Rehabilitation approaches to dysphagia that was developed for a patient who attempted to commit suicide by hanging: a case report.

We report our experience with a case of attempted suicidal hanging presenting with dysphagia, in which rehabilitation approaches resulted in improvement. A 36-year-old man was discovered collapsed at home. From the finding of a broken cord nearby, attempted suicide by hanging was suspected. He was transported to hospital after 40 minutes, and regained consciousness after emergency treatment. There were no noteworthy findings on brain magnetic resonance imaging, cervical spine computed tomography, or vocal cord examination. There were no noteworthy psychiatric disorders or cognitive abnormalities. On hospital day 10, he showed signs of dysphagia. Videofluoroscopic examination of swallowing revealed piriform sinuses residue and aspiration after ingestion of jelly in any posture. Rehabilitation approaches were started based on the diagnosis of dysphagia due to impaired transit through the piriform sinuses. The patient achieved independent oral intake by 40 days after the injury. In this case, dysphagia was considered attributable to compression of the vagus nerves running along the lateral aspects of the neck by the cord used in the hanging. If compression is brief, full functional recovery can be expected. Implementation of rehabilitation approaches is also important in this situation.

Effects of 5-HT(4) receptor agonists, cisapride and mosapride citrate on electrocardiogram in anaesthetized rats and guinea-pigs and conscious cats.

The purpose of this study was to examine the arrhythmogenic potential of 5-HT4 receptor agonists, cisapride and mosapride citrate (mosapride) in vivo. In anaesthetized rats, cisapride at intravenous infusion of 10 and 30 mg/kg/hr for 1 hr prolonged the electrocardiographic RR and QT intervals, whereas at 3 mg/kg/hr, it prolonged the RR interval without affecting the QT interval. Mosapride at 30 mg/kg/hr for 1 hr slightly, but not significantly, prolonged the QT interval. In anaesthetized guinea-pigs, cisapride at intravenous infusion of 0.3, 1 and 3 mg/kg over 15 min. prolonged the RR interval (18-44%), QT interval (18-42%) and the corrected QT interval (QTc; 8-19%). Mosapride at 3, 10 and 30 mg/kg over 15 min. little affected the QTc although at 30 mg/kg, it slightly prolonged the RR and QT intervals. With repeated oral administrations of 30 mg/kg twice a day for 7 days, cisapride prolonged the QT interval (11-35%) and QTc (11-32%) at the 3rd and 7th days in conscious cats. In addition, cisapride depressed the ST segment in two out of five cats. Mosapride at 60 mg/kg twice a day for 7 days did not affect the QT interval or QTc in cats. The maximal plasma concentrations of mosapride and its main metabolite (a des-4-fluorobenzyl-mosapride) at the 7th day in cats were 9.4+/-2.8 microM and 2.5+/-0.3 microM , respectively, being 100 and 30-60 times higher than those in man given therapeutic doses (Sakashita et al. 1993a&b). These results indicate that mosapride has little arrhythmogenic potential.

Retinopathy associated with Machado--Joseph disease (spinocerebellar ataxia 3) with CAG trinucleotide repeat expansion.

PURPOSE: To report characteristic atrophic maculopathy in a patient with Machado--Joseph disease (spinocerebellar ataxia 3) caused by trinucleotide repeat expansion of the relevant gene. METHODS: Case report. RESULTS: A 64-year-old Japanese man had suffered from slurred speech and gait disturbance since 57 years of age. Cerebellar ataxia, extensor plantar response, and other neurological signs were compatible with features of Machado--Joseph disease. Magnetic resonance imaging showed atrophies of cerebellum and cerebral cortex. Family history suggested an autosomal dominant inheritance of the disease. The patient presented with gaze-evoked nystagmus and limitations of eye movement in all directions. Ophthalmoscopy and fluorescein angiogram revealed symmetric changes in the posterior fundi, which consisted of patchy atrophies at the level of the retinal pigment epithelium. Scotopic electroretinogram showed no abnormalities with normal oscillatory potentials. Polymerase chain reaction analysis of the Machado--Joseph disease gene identified a heterozygous trinucleotide (CAG) repeat expansion. CONCLUSION: This case illustrates a rare association of atrophic maculopathy and external ophthalmoplegia in Machado--Joseph disease, contrasted with the common occurrence of retinal degeneration in spinocerebellar ataxia 7. Dystrophic changes in the retinal pigment epithelium have rarely been described but may be one of the characteristic complications of Machado--Joseph disease.

[Toxicity study of cefmatilen hydrochloride hydrate (S-1090) (1)--Single oral and intravenous dose toxicity studies in rats].

A single oral dose toxicity study of Cefmatilen hydrochloride hydrate (S-1090) and a single intravenous dose toxicity study of its sodium salt (S-1090-Na) were conducted in rats. One dose level of 2000 mg potency/kg was set in both studies. Single oral dose toxicity study of S-1090 No deaths occurred. Diarrhea occurred on the dosing day and slightly soft feces lasted until 6 days after administration. These changes were considered to result from changes of intestinal flora induced by the antibiotic activity of S-1090. Reddish-brown feces (due to chelated products of S-1090 or its decomposition products with Fe3+ in the diet) were also observed until the next day after administration. Body weights increased favorably, and no S-1090-related pathological changes were observed. The oral lethal dose of S-1090 was estimated to be more than 2000 mg potency/kg. Single intravenous dose toxicity study of S-1090-Na No deaths occurred. The rats showed characteristic clinical signs such as hypoactivity, abnormal gait and hypopnea immediately after dosing, and some rats showed prone position or paleness of eyeballs and ear auricles in due course. These signs disappeared by 4 hr after administration. Slightly soft feces and reddish-brown feces were observed much the same as in the orally-treated rats. Body weights increased favorably. In the pathological examinations, slight cecal enlargement and increased basophilia, dilatation and calcification of the renal tubules in the kidney were observed. The intravenous lethal dose of S-1090-Na was estimated to be more than 2000 mg potency/kg.

[Toxicity study of cefmatilen hydrochloride hydrate (S-1090) (6)--Six-month repeated oral dose toxicity study in dogs].

A six-month repeated oral dose toxicity study of Cefmatilen hydrochloride hydrate (S-1090) at dose levels of 40, 100 and 250 mg potency/kg/day was conducted in male and female beagle dogs. No toxicologically significant changes were observed in general conditions of all animals. Reddish-brown feces (due to chelated products of S-1090 or its decomposition products with Fe3+ in the diet) were observed in all treated groups. Plasma irons showed a tendency to increase in the males and females of the 250 mg potency/kg group. However, as no changes suggesting anemia or hepatic injury were observed in this group, the change of plasma iron was considered to have no toxicological significance. No toxicologically significant changes were observed in other examination items. The plasma S-1090 concentrations increased in a manner less than dose-proportional. Based on the above results, the NOAEL of S-1090 was assessed to be 250 mg potency/kg/day.

[Toxicity study of cefmatilen hydrochloride hydrate (S-1090) (8)--Nephrotoxicity study in rabbits by single oral administration].

A nephrotoxicity study of Cefmatilen hydrochloride hydrate (S-1090) was conducted in rabbits at single oral doses of 250, 500 and 1000 mg potency/kg. All treated groups showed a decreased food consumption and a tendency for the body weight to decrease. Urinary protein and glucose were detected and slight increases of plasma creatinine and urea nitrogen were observed in the 500 mg potency/kg group. Urinary protein was also detected in the 1000 mg potency/kg group. In the histopathological examination of the kidney, tubular necrosis was observed in the 500 and 1000 mg potency/kg groups. No nephrotoxic signs were observed in the 250 mg potency/kg group. The NOAEL on the nephrotoxicity of S-1090 in rabbits was estimated to be 250 mg potency/kg.

Effects of 5-HT4-receptor agonists, cisapride, mosapride citrate, and zacopride, on cardiac action potentials in guinea pig isolated papillary muscles.

The purpose of this study was to examine the effects of 5-HT4-receptor agonists cisapride, mosapride citrate (mosapride), and zacopride on action potentials (APs) in guinea pig isolated papillary muscles. Cisapride (0.1-3 microM) concentration-relatedly prolonged the duration of APs (APD) without affecting the other AP parameters. Mosapride and its main metabolite M1 (des-4-fluoro-benzyl-mosapride) did not affect APs at 10 microM. Zacopride at 10 microM shortened APD, and the APD-shortening effect was not affect by GR113808 (10 microM), a 5-HT4-receptor antagonist. The cisapride (1 microM)-induced prolongation of APD was not affected by GR113808 (10 microM), ritanserin (10 microM), a 5-HT2A/2C-receptor antagonist, or prazosin (10 microM), an alpha 1-receptor antagonist. The same concentrations of GR113808, ritanserin, and prazosin did not affect APD. Clofilium, a class III antiarrhythmic agent, prolonged APD; the effect was more pronounced at a stimulus frequency of 0.3 Hz than at 2.0 Hz. Cisapride did not exert such reverse use dependence, suggesting that its mechanism of action is different from that of clofilium. These results suggest that cisapride prolongs APD without involvement of 5-HT2, 5-HT4, or alpha 1 receptors. Mosapride is unlikely to induce the prolongation of electrocardiographic QT intervals correlated with the prolongation of APD in isolated ventricular muscles.

General pharmacology of recombinant human tumor necrosis factor. 1st communication: effects on cardiovascular, gastrointestinal, renal and blood functions.

The effects of recombinant human Tumor Necrosis Factor (rHu-TNF, PT-050), an antitumor agent, on the cardiovascular, gastrointestinal, renal and blood functions were examined in experimental animals. 1. PT-050 at 10(5) U/kg i.v. did not affect blood pressure and blood flow in anesthetized dogs. However, these were decreased 2-3 h after i.v. injection of 10(6) U/kg. A sustained decrease in blood pressure was seen in conscious dogs. PT-050 decreased systolic blood pressure and increased heart rate with a peak at 5-7 h after administration of 10 micrograms/kg (2.55 x 10(4) U/kg) i.v. and 10(5) U/kg s.c. PT-050 was without effect on perfusion volume in rabbit ear vessel preparations. 2. PT-050 enhanced gastric emptying in rats and intestinal charcoal meal propulsion in mice at 10(6) and 10(7) U/kg s.c., respectively. It decreased gastric juice volume and acid content with an increase of gastric juice pH in pyrolus ligated rats at 10(6) U/kg s.c. 3. PT-050 caused diarrhea at 10(5) U/kg i.v. in mice, while at 10(7) U/kg s.c., it did not exert the effect. 4. PT-050 increased urine volume and Na+ excretion at 3 x 10(3) U/kg i.v. and 10(5) U/kg s.c. in saline-loaded rats. 5. PT-050 decreased platelet counts at 10(5) U/kg i.v., depressed platelet aggregation responses to collagen and ADP at 10(6) U/kg i.v., and prolonged APTT and PT at 3 x 10(5) U/kg i.v. in rats, although it neither affected platelet aggregation nor blood coagulation in vitro. PT-050 neither affected platelet counts at 10(5) U/kg s.c., nor platelet aggregation at 10(7) U/kg s.c.(ABSTRACT TRUNCATED AT 250 WORDS)