Rosario A. Zappulla

Noncortical origins of the spinal motor evoked potential in rats.

&NA; Motor evoked potentials (MEPs) were recorded from the spinal cord, sciatic nerve, or both during transcortical electrical stimulation in the rat. Four peaks could be consistently identified in the spinal MEP. The latency and amplitude of the peaks varied differentially with intensity and polarity of stimulation. Conduction velocity for Peak 1 of the MEP was 43 m/sec. Bilateral sciatic nerve MEPs were present after unilateral cortical stimulation. The spinal MEP was elicited by stimulation of areas outside the motor cortex, and the response persisted during subcortical stimulation and after motor cortex ablation. We present evidence suggesting that components of the spinal MEP in rats arise from pathways outside the motor cortex.

Cerebral effects of low-flow cardiopulmonary bypass and hypothermic circulatory arrest

Although both hypothermic circulatory arrest (HCA) and low-flow cardiopulmonary bypass (CPB) are accepted techniques for the operative management of complex cardiovascular pathology, the potential for neurologic sequelae is still a concern. To assess the relative safety of these techniques, we compared cerebral hemodynamics and clinical outcome in two groups of puppies. Sixteen puppies underwent 45 minutes of either HCA or low-flow CPB (25 mL.kg-1.min-1) after cooling to 13 degrees C. Methodology included radioactive microsphere determination of cerebral blood flow; calculation of cerebral oxygen extraction (arteriovenous oxygen content difference) and consumption; measurement of glucose consumption, and determination of cerebrovascular resistance. Measurements were obtained at baseline (37 degrees C), 13 degrees C, and 30 degrees C and at 2, 4, and 8 hours after HCA or low-flow CPB. No neurologic deficits were observed in any of the survivors (15/16). In both groups, cerebral metabolic rate of oxygen was maintained at baseline or greater levels postoperatively. Cerebrovascular resistance rose slightly in the low-flow CPB group postoperatively in contrast to a marked elevation in the HCA group. During the period of high cerebrovascular resistance after HCA, cerebral metabolic rate of oxygen was maintained by increased oxygen extraction. After low-flow CPB, oxygen extraction was not significantly different from baseline, presumably because of less severe changes in cerebrovascular resistance. Glucose metabolism followed the same trends as oxygen metabolism in both groups. These data suggest that after HCA there is a vulnerable interval, lasting as late as 8 hours postoperatively, in which cerebrovascular resistance remains high and cerebral metabolism is maintained primarily by high oxygen and glucose extraction. Any additional stress during this interval (a decrease in arterial oxygen content or perfusion pressure) could result in cerebral injury.

Effects of selective spinal cord lesions on the spinal motor evoked potential (MEP) in the rat

The effects of selective spinal cord lesions on the motor evoked potential (MEP) in 21 rats were investigated. No significant change in peak amplitude was observed following lesions of the pyramidal tract. There was a significant decrease in peaks 1 and 2 with ventral funiculi lesions. All 4 peaks of the MEP were significantly reduced following lesions of the lateral funiculus. The most marked decrease in peak amplitude followed lateral funiculi lesions that involved the lateral grey of the spinal cord. In one animal where the lesion was confined to the grey matter in the cord there was a marked decrease in all peaks of the MEP. In 3 additional animals interruption of the descending tracts of the spinal cord via bilateral hemisections of the spinal cord failed to completely abolish the MEP. Increases in peak latency were also noted following spinal lesions. In some animals the increase in latency occurred in the absence of significant peak amplitude changes. The findings in this study refute the previously held position that the MEP in the rat arises from pyramidal tract activation. The role of the reticulospinal and propriospinal tracts in the generation and propagation of the MEP are discussed.

The effect of graded spinal cord injury on the extrapyramidal and pyramidal motor evoked potentials of the rat.

This study investigated the differential effects of graded spinal cord injury on the rat extrapyramidal motor evoked potential (exp-MEP) and pyramidal motor evoked potential (pyr-MEP) and the prognostic value of these effects in predicting postinjury motor performance in the rat model. In 20 rats subjected to graded spinal injury (10-100 g-cm), there was a differential injury threshold for ablation of exp-MEP and pyr-MEP. All peaks of the pyr-MEP were extinguished in the animals subjected to impact forces of 50 g-cm and above (n = 12). In contrast, the exp-MEP was completely abolished in only two animals at injuries of 80 g-cm or above. A residual exp-MEP response persisted in the remaining 18 animals. Motor performance was monitored in 16 additional animals for up to 1 week after spinal injury. The pyr-MEP was abolished in 100% of the rats subjected to a 50-g cm injury (n = 7), whereas the exp-MEP persisted up to the highest impact forces (80 g-cm). Hind leg paralysis was present in the five rats where the pyr-MEP was extinguished but with persistence of the exp-MEP. An 80% reduction in the amplitude of the pyr-MEP in four animals resulted in mild ataxia with motor improvement at the end of a week. An increase or a 70% loss in pyr-MEP peak amplitude resulted in no clinical motor deficits (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of spinal cord injury during simulated aneurysm repair in a chronic animal model

The pathogenesis of paraplegia after repair of thoracic aortic aneurysms is controversial. Using direct spinal cord evoked potential monitoring, critical intercostal arteries (CICA) were identified to evaluate the impact of backbleeding and ligation versus that of preservation during simulated aneurysm repair. Thirty pigs (40 kg) were randomly assigned to one of five groups. In groups 1 through 4, a thoracic segment containing CICA was cross-clamped for 60 minutes and distal aortic perfusion was provided by a centrifugal pump. In groups 1 and 2, the thoracic segment was vented, maintaining segment pressure at 0 mm Hg; CICA were ligated in group 1 and preserved in group 2. Thoracic segment was perfused at 70 mm Hg in groups 3 and 4; CICA were ligated in group 3 and preserved in group 4. Critical intercostal artery ligations were performed at the end of the cross-clamp period. In group 5 simple cross-clamping at the left subclavian artery was performed as a control. The combination of venting and ligation of CICA correlated with impaired neurologic outcome according to Tarlovs score (median, 1.5 in group 1 versus 3 in group 2; p = 0.015), indicated by a significant difference in median values of direct spinal cord evoked potential amplitude (expressed as a fraction of baseline values) at 120 minutes after cross-clamping (0.76 in group 1 versus 0.98 in group 2; p = 0.0082).(ABSTRACT TRUNCATED AT 250 WORDS)

Motor Evoked Potentials Elicited from Pyramidal Stimulation and Recorded from the Spinal Cord in the Rat

This study investigated the spinal evoked response to focal electrical stimulation of the sensorimotor cortex in 32 rats. The results demonstrate a long-latency response (beginning at 8 milliseconds) elicited by electrical stimulation, which is distinct from the short-latency motor evoked potential previously reported. The conduction velocity of this later response is similar to that reported for the pyramidal tract in the rat. Experiments confirm that the longer latency response depends upon the integrity of the pyramidal system. Focal stimulation outside the sensorimotor cortex failed to elicit a response. Experimental lesions of the pyramidal tract or ablating the sensorimotor cortex eliminated the spinal cord evoked response. The results demonstrate that focal stimulation of the sensorimotor cortex results in a spinal cord evoked response that represents activity within the pyramidal system. The utility of this response in the rat model for assessing experimental cord injury is discussed.

The protective effect of experimental subarachnoid haemorrhage on sodium dehydrocholate-induced blood-brain barrier disruption.

SummaryThe potential interactive effects between subarachnoid hemorrhage (SAH) and blood brain barrier (BBB) disruption were studied in a rat model. Experimental subarachnoid hemorrhage was produced in twenty rats (experimental group) by the intracisternal injection of blood. In ten additional rats (control group), saline was administered in place of blood. Analysis of mean blood pressure (MBP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) demonstrated an increase in ICP and MBP and a drop in CPP in all animals following intracisternal injection. Subsequent infusion of the left internal carotid artery with sodium dehydrocholate resulted in blood-brain barrier (BBB) disruption in both groups as evidenced by Evans blue staining of the infused cortex. The extent of BBB disruption was significantly greater in the control group than the experimental group.Analysis of the experimental group demonstrated that animals with the lowest pre-SAH MBP and the lowest CPP during the maximum blood pressure response to SAH demonstrated the greatest resistance to experimental BBB disruption.The possibility of ischemia as a contributing factor in BBB protection subsequent to SAH is discussed.

Isolated Central Nervous System Metastasis from Transitional Cell Carcinoma of the Bladder: Report of a Case and Review of the Literature

Although systemic metastases from transitional cell carcinoma of the bladder occur frequently, involvement of the central nervous system is uncommon. We describe a patient with an isolated cerebral metastasis who had previously undergone resection of a Grade III, Stage B2 carcinoma of the bladder. We have been able to find only one previous case report of a solitary intracerebral metastasis from transitional cell carcinoma of the bladder without evidence of primary recurrence or additional sites of spread. Central nervous system metastasis from bladder carcinoma must be considered in the differential diagnosis of solitary intracerebral lesions.

The Effects of Spinal Gray Activation by Strychnine on the Motor Evoked Potential in the Rat

Spinal motor evoked potentials were elicited by electrical stimulation of the motor cortex in 14 rats before and after the application of strychnine to the surface of the spinal cord. Strychnine applied to the high cervical cord resulted in the emergence of additional peaks at the site of application and in electrodes positioned distally on the middle and lower thoracic cord. The strychnine-induced peaks occurred earlier and were larger in amplitude (P less than 0.01) in the distal spinal cord. Strychnine applied to the lower thoracic cord resulted in similar peak generation in the lower thoracic cord and in the spinal cord proximal to the application of strychnine. These findings demonstrate that strychnine-induced motor evoked potential changes arise from spinal gray activity induced by efferent pathways activated during transcortical stimulation. The role of the propriospinal tract in mediating the distal effects of strychnine is discussed. In conclusion, the strychnine-induced peaks of the motor evoked potential may be used as a measure of spinal gray integrity in experimental spinal cord injury models.