Abnormal sensorimotor integration is related to disease severity in Parkinson's disease: a TMS study.

Hyperexcitability of the motor system has been reported in Parkinson's disease (PD). We evaluate how cutaneous afferents modulate motor excitability in PD patients and whether abnormal modulation is correlated to parkinsonian symptoms. Digital stimulation causes abnormal enhancement of motor responses in patients. This effect may be one of the features of motor hyperexcitability in PD. Cutaneomotor hyperexcitability correlates with clinical scores, suggesting that abnormal processing of cutaneous inputs might contribute to the pathogenesis of parkinsonian symptoms.     

Prediction of Remission of Acute Posttraumatic Stress Disorder in Motor Vehicle Accident Victims

One hundred forty five individuals who sought medical attention as a result of a motor vehicle accident (MVA), and who were initially assessed 1 to 4 months post-MVA, were followed up prospectively for 6 months to determine how many of the 55 with posttraumatic stress disorder (PTSD) and the 43 with sub-syndromal PTSD would remit and what variables would predict remission. Thirty (55%) of those with initial PTSD had remitted at least in part by 6 months while 67% of those with sub-syndromal PTSD had remitted (and 5% had worsened). Four variables, including severity of initial symptoms, degree of initial physical injury, relative degree of physical recovery by 4 months and whether a close family member suffered a trauma during the follow-up interval, combined to classify 6-month clinical status of 84% of those with initial PTSD secondary to MVAs.     

Stability of the Defibrillation Probability Curve with the Development of Ventricular Dysfunction in the Canine Rapid Paced Model

Most patients with implantable defibrillators have diminished cardiac function. Progressive heart failure might impair defibrillation efficacy, leading to interpreted device, failure. This study sought to determine the effect of ventricular dysfunction on defibrillation energy using a biphasic endocardial system. Eleven dogs were ventricularly paced at 225 pulses/min for 2 weeks to induce ventricular dysfunction, and five control dogs remained unpaced. Dose response defibrillation probability curves were generated for each animal at baseline, after 2 weeks (at which time the pacemakers were turned off in the paced group), and then 1 week later. The defibrillation thresholds, ED₂₀, ED₅₀, and ED₈₀ (the 20%, 50%, and 80% effective defibrillation energies, respectively) were determined for each dog at each study. In the paced dogs, the mean ejection fraction fell from 55% to 25% after pacing (P < 0.0001), and rose to 46% after its discontinuation (P = 0.0002). The defibrillation threshold, ED20, ED₅₀, and ED80 remained unchanged in both the control and paced groups for all three studies, even after adjustment for dog weight or left ventricular mass. Rapid pacing produced no change in left ventricular mass. It induced ventricular cavity dilatation and wall thinning, which had opposing effects on defibrillation energy requirements, resulting in no net change of the ED₅₀ in heart failure. In conclusion, the defibrillation efficacy of a biphasic transvenous system is not changed by the development of heart failure using the rapid paced canine model.     

Topography of cholinergic afferents from the nucleus basalis of meynert to representational areas of sensorimotor cortices in the rat

We investigated (1) the topography of projection neurons in the nucleus basalis of Meynert (NBM) with efferents to restricted regions of the primary somatosensory (SI), the second somatosensory (SII), and the primary motor (MI) cortices in the rat; (2) the percentage of these NBM projection neurons that were cholinergic; and (3) the collateralization, if any, of single NBM neurons to different subdivisions within SI, to homotopic areas of SI and SII, and to homotopic areas of SI and MI. Retrograde single-and double-labeling techniques were used to study NBM projections to electrophysiologically identified subdivisions of SI and to homotopic representational areas of SI and SII, and of SI and MI. Choline acetyltransferase immunocytochemistry was done to identify cholinergic NBM neurons. Of the retrogradely labeled NBM neurons that projected to selective subdivisions of SI, SII, and MI, 89%, 87%, and 88%, respectively, were cholinergic. We found a rostral-to-caudal progression of retrogradely labeled NBM neurons following a medial-to-lateral sequence of injections into subdivisions of SI. Overlapping groups of single-labeled NBM neurons were observed after injections of different tracers into adjacent subdivisions within SI or homotopic areas of SI and SII, and of SI and MI. We conclude that NBM innervation to SI, SII, and MI is mostly cholinergic in the rat, that each cortical area receives cholinergic afferents from neurons widely distributed within the NBM, and that each NBM neuron projects to a restricted cortical area without significant collateralization to adjacent subdivisions within SI or to homotopic areas of SI and SII, or SI and MI. © 1993 Wiley-Liss, Inc.     

刺激视上核对大鼠痛阈及电针镇痛的影响

以钾离子透引起的大鼠甩尾反应为痛指标，观察了电和化学刺激视上核（ＳＯＮ）对大鼠痛阈（ＰＴ）和电针（ＥＡ）镇痛的影响。电刺激ＳＯＮ后，ＰＴ明显高于假刺激组（Ｐ＜０．０５～０．００１），电刺激ＳＯＮ后电针足三里，镇痛效应明显提高，并有明显的量效关系。电刺激ＳＯＮ的近旁部位（０．５—１ｍｍ）对ＰＴ及电针镇痛无明显影响。ＳＯＮ内注射Ｌ－谷氨酸（Ｌ－Ｇｌｕ）后痛阈和电针镇痛效应都明显对照组，也有明显的量效关     

An inexpensive, self-assembly pressure algometer

We have developed a simple instrument for pressure algometry. It can be made easily using components found in most anaesthetic rooms. Ten students were able to make the device using written instructions. All the resulting algometers performed within 10% accuracy limits for values up to 4 kgcm⁻².     

Calcitonin gene-related peptide-like immunoreactivity, in botulinum toxin-paralysed rat muscles

Changes in calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) at the motor endplates of botulinum toxin-paralysed rat muscles were investigated using immunohistochemistry. One day following toxin injection, a dramatic increase in CGRP-LI was detected at the motor endplates and within preterminal axons of the soleus and gastrocnemius muscles. The upregulation of CGRP-LI persisted throughout the period during which muscle fibres were paralysed and new neuromuscular junctions were being formed by the growing sprouts. Decline of CGRP-LI at the motor endplates coincided with clinical recovery. Both up- and down-regulation of CGRP-LI took place earlier in the soleus than in the gastrocnemius muscle. Up-regulation of CGRP-LI was also detected in a subpopulation of motor axons in the sciatic nerves and in the spinal motor neurons innervating the paralysed muscles. These results indicate that levels of CGRP are regulated, at least partly, by changes in the target innervation. They also suggest an important role for CGRP in the regenerative processes following muscle paralysis.