Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 52-year-old male patient with Shy-Drager syndrome (SDS) complicated by an occurrence of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The patient first developed impotence at the age of 48, accompanied by urinary incontinence, and episodes of dizziness while standing. The following year, the patient had developed a staggering gait and speech became monotonous. At age 52, the patient was admitted to the hospital after experiencing frequent episodes of syncope associated with complete loss of consciousness. Upon examination, blood pressure was 100/70 in a recumbent position, and 80/60 when standing. The pulse rate varied from 60 per minute to 62. The patient was alert. The alternating Horner sign was observed, and a paucity of facial movements was visible. His speech was slow and monotonous. Muscle tone was increased bilaterally. There was incoordination. A laboratory examination revealed reduced serum sodium levels of 127 mEq/L and increased sodium excretion with plasma hypoosmolality (262 mOsm/kg/H), urine hyperosmolality and low serum renin activity (0.2 ng/ml/h). Renal functions were normal and the levels of adrenocortical and thyroid hormones were normal. There were no abnormalities observed in the chest roentgenogram taken. The level of antidiuretic hormone (ADH) was unreasonably high (5.74 pg/ml). A water-load test demonstrated failure of both water diuresis and inhibition of ADH secretion. These data suggested that hyponatremia in this case was caused by SIADH. The correlation between plasma osmolality and the concentration of ADH suggested that osmolality that initiates ADH release appeared to have been reset to around 230 mOsm/kg lower than normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Shy-Drager syndrome and the syndrome of inappropriate secretion of antidiuretic hormone]. 161 76

The effect of bifemelane hydrochloride on dementia in the elderly was studied in thirty-one patients having cerebrovascular disorders. Alzheimer's disease, Parkinsonism and related diseases. The drug (150 mg) was administered orally three times daily for 10 weeks. The final global improvement rating was 77.4% for all patients. The rates of improvement for Alzheimer's disease were higher than those for cerebrovascular disorders, suggesting that this drug affects Alzheimer's disease through a cholinergic potentiating action. Psychotic, neurological and subjective symptoms, and the activity of daily life, were rated before, during and after treatment. All mean rates of improvement were based on observations made in the 4th week after the start of treatment. Improvement rates for global symptoms were more than 80% for emotional incontinence and prejudice or querulous attitudes toward the nurses, and in headache, tinnitus and dizziness among the subjective symptoms. The improvement in intellectual function was evaluated by the dementia rating scale for the elderly (DRSE), and a significant increase was found in DRSE after treatment with this drug. Side effects attributable to the drug were noted in one patient developing urticaria. It is thus suggested that bifemelane hydrochloride is useful in the treatment of different symptoms of dementia.
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PMID:The clinical effect of bifemelane hydrochloride on dementia in aged patients. 179 96

The clinical effectiveness and safety of propiverine hydrochloride (P-4, 20 mg tablet) were studied on 29 patients with nervous pollakisuria, neurogenic bladder or unstable bladder, whose chief complaints were urinary frequency and/or urinary incontinence. The clinical efficacy was "good" or better in 62.1% and "fair" or better in 86.2%. Patients' impressions were "good" or better in 79.3%. There were a total of 4 cases (13.8%) of adverse reactions, namely, two cases of decreased urinary stream, one dry mouth, and one dizziness. These reactions disappeared rapidly after the completion or discontinuance of drug administration, and therefore, did not constitute significant safety problems. The clinical efficacy in the treatment of subjective symptoms was 74.1% for diurnal pollakisuria, 50.0% for nocturnal pollakisuria, 83.3% for urinary incontinence and 69.0% for urgent feeling of micturition. For objective symptoms, P-4 increased significantly the volume of maximum desire to void (MDV); however it did not increase significantly the residual urine volume. The results of this study suggest that propiverine hydrochloride is very useful for the treatment of urinary frequency and/or incontinence.
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PMID:[Experience in the use of propiverine hydrochloride (P-4) for patients suffering from urinary frequency and/or incontinence]. 237 10

We evaluated the effectiveness and side effects of long-term administration of terodiline hydrochloride in patients with chief complaints of pollakisuria or incontinence or both due to unstable bladder or neurogenic bladder associated with uninhibited contraction. The dose was 24 mg once daily. The symptoms such as pollakisuria and incontinence improved in 31 out of 41 patients (76%). Mild side effects were observed in 12 out of 47 patients (26%), which were thirst, dizziness, dysuria, urticaria and gastrointestinal symptoms. An increasing tendency of both maximum desire to void and compliance (p less than 0.10), and significant difference in maximum static pressure (p less than 0.05) were observed on urodynamic examinations before and after administration of this medicine. The results obtained from this study suggest that terodiline hydrochloride may be greatly recommended for patients with such symptoms as pollakisuria and incontinence.
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PMID:[Clinical evaluation of long-term administration of terodiline hydrochloride for the treatment of patients with pollakisuria and incontinence]. 340 May 52

Terodiline HCl was administered in a long-term study to 20 patients with neurogenic bladder and pollakisuria. Its efficacy on urinary frequency and urinary incontinence was studied together with its safety and changes in blood concentration. The dosing period extended from 2 through 53 weeks (21 weeks on the average). The drug was found effective in 62% of diurnal urinary frequency patients, 71% of nocturnal urinary frequency, 73% of urinary incontinence, and 69% of nocturnal enuresis. Side effects of dizziness and nasal obstruction were seen in only one case. The drug was judged to be useful in 75% of the patients studied. Terodiline HCl showed no further increase in plasma concentration due to the long-term administration, and it disappeared from plasma within one to two months after the last dosing.
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PMID:[Clinical evaluation of long-term administration with terodiline hydrochloride for the treatment of patients with neurogenic bladder]. 340 May 54

Seven cases of subacute central and peripheral neurologic dysfunction developed in 18 workers employed in the manufacture of reinforced plastic bathtubs. Cases were characterized by weight loss, dizziness, paresthesias, muscle weakness, incontinence, memory loss, and loss of peripheral, color, and night vision. Neuropathies began distally, involved both sensory and motor function, and were associated with prolonged sensory latency, muscle fibrillation, and reduced numbers of functioning motor units. One patient developed posterior lenticular cataracts. Slow improvement occurred on removal from exposure, but residual neuropathies persisted for as long as two years. Epidemiologic investigation disclosed that the first case developed approximately two weeks after introduction of a new plastic foaming agent, 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH). All cases occurred in workers exposed directly to BHMH. No new cases developed after use of BHMH was discontinued. A survey of the firm which produced BHMH and of 68 user firms found two additional clusters of mild neuropathy which may have been caused by BHMH. BHMH was withdrawn from distribution following discovery of these cases. Subsequently, BHMH has been shown in rats to be a potent neurotoxin. Adequate premarket testing could have averted this outbreak.
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PMID:Neurologic dysfunction from exposure to 2-t-butylazo-2-hydroxy-5-methylhexane (BHMH): a new occupational neuropathy. 398 40

Treatment with oestrogens in the perimenopause can regulate dysfunctional uterine bleeding and positively influence unpleasant subjective feelings such as sweating, dizziness, nervousness and lack or incapability of concentration. Oestrogens are especially successful in reactive depression and in the therapy of insomnia. Their positive effect on atrophic changes of the genitalia and in combating urge incontinence is also of therapeutic importance. Of particular socio-medical importance is their beneficial effect on postmenopausal osteoporosis. Side effects like weight gain, increase in blood pressure or changes in coagulation parameters are not observed during therapy with natural oestrogens in the usual doses. The incidence of thrombosis, embolism and myocardial infarction is not increased when oestrogens are given in the perimenopause. The controversy with respect to an increased incidence of endometrial carcinoma after long-term therapy with oestrogens may be based on an incorrect mode of administration as used on the Anglo-American scene. Excess dosage, continuous instead of intermittent therapy, lack of addition of progestational agents and a neglect of contraindications and risk factors may have led to the 3- to 8-fold increased incidence of endometrial carcinoma after oestrogen therapy in the studies from these areas.
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PMID:[Advances and risks in estrogen therapy in the perimenopause]. 665 19

Earlier nonselective alpha 1-adrenergic blocking drugs such as phentolamine and phenoxybenzamine are now restricted to the pharmacological management of alpha 1-adrenergic crisis and phaeochromocytoma. Prazosin, the first selective alpha 1-blocker approved for the treatment of hypertension, became available in the mid-1970s. Additional alpha 1-blockers such as doxazosin and terazosin have been introduced during recent years. The undesirable effects of all members of this class are similar. Most adverse events can be attributed to reversible competitive antagonism of postsynaptic alpha 1-adrenergic receptors in tissues that sustain high levels of alpha-adrenergic sympathetic tone, e.g. resistance arteries, capacitance veins and the urinary bladder outflow tract. Orthostatic hypotension with a sensation of intense faintness and occasional syncope, can occur shortly after the initial dose. Aggravating factors include upright posture, intravascular volume depletion and concurrent administration of other medications that lower blood pressure, including all other classes of antihypertensive drugs. The problem is reduced or avoided by the choice of low starting doses, beginning treatment at bedtime and by minimising other risks. Among overall adverse effects, asthenia, dizziness, faintness and syncope predominate and occur in 10 to 20% of patients, leading to discontinuation of therapy in about half that number. Infrequent adverse events include headache, drowsiness, palpitations, urinary incontinence and priapism. Some patients experience a 1 to 2kg bodyweight gain which may be associated with secondary hyperaldosteronism. Tolerance appears to develop to the benefits of alpha 1-blockade in patients with congestive heart failure, but not in hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effects of alpha 1-adrenergic blocking drugs. 791 78

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.
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PMID:[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords]. 795 87

A 55-year-old mildly hypertensive woman died after having developed a subcortical dementia during the past 9 years, with focal neurological signs. She presented at the age of 46 years with short episodes of dizziness and diplopia, suggesting that transient ischemic attacks involved the posterior fossa structures. Over the next 8 years, she developed difficulty in walking, urinary incontinence and seizures. On examination in 1989, she was severely demented. There was tetraparesis, bilateral arm and leg spasticity with hyperreflexia and bilateral Babinski signs. She showed epilepsia partialis continua involving the eyes, left hemiface and limbs. CT showed hypodensity of the white matter and lacunes in the basal ganglia and centrum semiovale, moderate hydrocephalus with cerebellar and cortical atrophy. Clinical and radiological features were similar to those of Binswanger's disease. Similar cases had occurred in the family affecting the patient's grandfather, father and two brothers, suggesting an autosomal dominant hereditary disease. Postmortem examination disclosed a Binswanger type of leukoencephalopathy caused by a peculiar microangiopathy characterized by a slightly basophilic small arterial granular degeneration of the medial sheath associated with the presence of ballooned smooth muscle cells with clear cytoplasm. Electron microscopic study revealed degenerative changes in the parietal vessels with notable increase of basal-membrane-type material and electron-dense granular deposits. These lesions could correspond to a specific familial pathology of the small arteries of the brain. They are identical to those reported in some patients with autosomal dominant inheritance. For other patients with similar clinical features and the same familial pattern, reported as "hereditary multi-infarct dementia'' and "chronic familial vascular encephalopathy'', there are no sufficient objective pathological facts to consider that they have the same disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Small arterial granular degeneration in familial Binswanger's syndrome. 814 Aug 99


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