Motoneuron survival after neonatal peroneal nerve injury in the rat-evidence for the sparing effect of reciprocal inhibition.

Sciatic nerve crush at birth results in the death of most of the motoneurons in the sciatic motor pool. It has been proposed that these cells die through excessive activation which can be explained partly by an increased susceptibility to NMDA. However, it is also possible that decreased inhibitory mechanisms resulting from nerve injury may contribute to overactivation of the motoneurons. In this study we compared the survival of motoneurons innervating two muscles in the peroneal motor pool, tibialis anterior and extensor digitorum longus, after either sciatic or common peroneal nerve crush. These two procedures both axotomize the motoneurons but differ in their effects on afferent input. Sciatic nerve crush severely reduces the afferent input from the antagonist muscles innervated via the tibial nerve, whereas common peroneal nerve crush preserves them. Using retrograde labeling with horseradish peroxidase, we found that almost twice as many motoneurons survived common peroneal nerve crush than sciatic nerve crush and that muscle weight showed a corresponding significant improvement. A control experiment excluded the possible involvement of increased stretch of the muscles as a result of common peroneal nerve crush alone as an explanation for the improvement. We therefore suggest that the increased survival of motoneurons after peroneal nerve crush was due to the preservation of their reciprocal inhibitory input. However, since even with this improvement the majority of motoneurons still died, loss of reciprocal inhibition probably does not play a major role in the death of motoneurons induced by overactivation.

Magnesium ions reduce motoneuron death following nerve injury or exposure to N-methyl-D-aspartate in the developing rat.

Developing motoneurons can be induced to die by target deprivation and there is evidence that this cell death involves the excitotoxic effects of N-methyl-D-aspartate. Treatment with dizocilpine maleate, an antagonist of this receptor, has been shown to rescue a proportion of those motoneurons destined to die following nerve injury at birth. However, this is a relatively toxic compound. In this study we examined whether systemic treatment with magnesium sulphate, a non-competitive antagonist of the N-methyl-D-aspartate receptor which is better tolerated than dizocilpine maleate, could prevent motoneuron death. Motoneurons were induced to die either by sciatic nerve injury at birth or by nerve injury at five days followed by exposure to N-methyl-D-aspartate. The number of surviving motoneurons reinnervating the tibialis anterior and extensor digitorum longus muscles were counted using retrograde labelling. Following nerve injury at birth and treatment with magnesium sulphate, there was a small increase in the survival of injured motoneurons, although this improvement was not significant. Nerve injury at five days does not result in motoneuron death, but when followed by treatment with N-methyl-D-aspartate, only 42 +/- 2.9% of motoneurons to these flexor muscles survived. Treatment with magnesium sulphate prior to injection of N-methyl-D-aspartate significantly increased motoneuron survival, so that 67 +/- 5.8% of motoneurons survived. Thus, systemic treatment with magnesium can prevent the death of motoneurons rendered susceptible to the excitotoxic effects of N-methyl-D-aspartate by nerve injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal aortic and multiple iliac aneurysms associated with crossed-fused ectopia of the kidney: a case report and review.

We report the first case of an infrarenal abdominal aortic aneurysm associated with crossed-fused ectopia of the kidney. This is the second most common fusion defect of the kidney with an incidence in the general population of 1 in 1000. The different types of crossed renal ectopia with and without fusion are described. The renal artery anomalies associated with crossed renal ectopia are emphasized. Abdominal ultrasonography or CT scanning must be used to uncover renal anomalies before surgery so that a selective preoperative aortogram can be obtained to determine the location of the arterial supply to the kidneys.

The high-risk angina patient. Identification by clinical features, hospital course, electrocardiography and technetium-99m stannous pyrophosphate scintigraphy.

We evaluated 193 consecutive unstable angina patients by clinical features, hospital course and electrocardiography. All patients were managed medically. Of the 193 patients, 150 (78%) had a technetium-99m pyrophosphate (Tc-PYP) myocardial scintigram after hospitalization. Of these, 49 (33%) had positive scintigrams. At a follow-up of 24.9 +/- 10.8 months after hospitalization, 16 of 49 patients (33%) with positive scintigrams died from cardiac causes, compared with six of 101 patients (6%) with negative scintigrams (p less than 0.001). Of 49 patients with positive scintigrams, 11 (22%) had had nonfatal myocardial infarction at follow-up, compared with seven of 101 patients (7%) with negative scintigrams (p less than 0.01). Age, duration of clinical coronary artery disease, continuing angina during hospitalization, ischemic ECG, cardiomegaly and a history of heart failure also correlated with cardiac death at follow-up. Ischemic ECG and a history of angina with a crescendo pattern also correlated with nonfatal infarction at follow-up. Patients with continuing angina, an ischemic ECG and a positive scintigram constituted a high-risk unstable angina subgroup with a survival rate of 58% at 6 months, 47% at 12 months and 42% at 24 and 36 months. We conclude that the assessment of clinical features, hospital course, ECG and Tc-PYP scintigraphy may be useful in identifying high-risk unstable angina patients.

Technetium-99m stannous pyrophosphate myocardial scintigrams in pericardial disease.

Technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial scintigrams were obtained in 35 acute pericarditis and in three chronic constrictive pericarditis patients. Thirteen of 35 acute pericarditis patients (37%) and one of three chronic constrictive pericarditis patients (33%) had abnormal scintigrams (a diffuse pattern in eight patients and a regional pattern in six patients). Of the 17 acute pericarditis patients with classic ST-segment changes of acute pericarditis, 10 (56%) had abnormal scintigrams compared to three of 17 patients (18%) without these ECG changes (P less than 0.02). These data indicate that pericardial disease may cause an abnormal scintigram. Therefore, one must rule out pericardial disease before concluding that a positive scintigram is due to acute myocardial infarction.