Publications (10)14.5 Total impact
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Article: Toward changing of the pathophysiological basis of acute hydrocephalus following subarachnoid haemorrhage: a preliminary experimental study.
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ABSTRACT: OBJECTIVE: Acute hydrocephalus (ventricular enlargement within 72 hours) is a relatively common complication in aneurysmal subarachnoid hemorrhage (SAH) patients. The cerebrospinal fluid secretion may be increased at the early phases of SAH, but it has not been proved definitely. We studied the histologic feature of choroid plexuses at the early and late phases of subarachnoid hemorrhage. METHODS: This study was conducted on twenty rabbits. Five, five and ten of them were used as control, SHAM and SAH groups, respectively. In SAH group, five of the animals were decapitated after two days. Other five animals were decapitated after fourteen days of injection. The choroid plexuses of lateral ventricles were obtained from coronary sections of brains at the levels of temporal horns of lateral ventricles. Sections were stained with haematoxylin-eosin and Masson's trichrome for subarachnoid haemorrhage-related damage and examined stereologically to determine the water filled vesicles which were counted, and compared statistically. RESULTS: The mean numbers of water vesicles were different after SAH between early decapitated group (Group III), and late decapitated group (Gropu IV). The mean numbers of water vesicles were found 2,80(±0,05)in control (Group I), 2,76(±0,02) in SHAM group (Group II), 14,68(±0,06) in early decapitated group (Group III), and 4,78(±0,13) in the late decapitated group Group IV). Total number of fluid-filled vesicles of choroid plexuses was also assessed by stereologically and found 840(±16) in control (Group I), 828 (±7) in SHAM group (Group II), 4404(±19) in early decapitated group (Group III), and 1434(±41) in the late decapitated group (Group IV). It was noted that the numbers of water filled cistern were significantly increased at the early phases of subarachnoid hemorrhage (p<0.05). CONCLUSIONS: In subarachnoid haemorrhage with aneurysm rupture, it seems that increased cerebrospinal fluid secretion is triggered by hemorrhage at the early phase, but it is not possible at the late phase because of choroid plexus degeneration. At the early phase of hemorrhage may be stimulated the irritant receptors glossopharyngeal and vagal nerve endings which innervate the healthy choroid plexuses epithelium and arteries. We stated that our findings may be accepted as being causative. It is likewise possible that CSF blockage per se leads to hydrocephalus and the morphological changes are sequelae further down the road. This is the first study to show the water vesicles of choroid plexus as a causative to the development of acute hydrocephalus following SAH.World Neurosurgery 12/2012; · 0.68 Impact Factor -
Article: Effects of haloperidol on striatal neurons: relation to neuronal loss (a stereological study).
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ABSTRACT: In the present work, we investigated the effect of chronic haloperidol administration on the number of striatal neurons in guinea pigs. For this purpose, adult male guinea pigs were given daily injections of 1, 2 or 3 mg/kg of haloperidol for 6 weeks. After treatment, the animals were anesthetized via brief inhalation of ether, the brains were removed and the corpus striatum was dissected. Then the tissues were processed and semi-thin sections were stained with toluidine blue for stereological and histopathological evaluation. The physical disector was used for measurements of nuclear height and numerical density of striatal neurons and also to evaluate both normal and degenerated neurons within the corpus striatum of treated animals and untreated controls. In the control group, the mean numerical density of neurons was calculated as 47.92 cell/mm3 and the mean nuclear height as 3.58 µm. Mean densities of all (both viable and degenerated) neurons were calculated to be 45.46 in the low-dose (p < 0.01), 39.73 in the medium-dose (p < 0.001) and 30.31 cell/mm3 in the high-dose group (p < 0.001). Mean densities of degenerated neurons in the low, medium and high dose group were 30.72, 22.93 (p < 0.001) and 15.56 cell/mm3 (p < 0.001) respectively. Mean nuclear heights were 2.804 (p < 0.0001), 2.78 (p < 0.0001) and 2.33 µm (p < 0.00001) in the low, medium and high dose group, respectively.Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences. 01/2011; 49(1):21-7. -
Article: Role of degenerated neuron density of dorsal root ganglion on anterior spinal artery vasospasm in subarachnoid hemorrhage: experimental study.
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ABSTRACT: The spinal arteries are innervated by several systems that contribute to the control of spinal cord blood flow. The sensory fibers of upper cervical nerves have vasodilatatory effect on the anterior spinal arteries (ASA). Subarachnoid hemorrhage (SAH) causes severe vasospasm by various neurochemical mechanisms. We examined whether there is a relationship between the neuron density of the C3 dorsal root ganglion and the severity of ASA vasospasm in SAH. This study was conducted on 20 rabbits. Four of them were used as baseline group. Experimental SAH has been applied to all of 16 animals by injecting homologous blood into cisterna magna. After 20 days of injection, ASA and C3 dorsal root ganglia (C3DRG) were examined histopathologically. ASA volume values and normal and degenerated neuron densities of C3DRG were estimated stereologically and the results were analyzed statistically. The mean ASA volume was 1.050±0.450 mm³, [corrected] and the mean neuronal density of C3DRG was 10,500 ± 850 in all animals. The mean volume value of ASA was 0.970±0.150 [corrected] mm³, and the normal neuron density of C3DRG fell to 8,600 ± 400/mm³ in slight vasospasm group. In severe vasospasm-developed animals, mean volume value of ASA was 0.540±0.90 [corrected]mm³ and the normal neuron density of C3DRG fell to 5,500 ± 360/mm³. An inverse relationship between the degenerated neuronal density of the C3DRG and ASA volume values may indicate the severity of ASA vasospasm. The neuron density of C3DRG may be an important factor on the regulation of ASA volume values and the continuation of spinal cord blood flow. Low neuron density of C3DRG may be considered as an important factor in the pathogenesis of severe ASA vasospasm in SAH.Acta Neurochirurgica 12/2010; 152(12):2167-72. · 1.52 Impact Factor -
Article: Erratum to: Role of degenerated neuron density of dorsal root ganglion on anterior spinal artery vasospasm in subarachnoid hemorrhage: experimental study.
Acta Neurochirurgica 11/2010; · 1.52 Impact Factor -
Article: The role of ischemic neurodegeneration of the nodose ganglia on cardiac arrest after subarachnoid hemorrhage: an experimental study.
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ABSTRACT: The heart is innervated by several systems that contribute to the control of the heart's rhythm. The cardiac fibers of the vagus nerve have an important role in the regulation of heart rhythm under many emotional and physical conditions. Severe electrocardiographic disturbances have been reported following subarachnoid hemorrhage (SAH), but ischemic neuronal degeneration of the nodose ganglion of the vagus nerve has not been previously investigated. We examined if there is a relationship between ischemic injury of the nodose ganglion of the vagus nerve and the severity of heart rhythm disorders after subarachnoid hemorrhage. This study was conducted on 20 rabbits. Four rabbits were used as a baseline group. Experimental subarachnoid hemorrhage was applied to half of the remaining animals (n = 8) by injecting homologous blood into the cisterna magna, and the others (SHAM group, n = 8) were injected with isotonic saline solution in the same manner. For 20 days after the injection, heart rhythm changes were observed daily. After the experiment, normal and ischemic neuron densities in the nodose ganglia of the vagus nerves were examined stereologically. The number of heart rhythm irregularities and the number of degenerated neurons in the nodose ganglia were compared statistically. The normal heart rhythm rate was 280 ± 45/min. At the beginning of the SAH, the average heart rate was 220 ± 30/min; about 10 hours later, it decreased to 189 ± 30/min, indicating severe bradycardia. However, after 7 days, the average heart rate had increased to 350 ± 30/min. Six animals died due to irregularities in cardiac function and respiration. Histopathological examinations showed that the average density of normal neurons in the nodose ganglion was 10,500 ± 2500 in the baseline animals and the SHAM group, but the normal neuron density was 8250 ± 1500 in survivors and 6450 ± 1330 in dead animals. The ischemic neuronal degeneration in the nodose ganglia was more severe in the dead animals than in the survivors (p < 0.0001). Afferent vagus nerves originating from the nodose ganglia have an important role in regulating heart rhythm via their afferent fibers and efferent connections. If neurons of the nodose ganglia are lesioned due to ischemic insult during subarachnoid hemorrhage, heart rhythm regulation by vagus afferent reflexes is disturbed. Vagus pathway paralysis may result in indirect sympathetic overactivity. The development of tachycardia causes depletion of the heart's reserves, and cardiac arrest may be inevitable following extensive subarachnoid hemorrhage.Experimental Neurology 09/2010; 230(1):90-5. · 4.70 Impact Factor -
Article: Haloperidol-Induced Neuronal Damage in Guinea Pig Hippocampus: A Microscopic Study
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ABSTRACT: Haloperidol, a neuroleptic drug, is still discussed if it is neurotoxic. In the present study, neurotoxic effects of haloperidol on guinea pig hippocampus were examined. Sixteen guinea pigs were randomly divided into two groups of 8 animals each. The animals of treatment group were given intraperitoneally (i.p.) haloperidol diluted in saline (dose of 5 mg/kg daily) for 6 weeks. Control animals received only the same volume of saline i.p. Hippocampi from both groups were examined by light and electron microscope. Numerous dark neurons with a heterochromatic nucleus and dense cytoplasm were observed in the hippocampi of the treatment group by light microscope and ultrastructural levels. Also some neurons have increased vacuolar contents and lysosomes. These findings suggest that haloperidol leads to prominent damage of hippocampal neuronsJournal of Neurological Sciences. 01/2010; -
Article: Mechanism of cerebral fat embolism in subarachnoid hemorrhage: an experimental study.
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ABSTRACT: Subarachnoid hemorrhage (SAH) may cause neurogenic pulmonary edema (NPE), and chylomicron metabolism may be destroyed in injured lungs. We aimed to investigate the effect of neurogenic pulmonary edema (NPE), if present, on the development of cerebral fat embolism. This study has been conducted on 20 rabbits. Experimental SAH has been applied to half of the animals by injecting homologous blood into the cisterna magna, and the remaining half was applied only isotonic saline solution in the same manner under general anesthesia. After 20 days, all animals were killed. Their lungs and brains were examined histopathologically. Six animals died of SAH between 16 and 20 days, and foamy hemorrhagic parenchymal lesions and intra-alveolar hemorrhage were observed in their lungs. Fat globules were abundantly found in cerebral arteries of six of all the non-surviving animals. But, minimal histopathological changes were found in the lungs and brains of the surviving animals. Cerebral fat embolism was detected in only one animal that was given isotonic solution. SAH may cause NPE and result in lung tissue destruction. Chylomicron metabolism may be disordered in the destructed lungs and leakage of chylomicrons into systemic circulation may be facilitated via destroyed lung barrier. These pathologic processes may lead to cerebral fat embolism.Neuropathology 01/2007; 26(6):544-9. · 2.02 Impact Factor -
Article: Histopathologic evaluation of neurogenic pulmonary edema after subarachnoid hemorrhage in rabbits.
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ABSTRACT: To investigate the effects of subarachnoid hemorrhage (SAH) on lung tissue. We conducted this study on 20 rabbits in the Ataturk University Medical Faculty, Erzurum, Turkey in 2005. Experimental SAH was applied to all animals under general anesthesia. After 20 days, all animals were sacrificed. Their lungs were examined histopathologically. Foamy hemorrhagic parenchymal lesions, alveolar rupture, and subintimal fluid collection in the pulmonary vasculature were observed in the lungs of the non-surviving animals. However, minimal changes were found in the lungs of the surviving animals (p<0.01). Our results suggest that luminal narrowing of the lung vessels due to subintimal fluid collection plays an important role in the development of pulmonary hypertension and neurogenic pulmonary edema in SAH.Neurosciences 07/2006; 11(3):158-61. · 0.12 Impact Factor -
Article: Disappearance of phantom limb pain during cauda equina compression by spinal meningioma and gradual reactivation after decompression.
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ABSTRACT: We describe a 65-yr-old woman, whose right lower limb had been amputated at the mid-femoral level because of complicated femur fracture sustained at the age of 5 yr. After amputation, she experienced phantom limb pain (PLP), which gradually decreased in intensity but persisted for 60 yr. At this point the pain diminished progressively, in parallel with the evolution of cauda equina compression caused by an intraspinal tumor. The PLP gradually reappeared over 3 mo after surgical removal of the tumor. IMPLICATIONS: We present a case in which phantom limb pain (PLP) in an amputated leg disappeared during cauda equina compression by meningioma and reactivated after surgical decompression. This case suggests that complete compression or blockade of nerves, a nerve plexus, the cauda equina, or the medullary cord may result in suppression of PLP, and decompression of or recovery from the block may cause reactivation.Anesthesia & Analgesia 11/2005; 101(4):1123-6, table of contents. · 3.29 Impact Factor -
Article: Malignant peripheral nerve sheath tumor of the orbit: case report and literature review.
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ABSTRACT: A 68-year-old woman with progressive visual loss and exophthalmos in her right eye had been operated on for a mass in her right calf 3 years earlier. Imaging showed a huge mass invading the orbital structures and temporal pole. The presumptive diagnosis was a malignant orbital tumor. The tumor was resected totally and eroded tissues such as the lateral rectus muscle and dural compartments were repaired. The histological diagnosis was a malignant peripheral nerve sheath tumor (MPNST). The patient recovered uneventfully and was discharged 8 days after surgery. Two years later she died from a liver tumor. Few MPNSTs involving the orbit have been reported.Skull Base Surgery 06/2004; 14(2):109-13; discussion 113-4. · 0.66 Impact Factor
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- Acta Neurochirurgica (2)
- Anesthesia & Analgesia (1)
- Neuropathology (1)
- Experimental Neurology (1)
- Neurosciences (1)
Institutions
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2004–2010
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Ataturk University
- Department of Neurosurgery
Erzurum, Erzurum, Turkey
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