Phanor L. Perot

A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury: Results of the second national acute spinal cord injury study

In 1990, the Second National Acute Spinal Cord Injury Study reported that high-dosage methylprednisolone improves neurologic recovery in spinal-injured humans. The study showed that patients who received the drug within 8 hr after injury improved, whereas those who received the drug later did not. The drug significantly increased recovery even in severely injured patients who were admitted with no motor or sensory function below the lesion, contradicting a long-held dogma that such patients would not recover. Some researchers, however, have questioned the stratification of the patient population, the use of summed neurologic change scores, and the absence of functional assessments. The stratification by injury severity and treatment time was planned a priori and based on objective criteria. Detailed analyses revealed no differences between groups attributable to stratification or randomization. While multivariate analyses of the summed neurologic scores were used, the conclusions were corroborated by other analytical approaches that did not rely on summed scores. For example, treatment with methylprednisolone more than doubled the probability that patients would convert from quadriplegia or paraplegia to quadriparesis or paraparesis, analgesia to hypalgesia, and anesthesia to hypesthesia. The treatment also significantly improved neurologic scores in lumbosacral segments, indicating that beneficial effects were not limited to segments close to the lesion site. The treatment did not significantly affect mortality or morbidity. The study strongly suggests that methylprednisolone has significant beneficial effects in human spinal cord injury, that these effects occur only when the drug is given within 8 hr, and that it helps even in patients with severe spinal cord injuries. These conclusions have important implications for spinal cord injury care and research.

A Randomized, Controlled Trial of Methylprednisolone or Naloxone in the Treatment of Acute Spinal-Cord Injury

Abstract Studies in animals indicate that methylprednisolone and naloxone are both potentially beneficial in acute spinal-cord injury, but whether any treatment is clinically effective remains uncertain. We evaluated the efficacy and safety of methylprednisolone and naloxone in a multicenter randomized, double-blind, placebo-controlled trial in patients with acute spinal-cord injury, 95 percent of whom were treated within 14 hours of injury. Methylprednisolone was given to 162 patients as a bolus of 30 mg per kilogram of body weight, followed by infusion at 5.4 mg per kilogram per hour for 23 hours. Naloxone was given to 154 patients as a bolus of 5.4 mg per kilogram, followed by infusion at 4.0 mg per kilogram per hour for 23 hours. Placebos were given to 171 patients by bolus and infusion. Motor and sensory functions were assessed by systematic neurologic examination on admission and six weeks and six months after injury. After six months the patients who were treated with methylprednisolone within eigh...

Alteration of thromboxane and prostacyclin levels in experimental spinal cord injury

We measured levels of thromboxane B2 and 6-keto-PGF10 in rabbit spinal cord and cat CSF after impact injury to spinal cord. Rabbit tiissue thromboxane B2 levels increased more than 6-keto-PGF10. In cat, CSF thromboxane B, was higher the first hour postinjury; CSF 6-keto-PGF10 also increased, but less so. These results imply activation of arachidonic acid metabolism. The relatively greater increase of thromboxane B, suggests that thromboxane-prostacyclin imbalance may contribute to post-traumatic ischemia.

Leukotriene B4 Release and Polymorphonuclear Cell Infiltration in Spinal Cord Injury

Abstract: Activation of arachidonic acid occurs after spinal cord injury. Leukotriene B4 is a lipoxygenase metabolite of arachidonic acid. In a rat model of experimental spinal cord injury, we found that the leukotriene B4 content was less than the sensitivity of our assay (8 pg/mg of protein) in non‐traumatized spinal cord. Leukotriene B4 was detectable in raumatized cord (mean ± SE, 25 ± 5 pg/mg of protein; n = 3). Release of leukotriene B4 from spinal cord slices into the incubation medium was also noted after trauma (9 ± 1 pg/mg of protein; n = 12) and was enhanced by exposure of traumatized spinal cord slices to the calcium ionophore A23187 (375 ± 43 pg/mg of protein; n = 12). The amount of leukotriene B4 released corresponded to the extent of post‐traumatic polymorphonuclear cell infiltration determined by a myeloperoxidase assay. Results from this study suggest that the source of leukotriene B4 in spinal cord injury is infiltrating polymorphonuclear cells.

Scalp recorded somatosensory evoked potentials to posterior tibial nerve stimulation in humans

The somatosensory evoked potentials (SEPs) produced by stimulation of the right and left posterior tibial nerves individually and also by their simultaneous stimulation were recorded in 84 adult normal subjects up to 150 msec after the stimulus by electrodes placed on the cranial vertex and by rows of electrodes over the sagittal and coronal lines using references on the ear or in the nasopharynx. The statistical distribution of the latencies of their different peaks was established. The effect of simultaneous stimulation of right and left posterior tibial nerves on the early SEP components was described. Some details of the anatomy of the rolandic sulcus were inferred from the amplitude distribution of these potentials.

Spinal Cord Glucose Utilization after Experimental Spinal Cord Injury

Metabolic alterations after experimental contusion injury of the spinal cord were evaluated by determining qualitative spinal cord glucose utilization (SCGU), SCGU was determined by the 2-deoxy-D-[14C] glucose technique. An increase in SCGU occurred at the site of maximal impact in the white matter after an injury causing paraparesis and in near trauma regions after an injury causing either paraparesis or paraplegia. These findings are most likely due to anaerobic glycolysis resulting from a reduction in blood flow that still allows delivery of substrate to tissue. Although an initial increase was observed at the site of maximal impact after a paraplegia-causing injury, SCGU in the white matter demonstrated a progressive deterioration by 4 and 8 hours after injury. A failure of substrate delivery resulting from ischemia is the most likely cause for this reduction in SCGU. The somatosensory evoked potential was found to be a very sensitive indicator of the remaining functional axons at the injury site.

Orthostatic hypotension with brainstem tumors

Three patients with brainstem tumors had orthostatic hypotension as the major presenting manifestation. Two patients had primary tumors that involved the dorsal medulla, pons, and rostra1 spinal cord; one was a malignant astrocytoma and the other a hemangioblastoma. The third patient had an oat cell carcinoma of the lung with subependymal spread to the medulla, pons, hypothalamus, and thalamus. Evaluation of baroreceptor function in the patient with the malignant astrocytoma showed a defect in the efferent sympathetic limb of the baroreceptor reflex arc.

The effects of low spinal injury on somatosensory evoked potentials from forelimb stimulation.

Spinal cord transection below C6 in anesthetized cats results in an alteration in the configuration of the SEP following direct or percutaneous stimulation of the median or radial nerves. The most significant alterations were in components occurring at latencies from 40 to 60 msec. The results of these experiments support the general conclusion that the spinal cord and supraspinal structures act as a functional unit and that the SEP is not solely determined by input over segmental pathways In addition, the alteration in the SEP produced by median nerve stimulation following spinal cord injury below C6 may serve clinically as a monitor of events at the site of injury in cases where an SEP from lower limb stimulation is no longer obtainable.

Trichinosis encephalitis: a study of electroencephalographic and neuropsychiatric abnormalities.

ESTIMATES of the incidence of trichinosis at autopsy in the United States range from 16 to 18 per cent.lr2 Approximately 350,000 persons each year acquire a new infection, and, of these, 16,000 manifest clinically detectable symptoms, with an over-all mortality rate estimated at 5 to 6 per It is well documented in the literature that the central nervous system may be involved in trichinosis.’3.7 The incidence of this complication is variously reported as 10 to 17 per cent.*p3 The mortality in cases with neurologic involvement has been found to be as high as 35 per cent.gJ0 The importance of recognizing this clinical syndrome is obvious. With the advent in recent years of an effective, although nonspecific, treatment in the form of steroid hormones, one feels even more urgently the necessity of early diagnosis.

History and current state of neurosurgery at the Medical University of South Carolina.

We review the development of neurosurgery at the Medical University of South Carolina (MUSC) and the emergence of MUSC as a leading academic neurosurgical center in South Carolina. Historical records from the Waring Historical Library were studied, former and current faculty members were interviewed, and the personal records of Dr Phanor J Perot were examined. Dr Frederick E Kredel was the first to perform cerebral revascularization in stroke patients using omental flaps and the first to culture glioma cells in artificial media. The MUSC Neurosurgery residency program was established in 1964 by its first formally trained neurosurgeon, Julian Youmans, MD. The first graduate of the program, Dr Russell Travis, went on to become the President of the American Association of Neurological Surgeons. In 1968, the longest serving chairman, Dr Perot, joined the department and conducted significant research in spinal cord injury, receiving a continuous, 20-year award from the National Institute of Neurological Disorders and Stroke. A major change in the neurosurgery program occurred in 2004 when Dr Sunil Patel accepted the chairmanship. He integrated neurosurgery, neurology, and basic neuroscience departments into a comprehensive Department of Neurosciences to provide integrated clinical care. This department now ranks second in the country in National Institutes of Health research funding. Recently, the Center for Global Health and Global Neurosurgery was established with a vision of caring for patients beyond national borders. Neurosurgery at MUSC has been influenced by Drs Kredel and Perot and the current leadership is moving forward with a uniquely integrated department with novel areas such as global neurosurgery.