Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

The authors report the cases of three men who presented for evaluation of a rapidly progressing dementia. All were found to have a giant aneurysmal mass in the basifrontal region, and all were successfully treated by surgical excision of the mass. The presenting syndrome included rapidly progressive and severe loss of recent memory associated with confusion, chronic headache, wide-based staggering gait disturbance, urinary urgency, frequency, and incontinence, and a fine tremor of the hands exacerbated by purposeful movements. The clinical presentation, radiological assessment, and surgical treatment are discussed.
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PMID:Aneurysmal tumors of the basifrontal region. 84 29

1. Acute toxicity: Empenthrin ((RS)-(EZ)-1-ethynyl-2-methyl-2-pentenyl (1R)-cis/trans-chrysanthemate) caused some toxic signs such as muscular fibrillation, tremor, hypersensitivity, decrease of spontaneous activity, ataxic gait, lymb paralysis, irregular respiration, excretion of oily substance, loose stool and urinary incontinence in oral acute toxicity studies at 1000 mg/kg and above in rats, and at 2000 mg/kg and above in mice. The oral LD50 value was estimated greater than 5000 mg/kg (male) and greater than 3500 mg/kg (female) in rats and greater than 3500 mg/kg (both sexes) in mice. In both rats and mice, the toxic signs were not found at 2000 mg/kg by dermal administration. The dermal LD50 value was estimated greater than 2000 mg/kg (both sexes) in both rats and mice. The LC50 value in rats for the acute inhalation toxicity of empenthrin was estimated to be greater than 4610 mg/m3 for both sexes. The LC50 value in mice was determined to be 2700 mg/m3 for male and 2300 mg/m3 for female. Mice showed higher sensitivity to empenthrin than rats. 2. Reproductive and developmental toxicity: Empenthrin was orally administered to fetal organogenesis periods of rats at the dose levels of 50, 150 and 500 mg/kg, and of rabbits at 100, 300 and 1000mg/kg. Maternal toxicity was found at 500 mg/kg in rats and at 300 mg/kg or more in rabbits. There were no teratogenicity, no embryotoxicity and no fetal retardation in rats or rabbits. In addition, there were no adverse effects on F1 pups growth, development or reproductive performance. 3. Subchronic toxicity: Empenthrin was orally administered to male and female SD rats at dose levels of 0 (corn oil), 10, 100 and 300 mg/kg for 26 weeks. Clinical signs, body weight, food and water consumption were monitered, and hematological, blood biochemical, ophthalmological and histopathological examination were carried out. As a result, changes related to administration of empenthrin were observed mainly in the liver and kidneys in rats receiving 100 mg/kg or more. Therefore, the no-effect-level of empenthrin is determined to be 10 mg/kg in both sexes of rats in this study.
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PMID:[Mammalian toxicity of empenthrin (Vaporthrin, S-2852F)]. 129 29

We report a 41-year-old male of citrullinemia associated with argininosuccinate acid synthetase deficiency. He was admitted to the Hitachi General Hospital because of finger tremor, restlessness and urinary incontinence. He had short stature and a poor appetite. Laboratory evaluation was summarized as follows: mild hypoglycemia, low plasma cortisol levels, delayed response of 17-OHCS and 17-KS to ACTH administration in urine, and delayed response of plasma ACTH level to insulin administration. In this case, ACTH deficiency is estimated to be a dysfunction of the hypothalamus. Replacement therapy of hydrocortisone improved his symptoms. He was readmitted to the hospital because of delirium and confusion, two weeks after the hydrocortisone administration. At that time, he had flapping tremor. Laboratory examination revealed hyperammonemia (NH3: 231 micrograms/dl) and mild elevation of GOT and GPT. Serum and urinary amino acid determination showed marked elevation of citrulline (478.1 nmol/ml in serum, 4681.2 mumol/day in urine). Lactulose administration, low protein diet and plasmapheresis were started, but he went into a coma. Without any improvement, he died on the 29th hospital day. Autopsy examination of the liver disclosed fatty change. Adrenal cortex depicted severe atrophy. Biochemical analysis of urea cycle enzymes of the liver and kidney showed decreased activity of argininosuccinate synthetase (liver: 0.0022 U/mg protein, 5% of that normal liver, kidney: 0.003 IU/mg protein, 20% of that in normal kidney). Citrullinemia associated with ACTH deficiency have not reported in the literature. It may be presumed that ACTH deficiency is concerned with the delayed onset of hyperammonemia. The relation between citrullinemia and endocrinological abnormalities is also discussed.
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PMID:[A case of citrullinemia associated with isolated ACTH deficiency, rapidly developing coma]. 133 25

2,2'-Isobutylidene-bis(4,6-dimethylphenol), an antioxidant, was given orally to pregnant Wistar rats by stomach intubation at the dose levels of 5, 15 or 45 mg/kg body weight during days 7 to 17 of gestation, and the effects of the compound on dams and fetal developments were examined. In the dams at the two higher dose levels of 15 and 45 mg/kg, toxic signs (tremor, startle reflex, salivation, involuntary urination, wheezing and nostril discharge) were observed. Moreover, at the highest dose level, additional toxic signs (lacrimation and vaginal bleeding), suppression in maternal body weight gain and food consumption were observed. However, there was no evidence of an increase in malformations attributable to the treatment with 2,2'-isobutylidene-bis(4,6-dimethyl-phenol) in any of the treated groups. It was concluded that 2,2'-isobutylidene-bis(4,6-dimethylphenol) has no teratogenic effect in rats, though toxic signs were observed in treated dams of the 15 and 45 mg/kg groups.
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PMID:[Studies on the teratogenic potential of 2,2'-isobutylidene-bis (4,6-dimethylphenol) in rats]. 136 2

A Japanese woman, aged 42, was admitted because of paroxysmal attacks consisting of paresthesia of the left face, tremor in the right hand, epigastric pain and urinary incontinence. A year prior to the admission, she noticed some difficulty in writing, dysarthria and unsteadiness of walking. These symptoms had been persistent since then. At the end of March, 1991, these symptoms rapidly worsened, and she fell down frequently. She also experienced pain behind both eyes, numbness in her left fingers and toe, urinary frequency and the above-mentioned attacks. Neurological examination disclosed bilateral internuclear ophthalmoplegia and upbeating nystagmus on upward gaze, titubation in the head, scanning speech, dysmetria in all limbs, exaggerated reflexes in jaw and both legs, bilateral extensor plantar reflexes and ankle clonus. SEP showed delayed cortical response with stimulation of the median nerves bilaterally and of the right posterior tibial nerve. P40 was absent with the left posterior tibial nerve stimulation. VEP was normal. T2-weighted image of MRI showed multiple high intensity areas located around the third ventricle, crus cerebri and the right upper part of the pons. The diagnosis of multiple sclerosis was made. Each paroxysmal attack started with numbness in the left face and burning sensation in the neck. Almost simultaneously tremor in the right hand began. The surface EMG showed the rhythmic contractions in the dorsal hand muscles and wrist extensors at a frequency of 6-7 Hz, and sometimes it revealed synchronized contractions of finger flexors and the dorsal hand muscles. A few seconds later she felt painful sensation in the epigastric region, and the tremor gradually increased in its intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of multiple sclerosis with paroxysmal attacks of facial paresthesia, unilateral hand tremor, epigastric pain and urinary incontinence]. 162 36

We report an autopsy case of a 73 year-old female with idiopathic parkinsonism, characterized pathologically by the wide spread appearance of Lewy bodies (LBs) not only in the pigmented neurons in the midbrain and brainstem but also in the cerebral cortex. Initial symptoms at the age of 62 were finger tremor and gait disturbance, which were followed mainly by mental deterioration, such as regression, dependency, auditory hallucination, depression, emotional incontinence, and a personality change. In the terminal stage, nuchal stiffness in extension, one of the hallmarks of progressive supranuclear palsy, and slow and generalized tremor in all 4 extremities were noted. She died of aspiration pneumonia. The brain was somewhat small and weighed 1100 g after the fixation by formalin. Macroscopical findings included mild cerebral atrophy with mild pial thickening both in the frontal and temporal lobes and slight expansion of the ventricular system. Histopathologically, severe loss of neuronal cells in both the pallidum and Luy's body and moderate loss of large cells in the putamen were noted in addition to the typical findings of Parkinson's disease in the substantia nigra and locus caeruleus including neuronal cell loss, depigmentation, and gliosis. These findings in the basal ganglia were more conspicuous than the two controls of classical Parkinson's disease. The distribution, stainability in the routine methods of staining, and shape of Lewy bodies in the cerebral cortex conformed to those of previous reports. The similar case reports in the literatures do not seem to have paid much attention to the findings of the basal ganglia observed in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsy case of idiopathic parkinsonism with numerous Lewy bodies in the cerebral cortex--diffuse Lewy body disease]. 165 48

The clinical effectiveness and safety of terodiline hydrochloride and clenbuterol hydrochloride were studied on 51 patients with neurogenic bladder, stress incontinence, unstable bladder and others, the chief complaints of which were urinary frequency or urinary incontinence. Overall improvement was graded as marked in 6 patients (11.8%), moderate in 20 patients (39.2%), slight in 11 patients (21.6%), unchanged in 13 patients (25.5%) and aggravated in one. The patients impression was "good" or better in 56.9%. There were a total of 13 cases (25.5%) of adverse reactions, namely, 7 cases of finger tremor, 3 cases of dry mouth and others. These reactions disappeared rapidly after the discontinuance of drug administration. The clinical efficacy in the treatment of subjective symptoms was 71.4% for urinary incontinence, 56.4% for diurnal pollakisuria. The examination of lower urethral functions demonstrated a significant (p less than 0.01) increase in bladder capacity at first desire and maximum desire to void. However, we found no significant increase in urethral clossure pressure. The findings of this study suggest that terodiline hydrochloride and clenbuterol hydrochloride are very useful for the treatment of urinary frequency and incontinence.
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PMID:[Clinical studies of terodiline hydrochloride and clenbuterol hydrochloride for urinary frequency and incontinence]. 176 84

A total of 49 patients complaining of pollakisuria and incontinence; 20 patients with overactive neurogenic bladder and 29 patients with stress incontinence, were treated with clenbuterol, and the effects of the drug were studied. Subjective symptoms were improved markedly in 8 patients (17%), moderately in 14 patients (29%), and slightly in 10 patients (21%). The symptoms were unchanged in 15 patients (31%) and aggravated in 1 patient (2%). In objective observation, the volume at first desire to void (P less than 0.01) and the maximum urethral closure pressure (P less than 0.05) significantly increased. The objective symptoms were improved markedly in 2 patients (5%), moderately in 12 patients (27%), and slightly in 11 patients (25%). The symptoms were unchanged in 15 patients (34%) and aggravated in 4 patients (9%). Overall improvement was graded as marked in 7 patients (15%), moderate in 17 patients (35%), slight in 11 patients (23%), unchanged in 13 patients (27%) and aggravated in none. In neurogenic bladder, the overall improvement was graded as marked in 2 patients (11%), moderate in 4 patients (21%), slight in 4 patients (21%), unchanged in 9 patients (47%) and aggravated in none. In stress incontinence, the overall improvement was graded as marked in 5 patients (17%), moderate in 13 patients (45%), slight in 7 patients (24%), unchanged in 4 patients (14%) and aggravated in none. Side effects were noted in 12 patients (25%) and they were all not serious. Finger tremor was the most common side effect (5 patients).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical effects of clenbuterol-HCL in urge incontinence and stress incontinence]. 234 15

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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PMID:The AIDS dementia complex: I. Clinical features. 372 8


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