Studies of lesions of the primate cerebellum leave little doubt that the cerebellum is necessary for the execution of smooth and accurate movements. How the cerebellum fulfills this role at a neuronal level remains unknown. It is likely that the cerebellum exerts the same effect on a number of different efferent targets. In order to influence voluntary movement, a major output from the cerebellum projects to the motor cortex via the cerebello-thalamo-cortical (CTC) pathway. By examining neuronal activity in the cerebellar thalamus, and comparing this with activity recorded from its connections with the deep cerebellar nuclei and motor cortex, conclusions can be made regarding cerebellar function. Current data does not support a role for the CTC pathway in the initiation of movement or the control of trans-cortical reflexes. Also, the evidence does not support the hypothesis that the cerebellum prevents terminal movement oscillations by predictively sending a message to the antagonist muscle to brake the movement. The available literature supports the Eccles theory that during normal movement, the CTC pathway receives a form of efference copy from the motor cortex and compares this message with that derived from peripheral afferents about the actual progress of the movement. However, there is not a significant degree of kinematic information passing through this pathway in the course of a voluntary movement. Therefore the actual site of comparison or error-detection in this system awaits further elucidation.

Background: The opioid epidemic is a health crisis in the United States. Physicians contribute to this problem by overprescribing opioids. Ambulatory hand surgery (AHS) is common in the United States and associated with overprescribing of opioids. Education and guidance regarding the effectiveness of nonopioid compared with opioid interventions for pain management following ambulatory hand procedures are lacking. We assessed the current literature to suggest evidence-based protocols for postoperative analgesia. Methods: A systematic review was performed using PubMed, Web of Science, and Cochrane Library. Studies comparing nonopioid with opioid treatments for pain management following AHS were identified. Studies investigating opioid-sparing strategies after AHS were also identified. Evidence was examined to determine efficacy of nonopioid interventions and to provide recommendations for optimal nonopioid protocols and opioid-sparing strategies. Results: A total of 510 studies were identified in the search with 18 meeting inclusion criteria. High-level evidence demonstrated efficacy of nonopioid interventions for pain management following AHS (levels I and II evidence). Results provided evidence-based guidelines for recommendations of nonopioid treatment protocols and opioid-sparing strategies (levels I and II evidence). Conclusions: Our review demonstrated nonopioid interventions are adequate in multiple aspects of pain management compared with opioid treatments. Recommendations were established for two nonopioid treatment protocols, and for an opioid-sparing intervention (levels I and II evidence). The evidence provided in this review should be strongly considered for pain management guidance following AHS and provides a means to decrease opioid overprescribing in the United States.

The case is reported of a 46-year-old woman with congenital right ventricular hypoplasia, severe tricuspid stenosis, pulmonary hypoplasia, and an intact ventricular septum. This cardiac malformation is extremely rare in adults. Pulmonary circulation was augmented by bronchial collaterals.The recently designated 'hypoplastic right heart complex' (Khoury et al., I969), consisting of various degrees of right ventricular hypoplasia, congenital tricuspid stenosis, and pulmonary stenosis, is extremely rare beyond childhood (Sackner et al., I96I; Williams, and Lowe, I963). This report is of a woman who survived 46 years with this complex. Case reportThe patient had been cyanotic since birth. She was first evaluated at Duke University Medical Center when she was 20 years old at which time her heart was slightly enlarged but no murmurs were heard. At the age of 24 she developed pelvic thrombophlebitis which resulted in paradoxical emboli and an acute diaphragmatic myocardial infarction. Shortly thereafter she began to have occasional chest pain, but she did not require cardiac medication.Deterioration of cardiac function, in fact, did not begin until six months before death when the chest pain became more frequent and signs of congestive heart failure appeared. A phonocardiogram one month before death disclosed an apical systolic murmur, a widely split second heart sound which moved slightly with respiration, and an early pulmonary ejection murmur.Three weeks later the patient was admitted to hospital with congestive heart failure. Her Radiological examination of the heart showed left ventricular and biatrial enlargement. The pulmonary vasculature was diminished. There was evidence, however, of prominent bronchial circulation.Cardiac catheterization revealed bidirectional shunting across a large atrial septal defect. Mean pressures in the right and left atria were 20 and 2 I mm. Hg, respectively, with a left ventricular pressure of II5/4-22 mm. Hg. The catheter could not be passed through the tricuspid valve. Oxygen Angiocardiography showed sequential opacification of the right atrium, left atrium, left ventricle, and the aorta. The right ventricle and a small pulmonary artery could be detected only on the last films of left ventriculography.After injection of the contrast material the patient suddenly became unresponsive and more cyanotic. Three days later she died in ventricular fibrillation.Necropsy findings The heart weighed 480 g. The great vessels arose normally, but the pulmonary artery was small and the aorta was dilated. An atrial septal defect, 2 cm. in diameter, was present. The ring of the tricuspid valve was hypoplastic, 6-9 cm. in circumference (Fig.). The valvular cusps had apparently never separated, so that a single circumferential leaf was present, leaving a stenotic orifice I cm. in diameter. The right ventricle was small. Though the pulmonary valve was hypoplastic with a ring circumference of 4.1 cm., the valve leaflets appeared normal

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