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 an autopsied case of Parkinson's disease manifesting Shy-Drager syndrome. At the age of 63 years, the patient noticed an onset of progressive orthostatic dizziness, which was followed by constipation, dysuria, and sexual impotence. When he was 66 years old, syncopal attack for a few minutes, tremor in the bilateral hands, and memory disturbance developed. On admission, his blood pressure was 142/72 mmHg in supine position, which fell to 58/42 mmHg on standing with appropriate increase of heart rate. Neurological examination revealed hallucination, memory disturbance, masked face, muscular rigidity, bradykinesia, mild postural tremor, and autonomic dysfunction including severe orthostatic hypotension, hypohydrosis, constipation, dysuria, and sexual impotence. Electroencephalogram showed diffuse slowing. Brain CT demonstrated absence of severe atrophy of the cerebellum, and brain stem. Pharmacological study revealed denervation hypersensitivity to the intravenously administrated noradrenaline. A diagnosis of Shy-Drager syndrome was made, and he was treated with anti parkinsonian drugs. However, no improvement was observed in his clinical symptoms. Seven months later, he died of pneumonia. Neuropathological examination revealed marked neuronal cell loss and gliosis in the substantia nigra and locus ceruleus. Lewy bodies were seen in those pigmented nuclei, dorsal vagal nucleus, hypothalamus and nucleus basalis of Meynert. No abnormality was found in the intermediolateral nucleus of the spinal cord. This is the first report on a Japanese patient who presented clinically Shy-Drager syndrome and pathologically typical Parkinson's disease. In this patient, from the pharmacological and pathological findings, sympathetic ganglia were supposed to be the responsible lesion for orthostatic hypotension.
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PMID:[An autopsied case of Parkinson's disease manifesting Shy-Drager syndrome]. 130 25

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

Shy-Drager syndrome is characterized by severe orthostatic hypotension and other autonomic dysfunctions, cerebellar ataxia, parkinsonism, and upper and lower motor neuron symptoms. The disease starts in the 4th to 6th decades with severe dizziness, blackout or syncopi on standing up, and the duration of the illness is 6-7 years in the majority of the cases. The pathological lesions responsible for the autonomic dysfunctions are in the hypothalamus, locus saeruleus, Edinger-Westphal and other nuclei in the brain stem, intermediolateral column and Onuf's nuclei in the spinal cord. Oppenheimer has postulated a concept of multiple system atrophy to such widely distributed degenerative neurological disorders. However, olivopontocerebellar atrophy of Dejerine and Thomas, striatonigral degeneration and this syndrome can be distinguished clinically as well as pathologically.
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PMID:[Shy-Drager syndrome]. 161 60

Progressive or primary autonomic failure (AF) is a disease of unknown-etiology, and presents generalized and extensive autonomic disturbances because of selective neuronal degeneration in the whole of autonomic nervous system. AF is classified into three categories; (1) pure autonomic failure, without associated neurological disorders, (2) AF with Parkinson's disease (PD), and (3) AF with multiple system atrophy (Shy-Drager syndrome) (Bannister, 1988). AF with PD is pathologically characterized by neuronal cell degeneration in the intermediolateral column and the substantia nigra, together with Lewy bodies mainly in the pigmented nuclei in the brain stem. Patients with PD occasionally develop syncope or dizziness due to orthostatic hypotension and/or postprandial hypotension as well as urorectal disturbances as the initial symptoms, and are followed by parkinsonism. Levodopa is usually effective for parkinsonism but the prognosis is rather poor. AF with PD could be regarded as a form of 'the Lewy body disease' according to Kosaka's clinicopathological entity (1984).
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PMID:[Progressive autonomic failure with Parkinson's disease]. 161 62

Three patients with the chief complaints of dizziness while standing up or blackouts were diagnosed correctly as having the Shy-Drager syndrome at the Department of Otolaryngology. Both the electrocardiogram R-peak to R-peak interval and the Schellong test revealed disorders of the autonomic nervous system in each of these cases. Electronystagmography also demonstrated pathology of the oculomotor system and/or central vestibular system. Postural balance was also abnormal in one of the cases. Auditory brain-stem responses were normal in all three cases.
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PMID:Otoneurological manifestations of the Shy-Drager syndrome. 202 94

Encainide is a class IC antiarrhythmic agent having little or no effect on action-potential duration or maximum diastolic potential but decreasing the maximum rate of phase O depolarization as well as increasing atrial and ventricular effective refractory periods. In intact animals or humans, encainide increases the AH, PR, QRS, and H-V intervals while not affecting the sinus node cycle length or JT interval. QT interval increases only by the concomitant increase in the QRS interval. Encainide is metabolized to O-demethyl encainide (ODE) and 3-methoxy-ODE (MODE), both of which are also antiarrhythmics with similar pharmacology to encainide. Encainide and its metabolites have little negative inotropic activity and ancillary pharmacology. Consequently, encainide has little or no effect on hemodynamic variables in patients with either normal or compromised cardiac function. The drug is well tolerated, with side effects being mainly those associated with its local anesthetic activity such as blurred vision and dizziness. Encainide is particularly effective in patients with excessive premature ventricular complexes (PVCs) and less so in patients with sustained ventricular tachycardia (VT). Like all antiarrhythmics, encainide may aggravate or precipitate new arrhythmias (proarrhythmia). The overall incidence of proarrhythmia is about 10%, with less occurring in patients with PVCs and more in those with sustained VT; also, the incidence of proarrhythmia is higher in patients with underlying heart disease. Encainide is also effective for the treatment of supra-ventricular arrhythmias, including atrial fibrillation, PSVT (both PAF as well as reentry of the nodal or W-P-W type), and ectopic atrial tachycardia. Its dosage and role in antiarrhythmic therapy are discussed.
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PMID:Encainide. 251 80

A 64-year-old carpenter had an unsteady gait, severe dizziness, nocturia, and a loss of erection for more than 4 years. The neurological manifestations consisted of a wide-based ataxic gait, bilateral dysmetria with intentional tremor, staccato speech, rigidity, bradykinesia, and an iris-thinning. There was reproducible orthostatic hypotension. A sweat test revealed severe anhidrosis. Nicotine and methylbenzene sensitivity was absent, whereas norepinephrine infusion test showed a significant elevation of blood pressure. The resting plasma norepinephrine level on recumbency was low and a subnormal surge was noted on standing or exercise. We conclude that the clinical features caused by a degenerative process involving both the central and peripheral autonomic systems, together with atrophy of other systems in this patient, constitute the Shy-Drager syndrome.
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PMID:Abnormal cardiovascular responses to postural changes and pharmacologic agents in a case of Shy-Drager syndrome. 262 36

Neurogenic orthostatic hypotension is a severely disabling condition due to deficient peripheral vasoconstrictor tone in response to the upright position and is characterized by a decrease in blood pressure upon standing associated with symptoms of lightheadedness, dizziness, visual "white-out", weakness, lack of energy, near syncope or even syncope. Previous pharmacologic treatment of neurogenic orthostatic hypotension has been problematic. Midodrine, a new specific alpha-1-agonist has been shown to produce arteriolar constriction and decrease in venous pooling via a constriction of venous capacitance vessels. Therefore, a recent multicenter study evaluated the safety and efficacy of midodrine therapy in 97 patients with neurogenic orthostatic hypotension due to various etiologies: Shy Drager syndrome (No. 18); Bradbury Eggleston syndrome (idiopathic orthostatic hypotension) (No. 20); diabetic autonomic neuropathy (No. 27); Parkinson's disease (No. 22); and miscellaneous (No. 10). Following one week of placebo therapy, the patients were randomized into 4 groups for a 4 week period of time; placebo, 2.5 mg, 5 mg, or 10 mg three times daily. The BE/SDS subgroup demonstrated a 27 +/- 8% (22 mmHg) increase in standing systolic blood pressure for the 10 mg dose. Diabetics achieved a significant increase at 5 mg. Similar increases were observed for the entire group on the 10 mg dose (p < 0.001). Symptoms or fainting, blurred vision, improved energy level, standing time, and depressed feelings were also significantly improved even at lower doses (p < 0.05 or less). Side effects were mild. Therefore, midodrine is an effective and safe agent for the treatment of neurogenic orthostatic hypotension.
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PMID:Midodrine in neurogenic orthostatic hypotension. A new treatment. 769 Mar 83

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

This chapter reports the clinical and neuropathological findings of eight cases of "diffuse Lewy body disease" verified by autopsy. The age at onset was between 60 and 82 years; the age at death was between 75 and 92 years. The initial symptoms were amnesia in three cases, orthostatic dizziness in three, visual hallucination in two, but parkinsonism in none. The cardinal clinical symptoms included dementia in all cases, hallucinatory-delusional state in six, akinesia and rigidity in five, and orthostatic hypotension in five. Antemortem diagnoses were senile dementia in five, and hallucinatory-delusional state, Parkinson's disease and Shy-Drager syndrome in one each. Despite the clinical symptoms differences from each other, neuropathological findings were alike. Abundant Lewy bodies were present in the neurons of the cerebral cortex as well as in the brainstem nuclei and diencephalon. Concomitant senile changes including senile plaques and Alzheimer's neurofibrillary tangles (NFTs) were also present in varying degree. Immunocytochemical study with anti-ubiquitin for Lewy body, anti-tau protein for NFT, and beta-protein of amyloid for senile plaque suggested that dementia of DLBD might have resulted not from a single pathology but from the complex of Lewy bodies, NFTs and senile plaques.
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PMID:Clinical and neuropathological aspects of diffuse Lewy body disease in the elderly. 842 Jan 71


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