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We studied the relationship between petrous ganglion cells of the GPN and water vesicles of CP in the early and late phases of SAH, and found that CP vesicles are increased in the early phase of SAH due to irritation of GPN, and decreased in the late phase due to ischemic insult of the petrous ganglion and parasympathetic innervation of the CP.

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AIM: To examine ischemic neurodegeneration of the ciliospinal center on permanent miosis following subarachnoid hemorrhage (SAH). MATERIAL and METHODS: Nineteen rabbits were examined in this study. The animals were divided into three groups, as control (GI, n=5), sham (GII, n=5) and study group (GIII, n=9). Pupil diameters were measured after giving 0.5 mL physiological saline for sham and autologous arterial blood for the study group into the cervico-thoracic subarachnoid space. After three weeks of follow up, the cervico-thoracic cord and bilateral superior cervical sympathetic ganglia were removed. The pupil diameter values were compared with degenerated neuron volumes of sympathetic ganglia and degenerated neuron densities of thoracic sympathetic nuclei which were studied by stereological methods. RESULTS: The mean pupil diameter was 5180 ± 370 µm and the mean degenerated neuron density of the ciliospinal center was 4 ± 1/mm 3 in animals of the control group (GI). These values were 9850 ± 610 µm, 10 ± 3/mm 3 in sham (GII), and 7.010 ± 440 µm and 98 ± 21/mm 3 in the study (GIII) groups. There was an inverse relationship between degenerated neuron density of the ciliospinal nuclei and pupil diameters. CONCLUSION: We showed and reported for the first time that ciliospinal sympathetic center ischemia-induced neurodegeneration may have been responsible for permanent miosis following SAH.

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AIm: Cerebral vasospasm after subarachnoid hemorrhage (SAH) may lead to a devastating neurological outcome by inducing cerebral ischemia. However the role of external carotid artery (ECA) vasospasm has been rarely reported in the literature. The aim of this study was to elucidate the effect of ECA vasospasm on cerebral ischemia related neurodegeneration in the cerebral cortex after SAH. mATERIAl and mEThODS:This study was performed on 23 rabbits, divided into three groups: control (n=5), sham (n=5), and SAH (n=13). Experimental SAH was performed by injecting 0.75 mL auricular arterial homologous blood into the cisterna magna. After three weeks, the animals were decapitated and the common carotid arteries with their external and internal branches and the brains were examined histopathologically. Vasospasm indexes (VSI) of ECAs and internal carotid arteries (ICAs) and degenerated glial cell numbers of temporal cortices (n/mm 3 ) were estimated stereologically and the results were compared statistically. CONClUSION: ECA vasospasm was observed to have a more important predictive role on the serious cerebral ischemia and neuronal degeneration after SAH. The mechanism may be related to ischemia of the parasympathetic ganglia of the lower cranial nerves and dorsal root ganglion. RESUlTS

Four cases of alveolar hydatid disease of the brain encountered within 27 months in eastern Turkey are reported. All of the patients were male farmers who presented with signs of cerebral tumor. Two of the patients were shown to harbor hepatic lesions and one of them had pulmonary metastases. The cerebral lesions were removed in toto and neurological recovery was obtained in all four patients. A review of the literature revealed only five previously reported cases treated surgically. It is concluded that cerebral Echinococcus multilocularis lesions are amenable to surgery, and that their removal provides useful prolongation of life despite the presence of hepatic or pulmonary disease.

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