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Öğe Are unresponsive dilated pupils an indicator for brain death? an evaluation of Edinger Westphal nucleus in rabbits with brain death(2019) Ozmen, Ozgur; Aksoy, Mehmet; Aydin, Mehmet Dumlu; Atalay, Canan; Dostbil, Aysenur; Ince, Ilker; Sener, EbruAim: To investigate a relationship between unresponsive pupils and severity of neurodegeneration in Edinger Westphal nucleus (EWN) of animals diagnosed with brain death.Material and Methods: A total of 24 New Zealand white rabbits were used. The animals were divided into three groups, as control group (n=5), sham (n=5) and subarachnoid hemorrhage (SAH) group (n=14). Pupil diameters were measured after giving 2 mL of physiological saline for sham and 2 ml non‑heparinized autologous arterial blood for the study group into the cisterna magna. Brain death was diagnosed in 10 rabbits in the SAH group. Then all animals were sacrificed. The brains, oculomotor nerves of all animals were extracted and stored in 10% formalin solutions for histopathological examination.Results:TThe mean neuron numbers of Edinger Westphal nucleus was 253±43/mm3 in the control group; 244±12/mm3 in the sham group and 236±12/mm3 in dead unresponsive animals. Pupil diameters and degenerated neuron density of EWN in control, sham and SAH groups were found as follows, respectively: 8960±990µm-3±1/mm3; 10543±1.123µm-13±4/mm3 and 13540±1.356µm-63±11/mm3 (P0.005). There was a positive relationship between degenerated neuron density of the EWN and pupil diameters (P0.001). The mean nondegenerated neuron numbers were 170±32/mm3 in unresponsive pupils of examined animals.Conclusion: In the absence of electrocardiographic/electroencephalographic functions, unresponsive pupils could not indicate real brain death.Öğe The role of vagal nerve injury on respiration disturbances in subarachnoid hemorrhage(Turkısh Neurosurgery, 2014) Çakır, Murteza; Atalay, Canan; Çakır, Zeynep; Emet, Mücahit; Aydın, Mehmet Dumlu; Aydın, Nazan; Önder, Arif; Çalık, MuhammedWe examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). MaterIal and Methods: This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. Results: Normal respiration rate, as measured in the control group, was 30±6 bpm. In the SAH-induced group, respiration rates were initially 20±4 bpm, increasing to 40±9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28500±5500 in both control and sham animals, whereas axon density was 22250±3500 in survivors and 16450±2750 in dead SAH animals. The severity of axonal degeneration of vagal nerves was greater in the six dead animals than in the survivors. ConclusIon: If vagal nerves are lesioned, the muscles of respiration are paralyzed and respiratory reflexes are disrupted. That the ischemic and mechanical factors created by SAH cause vagal nerve root injury and respiration disorders may be inevitable and fatal.