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Robert A. Feldman and Richard C. Karl

✓ Three patients who developed Ogilvie's syndrome following lumbar spinal surgery are described. Ogilvie's syndrome, also known as pseudo-obstruction of the colon, is characterized by massive cecal distention without mechanical obstruction. If this condition is not recognized and not promptly treated, it may be complicated by cecal perforation, a life-threatening hazard. The etiology, diagnosis, management, and potential relationship between lumbar spinal surgery and Ogilvie's syndrome are discussed.

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Ronald F. Young, Richard Kroening, Wayne Fulton, Robert A. Feldman and Israel Chambi

✓ Forty-eight patients underwent electrical stimulation of the brain for treatment of chronic pain between 1978 and 1983. Average pain duration prior to treatment was 4.5 years. Before selection for this procedure patients underwent pain treatment in a multidisciplinary pain center, intensive psychological and psychiatric evaluation, and assessment of pain responsiveness to intravenous administration of placebo, morphine, and naloxone. A total of 71 electrodes were placed in the 48 patients at a variety of stimulating targets, including the periaqueductal gray matter, periventricular gray matter, thalamus, and internal capsule.

Seventy-two percent of patients experienced complete or partial pain relief. In addition, 59% of patients were able to discontinue narcotic usage. Twenty-five percent of patients returned to normal physical activities and another 33% showed marked improvement in functional capacity. Follow-up periods ranged from 2 to 60 months; with a mean follow-up period of 20 months. A variety of relatively minor complications occurred, but no mortality or permanent sequelae were experienced. No patient's pain was made worse as a result of electrical stimulation. Electrical stimulation of the brain offers a safe and relatively effective method for the treatment of chronic pain in appropriately selected patients, who are unresponsive to other forms of therapy.

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Robert A. Feldman and Ghassan F. Khayyat

✓ The authors report a case in which skeletal traction was applied with Gardner-Wells tongs and one of the pins perforated the inner table of the skull.

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Robert A. Feldman, David Yashon, George E. Locke and William E. Hunt

✓ Eleven anesthetized dogs underwent bilateral craniectomies. Four control dogs had serial resections of cerebral tissue in the normotensive state. After one control sample was removed from the remaining seven dogs, they were bled to a mean arterial pressure of 30 to 35 mm Hg and had cerebral tissue samples resected at 0, 30, and 60 min after the onset of hypotension. The tissue samples from the four normotensive dogs averaged 4.83 mM lactate/kg tissue with a range of 4.67 to 7.22 mM/kg. At 0 time post-shock the samples averaged 7.18 mM/kg, at 30 min post-shock 14.31 mM/kg, and at 60 min 18.76 mM/kg. It can be concluded that hemorrhagic shock causes a progressive elevation in cerebral tissue lactate, which correlates with the duration of shock. At low mean arterial pressures the brain is susceptible to the effects of poor tissue perfusion, which results in both inadequate oxygenation and lactate washout in spite of well-established mechanisms for preferential shunting of blood to the brain.

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George E. Locke, David Yashon, Robert A. Feldman and William E. Hunt

✓ Lactate accumulation in spinal cord tissue following trauma was determined to ascertain the role and magnitude of ischemia. High thoracic and low thoracic laminectomies were performed on each of nine rhesus monkeys. The lower exposed cord was traumatized with a calibrated blow of 300 gm cm. The upper exposed cord served as a nontraumatized control. At time intervals of 1.5 min to 48 hrs after trauma, both cord segments were removed and assayed for lactic acid. Lactate in nontraumatized segments averaged 3.64 mM/kg tissue, with a range of 2.20 to 4.95. Lactate in traumatized segments removed in from 1.5 min to 12 hrs from six monkeys averaged 5.50 mM/kg tissue, with a range of 4.32 to 6.46. Lactate in traumatized segments from three monkeys 18 to 40 hrs after trauma averaged 4.07 mM/kg, with a range of 3.20 to 5.18. This finding supports the concept that ischemia plays a role early in the traumatic process in spinal cord injury.

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Robert A. Feldman, David Yashon, George E. Locke and William E. Hunt

✓ In rhesus monkeys subjected to circulatory arrest, studies were made of the relationship of lactate production in the spinal cord to the duration of circulatory arrest and magnitude of lactate accumulation, and the results were compared to the magnitude of rise in cerebral tissue lactate. Both high and low thoracic laminectomies were performed on each of eight rhesus monkeys. Spinal cord tissue was excised for lactate assay at the upper laminectomy as a control, and a second tissue specimen was excised at the lower laminectomy site at time increments of 30 sec to 30 min after circulatory arrest. Tissue was excised from each site without circulatory arrest in one monkey and showed negligible increase in lactate production, indicating that excision of tissue itself does not result in increased lactate. Nonanoxic samples from seven monkeys averaged 4.60 millimoles (mM)/lactate/kg tissue, with a range of 2.22 to 6.49. Postcirculatory arrest samples from these monkeys averaged 11.10 mM lactate/kg tissue, with a range of 3.62 (at 30 sec) to 14.33 (at 10 min). Anoxic spinal tissue lactate was elevated above controls in each instance, and tissue lactate peaked between 5 to 10 min after circulatory arrest and remained stable with mild fluctuations beyond that time. Thus, the spinal cord responds to circulatory arrest much as cerebral tissue, but with some delay in the accumulation of lactic acid.