Accessory nerve neurotization in infants with brachial plexus birth palsy

We report the surgical results of 13 accessory nerve neurotizations in brachial plexus birth palsy. The mean age at operation was 5.9 months. The accessory nerve was transferred to three C5 roots, to three C6 roots, to four posterior division of the middle trunks, to one musculocutaneous nerve, and to two suprascapular nerves. Sixty-seven percent of the cases acquired M4 or more in the deltoid muscle, 88% in the infraspinatus muscle, and 100% in the biceps brachii muscle. Twenty-five percent of the cases acquired M4 or more in the triceps brachii muscle and the wrist extensor muscles. These results were much better than formerly reported for adult cases by other authors. No functional compromise of the trapezius muscle was noted. The accessory nerve neurotization can be used safely and effectively in neurosurgical reconstruction of the brachial plexus palsy in infants. © 1994 Wiley-Liss, Inc.     

Retroperitoneal schwannomas simulating adrenal tumors.

Tumors in the area of the adrenal were detected by chance in two patients who underwent a regular physical check-up. On arteriography the tumors were found to be fed by the adrenal artery. The diagnosis was retroperitoneal schwannoma, but in both patients it was difficult to differentiate the schwannoma from an adrenal tumor preoperatively.     

Expression and growth-promoting effect of adult T-cell leukemia-derived factor. A human thioredoxin homologue in hepatocellular carcinoma.

Adult T-cell leukemia-derived factor (ADF), originally defined as an interleukin-2 receptor inducer, is a human thioredoxin homologue. ADF is detected in many malignant tissues and has a growth-promoting effect on transformed cells. In this study, ADF expression was examined immunohistochemically in human liver cell lines and liver tissues, and its growth-promoting effect was tested on human hepatoma cells. On three liver cell line--PLC/PRF/5, HepG2, and Chang liver cells--ADF stained positively and also was detected by immunoblotting. ADF had strong staining in the fetal liver (n = 8), although it was faint in the normal adult liver (n = 6). In hepatocellular carcinoma (n = 25), ADF expression generally was enhanced and was very strong in 52% (13 of 25) of the cases, although it was moderate in cases of chronic hepatitis or cirrhosis. ADF augmented the growth of PLC/PRF/5 cells and showed an additive effect with epidermal growth factor. These results indicate possible involvement of ADF in cell activation and growth of hepatocytes, as is the case with lymphocytes.     

Transverse myelopathy in a patient with systemic lupus erythematosus associated with positive anticardiolipin antibody--a case report]

A 52-year-old woman who developed acute transverse myelopathy following systemic lupus erythematosus (SLE) was reported. At the age of 46, she was diagnosed as having atypical psychosis. Neurological examination revealed mild depressive state, paraparesis, diffuse hyperreflexia, hypesthesia below the breasts, and urinary disturbance. Gait was slightly ataxic and Romberg sign was positive. Laboratory study disclosed lymphocytopenia, positive antinuclear antigen, false positive Venereal Disease Research Laboratories flocculation test and prolonged activated partial thromboplastin time. IgG anticardiolipin antibody (aCLA) was positive, whereas IgM aCLA was negative. Cerebrospinal fluid was normal except the elevation of %IgG. Nerve conduction studies were normal and no abnormality was detected in the brain and spinal cord by MRI and CT. We treated her by two series of steroid pulse therapy, which resulted in marked improvement of symptoms and disappearance of aCLA. Before and after the pulse therapy, symptoms were fluctuated in parallel with the levels of aCLA. These findings suggest the relation of aCLA to the transverse myelopathy in SLE. This is the first case report of a good prognosis of myelopathy in a SLE patient who was treated by steroid pulse therapy with the aim of disappearance of aCLA.     

Intraosseous ganglion about to cause a fracture of the glenoid: a case report

Intraosseous ganglia of the glenoid are rare, and their etiology is unknown. This report describes a case of an intraosseous ganglion about to cause fracture of the glenoid. The patient was a 61-year-old woman with a painful left shoulder with a limited range of motion. Her symptoms did not improve after non-operative treatment. Arthroscopic examination showed a cartilage defect and erosion in the posteroinferior portion of the glenoid, behind which computed tomography (CT) showed a cystic lesion of the glenoid. There was no communication between the cyst and the joint space. The patient was treated by curettage and an autogenous cancellous bone graft from the iliac crest. Two years after the operation, the patient was almost free from pain, and CT showed good integration of the bone graft.     

Axonal dystrophy in the posterior column nuclei of young adult epileptics with chronic phenytoin intoxication

Axonal spheroids in the posterior column nuclei of phenytoin-intoxicated epileptics were classified according to their predominant subcellular components into six types, and their incidences were compared with those in controls. Spheroids from phenytoin-intoxicated epileptics showed significantly higher proportions of the tubulomembranous (TM) and layered membrane loop (LML) types in the gracile nucleus, appearance of the same types in the cuneate nucleus, and a significant decrease of the neurofilamentous (NF) type in both nuclei. The incidences of the complex body (CB) and granular material types and of the homogeneous dense-body (HDB) type, which appeared only in the gracile nucleus, showed no difference between the intoxicated patients and the controls. The NF, CB and HDB types were therefore considered to be nonspecific. It was thought that chronic phenytoin intoxication might induce dystrophic changes, such as those characterized by the presence of the TM and LML types, in the axon terminals of the gracile and cuneate nuclei, possibly due to some abnormalities of the axoplasmic transport system.     

PFK inhibition test for cancer detection: clinical applications and mechanisms of PFK inhibition

A newly established cancer marker, the PFK inhibition test, has been further examined for its capacity to detect malignant neoplasms irrespective of the organs in which cancer cells start proliferating. We tested 1,160 sera from cancer patients and compared them with 756 normal sera, using histograms and normal paper for analysis of accumulated frequency. PFK activity through the influence of normal sera showed normal distribution, and cancerous sera shifted to the inhibitory site with an irregular shape. From these analyses, the patients were classified into the following types: normal range: PFK greater than SD (standard deviation of PFK activity in normal sera); suspicious range: SD greater than PFK greater than 2SD, must be given the PFK test again; and dangerous range: PFK less than 2SD, further examination must be carried out to detect cancer. Fifty percent of the sera from all the cancer patients inhibited PFK beyond 2 SD of normal sera. We also analyzed organ-associated PFK distribution, eg, gastric, colorectal, and mammary cancer. In gastric cancer, PFK inhibition was stronger in accordance with how far a particular stage of cancer had progressed. However, 50% of sera from stage I gastric cancer patients was positive beyond the cut-off line of 2 SD. We examined 104 sera from patients diagnosed as benign prostatic hypertrophy and found malignant cells in 10 patients whose sera tended to be positive in PFK inhibition. The PFK inhibitory factor in the body fluids of cancer patients was fractionated by Sephadex G-75 gel filtration and DEAE ion exchange chromatography. The approximate molecular weight of this factor was 13,000 daltons. The factor was resistant to heat and acid (0.1 N HCl and H2SO4) and was sensitive to 0.1 N NaOH and phosphate buffer. Diluted sulfuric acid and ammonium sulfate made an inactive NaOH-treated sample active when lyophilized following dialysis against distilled water. PFK inhibition by cancerous sera was eliminated by fructose-2,6-bisphosphate (the strongest activator of PFK) in a dose-dependent manner. PFK attached to agarose beads was found to be reversible even after being inhibited by cancerous body fluids and ATP water solution. Although PFK is apt to decay in a low pH range, the established procedure did not destroy PFK, but induced a direct inhibition of PFK by ATP through the ATP inhibition site on the PFK molecule. The PFK inhibitor may possibly function as a proton carrier and release protons to activate the ATP inhibition site.(ABSTRACT TRUNCATED AT 400 WORDS)     

Competitiveness in sports activities of the psychiatrically disabled]

In 2002, psychiatrically disabled athletes joined an historic first open game of volleyball at the national sports games for the disabled. Compared to the competitive sports and Paralympic Games that physically and intellectually disabled athletes have participated in, activities for the psychiatrically disabled have not been well-organized. In this paper, we examine a number of problems that have arisen when the psychiatrically disabled joined competitive sports games. We identify two major characteristics of the psychiatrically disabled of particular relevance when organizing competitive sports activities. First, all psychiatrically disabled athletes need treatment of their individual diseases. For example, psychiatric symptoms fluctuate markedly over time, unlike physical or intellectual disabilities, whose symptoms are much more stable. Exacerbations of psychiatric illness are also likely to occur due to the stresses of competitiveness. Second, psychiatric disabilities are manifestations of disorders in the central nervous system, which makes the classification of psychiatric disabilities less straightforward than classification of the physically disabled. These two characteristics require special attention when organizing competitive athletic challenges that include the psychiatrically disabled. However, promoting sports activities that include the psychiatrically disabled would be expected to reduce the prejudice toward and subsequent social disadvantages experienced by psychiatric patients. Thus, with careful planning to successfully integrate psychiatrically disabled athletes, we expect increased promotion of such sports activities in the future.     

An immunohistochemical study of MAP2 and clathrin in gerbil hippocampus after cerebral ischemia

Changes in MAP2 and clathrin immunoreactivity were studied in gerbil hippocampus after transient cerebral ischemia. MAP2 immuno-reactivity decreased significantly by 1 h in the subiculum-CA1 and CA2 areas which correspond to reactive change, while no decrease was observed in CA1 until day 4. Before the initiation of delayed neuronal death, MAP2 immunoreactivity was not changed in CA1. On the other hand clathrin immunoreactivity increased in the pyramidal cell layer of CA1 by 3 h after ischemia and remained high for 2 days. Clathrin immunoreactivity in the pyramidal cell layer of CA1 diminished after delayed neuronal death. The transient change of clathrin was noted especially in CA1 in the period prior to delayed neuronal death. These results imply an abnormal change in clathrin turnover after ischemia, which may participate in the pathogenesis of delayed neuronal death.