No abstract

The distribution of sitting pressure and ability to respond with reactive hyperaemia were studied in a group of paraplegic and tetraplegic patients (n = 8) with spinal cord lesions and healthy controls (n = 10) using a pressure sensitive plate and laser Doppler perfusion imager. The results show that the mean sitting pressure of the patients was 9.9 N/cm2 (left) and 11.7 N/cm2 (right) compared with 3.5 N/cm2 (left) and 3.6 N/cm2 (right) in controls. The differences were significant on both the left (p < 0.01) and right (p < 0.05) sides. The maximum pressure in patients was 42.9 N/cm2 (left) and 48.7 N/cm2 (right), and in controls 12.0 N/cm2 (left) and 12.9 (right) (p < 0.01). Both groups showed a reduction in skin perfusion in the seat area during sitting compared with unloaded resting, and in the controls it was significantly increased (p < 0.001 on both sides) during the reactive hyperaemic phase immediately after sitting. Compared with the preload values, the patients showed a similar but slightly weaker picture significant on the right side (p < 0.05), but not on the left. The hyperaemia was not uniformly distributed, but occurred where the pressure was greater than 2 N/cm2. There was no correlation between the amount of reactive hyperaemia and absolute values of sitting pressures. We conclude that tetraplegic and paraplegic patients have significantly higher sitting pressures than normal controls, and that the hyperaemic response in the buttock region in the upright position after pressure load is slightly weaker in the patients, which could be of importance for the development of decubitus ulcers.

The vessel wall regeneration and the inflammatory response in the rabbit femoral artery and vein the first three months after microvascular end-to-end suture anastomosis was assessed histologically. The initial damage consisted of endothelial loss and partial necrosis of media and adventitia. The luminal surface was reendothelialized and the adventitial layer restored by 20 days, but the necrotized part of the media did not regenerate. Instead, the vessel wall diameter was maintained by an intimal hyperplastic response. At the anastomotic site a characteristic slight dilatation was persistent. Consequently, the vessel wall architecture was not restored to the preoperative state after microvascular anastomosis.

This study describes changes in a rat facial muscle innervated by the mandibular and buccal facial nerve branches 4 months after nerve injury and repair. The following groups were studied: (A) normal controls; (B) spontaneous reinnervation by collateral or terminal sprouting; (C) reinnervation after surgical repair of the mandibular branch; and (D) chronic denervation. The normal muscle contained 1200 exclusively fast fibers, mainly myosin heavy chain (MyHC) IIB fibers. In group B, fiber number and fiber type proportions were normal. In group C, fiber number was subnormal. Diameters and proportions of MyHC IIA and hybrid fibers were above normal. The proportion of MyHC IIB fibers was subnormal. Immediate and delayed repair gave similar results with respect to the parameters examined. Group D rats underwent severe atrophic and degenerative changes. Hybrid fibers prevailed. These data suggest that spontaneous regeneration of the rat facial nerve is superior to regeneration after surgical repair and that immediacy does not give better results than moderate delay with respect to surgical repair. Long delays are shown to be detrimental.

The combined loss of the Achilles tendon and the overlying soft tissue in the young ambulant patient with expectations of a normal life is a challenge. These patients need not only skin coverage but also dynamic, functioning repair. Two cases of major defects after tumour resection are presented. In each case the tendon was reconstructed using the remaining gastrocnemius aponeurosis reinforced with fascia lata. This was covered by a free tensor fascia lata (TFL) flap. In one of the cases the flap was transferred as a neurovascular free flap.