Biomedical subjects
Publications and source records attributed to M Kaoutzanis.
A simple instrument used in the detachment of the dura mater from the inner surface of the skull is presented. This separator is a hollow tube attached to a syringe. It bears a convex tip lightly pressing and detaching the dura. Saline solution given through the syringe comes out at the tip of the separator and easily, safely, and effectively detaches the dura.
The pathophysiology of cerebral vasospasm is complex and multifactorial. The present study sought to identify the degree of correlation between cerebral vasospasm as observed angiographically and clinical evaluation of an animal's neurologic status in the canine model following a single and double experimental subarachnoid hemorrhage (SAH) protocol. Nineteen mongrel dogs underwent single or double experimental SAH by percutaneous needle puncture of the cisterna magna and placement of a subarachnoid blood clot in the basal cistern on day 1 and day 4, respectively. At 72 h after each experimental SAH, vertebral angiography was performed and compared to control angiography. Basilar artery diameter measured at multiple positions was expressed as percentage of control diameter. Clinical evaluation of the animals was performed every day throughout the experiments. To assess the degree of neurologic impairment we developed a coma scale that efficiently estimated motor ability, eye response and eating habits of the animals. Vasoconstriction after experimental SAH reduced mean basilar artery diameter to 79.1% (+/- 5.4) of control diameter following single SAH and to 69.0% (+/- 2.1) of control diameter following double SAH. No changes were observed in the neurologic behavior of the animals throughout the experiment. Since a principal characteristic of human cerebral vasospasm is the close correlation between arterial constriction and neurological deficit, we believe that the canine model of SAH, although good in creating cerebral arterial vasoconstriction, does not fully represent the best model of human cerebral vasospasm.
We used monoclonal antibodies to examine the immunohistochemical distribution of the three major Ca(2+)-dependent protein kinase C (PKC) isozymes (I, II, and III) in ischemic gerbil hippocampus. Groups of four animals were sacrificed at 15 min, 4 h, 1 day, 2 days, 3 days, and 7 days after a 10-min episode of global forebrain ischemia. In control animals, PKC-I immunoreactivity was greater in CA1 neurons than in CA3-4. Terminal-like staining was not evident. PKC-II immunoreactivity was observed in all CA fields and in the outer molecular layer of the dentate gyrus. PKC-III staining was present in the CA fields, the inner molecular layer of the dentate gyrus and the subiculum. Dentate granule cells and mossy fibers were not stained with any of the PKC antibodies. Fifteen minutes and 4 h after ischemia, PCK-I, -II and -III immunoreactivity were all increased in CA1 neurons and PKC-III immunoreactivity alone was visualized in granule cells and mossy fibers. Staining patterns returned to baseline one day after ischemia. PKC-II and -III terminal-like staining were preserved in the stratum lacunosum-moleculare for 3 days and 2 days after ischemia respectively and then disappeared. The altered patterns of PKC staining in the hippocampus may reflect activation and/or down-regulation of PKC isozymes. Ca(2+)-dependent PKC isozymes may, therefore, potentially play a role in the pathogenesis of delayed ischemic neuronal death.
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Six cases of hydatid disease affecting the vertebrae are described. Four patients presented with paraparesis and sphincter disturbances while the other two presented with low back pain and sciatica. Myelographic findings were positive in all six patients. The CT scans showed a paravertebral mass with destruction of bone in two cases. The nuclear magnetic resonance performed in one patient showed the exact extent of the disease all along the spine. Posterior laminectomy with decompression of the spinal cord and removal of the hydatid cysts was performed in all six patients. After the operation four patients received oral treatment with mebendazole. The patients with paraparesis showed little improvement of their neurological status. The two patients with low back pain and sciatica showed marked improvement. Hydatid disease affecting the vertebrae presents with neurological complications due to cord compression. The prognosis remains poor in spite of laminectomy, although removal of the hydatid cysts and long-term mebendazole medication may result in relief of symptoms.