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Loss of somatosensory evoked potentials during intramedullary spinal cord surgery predicts postoperative neurologic deficits in motor function [corrected].

STUDY OBJECTIVES: To estimate the sensitivity and specificity of somatosensory evoked potentials (SSEPs) for predicting new postoperative motor neurologic deficits during intramedullary spinal cord surgery; to establish whether SSEPs more accurately predicted postoperative deficits in position and vibration sense than in strength. DESIGN: Prospective open and retrospective study. SETTING: University-affiliated hospital. PATIENTS: 20 patients with intramedullary spinal cord tumors scheduled for surgery with intraoperative SSEPs. INTERVENTIONS: Median, ulnar, and tibial nerve cortical and subcortical SSEPs were recorded continuously. MEASUREMENTS AND MAIN RESULTS: Conventional intraoperative SSEP criteria considered indicative of neurologic injury were modified and defined as either the complete and permanent loss of the SSEP or the simultaneous amplitude reduction of 50% or greater in the nearest recording electrode rostral to the surgical site and 0.5 millisecond increase in the central latency. Our definition required confirmation of both amplitude and latency changes on a repeated average. All patients had 1 or more SSEPs, which were reproducible and sufficiently stable for analysis throughout the operation. Six patients developed new postoperative neurologic deficits. One had new motor deficits in an extremity from which no baseline SSEPs could be elicited. In each of the other 5 patients, significant SSEP changes preceded the postoperative motor deficits in the extremity or extremities monitored. In no patient without a new postoperative motor deficit was there a significant change in the SSEP. In only 2 of these 5 patients was there a documented postoperative loss or diminution in vibration or position sense. CONCLUSIONS: Intraoperative SSEP changes during intramedullary spinal cord surgery are a sensitive predictor of new postoperative motor deficits, but such changes may not correlate reliably with postoperative deficits in position or vibration sense. In this setting SSEP monitoring serves primarily to reassure the operating team that, when the SSEPs remain constant, the surgery has not caused additional injury.

Adult↗

Brain stem mechanism in ocular motor function.

The progress of clinical and experimental neuro-ophthalmology during the last two decades was reviewed. The ocular motor system in the brain stem was described firstly based on anatomical, neurophysiological and clinical evidences. Clinical syndromes in cerebrovascular brain stem impairments which present ocular motor dysfunction were analyzed briefly.

Animals↗

[Motor function of the stomach and small intestine and gastric secretory activity in smokers and alcoholic patients with duodenal ulcer].

The dependence of the parameters of the electromyogastroenterogram, basal and maximal histamine secretion of HCl and pepsin on alcohol consumption and smoking (separately and in combination) was studied in 248 duodenal ulcer patients. The amplitude parameters of the digestive motor gastric and small intestinal function, HCl secretion in the basal period and in response to maximal histamine stimulation were found to be significantly increased in habitual alcoholics and smokers, while the level of the basal and stimulated pepsin secretion in smokers was also increased. In addition, in 15 males without ulcer a single intake of large doses of alcoholic drinks containing more than 200 g of ethanol caused significant increase in the amplitude parameters of the electromyogastroenterogram which normalized in 48 hours. Since alcohol and smoking significantly enhance hypermotor gastroenteral dyskinesis and gastric hypersecretion in duodenal ulcer patients, prophylaxis and treatment should be aimed at the removal of these factors.

Adolescent↗

The effects of unilateral removal of the cerebellar hemispheres on motor functions and weight gain in rats.

Left or right unilateral removal of a cerebellar hemisphere resulted in a high mortality rate caused by anorexia, not previously seen in cerebellectomized animals. The reduced post-surgical gain in body weight may be explained by oropharyngeal dyspraxia or a loss in appetite. However, the growth rate of the surviving animals was similar to that of controls. After unilateral damage of the cerebellum, deficits were observed in motor coordination tasks, such as the rotorod, the hole-board, and the stationary beam, and the left hemisphere group fell from a suspended wire sooner than controls. The motor deficits were more pronounced after left as opposed to right cerebellar damage on the rotorod, implying a certain degree of functional lateralization for this test.

Animals↗

Analysis of kinesin motor function at budding yeast kinetochores.

Accurate chromosome segregation during mitosis requires biorientation of sister chromatids on the microtubules (MT) of the mitotic spindle. Chromosome-MT binding is mediated by kinetochores, which are multiprotein structures that assemble on centromeric (CEN) DNA. The simple CENs of budding yeast are among the best understood, but the roles of kinesin motor proteins at yeast kinetochores have yet to be determined, despite evidence of their importance in higher eukaryotes. We show that all four nuclear kinesins in Saccharomyces cerevisiae localize to kinetochores and function in three distinct processes. Kip1p and Cin8p, which are kinesin-5/BimC family members, cluster kinetochores into their characteristic bilobed metaphase configuration. Kip3p, a kinesin-8,-13/KinI kinesin, synchronizes poleward kinetochore movement during anaphase A. The kinesin-14 motor Kar3p appears to function at the subset of kinetochores that become detached from spindle MTs. These data demonstrate roles for structurally diverse motors in the complex processes of chromosome segregation and reveal important similarities and intriguing differences between higher and lower eukaryotes.

Chromosome Segregation↗

How can corticospinal tract neurons contribute to ipsilateral movements? A question with implications for recovery of motor functions.

In this review, the authors discuss some recent findings that bear on the issue of recovery of function after corticospinal tract lesions. Conventionally the corticospinal tract is considered to be a crossed pathway, in keeping with the clinical findings that damage to one hemisphere, for example, in stroke, leads to a contralateral paresis and, if the lesion is large, a paralysis. However, there has been great interest in the possibility of compensatory recovery of function using the undamaged hemisphere. There are several substrates for this including ipsilaterally descending corticospinal fibers and bilaterally operating neuronal networks. Recent studies provide important evidence bearing on both of these issues. In particular, they reveal networks of neurons interconnecting two sides of the gray matter at both brainstem and spinal levels, as well as intrahemispheric transcallosal connections. These may form "detour circuits" for recovery of function, and here the authors will consider some possibilities for exploiting these networks for motor control, even though their analysis is still at an early stage.

Animals↗

Magnetic stimulation: examination of motor function in patients with cervical spine or cord lesion.

In 20 patients with cervical spine or cord lesions, we examined motor evoked potentials (MEPs) by transcranially applied magnetic stimulation to the motor cortex. We used a large-diameter (12 cm) coil to induce equal current in both left and right hemispheres. The MEPs were recorded simultaneously from multiple muscles covering the C5 to C8 myotome distribution bilaterally. The MEP abnormalities correlated well with clinical muscle weakness in 15 patients. In two patients, MEP revealed abnormalities in muscles of normal strength. Three patients with sensory but without motor deficit had normal MEPs. We conclude that magnetic stimulation is a useful adjunct in confirming and objectifying motor weakness, and in localizing the level of dysfunction in cervical spine lesions.

Adult↗

Esophageal motor function in primary Sjögren's syndrome: correlation with dysphagia and xerostomia.

The incidence of dysphagia in patients with primary Sjogren's syndrome (pSS) has been underestimated and all too often ascribed to xerostomia, without considering the possible presence of esophageal motor abnormalities affecting other nonscleroderma connective tissue diseases. Esophageal and salivary functions were prospectively evaluated in 27 females who met the four criteria proposed by Fox for the diagnosis of pSS, using esophageal manometry after wet swallows and Saxon's test, respectively. Dysphagia was graded using a standard symptoms questionnaire and results were compared with those obtained in a group of 21 healthy controls. Seven patients with pSS (26%) had no swallowing discomfort, 2 (7.4%) had mild dysphagia, 7 (26%) had moderate dysphagia, and 11 (40.6%) had severe dysphagia. Saxon's test revealed an overall decrease in the salivary flow rate compared to controls, with no difference between patients with or without dysphagia. Esophageal manometry demonstrated the absence of any lower or upper esophageal sphincter function abnormalities in all patients. In the patients with pSS as a whole, manometric study of the esophageal body showed a motor pattern comparable with that of controls, with no difference between patients with and without dysphagia. Defective peristalsis, ie, the presence of simultaneous contractions in more than 30% of wet swallows was detected, however, in the distal tract of the esophagus of six patients (22.2%) and in the proximal tract of three (11.1%). All these patients had severe dysphagia and the modified Saxon's test revealed a salivary secretion comparable with that of patients with a normal peristalsis. Dysphagia is a very common complaint in patients with pSS and does not seem to correlate with xerostomia, which is a constant and typical finding of the disease. About one third of patients with pSS have an abnormal esophageal peristalsis that is responsible for severe dysphagia, whereas decreased salivary outflow exacerbates the swallowing discomfort. This has to be taken into account and justifies the routine use of esophageal manometry in patients with pSS. The cause of dysphagia in pSS patients without peristaltic disorders of the esophagus has to be investigated.

Adult↗

Median nerve somatosensory evoked potentials and upper limb motor function in hemiparesis.

The purpose of this study is to describe the relationship between median nerve somatosensory evoked potential (SEP) parameters and clinical measures of motor impairment and physical disability in the affected upper limb of patients with hemiparesis. SEP assessments were carried out in 28 long-term survivors of stroke. Stroke survivors with preserved SEPs over the affected hemisphere exhibited significantly lower motor impairment and physical disability than those with absent waveforms. Among those with preserved waveforms, SEP amplitude exhibited a weak correlation with degree of upper limb motor impairment. The correlation between SEP amplitude and physical disability was not statistically significant. Contrary to prior reports, median nerve SEP appears to have a weak correlational relationship with clinical measures of upper limb function in hemiparesis.

Adult↗

Recovery of motor functions following hemiparetic stroke: a clinical and magnetic resonance-morphometric study.

Predictors for the degree of clinical recovery after stroke are still poorly defined. In this study we tried to assess the predictive value of clinical data and of lesion size for motor recovery after ischemic stroke. In 52 hemiparetic patients we monitored the course of clinical recovery by a dedicated score of sensorimotor hand function after their first stroke. The course of the lesion size was measured in proton density magnetic resonance images. Three groups of patients were identified. Patients with moderate initial motor deficit recovered almost completely within 9 days (17/17, group 1). From the patients with severe initial motor deficit, about equal numbers recovered (16/35, group 2) or remained severely impaired during the entire observation period of more than 6 months (19/35, group 3). There was no correlation between changes of lesion size and motor deficit. Logistic regression of probability of good clinical outcome on initial lesion size, initial motor score and subcortical versus cortical location of lesion showed that only the initial motor score was predictive (p = 0.006). A relative improvement of the initial motor score of about 20% in the first 4 weeks after stroke appeared to be a relevant cut point for good outcome. The data indicate that patients with mild initial motor deficits recover well, whereas severely affected patients may differ in outcome. Since lesion size was not correlated with outcome the amount of spared residual function appeared as major determinant for the capacity for motor recovery.

Activities of Daily Living↗

Mice with the deleted neurofilament of low molecular weight (Nefl) gene: 2. Effects on motor functions and spatial orientation.

Mice with a null mutation of the Nefl gene were compared with normal controls in tests of motor activity, equilibrium, and spatial orientation. Despite a normal capacity to ambulate, NFL -/- mice had fewer rears in an open field, crossed fewer segments on stationary beams, and fell more frequently when suspended on a horizontal bar. In addition, the distance swum before reaching the escape platform was greater in NFL -/- mice than in controls during acquisition of place learning in the Morris water maze at the start of training. The motor impairments were linearly correlated with increased cytochrome oxidase activity seen in cerebellum and brainstem. These results indicate that, as early as 6 months, depletion of the NFL protein is sufficient to cause mild sensorimotor dysfunctions and spatial deficits, but without overt signs of paresis.

Amyotrophic Lateral Sclerosis↗

Epidural cortical stimulation enhances motor function after sensorimotor cortical infarcts in rats.

This study examined whether epidurally delivered cortical electrical stimulation (CS) improves the efficacy of motor rehabilitative training and alters neuronal density and/or cell proliferation in perilesion cortex following ischemic sensorimotor cortex (SMC) lesions. Adult rats were pre-trained on a skilled reaching task and then received partial unilateral SMC lesions and implantation of electrodes over the remaining SMC. Ten to fourteen days later, rats received daily reach training concurrent with anodal or cathodal 100 Hz CS or no stimulation (NoCS) for 18 days. To label newly generated cells, bromodeoxyuridine (BrdU; 50 mg/kg) was administered every third day of training. Both anodal and cathodal CS robustly enhanced reaching performance compared to NoCS controls. Neuronal density in the perilesion cortex was significantly increased in the cathodal CS group compared to the NoCS group. There were no significant group differences in BrdU-labeled cell density in ipsilesional cortex. Staining with Fluoro-Jade-B indicated that neurons continue to degenerate near the infarct at the time when cortical stimulation and rehabilitation were initiated. These data indicate that epidurally delivered CS greatly improves the efficacy of rehabilitative reach training following SMC damage and raise the possibility that cathodal CS may influence neuronal survival in perilesion cortex.

Analysis of Variance↗