The vascular anatomy of the lumbrical muscles in the hand.

The lumbrical muscles are located in the midpalm, dorsal to the palmar aponeurosis. The main function of these muscles is an indirect contribution to interphalangeal joint extension by decreasing the flexor effect of the flexor digitorum profundus muscle. Due to their minor biomechanical functions and suitable constructions, these muscles have been preferred in reconstructive surgery as local transposition flaps or pedicled flaps. Despite the surgical and clinical importance, vascular anatomical studies of these muscles are not well represented in the current literature. This study was performed in the Department of Anatomy of the Faculty of Medicine of the Ege University. Thirty-four cadaver hands, injected with red-coloured latex were used, and we aimed to describe the morphometry and vascular anatomy of the lumbrical muscles. We measured the length and width of the muscles, after removing their epimisium, and the diameter and length of the arteries to the muscles. The outcomes of our study determined that the length and width of the lumbrical muscles were reduced significantly from radial towards ulnar sides. The lumbrical muscles were supplied from both their palmar and dorsal surfaces by both superficial and deep palmar arches and/or their branches. We also described the level of entry of the dominant arteries for each lumbrical muscle and measured the size of the vessels and muscles to guide some surgical approaches. This anatomical study could guide for some surgical approaches and reduce the deficiency about the vascular anatomical patterns of the lumbrical muscles in the literature.     

Evaluation of neointimal hyperplasia on tranilast-coated synthetic vascular grafts: an experimental study.

Tranilast is an antiallergic drug that interferes with proliferation and migration of vascular smooth muscle cell induced by platelet-derived growth factor (PDGF) and transforming growth factor-beta1 (TGF-beta1). We investigated the local effect of tranilast on neointimal hyperplasia using tranilast-coated prosthetic grafts. The inner sides of the thin-walled polytetrafluoroethylene (PTFE) grafts were coated with chitosan and tranilast containing chitosan solution. Wistar albino rats (32) were used in the study. Patches (1 x 2 mm) for vascular grafts were prepared. Three groups were tested: group 1 (n = 12; tranilast coated), group 2 (n = 10; adhesive-only film-layer-coated), and group 3 (n = 10; normal ePTFE patch grafts sutured to the carotid arteries of the rats). Recipient sites of the carotid arteries were excised 4 weeks after surgery. All sections were examined histologically for graft patency, thrombus formation, and neointimal thickness. Expression of PDGF, fibroblast growth factor, and TGF-beta1 on cross-sections of the neointima were evaluated by immunohistochemistry. No significant differences were found regarding mean neointimal thicknesses. PDGF and TGF-beta-1 expressions were significantly lower in group 1. Although a decrease in local effect of tranilast was observed for growth factor expressions at a drug concentration of 0.05 mg/cm(2), a significant reduction in neointimal hyperplasia was not achieved. The coating concentration of 0.05 mg/cm(2) may have been too low to produce an antiproliferative effect. Given our promising results, further studies are recommended and planned using different drug concentrations and time intervals.     

Apoptosis in perinatal hypoxic-ischaemic cerebral damage

Perinatal hypoxia-ischaemia induces a biphasic cerebral injury: the depletion in high energy phosphates during the insult returns to normal soon after resuscitation. However, some 8–15 h later a second phase of impaired energy metabolism begins, which is related to the severity of later neurodevelopmental impairment. Delayed injury differs from acute hypoxia-ischaemia because intracellular acidosis does not occur. Apoptosis may be a mechanism of delayed cellular injury. Apoptotic cells and typical DNA fragmentation have been found after perinatal hypoxia-ischaemia. In newborn piglets, fraction of apoptotic cells was directly related to the degree of high energy phosphate depletion during hypoxia-ischaemia. Apoptosis may be interrupted: in piglets, brain cooling for 12 h following resuscitation reduced the fraction of apoptotic but not necrotic cells. These results have implications for both the understanding of cerebral injury and the use of hypothermia as a neural rescue strategy in the developing brain.     

Neuroleptic malignant syndrome induced by ziprasidone on the second day of treatment.

Neuroleptic malignant syndrome (NMS) is the rarest and most serious of the neuroleptic-induced movement disorders. We describe a case of neuroleptic malignant syndrome (NMS) associated with the use of ziprasidone. Although conventional neuroleptics are more frequently associated with NMS, atypical antipsychotic drugs like ziprasidone may also be a cause. The patient is a 24-year-old male with a history of schizophrenia who developed signs and symptoms of NMS after 2 days of treatment with an 80-mg/day dose of orally administrated ziprasidone. This case is the earliest (second day of treatment) NMS due to ziprasidone reported in the literature.     

Effect of caffeic acid phenethyl ester on survival of axial pattern flaps in rats with ischaemia-reperfusion injuries.

Oxygen-derived free radicals have been implicated in the pathogenesis of tissue injury after ischaemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active ingredient of honeybee propolis, has been identified as having potent antioxidant and anti-inflammatory properties. We evaluated the ability of CAPE applied intraperitoneally in reducing tissue injury after ischaemia-reperfusion. To investigate whether treatment with CAPE modifies the concentrations of the endogenous indices of oxidant stress, we examined its effects on a model of flap ischaemia-reperfusion injury in rats. CAPE (10 micromol/kg) was given through the peritoneum before reperfusion. CAPE given intraperitoneally had an inhibitory effect on tissue injury after ischaemia-reperfusion comparable to that of a control group. The anti-inflammatory and antioxidant properties of CAPE may contribute to its suppression of tissue injury.     

Acute subdural hematoma: Outcome and outcome prediction

Patients with traumatic acute subdural hematoma were studied to determine the factors influencing outcome.Between January 1986 and August 1995, we collected 113 patients who underwent craniotomy for traumatic acute subdural hematoma. The relationship between initial clinical signs and the outcome 3 months after admission was studied retrospectively.Functional recovery was achieved in 38% of patients and the mortality was 60%. 91% of patients with a high Glasgow Coma Scale (GCS) score (9–15) and 23% of patients with a low GCS score (3–8) achieved functional recovery. All of 14 patients with a GCS score of 3 died. The mortality of patients with GCS scores of 4 and 5 was 95% to 75%, respectively. Patients over 61 years old had a mortality of 73% compared to 64% mortality for those aged 21–40 years. 97% of patients with bilateral unreactive pupil and 81% of patients with unilateral unreactive pupil died. The mortality rates of associated intracranial lesions were 91% in intracerebral hematoma, 87% in subarachnoid hemorrhage, 75% in contusion.Time from injury to surgical evacuation and type of surgical intervention did not affect mortality. Age and associated intracranial lesions were related to outcome. Severity of injury and pupillary response were the most important factors for predicting outcome.