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.     

Pattern electroretinography and visual evoked potentials in optic nerve diseases.

BACKGROUND: To evaluate transient pattern electroretinography (PERG) and pattern visual evoked potential (VEP) for the diagnosis, differential diagnosis and follow-up of optic nerve diseases. METHODS: Twenty-nine consecutive patients (14 female, 15 male) with the diagnosis of ischaemic optic neuropathy (n=14) and optic neuritis (n=15) were included in this study. Mean age of the patients with ischaemic optic neuropathy was 63.3+/-3.3 (60-78) years and the mean age of the patients with optic neuritis was 28.3+/-8.4 (19-43) years. In each patient ophthalmological examination and systemic evaluation were done and VEP and PERG were recorded. As a control group, VEP recordings of 35 healthy subjects were included. RESULTS: In the ischaemic optic neuropathy group (group 1), mean VEP amplitude (+/-SD) (1.96+/-0.95 microV) was found to be decreased significantly in the affected eyes in comparison to the control group and the unaffected eyes. The delay in latency (116.3+/-20.14 msec in the affected eyes compared with 101.31+/-6.19 msec in unaffected eyes) was statistically significant when compared with the healthy subjects. In the optic neuritis group (group 2), VEP amplitude was decreased (4.13+/-4.04 microV vs 6.97+/-3.35 microV and 6.97+/-4.43 microV) and latency was increased (122.59+/-20.09 msec vs 101.31+/-6.19 msec and 108.76+/-13.57 msec) in affected eyes significantly in comparison to the unaffected eyes and control group, respectively. Even though there were no significant differences for P50 latency and N95/P50 ratios between affected and unaffected eyes in both groups, N95 amplitude decreased significantly in the affected eyes of the ischaemic optic neuropathy patients and N95 latency was found to be decreased in optic neuritis patients. There was no correlation between VEP and PERG findings in both groups. CONCLUSION: VEP amplitude decreased significantly in ischaemic optic neuropathies while latency delay was more significant in patients with optic neuritis. PERG findings showed decreased N95 amplitude in ischemic optic neuropathy without associated latency changes.     

Evaluation of leukocyte arylsulphatase a, serum interleukin-6 and urinary heparan sulphate following tamoxifen therapy in breast cancer.

Leukocyte arylsulphatase A (AS-A) was shown to be significantly high in newly-diagnosed breast cancer patients. Previous reports imply a connection between serum interleukin-6 (IL-6) and breast cancer, possibly through a modulation of enzymes involved in estrogen synthesis. Abnormal distribution of heparan sulphate proteoglycans (HSPGs) in malignant breast epithelial cells suggests that they play a key role in the regulation of cell growth. Estradiol is believed to be effective in modulating glycosaminoglycans (GAGs) and their depolymerizing enzymes. Therefore, in this study, attempts were made to evaluate the activity of leukocyte arylsulphatase A, serum interleukin-6, urinary GAGs and heparan sulphate (HS) in response to tamoxifen (TAM) therapy in mastectomised breast cancer patients. Thirty-four patients (aged 30-82 years) were administered TAM (20 mg twice daily). Blood and urine samples of each patient were collected three times (at the beginning, and in third and sixth month of TAM therapy), and biochemical parameters were measured. There was no difference between baseline leukocyte AS-A activity and that measured after three months. At the end of six months, enzyme activity was significantly higher than the former values (p=0.022), but within the reference intervals reported in the literature. Although this increase might imply a normalization, the duration of TAM therapy is not long enough to make a decision about either regression or aggravation of the disease. TAM did not have any effect on serum IL-6, urinary HS and GAG levels which may be due to insensitivity of these variables to TAM during the short period of therapy. Both urinary GAG and HS levels measured at sixth month exhibited a positive correlation with the baseline level of leukocyte AS-A (p=0.005 and 0.009, respectively), suggesting that positive responses to the drug might be seen in patients with low AS-A activity.     

Autonomic denervation in jejunal mucosa of homosexual men infected with HIV.

Autonomic nerves in jejunal mucosa of HIV-infected patients show severe structural damage on electron microscopic examination. The aim of this study was to quantify loss of autonomic axons from the lamina propria of HIV-infected patients in different clinical stages of disease. Jejunal biopsies were taken from 19 HIV-antibody-positive homosexual men and from 10 control patients. Autonomic fibres in the mucosa were stained with a neurone-specific polyclonal antibody, PGP 9.5. The density of axons was quantified by a point-counting technique using a Lennox eyepiece graticule under light microscopic examination. There was significant reduction in axonal density in the villi of HIV-infected patients [mean, 9.0; standard deviation (s.d.), 4.7] compared with controls (mean, 15.3; s.d., 5.2; P = 0.003), and in the pericryptal lamina propria of HIV-infected patients (mean, 17.8; s.d., 5.4) compared with controls (mean, 27.3; s.d., 6.2; P = 0.0002). Although autonomic denervation occurs throughout the jejunal mucosa of HIV-infected patients, there was no correlation between the clinical stage of HIV disease and the degree of denervation. The denervation was greatest in patients with the most severe diarrhoea, but this difference was not significant. This study provides the first quantitative morphological evidence for depletion of autonomic nerves in the jejunum of patients infected with HIV. Autonomic neuropathy may contribute to chronic diarrhoea in HIV disease.