The purpose of the study was to determine anatomical variations at the suprascapular notch for better understanding of possible predisposing factors for suprascapular nerve entrapment. We dissected 32 shoulders of 16 cadavers between the ages of 39 and 74 years. We observed abnormally oriented superior fibers of the subscapularis muscle in five shoulders of the 16 cadavers, which were covering the entire anterior surface of the suprascapular notch and significantly reducing the available space for the suprascapular nerve. We also detected anterior coracoscapular ligament in six of the 32 shoulders, and calcified superior transverse scapular ligament in four of the shoulders. In this study, we classified the variations for the superior transverse scapular ligament. In conclusion, knowing the anatomical variations in detail along the course of the suprascapular nerve might be important for better understanding of location and source of the entrapment syndrome, especially for individuals who are involved in violent overhead sports activities such as volleyball and baseball. To our knowledge, close relationship of subscapularis muscle with the suprascapular nerve as a possible risk factor for suprascapular nerve entrapment has not been mentioned previously.

Parkinson's disease (PD) is associated with increased excitatory activity within the subthalamic nucleus (STN). We sought to inhibit STN output in hemiparkinsonian macaques by transfection with adeno-associated virus (AAV) containing the gene for glutamic acid decarboxylase (GAD). In total, 13 macaques were rendered hemiparkinsonian by right intracarotid 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine injection. Seven animals were injected with AAV-GAD into the right STN, and six received an AAV gene for green fluorescent protein (GFP). Videotaped motor ratings were performed in a masked fashion on a weekly basis over a 55-week period. At 56 weeks, the animals were scanned with (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET). Histological examination was performed at the end of the study. No adverse events were observed after STN gene therapy. We found that the clinical rating scores for the two treatment groups had different patterns of change over time (group x time interaction, P<0.001). On FDG PET, the GAD animals exhibited an increase in glucose utilization in the right motor cortex relative to GFP controls (P<0.001). Metabolism in this region correlated with clinical ratings at end point (P<0.01). Histology confirmed GAD expression in treated animals. These findings suggest that STN AAV-GAD is well tolerated and potentially effective in a primate model of PD. The changes in motor cortical glucose utilization observed after gene therapy are consistent with the modulation of metabolic brain networks associated with this disorder.

Previous nonhuman primate stroke models have employed temporary occlusion of arteries, had limited behavioral testing and imaging, and focused on the short-term outcome. Our goals were 1. to develop a stable model of chronic stroke in the nonhuman primate, 2. to study in vivo the long-term biochemical changes in the area adjacent to the infarct, using proton magnetic resonance spectroscopy (H MRS), and 3. evaluate these changes in relation to the histopathological effects of stroke. Four adult cynomologous monkeys had an occlusion of the M1 segment of the right MCA. Behavioral tests included a clinical rating scale, motor planning task, fine motor task, and activity monitoring. Eight months afterwards, MRI and 1H MRS were performed. Following the imaging studies the monkeys were perfused transcardially, their brains extracted and processed. Nissl staining and immunohistochemistry for neuronal markers (NeuN) were performed and used to measure the lesion volume and neuronal optical density (OD). All animals developed a left hemiparesis and were unable to perform a fine motor task with the left hand. There was a significant (31%) decline in the motor planning ability with the nonparetic extremity. Monkeys displayed a stooped posture, episodes of rotation to the side of the lesion, partial left hemianopsia, and transient changes in activity. The clinical signs improved over the first 6-8 weeks but the deficits remained stable for the remaining six months of follow up. MRI demonstrated a subcortical and cortical infarction in the right MCA distribution. 1H MRS data detected a significant decrease in the N-acetyl-aspartate (NAA)/creatine (Cr) ratio in the area adjacent to the infarction (VOl-St) compared to a mirror area in the contralateral hemisphere (VOl-Co). Histopathological measurements revealed a significant decline in neuronal cross-sectional area and neuronal optical density in the region of the VOl-St. We established a stable and reproducible model of chronic stroke in the MCA distribution, in the macaque monkey. Our data indicate that NAA detected by 1H MRS can be used to measure neuronal loss in vivo and help target this area for intervention. Our model may be particularly suitable for studies testing the effects of therapeutic strategies involving neural or stem cell transplantation, trophic factors or gene therapy.

Temporoparietal fascia constitutes a very important structural unit from both an aesthetic and a reconstructive surgical point of view. A histologically supported anatomic study was conducted for the reappraisal of the anatomic relationships and clinical application potentials of the data obtained. Anatomy of the temporoparietal fascia was investigated on 20 sides from 10 cadavers. After dissections, necropsies were obtained to demonstrate histologic features of the temporoparietal fascia. The outer part of the temporoparietal fascia is continuous with the superficial musculoaponeurotic system (SMAS) in the inferior border and with orbicularis oculi and frontalis muscles in the anterior border. Therefore, plication of the temporoparietal fascia can increase tightness of the SMAS, orbicularis oculi, and frontalis muscle in rhytidectomy. The frontal branches of facial nerve were noted to course parallel to the frontal branch of the superficial temporal artery, lying deeper to the temporoparietal fascia within the innominate fascia. In the view of these findings, conventional subfascial dissection, which is performed to protect frontal branches of the facial nerve, is not reasonable during the temporal part of rhytidectomy. Careful subcutaneous dissection just under the hair follicles is more appropriate to avoid nerve injury and also provides excellent exposure of the temporoparietal fascia for plication in rhytidectomy with protection of the auriculotemporal nerve and the superficial temporal vessels. Furthermore, two layered structures of the temporoparietal fascia are very suitable to insert a framework into the temporoparietal fascia for ear reconstruction to eliminate some of the shortcomings of Brent's technique. A thin muscle layer was also noted within the outer part of the temporoparietal fascia below the temporal line; the term "temporoparietal myofascial flap" would, therefore, be more accurate than "temporoparietal fascial flap." Finally, the innominate fascia and the deep temporal fascia can be elevated with the two layers of the temporoparietal myofascial flap to obtain a well-vascularized, four-layered myofascial flap based on the superficial temporal vessels. This multilayered flap can be used to reconstruct all defects when fine, pliable, thin, multilayered flaps are required.