from the basilar artery, which were collected at different intervals after experimental SAH.Results: Endothelin-1 levels in brain tissue and serum were higher in the vasospasin group than in the control group (P < .05). In group 3 rats, the administration of resveratrol resulted in significantly lower ET-1 values than those in group 2. Brain and serum lipid peroxidation levels were markedly elevated in group 2 rats but decreased significantly after resveratrol treatment in group 3 rats (P < .05). Superoxide dismutase expression in brain tissue and scrum was lower in group 2 rats than in sham-operated controls, and a significant increase in the SOD level was associated with resveratrol treatment. On examination via light microscopy 72 hours after SAH, the mean perimeters of the arterial lumen in groups 1, 2, and 3 were 719 +/- 16, 411.6 +/- 9, and 590.1 +/- 5.6 mu m, respectively. The mean thickness of the arterial wall was as follows: in group 1, 11.1 +/- 0.8 mu m; in group 2, 16.1 +/- 1.2 mu m; and (after resveratrol treatment) in group 3, 13.4 +/- 0.6 mu mConclusions: The results Of Our study showed that resveratrol induced the relaxation of smooth muscle in the wall of the basilar artery and may be provided with neuroprotection against cerebral ischemia in a rat model. These effects may be associated with the antioxidant and vasodilatory effects of resveratrol, which could prove to be an agent prophylactic against CV and to be therapeutic for individuals who experience that event. (C) 2008 Elsevier Inc. All rights reserved.

Background: Apoptosis as a cell death mechanism is important in numerous diseases, including traumatic SCI. We evaluated the neuroprotective effects of Ac.YVAD.cmk and functional outcomes in a rat SCI model.Methods: Thirty rats were randomized into 3 groups of 10: sham-operated, trauma only, and trauma plus Ac.YVAD.cmk treatment. Trauma was produced in the thoracic region by a weight-drop technique. Group 3 rats received Ac.YVAD.cmk (1 mg/kg, ip) 1 minute after trauma. The rats were killed at 24 hours and 5 days after injury. Efficacy was evaluated with light microscopy and TUNEL staining. Functional outcomes were assessed with the inclined plane technique and a modified version of the Tarlov grading system.Results: At 24 hours postinjury, the respective mean number of apoptotic cells in groups 1, 2, and 3 were 0, 5.26 +/- 0.19, and 0.97 +/- 0.15. Microscopic examination of group 2 tissues showed widespread hemorrhage, edema, necrosis, and polymorphic nuclear leukocyte infiltration and vascular thrombi. Group 3 tissues revealed similar features, but cavitation and demyelination were less prominent than those in group 2 samples at this period. At 5 days postinjury, the respective mean 5 inclined plane angles in groups 1, 2, and 3 were 61.5 +/- 2.09, 42.00 +/- 2.74, and 52.5 +/- 1.77. Motor grading of animals revealed a similar trend. These differences were statistically significant (P < .05).Conclusions: Ac.YVAD.cmk inhibited postraumatic apoptosis in a rat SCI model. This may provide the basis for development of new therapeutic strategies for the treatment of SCI. (C) 2008 Elsevier Inc. All rights reserved.

Apoptosis is an important element of the secondary processes that occur after spinal cord injury. Calpain and caspases are key proteases in apoptotic cell death. We evaluated the neuroprotective effects of SJA6017 (a calpain inhibitor) and measured functional recovery in a rat spinal cord injury model. Thirty Wistar albino rats were divided into three groups of 10 animals each: sham-operated (group 1), trauma control (group 2) and trauma-plus-SJA6017 treatment (group 3). Spinal cord trauma was produced in the thoracic region of the animals. Rats in group 3 received SJA6017 1 min after trauma. Treatment efficacy was evaluated after injury using light microscopy and TUNEL staining. Neurological performance was assessed using an inclined plane and a modified version of the Tarlov's grading scale. Group 2 rats showed moderate trauma with widespread edema, hemorrhage, vascular thrombi and necrosis 24 h after injury. Group 3 rats had significantly reduced tissue injury and apoptosis. Tarlov scores revealed that group 3 rats also had ameliorated recovery of limb function. Our results demonstrate that treatment with SJA6017 reduces apoptotic cell death, preserves spinal cord tissue and improves functional outcome. Treating calpain-induced apoptosis with this agent may be a feasible therapeutic strategy for patients with spinal cord injury.

Özet: Amaç: Bu deneysel çalismada bir antiplatelet ajan olup Platelet Glikoprotein (GP) IIb/IIIa reseptör antagonisti olarak etki eden tirofibanin ratlarda olusturulan geçici serebral iskemi modelindeki nöroprotektif etkinligi incelenmistir. Yöntemler: Deneyler, sham-operated kontrol, iskemi ve tedavi grubu olmak üzere 3 gruba ayrilan 24 adet wistar albino ratta yapilmistir. Geçici serebral iskemi, bilateral carotis communis arterlerin 10 dakika süreyle oklüzyonu ile olusturulmustur. Tedavi grubundaki deneklere iskemi sonrasinda Iv 0,4 /-lgr/kg/dakika dozunda 30 dakika süreyle infüzyon seklinde tirofiban verilmistir. Denekler iskemiden 3 saat sonra sakrifiye edilerek beyin dokulari çikarilmistir. Iskeminin etkileri ve tirofiban tedavisinin etkinligi biyokimyasal parametrelerle (doku lipid peroksidasyonu-malondialdehit (MDA), nitrik oksit (NO), superoksit dismutaz (SAD) ve ATP düzeyleri ile) incelenmistir. Bulgular: Ortalama doku lipit peroksidasyon düzeyleri, 1. grupta 129,12 ± 2,69, iskemi grubunda 233,00 ± 3,25 ve tirofiban tedavi grubunda ise 163,62 ± 3,96 nmol/ gr yas doku idi. Ortalama doku NO düzeyleri ise 1. grupta 0,51 ± 0,02, iskemi grubunda 0,73 ± 0,02 ve tedavi grubunda 0,58 ± 0,02J.lmol!mg olarak ölçüldü. Bir baska degisle doku lipit peroksidasyon ve NO düzeyleri tirofiban tedavisi ile istatikselolarak ileri derecede anlamli bir sekilde düsmüstür (p

OBJECT:Apoptosis is considered one of the most significant mechanisms in the pathogenesis of neuronal damage after spinal cord injury (SCI). This form of cell death occurs via mediators known as caspases. The aim of this study was to evaluate the neuroprotective effect of the caspase-9 inhibitor, z-LEHD-fmk, in a rat model of spinal cord trauma.METHODS:Fifty-four Wistar albino rats were studied in the following three groups of 18 animals each: sham-operated controls (Group 1); trauma-only controls (Group 2); and trauma combined with z-LEHD-fmk-treated animals (0.8 microM/kg; Group 3). Spinal cord injury was produced at the thoracic level by using the weight-drop technique. Responses to SCI and the efficacy of z-LEHD-fmk treatment were determined on the basis of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining and light and electron microscopy findings in cord tissue at 24 hours and 7 days posttrauma. Six rats from each group were also assessed for functional recovery at 3 and 7 days after SCI. This was conducted using the inclined-plane technique and a modified version of the Tarlov motor grading scale. At 24 hours postinjury, light microscopic examination of Group 2 tissue samples showed hemorrhage, edema, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. Those obtained in Group 3 rats at this stage showed similar features. At 24 hours postinjury, the mean apoptotic cell count in Group 2 was significantly higher than that in Group 3 (90.25 +/- 2.6 and 50.5 +/- 1.9, respectively; p < 0.05). At 7 days postinjury, the corresponding mean apoptotic cell counts were 49 +/- 2.1 and 17.7 +/- 2.6, also a significant difference (p < 0.05). Electron microscopy findings confirmed the occurrence of programmed cell death in different cell types in the spinal cord and showed that z-LEHD-fmk treatment protected neurons, glia, myelin, axons, and intracellular organelles.CONCLUSIONS:Examination of the findings in this rat model of SCI revealed that apoptosis occurs not only in neurons and astrocytes but also in oligodendrocytes and microglia. Furthermore, immediate treatment with the caspase-9 inhibitor z-LEHD-fmk blocked apoptosis effectively and was associated with better functional outcome. More in-depth research of the role of programmed cell death in spinal cord trauma and further study of the ways in which caspases are involved in this process may lead to new strategies for treating SCI.

Background: Apoptosis is one of the most important forms of cell death seen in a variety of physiological and pathological conditions, including traumatic injuries. This type of cell death occurs via mediators known as caspases. Previous studies have investigated the roles that apoptosis and different caspases play in the pathogenesis of secondary damage after spinal cord injury (SCI). The aim of this research was to assess the neuroprotective effect of z-DEVD.frnk, a caspase-3 inhibitor, in a rat model of SCI.Methods: Forty-five Wistar albino rats were studied in 3 groups of 15 animals: sham-operated control animals (group 1); trauma-only control animals (group 2); and rats subjected to trauma + z-DEVD.ftnk treatment (group 3). Spinal cord injury was produced at the thoracic level using the weight-drop technique. Responses to injury and the efficacy of z-DEVD.fmk were assessed by light microscopy and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling staining in cord tissues collected at 4 and 24 hours posttrauma. Five rats from each group were used to assess functional recovery at 7 days after SCI. The functional evaluations were done using the inclined-plane technique and a modified Tarlov motor grading scale.Results: At 4 hours postinjury, the mean apoptotic index in groups 1, 2, and 3 was 0, 33.01 +/- 6.62, and 16.40 +/- 4.91, respectively. The group 3 count was significantly lower than the group 2 count (P <.01). At 24 hours postinjury, light microscopic examination of group 2 tissues showed widespread hemorrhage, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. The group 3 tissues showed similar features. The prominent findings in group 2 were hemorrhage and necrosis, whereas the prominent findings in group 3 were focal hemorrhage and leukocyte infiltration. The mean inclined-plane angles in groups 1, 2, and 3 were 64.5 +/- 1.0, 41.5 +/- 1.3, and 47 +/- 2.0, respectively. Motor scale results in all groups showed a similar trend.Conclusion: Local application of z-DEVD.fmk after SCI in rats reduces secondary tissue injury and helps preserve motor function. These effects can be explained by inhibition of apoptotic death in all cell types in the spinal cord. (c) 2005 Elsevier Inc. All rights reserved.

Summary Background. The secondary injury process following spinal cord trauma has been shown to involve different mechanisms such as excessive release of excitatory amino-acids, and induction of free radical induced lipid peroxidation. In this experimental study, the time-level relationship of the nitric oxide and the neuroprotective effects of aminoguanidine were investigated in a rat spinal cord trauma model. Methods. The experiments were performed on 63 Wistar albino rats divided into three groups; sham-operated control (Group 1), trauma created control (Group 2) and aminoguanidine group (Group 3). In groups 2 and 3, spinal cord trauma was produced at thoracic level by using weight the drop technique (at a severity of 50 gr-cm). After the trauma, the rats in Group 3, received an intraperitoneal injection of 100 mg=kg aminoquanidine twice a day for 3 days. The effects of the injury and the efficacy of aminoguanidine were determined based on biochemical parameters (lipid peroxidation and nitric oxide levels in tissue), and on light microscopy findings in cord tissue collected at different times post-injury. Biochemical parameters were performed one hour, three and five days after injury. Functional recovery was assessed at 3, and 5 days after cord trauma with the inclined-plane technique and Tarlov’s motor grading scale. Findings. Although there was no statistically significant difference at the 1 st hour, the values of the tissue nitric oxide in trauma created controls were 42% higher on the 3 rd day and 40% higher on the 5 th day when compared with those in sham controls. The levels of the tissue lipid peroxidation in trauma created controls were 88% higher at the 1 st hour and 52.8% higher on the 5 th day when compared with shame

OBJECT:The toxic effects of glutamate in the central nervous system are well known. This neurotoxicity occurs through metabotropic and ionotropic receptors, the latter group composed of N-methyl-D-aspartate, alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA), and kainate receptors. The authors investigated the neuroprotective effects of GYKI 52466, a 2,3-benzodiazepine that is a selective and potent AMPA receptor antagonist, in a rat spinal cord trauma model.METHODS:Sixty Wistar albino rats were studied in three groups of 20 animals each: sham-operated controls (Group 1); spinal cord-injured rats (Group 2); and spinal cord-injured plus GYKI 52466-treated rats (Group 3). In Groups 2 and 3, spinal cord injury (SCI) was induced at the thoracic level by applying an aneurysm clip to the cord for 1 minute. One minute after the clip was removed, the rats in Group 3 received an intraperitoneal injection of 15 mg/kg GYKI 52466. Responses to injury and treatment were evaluated based on biochemical parameters (lipid peroxidation and adenosine 5'-triphosphate [ATP] levels in tissue), and on light and transmission electron microscopy findings in cord tissue collected at different times post-SCI. Five rats from each group underwent assessment of functional recovery at 1, 3, and 5 days after SCI; evaluation was performed using the inclined-plane technique and Tarlov motor grading scale. The mean lipid peroxidation levels in Groups 1 and 2 were 21.73 +/- 4.35 and 35.53 +/- 2.99 nmol/g of wet tissue, respectively. The level in Group 3 was 27.98 +/- 3.93 nmol/g of wet tissue, which was significantly lower than that in Group 2 (p < 0.01). The mean ATP levels in Groups 1 and 2 were 166.21 +/- 25.57 and 41.72 +/- 12.28 nmol/g of wet tissue, respectively. The ATP level in Group 3 was 85.82 +/- 13.92 nmol/g of wet tissue, which was significantly higher than that in Group 2 (p < 0.01). Light microscopic examination of Group 2 tissues showed hemorrhage, necrosis, polymorphonuclear leukocyte infiltration, and vascular thrombi. In contrast, the examination of Group 3 tissues showed limited hemorrhage and no necrosis or vascular thrombi. The most prominent findings in Group 2 were hemorrhage and necrosis, whereas the most prominent findings in Group 3 were focal hemorrhage and leukocyte infiltration. Electron microscopy demonstrated that GYKI 52466 protected the neurons, myelin, axons, and intracellular organelles. The mean inclined-plane angles in Groups 1, 2, and 3 were 65 degrees, 40 to 45 degrees, and 55 degrees, respectively. Motor scale results in all groups showed a similar trend.CONCLUSIONS:The findings in this rat model suggest that GYKI 52466 may provide significant therapeutic protection from secondary damage after acute SCI. This agent may be a viable alternative treatment for SCI.

A solitary plasmacytoma of the calvarium was removed radically without postoperative radiotherapy. A 69-year-old female patient was operated for a giant solitary plasmacytoma in the frontal region and the follow-up over 10 years revealed no recurrence. The authors discuss that solitary plasmacytoma of the calvarium may have a good prognosis if radically removed and the radiotherapy may not be necessary.

A surgically confirmed primary leptomeningeal malignant melanoma (PLMM) discovered at the parietal region is reported in a 72-year-old male. He developed progressive right hemiparesis and speech disorders caused by a parietal large mass that simulated a growing meningioma. A well-defined, dark-black tumor was removed completely and was histopathologically diagnosed as a malignant melanoma. No melanomas were detected by systemic clinical and radiological examination, including dermatological and ophthalmologic examinations. Follow-up examination 18 months postoperatively showed no evidence of recurrence of the tumor. The patient gradually became bedridden probably because of decreased general activity possibly due to brain atrophy and died of cardiac failure without any evidence of recurrence. Because of the absence of other systemic localizations, we consider this melanoma as primary. A favorable outcome was obtained by surgical treatment alone.

A rare case of distal aneurysm of the posterior inferior cerebellar artery (d PICA) found in association with distal anterior cerebral artery (d ACA) and middle cerebral artery (MCA) aneurysms is described. d PICA aneurysm causing subarachnoid hemorrhage was successfully clipped. The aneurysmal sac was excised and examined pathologically; no infectious etiology was found. Aneurysms at other locations were not operated. The association of vascular anomalies with d PICA aneurysms is discussed.

Eosinophilic granuloma of bone is the localised and most benign form of Langerhans-cell histiocytosis, previously known as histiocytosis X and is characterised by lytic lesions of one or more bones. It is a disease of children and adolescents, and very rarely affects adults. We report a 34-year-old patient with a solitary eosinophilic granuloma involving the fifth lumbar vertebra which produced sciatica. Operative treatment performed by a single extended posterior approach consisted of total resection of the tumour with hemicorporectomy, L4-5 and L5-S1 discectomy, interbody fusion with an iliac bone graft, and interpedicular fixation. Postoperatively, the symptoms resolved and the patient continues to do well at 21/2 years follow-up.

Damage which occurs following spinal traumas is often irreversible. During recent years free oxygen radicals formed due to the pathological changes following neural tissue ischemia have been identified as being responsible for the ethio-pathogenesis of such damage.

Primary multiple hydatid cyst in the brain is uncommon. We report two large primary multiple hydatid cysts of the brain in an adult, which were removed without rupture by two separate operations.

In this report we present two families with von Hippel-Lindau syndrome. We operated on haemangioblastomas in two members, one from each, in our clinic. In the first family we saw 17 lesions in 9 members. Although in the first family carcinoma of the kidney was often observed, in the second family retinal haemangioma was found to be predominant, namely, in eight out of nine patients. In both families there were 11 patients with retinal haemangioma; of these, 9 patients were blind (82 %). In 6 patients with retinal haemangioblastoma blindness was unilateral and bilateral only in one. All the patients with renal carcinoma were male and died young. In one of our patients with renal carcinoma we found metastatic lesions in the distal and proximal parts of the femur, vertebral arch, cranium and the thoracic wall. In these two families 23 members had 32 lesions, from which eleven were retinal haemangiomas (3 + 8), nine haemangioblastomas of CNS (5 + 4), one a renal cyst (0 + 1), eight renal carcinomas (7 + 1), two pancreatic cysts (1 + 1) and one liver cyst (0 + 1).

In this report we present two families with von Hippel-Lindau syndrome. We operated on haemangioblastomas in two members, one from each, in our clinic. In the first family we saw 17 lesions in 9 members. Although in the first family carcinoma of the kidney was often observed, in the second family retinal haemangioma was found to be predominant, namely, in eight out of nine patients. In both families there were 11 patients with retinal haemangioma; of these, 9 patients were blind (82%). In 6 patients with retinal haemangioblastoma blindness was unilateral and bilateral only in one. All the patients with renal carcinoma were male and died young. In one of our patients with renal carcinoma we found metastatic lesions in the distal and proximal parts of the femur, vertebral arch, cranium and the thoracic wall. In these two families 23 members had 32 lesions, from which eleven were retinal haemangiomas (3 + 8), nine haemangioblastomas of CNS (5 + 4), one a renal cyst (0 + 1), eight renal carcinomas (7 + 1), two pancreatic cysts (1 + 1) and one liver cyst (0 + 1).