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Biomedical subjects

P L Perot

Publications and source records attributed to P L Perot.

At least 37 records · Page 2Linked to original sources
PubMed1982

Treatment of nontraumatic atlantoaxial dislocation and fibrous fusion. Case report.

The authors describe a case of nontraumatic atlantoaxial dislocation secondary to acute rheumatic fever, in which there appeared to be fibrous fusion between the axis and the atlas in the subluxed position. The dislocation was reduced by means of combined traction and steroid therapy. Fibrous fusion occurred in the realigned position after immobilization.

Axis, Cervical Vertebra↗
PubMed1981

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.

Animals↗
PubMed1979

Pressor response resulting from experimental contusion injury to the spinal cord.

Experimental contusion paraplegic injury to the posterior spinal cord in cats results in a sudden increase of systemic blood pressure to between 200 and 250 mm Hg, and an increase in pulse pressure and a slowing of pulse rate. This initial hypertensive phase lasts approximately 3 to 4 minutes, and then is followed by a hypotensive phase. This pressor response is mediated by the alpha adrenergic receptor sites of the peripheral sympathetic nervous system and can be blocked by intravenous phenoxybenzamine, an alpha adrenergic blocking agent. The hypotensive phase is the result of an overall reduction in alpha adrenergic vascular tone and can be reversed by the infusion of metaraminol or intravenous fluids. The alterations in blood pressure that follow impact injury are most likely related to alterations of peripheral arteriolar resistance and venous return of blood to the heart.

Adrenalectomy↗
PubMed1978

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.

Animals↗
PubMed1978

The histopathology of experimental spinal cord trauma. The effect of systemic blood pressure.

The early sequential histopathological alterations following a concussive paraplegic injury to the posterior thoracic spinal cord in cats were studied. The lack of significant progression of hemorrhages over a 4-hour period after injury indicates that most hemorrhages probably occur within the first hour. The marked enhancement or retardation of hemorrhages in the post-injury period, when the blood pressure was increased or decreased, respectively, demonstrates the loss of autoregulation of spinal cord vasculature at the trauma site after a concussive paraplegic injury. Progressive edema formation was evident over a 4-hour period following injury, and it could be enhanced or retarded by elevation or reduction of the systemic blood pressure.

Animals↗
PubMed1978

Experimental spinal cord trauma, I: Correlation of blood flow, tissue oxygen and neurologic status in the dog.

Spinal cord blood flow and tissue oxygen were measured concurrently in a series of paraplegic dogs subjected to experimental spinal cord trauma. Injury to the spinal cord sufficient to cause clinical paraplegia is associated with a significant (P less than 0.01) decrease in blood flow in the central spinal cord from 15.2 to 6.1 ml/min/100gms at two to three hours following injury. Also, at two and three hours post-injury, paraplegic dogs demonstrate a significant (P less than 0.01) decrease in tissue oxygen levels from 35-39 mm Hg to 17-24 mm Hg. No significant changes occurred in systemic blood pressure or carotid blood flow. A delay often precedes the significant onset of blood flow and tissue oxygen alterations, which suggests that therapeutic efforts could be directed during this critical interval.

Animals↗
PubMed1978

Experimental spinal cord trauma, II: Blood flow, tissue oxygen, evoked potentials in both paretic and plegic monkeys.

Graded clinical motor deficits were produced in a series of Rhesus monkeys subjected to experimental spinal cord trauma from a variety of impact loads. An argon washout technique was used to measure spinal cord blood flow; tissue oxygen carbon dioxide, and somatosensory evoked potentials (SEPs) were also monitored. Each animal received a clinical grade and, after a week of study, the spinal cords were removed for histopathological grading. Blood flow in paraplegic animals was significantly decreased at two hours and seven days following injury (5 ml/min/100 gms tissue); paraparetic animals showed no significant difference from preinjury levels (14 ml/min/100 gms tissue). Animals which completely recovered demonstrated increased flow (27 ml/min/100 gms tissue). Composite tissue oxygen was generally depressed in paraplegic animals (28 mm Hg/kg) but showed no clear pattern in other groups. Only 8% of monkeys rendered paraplegic preserved a somatosensory evoked potential (SEP) at five minutes after injury. Paraparetic animals were more likely (40%) to show initial preservation of the SEP and in normal animals, the SEP always returned by three hours. Histopathological grading tended to parallel clinical grading in 92% of the cases. Although the extremes of possible postinjury deficits (complete paraplegia or recovery) can be predicted from a combination of these measurements, incomplete lesions (whether judged clinically or pathologically) present a more variable picture.

Animals↗
PubMed1976

Myelotomy for control of mass spasms in paraplegia.

A new myelotomy knife is described and a procedure, designed to sever certain reflex connections while preserving as many corticospinal connections as possible, is presented. Through intermittent dorsal midline incisions the gray matter lateral to the central canal is severed bilaterally under the microscope from L-1 to S-1. This procedure relieved mass spasms and hyperactive reflexes in 14 paraplegic or tetraplegic patients, but preserved postural reflexes and whatever voluntary motor power the patients had prior to myelotomy. Before myelotomy all patients were bedridden. Afterward nine patients were able to use a wheel chair and five were able to walk with the use of parallel bars or crutches.

Adult↗
PubMed1975

Dynamic changes of cerebrospinal fluid in upright and recumbent shunted experimental animals.

The effect of positional change on intracranial CSF pressure, valve flow rates and atrial pressures were studied in 40 experimental dogs. The flow rate with a 30 to 60 mm H2O Holter valve changed from the recumbent to the head-up position: during the first minute it increased 2 1/2 times and then progressively decreased to become stabilized 20-30 min later at a value slightly lower than the head-up value. At the same time pressure dropped rapidly to -23 mm H2O and then slowly, during 30 min to -120 mm H2O. In dogs without a shunt the pressure drop was initially similar to that of shunted dogs but recovered to almost the initial positive pressure in 30 min. The flow rate from a reservoir to the atrium through a shunt system when changing to the head-up position showed a siphon effect. Atrial pressure does not change with positioning. The findings were similar with cisternal-peritoneal shunts. Flow rate, therefore, increase in the head-up position. Negative intracranial CSF pressure was due to a siphon effect through the shunt system.

Animals↗