Sanser Gul

Intramedullary spinal cord metastases: diagnosis and treatment – an illustrated review

Summary.Background. Intramedullary spinal cord metastases (ISCM) are rare but, with increasing use of magnetic resonance imaging (MRI) are being encountered with increasing frequency. Optimum treatment remains controversial. On the basis of a review of previous reports and experience with a patient with an ISCM from a large cell lung cancer, we propose practical diagnostic and therapeutic approaches.Findings. We found 284 patients who had an Intramedullary spinal cord metastasis reported in English literature up to February 2004. 32 had been treated surgically. The mean survival in these patients was two times longer than in those treated by a conservative approach. Improvement and prolonged survival occurred in patient we treated by microsurgical dissection of the metastasis.Conclusion. Early diagnosis and early surgical resection can result in improvement in neurological deficits and in the quality of life of patients with a Intramedullary spinal cord metastasis.

Effects of dexmedetomidine or methylprednisolone on inflammatory responses in spinal cord injury

Background: The aim of this study was to compare the anti‐inflammatory response of methylprednisolone and the α2‐agonist dexmedetomidine in spinal cord injury (SCI).

Effect of coenzyme Q10 on ischemia and neuronal damage in an experimental traumatic brain-injury model in rats.

BackgroundHead trauma is one of the most important clinical issues that not only can be fatal and disabling, requiring long-term treatment and care, but also can cause heavy financial burden. Formation or distribution of free oxygen radicals should be decreased to enable fixing of poor neurological outcomes and to prevent neuronal damage secondary to ischemia after trauma. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is a strong antioxidant that plays a role in membrane stabilization. In this study, the role of CoQ10 in the treatment of head trauma is researched by analyzing the histopathological and biochemical effects of CoQ10 administered after experimental traumatic brain injury in rats. A traumatic brain-injury model was created in all rats. Trauma was inflicted on rats by the free fall of an object of 450 g weight from a height of 70 cm on the frontoparietal midline onto a metal disc fixed between the coronal and the lambdoid sutures after a midline incision was carried out.ResultsIn the biochemical tests, tissue malondialdehyde (MDA) levels were significantly higher in the traumatic brain-injury group compared to the sham group (p < 0.05). Administration of CoQ10 after trauma was shown to be protective because it significantly lowered the increased MDA levels (p < 0.05). Comparing the superoxide dismutase (SOD) levels of the four groups, trauma + CoQ10 group had SOD levels ranging between those of sham group and traumatic brain-injury group, and no statistically significant increase was detected. Histopathological results showed a statistically significant difference between the CoQ10 and the other trauma-subjected groups with reference to vascular congestion, neuronal loss, nuclear pyknosis, nuclear hyperchromasia, cytoplasmic eosinophilia, and axonal edema (p < 0.05).ConclusionNeuronal degenerative findings and the secondary brain damage and ischemia caused by oxidative stress are decreased by CoQ10 use in rats with traumatic brain injury.

Demonstration of the histopathological and immunohistochemical effects of a novel hemostatic agent, ankaferd blood stopper, on vascular tissue in a rat aortic bleeding model

BackgroundAnkaferd Blood Stopper® (ABS) is a folkloric medicinal plant extract used as a hemostatic agent in traditional Turkish medicine. This experimental study investigated the histopathological and immunohistochemical effects of ABS on vascular tissue in a rat model of aortic bleeding.MethodsFour groups of 11 Wistar albino rats were used. The abdominal aortas of the rats were wounded; an ABS-soaked tampon was applied to rats in Groups 1 and 3, and a plain gauze tampon was applied to rats in Groups 2 and 4 until the bleeding stopped. The bleeding time was recorded. Immediately following sacrificing, the arteriotomy sites from Groups 1 and 2 were removed. The abdominal incisions in Groups 3 and 4 were closed following hemostasis. On Day 7 of the study, Group 3 and 4 rats were sacrificed and the abdominal aorta arteriotomy sites were removed for histopathological and immunohistochemical evaluation.ResultsThe mean bleeding time in 15 animals in Groups 2 and 4 was 4.9 ± 0.6 s, and in 22 animals in Groups 1 and 3 was 3.1 ± 0.6 s. Distal aortic occlusion was not observed on either Day 1 or 7 in any group. Significantly more widespread and dense endothelial nitric oxide synthase (eNOS) staining was observed in Group 1 animals than Group 2. On Days 1 and 7 after application of ABS, histopathological changes, consisting of necrosis, inflammation, and endothelial cell loss, in the rat abdominal aortas did not differ between Groups 1 and 2. The basophilic discoloration in the ABS group on the operation day was a result of a foreign body reaction and hemosiderin-loaded histiocyte accumulation, which occurred on Day 7.ConclusionsIn this study, hemostasis was successfully achieved with ABS in rat abdominal aortas. No histopathological change was found in the rat abdominal aortas between the ABS and control groups on Days 1 and 7. Further studies on the long-term effects of foreign body reactions and hemosiderin-loaded histiocyte accumulation are required.

The effects of dexmedetomidine dosage on cerebral vasospasm in a rat subarachnoid haemorrhage model.

We investigated the effect of two different doses of dexmedetomidine on vasospasm in a rat model of subarachnoid haemorrhage (SAH). SAH was induced by injecting 0.3 mL blood into the cisterna magna in all rat groups except the control (Group C). At 1 hour and 24 hours after SAH, 5 microg/kg dexmedetomidine was given to group D5, and 10 microg/kg dexmedetomidine was given to group D10. No medication was administered to the haemorrhage group (Group H). Malondialdehyde (MDA) and paraoxonase (PON) levels were measured at 48 hours after SAH. Mean wall thickness (MWT), mean luminal diameter (MLD), and proliferating cell nuclear antigen (PCNA) expression of the basilar artery were evaluated. MDA levels and MWT were lower in the dexmedetomidine groups. The lowest MDA levels and MWT were found in Group D10. The MLD was lowest in Group H. PCNA expression was observed only in Group D10. We concluded that dexmedetomidine reduces oxidative stress and vasospasm following SAH in a dose-dependent manner.

The effectiveness of dexmedetomidine in experimental spinal cord injury compared to methylprednisolone in rats.

The present study aimed to investigate the neuroprotective efficacy of dexmedetomidine in a rat experimental spinal cord injury model. The rats (n=40) were equally divided into four groups: G1, G2, G3, and G4. Rats in the G1 group underwent a laminectomy only. For the rats in the G2, G3, and G4 groups, spinal cord injury was induced by placing an aneurysm clip extradurally for 60 s at T10. The rats in G2 did not receive any post-injury treatment. Immediately after trauma was induced, rats in G3 were given methylprednisolone (30 mg/kg) and in G4, dexmedetomidine (10 microg/kg), both intraperitoneally. The rats were sacrificed under anesthesia 24 hours later and 1.5 cm lengths of injured spinal cord were obtained. Malonyldialdehyde values were significantly increased in G2 compared to G1, G3 and G4 (p<0.05). The neuronal cell count in G1 was significantly higher than in G2 and G3 (p=0.0001; p=0.007). G4 had higher cell counts compared to G2 and G3 (p=0.0001; p=0.05). These findings indicated that dexmedetomidine might have neuroprotective effects in spinal cord injury.

A rare complication of spinal surgery: cerebellar hemorrhage.

Remote cerebellar hemorrhage (RCH) after spinal surgery is encountered extremely rarely. A 64 year-old female patient developed symptoms of deteriorating consciousness and diplopia arising on the first postoperative day after recurrent spinal surgery. Cranial CT scan showed cerebral edema and evidence of a cerebellar hemorrhage. Urgent suboccipital decompressive craniectomy and expanded duraplasty were performed. Repeat CT at 24 h revealed hydrocephalus and an external ventricular drain (EVD) was inserted for 20 days. The patients consciousness deteriorated after withdrawal of the EVD and a ventriculoperitoneal shunt was placed. The patient recovered completely except for gait ataxia and left foot drop. Although the exact cause is unknown iatrogenic dural opening resulting in excessive cerebrospinal fluid (CSF) drainage and secondary development of venous infarction have been suggested to lead to RCH.

A training model for lumbar discectomy

Training models are becoming increasingly important for gaining surgical skills. We present an easy to prepare and cheap model using cadaver sheep spine appropriate to learn and practice various discectomy procedures.

Syringomyelia and intradural extramedullary tuberculoma of the spinal cord as a late complication of tuberculous meningitis.

Intradural extramedullary (IDEM) tuberculomas account for only 1% of all spinal tuberculomas. Concurrent IDEM tuberculoma and syringomyelia arising as a complication of tuberculous meningitis (TM) is extremely rare and only two cases have been reported to date. There is yet no report in the literature describing syringomyelia presenting as a delayed complication of IDEM tuberculoma. Here we present such a case. A 21 year-old male patient underwent partial decompression for thoracolumbar IDEM tuberculoma as a late complication of tuberculous meningitis. Spinal magnetic resonance imaging (MRI) of the patient suffering from progression of paraparesia six months after the operation revealed a syringomyelia occupying the space from T1 to T9, remote from the operation site, and syringo-peritoneal shunt placement was performed.

Effect of vardenafil on cerebral vasospasm following experimental subarachnoid hemorrhage in rats

We examined the effects of the phosphodiesterase 5 (PDE-5) inhibitor vardenafil on cerebral vasospasm in an experimental rat subarachnoid hemorrhage (SAH) model. Thirty-two albino Wistar rats were divided into five groups: G1, no experimental intervention; G2, administered subarachnoid physiological saline after sham surgery; G3, subjected to SAH; G4, subjected to SAH and administered low-dose (0.5 mg/kg) vardenafil treatment; and G5, subjected to SAH and administered high-dose (5 mg/kg) vardenafil treatment. For animals in G3, G4 and G5, SAH was induced by an injection of autologous non-heparinized blood into the cisterna magna. Immediately after SAH, for animals in G4 and G5, vardenafil was administered by gavage at intervals of 8 hours for 2 days. The rats were then decapitated, and basilar arteries and blood samples were taken for biochemical and histopathological examination. Malonyldialdehyde values in G2 (p = 0.004) and G3 (p = 0.002) were significantly higher than those in G1. G4 and G5 had significantly lower values than G2 and G3 (p = 0.014, G4 v. G2; p = 0.005, G4 v. G3; p = 0.005, G5 v. G2; p = 0.002, G5 v. G3). Total antioxidant capacity (TAC) values in G3 were significantly lower than those in G1 (p = 0.041). TAC values in G4 and G5 were significantly higher than those in G3 (p = 0.043). Mean luminal diameter in G3 was significantly smaller compared with G1 and G2 (p = 0.002), but larger in G4 (p = 0.002) and G5 (p = 0.001) compared with G3. Mean luminal diameter was also significantly larger in G5 than in G2 (p = 0.008) and G4 (p = 0.038). Mean wall thickness in G2 (p = 0.015) and G3 (p = 0.002) was significantly thicker compared with G1. Wall thickness was significantly thinner in G4 and G5 compared with G2 and G3 (p = 0.008, G4 v. G2; p = 0.001, G4 v. G3; p = 0.005, G5 v. G2; p = 0.001, G5 v. G3). Our results confirm that vardenafil may induce vasodilatation and provide potential benefits in SAH therapy by preventing vasospasm.