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Öğe Cervical hematomyelia(Karger, 2002) Önal, Ç; Yakinci, C; Kocak, A; Erguvan, R; Tekiner, A; Kutlu, R; Özcan, CSpinal cord injury with or without trauma has been reported in the perinatal period. The prognosis depends primarily on diagnosis of the level, extent and nature of the lesion, established by correlations between clinical, imaging and electrophysiological data. A 25-day-old boy with normal birth weight delivered at term by cesarean section was transferred to Inonu University Turgut Ozal Medical Center because of respiratory distress and brachial diplegia. A suspicious medullary lesion on cervical computerized tomography was confirmed as an intramedullary lesion extending from C3 to D1 on magnetic resonance imaging (MRI). Emergent surgery consisting of exposure of the lesion site and interlaminar direct puncture of the lesion under fluoroscopy revealed that the pathology was an intramedullary hematoma. The partial evacuation of the lesion with direct puncture, the patient's neurological improvement and close follow-up of the patient with ultrasonography, electrophysiology and MRI are discussed in the light of recent literature. Copyright (C) 2002 S. Karger AG, Basel.Öğe Effect of combined treatment with melatonin and methylprednisolone on neurological recovery after experimental spinal cord injury(Springer, 2004) Cayli, SR; Kocak, A; Yilmaz, U; Tekiner, A; Erbil, M; Ozturk, C; Batcioglu, KSpinal cord injury (SCI) results in the loss of function below the lesion. Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death. Methylprednisolone (NIP), by reducing edema and protecting the cell membrane against peroxidation, is the only pharmacological agent with a proven clinically beneficial effect on SCI. Melatonin, known as a free radical scavenger, has been shown to have an effect on lipid peroxidation following experimental SCI. The purpose of this study was to examine the effect of MP and melatonin on neurological, ultrastructural, and electrophysiological recovery. Female albino rats weighing 200-250 g were randomized into five groups of 18 rats each and six rats for the control group. Weight-drop trauma was performed for each group and a 30-mg/kg single dose of NIP for rats in group 1, a 10-mg/kg single dose of melatonin for rats in group 2, and MP and melatonin in the same doses for rats in group 3 were administered immediately after trauma. The rats in group 4 were the vehicle group (treated with ethanol) and group 5 was the trauma group. The motor and somatosensory evoked potentials were recorded at the 4th hour, the 24th hour, and on the 10th day of the study for six rats in each group. Posttraumatic neurological recovery was recorded for 10 days using motor function score and inclined plane test. After electrophysiological study the rats were terminated for an analysis of lipid peroxidation level of the injured site of the spinal cord. Electron microscopic studies were performed to determine the effects of melatonin, MP, and the combined treatment with MP and melatonin on axons, neurons, myelin, nucleus, and intracytoplasmic edema. The groups treated with MP, melatonin, and a combination of both had significantly enhanced electrophysiological, biochemical, and neurological recovery and also showed better ultrastructural findings than the trauma and vehicle groups. Although combined treatment was significantly more effective on lipid peroxidation than melatonin or MP treatments alone, at the 10th day, neurobehavioral, electrophysiological, and ultrastructural recovery were at the same level. In conclusion, MP, melatonin, and MP and melatonin combined treatment modalities improved functional recovery at the same level. Future studies involving different doses of melatonin and different dose combinations with MP could promise better results since each drug has a different anti-oxidative mechanism of action.Öğe Endodermal sinus tumor and spinal cord compression(Amer Assoc Neurological Surgeons, 1997) Colak, A; Tekiner, A; Kocak, A[Abstract Not Available]Öğe Intraorbital encephalocele: An important complication of orbital roof fractures in pediatric patients(Karger, 2003) Cayli, S; Kocak, A; Alkan, A; Kutlu, R; Tekiner, A; Ates, O; Sahinbeyoglu, BOrbital roof fractures are uncommon, and traumatic intraorbital encephalocele formation is a very rare complication of this type of injury. We treated 43 pediatric patients with orbital roof fractures at our center over a 4-year period. The aim of this study was to retrospectively investigate conditions that may lead to intraorbital encephalocele formation in children with orbital roof fractures. Each case was reviewed, and the cause of injury, associated clinical and computerized tomography findings, the Glasgow Coma Scale score on admission, neurological status, other bodily injuries, hospitalization time and type and width of the orbital roof fracture were recorded. The findings in 6 patients who developed encephaloceles were compared to corresponding findings in the 37 patients who did not develop this complication. A total of 44 orbital roof fractures were diagnosed by axial and coronal computed tomography scanning. Six of the 43 children developed intraorbital encephaloceles in the first month after head trauma. In each of these cases, magnetic resonance imaging demonstrated the intraorbital cystic lesion in communication with the subarachnoid space. The width of each orbital roof fracture was measured on axial and coronal computed tomography slices and was confirmed by measurements during surgery. The width of the fractures in the encephalocele cases ranged from 2-4 mm. Duraplasty and orbitoplasty were performed in all the patients with encephalocele. Pediatric patients with orbital roof fractures that exhibit more than 2 mm diastasis and are associated with frontal cerebral contusion may be at greater risk for developing intraorbital encephalocele. All such cases should be monitored closely and investigated further with magnetic resonance imaging. Copyright (C) 2003 S. Karger AG, Basel.Öğe Melatonin as a free radical scavenger in experimental head trauma(Karger, 1999) Cirak, B; Rousan, N; Kocak, A; Palaoglu, O; Palaoglu, S; Kilic, KHead trauma causes two kinds of injury in the neural tissue. One is the primary injury which occurs at the time of impact. The other one is a secondary injury and is a progressive process. Free radicals are produced during oxidative reactions formed after trauma. They have been thought to be responsible in the mechanism of the secondary injury. Some studies have been conducted to demonstrate the role of free oxygen radicals in neuronal injury. The alterations in the free radical level during the early posttraumatic period and the effect of a free radical scavenger on these alterations have not been studied as a whole. We aimed to demonstrate the free oxygen radical level changes in the early posttraumatic period and the effect of melatonin, which is a potent free radical scavenger, on the early posttraumatic free radical level. A two-staged experimental head trauma study was designed. In stage one, post-traumatic free radical level changes were determined. In the second stage, the effect of melatonin on the free radical level changes in the post-traumatic period was studied. Two main groups of rats each divided into four subgroups were studied. Rats in one of the main groups underwent severe head trauma, and malondealdehyde (MDA) levels were measured in the contused cerebral tissue at different time points. Rats in the other main group also underwent the same type of trauma, and melatonin was injected intraperitoneally at different time points after trauma. The MDA level alteration in the tissue was determined after the injection of melatonin. The MDA level increased rapidly in the early posttraumatic period. But in time, it decreased in the groups with only trauma. In the melatonin-treated group, the MDA level decreased after the injection of melatonin, when injected in the early posttraumatic period, compared to the control and trauma groups. However, melatonin increased MDA to a higher level than in the groups with only trauma and the control group when injected later than 2 h after trauma. The MDA level increases in the very early posttraumatic period of cerebral trauma and decreases in time. Melatonin, which is the most potent endogenous free radical scavenger, when injected intraperitoneally to the cerebral traumatized rats in the very early posttraumatic period, causes a significant decrease in the MDA level. But, melatonin, when injected more than 2 h after trauma, increases the MDA level in experimental cerebral trauma in rats. Copyright (C) 2000 S. Karger AG, Basel.Öğe A new model for tethered cord syndrome: A biochemical, electrophysiological, and electron microscopic study(Karger, 1997) Kocak, A; Kilic, A; Nurlu, G; Konan, A; Kilinc, K; Cirak, B; Colak, AIn order to investigate the pathophysiology of the tethered cord syndrome, a few experimental models have been developed and used previously. In this study, the authors present a new experimental model to investigate the biochemical, electrophysiological, and histopathological changes in the tethered spinal cord syndrome. A model was produced in guinea pigs using an application of cyanoacrylate to fixate the filum terminale and the surrounding tissue to the dorsal aspect of the sacrum following 5-gram stretching of the spinal cord. The experiments were performed on 40 animals divided into two groups. The responses to tethering were evaluated with hypoxanthine and lipid peroxidation, somatosensory and motor evoked potentials, and transmission electron microscope examination. The hypoxanthine and lipid peroxidation levels significantly increased, indicating an ischemic injury (p < 0.01). The average hypoxanthine level in the control group was 478.8 +/- 68.8 nmol/g wet tissue, while ii, was 651.2 +/- 71.5 nmol/g in the tethered cord group, The lipid peroxidation level in group I Nas 64.0 +/- 5.7 nmol/g wet tissue, whereas it Nas 84.0 +/- 4.7 nmol/g in group II. In the tethered cord group, the latencies of the somatosensory and motor evoked potentials significantly increased, and the amplitudes decreased. These changes indicated a defective conduction in the motor and sensorial nerve fibers. In the transmission electron microscopic examinations, besides the reversible changes like edema and destruction in the gray-white matter junction, irreversible changes like scarcity of neurofilaments and destruction in axons and damage in myelin sheaths were observed. We consider that this work can be used as an experimental model for tethered cord syndrome.Öğe Protective effect of melatonin on experimental spinal cord ischemia(Springernature, 2003) Erten, SF; Kocak, A; Ozdemir, I; Aydemir, S; Colak, A; Reeder, BSStudy design: Experimental animal model to assess ischemic spinal cord injury following occlusion of the thoraco-abdominal aorta. Objectives: To measure whether melatonin administered to rabbits before and after occlusion exerts an effect on the repair of ischemia-reperfusion (IR) injury. Setting: Medical Biology Laboratory, Inonu University, Malatya, Turkey. Methods: Rabbits were divided into three IR treatment groups and one sham-operated (ShOp) control group. The three treatment groups had their infrarenal aorta temporarily occluded for 25 min, while the ShOp group had laparotomy without aortic occlusion. Melatonin was administered either 10 min before aortic occlusion or 10 min after the clamp was removed. Physiologic saline was administered to the control animals. After treatment, the animals were euthanized and lumbosacral spinal cord tissue was removed for the determination of relevant enzyme activities. Results: Malondialdehyde levels, indicating the extent of lipid peroxidation, were found to be significantly increased in the nonmelatonin treated (IR) group when compared to the ShOp group. Melatonin, whether given to pre- or post occlusion groups, suppressed malondialdehyde levels below that of the ShOp group. Catalase (CAT) and glutathione peroxidase (GSH-Px) enzyme activities were increased in the IR group compared to the ShOp group. Melatonin given preocclusion resulted in a significant decrease in both CAT and GSH-Px enzyme levels. The superoxide dismutase ( SOD) enzyme activity was decreased in the ischemia-reperfusion treatment group. However, the melatonin treatment increased SOD enzyme activity to levels approximating that of the ShOp group. Conclusion: To our knowledge, this is the first study that shows the effects of melatonin administered both pre- and postischemia on induced oxidative damage to injured spinal cords. Our data also expands on reports that melatonin administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.Öğe Thrombolysis and mechanical fragmentation to treat massive pulmonary embolism in a patient with an anterior communicating artery aneurysm(Alliance Communications Group Division Allen Press, 2003) Kutlu, R; Alkan, A; Kocak, A; Sarac, KPurpose: To describe successful management of massive pulmonary embolism suffered by a patient with an unsecured intracranial aneurysm. Case Report. An anterior communicating artery aneurysm was found 10 days after a 50-year-old woman was admitted to the intensive care unit with subarachnoid hemorrhage. The patient developed severe acute dyspnea before planned surgery; imaging demonstrated thrombus in the right and left pulmonary arteries. Heparin was contraindicated, so an emergent coil embolization procedure was undertaken. In the same session, recombinant tissue plasminogen activator was administered directly into the thrombus. After 2 hours of thrombolysis and intermittent mechanical fragmentation, lung perfusion improved, and the patient's symptoms abated. Conclusions: Mechanical fragmentation together with fibrinolytic agent administration is a safe and effective treatment for pulmonary embolism after securing cerebral aneurysms.Öğe Unusual presentation of a sinonasal carcinoma mimicking an aneurysm rupture(Springer Verlag, 1998) Kocak, A; Erten, SF; Mizrak, B; Akbasak, A; Colak, AAlthough the association of subarachnoid hemorrhage (SAH) and tumoral lesions in adult is well known, hemorrhage from a sinonasal carcinoma extending to the intracranial cavity is exceedingly rare. In this paper, the authors report on a 12-year-old girl who presented with SAH caused by a sinonasal carcinoma located in the anterior skull base area. To our knowledge, this is the first report of a sinonasal carcinoma concomitant with SAH.
