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Three patients with a history of anterior spinal surgery treated with a polymethylmethacrylate construct had extrusion of their constructs. In two instances, there were life-threatening esophageal fistulas, mediastinitis, and sepsis 3 months to 10 years after the original surgery. Surgical treatment required removal of the construct, treatment of the esophageal injury, and use of new spinal stabilization. Based on their experience and a review of the literature, the authors strongly recommend against the use of polymethylmethacrylate alone in anterior procedures involving the cervical spine except to treat malignancies in patients with a short life expectancy.

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A patient with a gunshot wound to the spinal cord with an incomplete neurologic deficit is presented. The neurologic examination revealed a combination of a central cord injury and the Brown-Séquard Syndrome. The authors suggest that the Brown-Séquard portion of the syndrome was caused by compression of tracts within the spinal cord caused by the mass of the bullet and the central cord injury was produced by the kinetic energy of the bullet during penetration into the spinal canal. They conclude that with incomplete neurologic lesions following gunshot wounds the bullet be removed.

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Experimental subarachnoid haemorrhage and intraparenchymal haematoma were produced in 20 cats serving as a model for parenchymal cell injury in patients with head trauma. There was a typical and constant cellular membrane dysfunction characterized by K+ outflux and Ca2+ influx. It appears that both of these events have a major influence on subsequent development of cellular dysfunction, anatomically characterized as cellular swelling. In addition, the calcium influx appears to have a specific role in the cell membrane destruction process by initiating an autolytic destruction of cell membranes. This mechanism may be crucial in the development of secondary irreversible injuries in cells destabilized, but not completely destroyed, at the time of the initial trauma.

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A total of 17 patients with arteriovenous malformations (AVMs) in sensitive areas of the brain were operated on and the AVMs were completely resected using perivenous techniques. No patient suffered a new neurological deficit following surgery. The perivenous surgical technique is most suitable for small AVMs in sensitive cortex. It differs from the standard approach in that it places emphasis on perivenous microsurgical dissection, identification of the nidus before major arterial feeders, and early ligation of selected venous channels. Three different types of venous drainage--single, multiple, and dual--were identified. Each different type of venous drainage requires a different surgical approach for the best results.

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Acute subarachnoid hemorrhage (SAH) and intraparenchymal hematoma (IPH) in cats are accompanied by massive cellular depolarization. This depolarization, characterized by potassium (K+) efflux and calcium (Ca++) influx, results in membrane destabilization, osmotic imbalance, and a decrease in electrical conduction. The Ca++ influx appears to initiate a chain reaction that, in some instances, may result in delayed cell destruction. The ionic dysequilibrium probably contributes to both brain engorgement and spasm in large vessels. The cellular depolarization and calcium-induced cell membrane injury at the moment of impact may play a greater role in the pathophysiology of head trauma than previously thought.

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A model of intraparenchymal hemorrhage was created in 11 cats. The development of the parenchymal hemorrhage was accompanied by a massive cellular depolarization and K+ release in anatomically intact areas in the vicinity of the hematoma. The K+ clearance was rapid and in most instances total. This initial K+ release was not ischemic in origin but was the result of mechanical and chemical factors of the extravasated blood on cellular membranes. In contrast, an increased water content of the white matter did not affect the cellular function or levels of K+ in the extracellular space of the cerebral cortex in the recording area. The experimental results suggest that K+ release takes place at the onset of trauma in subcritically injured cellular areas in the vicinity of a hemorrhage. The cellular elements undergo massive depolarization which is accompanied by a number of chemical and biochemical changes that lead to cellular swelling. Cellular depolarization and K+ release appear to be the initial response of the central nervous system to trauma. The extent of this response may strongly influence the final degree of cellular damage and, thus, the neurological deficit in patients with head trauma.

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Local experimental subarachnoid hemorrhage (SAH) was produced over the cerebral cortex in 15 cats. The cellular response was monitored using ion-specific electrodes for extracellular potassium (K+) and calcium (Ca++) activity, DC cortical potential, and electrocorticogram. The response was characterized by a profound cellular depolarization and extracellular calcium (Ca++) depletion which accompanied extracellular potassium (K+) accumulation. The prehemorrhage baseline calcium levels measured 1.14 +/- 0.11 mM, and were lowered to 0.4 to 0.7 mM/liter in different experiments. The K+ accumulation reached levels between 16 and 31 mM from a baseline of 3.17 +/- 0.52 mM and were cleared to normal or nearly normal within 5 minutes. The Ca++ levels also returned to normal within 5 minutes, but remained depressed for the duration of the experiment in two animals. These results confirm that blood extravasated into the subarachnoid space had a direct effect on parenchymal elements. The combination of transient K+ elevations and calcium depression may play an important role in the development of vascular spasm by inducing or facilitating a contraction in the muscular layer in the wall of major intracranial vessels.

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This paper presents a report of a case with vertebral metastatic chemodectoma with neurological complication who was treated successfully. A review of the literature on vertebral metastatic chemodectoma is also presented.

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Employing the techniques of electrogoniometry and force measurement, the authors devised a system that provides rapid, reliable, and objective evaluation of a motor task. Utilizing a high-speed minicomputer, various parameters of a motor task were recorded, analyzed, and displayed. This system was used to monitor recovery of motor function after surgery, during a drug regimen, and during electrical stimulation of specific sites in the central nervous system.

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The association of a recurrent cerebellar hemangioblastoma, retinal angioma, pheochromocytoma, renal carcinoma, and multiple renal and pancreatic cysts in one patient is reported, and the pertinent diagnostic studies are discussed briefly. Awareness of the possibility of late manifestations of various components of this syndrome in patients treated successfully for cerebellar hemangioblastoma will lead to their early identification and successful surgical treatment. Genetic counseling for patients affected by this syndrome and their families is recommended.

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