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

1. Three oral glucose tolerance tests were performed in each of 32 symptomatic postprandial hypoglycaemic patients (before placebo, before doxepin therapy and after doxepin therapy). Plasma neurotransmitters were determined in parallel with assays of plasma insulin and glucose levels. 2. Three different types of patients were distinguished. Type I showed a low noradrenaline/adrenaline ratio, high dopamine levels and low platelet 5-hydroxytryptamine (serotonin) levels during basal periods. After a glucose load, late peaks of dopamine and free 5-hydroxytryptamine, which coincided with the symptoms but not with the nadir of plasma glucose, were observed. Type II showed a low basal plasma noradrenaline/adrenaline ratio. After a glucose load, progressive increases in adrenaline and decreases in glucose were seen. Adrenergic symptoms coincided with the nadir of glucose. Although type III patients showed hyperinsulinaemia after a glucose load similar to the other types of patient, they did not show hyperglycaemia, but rather exhibited a sustained and progressive reduction in plasma glucose. These patients were characterized by a high basal plasma noradrenaline/adrenaline ratio, high basal plasma levels of 4-hydroxy-3-methoxyphenylethyleneglycol and high basal levels of platelet 5-hydroxytryptamine, all of which increased after a glucose load. Systolic and diastolic blood pressure decreases paralleled reductions in heart rate and glucose. The nadir of plasma glucose occurred simultaneously with the appearance of symptoms (weakness, heartburn, oppressive chest pain, tension headache, abdominal cramps, dizziness, etc.). Therapy with doxepin led to disappearance of the symptoms within 3-4 weeks. Normalization of all other disordered variables (cardiovascular, metabolic and neurochemical, and the clonidine test) paralleled the disappearance of the symptoms. 3. Symptoms varied in the three types of patients and we conclude that they are related to hypoglycaemia-induced disorders of plasma neurotransmitters, rather than to hypoglycaemia per se. We postulate that an uncoping stress situation (type I and II patients) and depression (type III patients) underlie the physiopathological mechanisms.
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PMID:Doxepin therapy for postprandial symptomatic hypoglycaemic patients: neurochemical, hormonal and metabolic disturbances. 167 82

A 30-year-old woman with longstanding dizziness was found to have a severe postural fall in blood pressure and a reduced skin axon-reflex flare response. Autonomic tests indicated selective impairment of adrenergic sympathetic function. Plasma noradrenaline, adrenaline, dopamine, and dopamine beta hydroxylase were undetectable. Skin biopsy specimens showed loss of tyrosine hydroxylase and neuropeptide Y (markers of adrenergic sympathetic fibres) and of substance P and calcitonin gene-related peptide (sensory neuropeptides). A sural nerve biopsy specimen showed severe depletion of unmyelinated fibres. The constellation of losses were compatible with nerve growth factor (NGF) deprivation, which was confirmed on assay. This new syndrome may be explained by loss of trophic action of NGF.
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PMID:New autonomic and sensory neuropathy with loss of adrenergic sympathetic function and sensory neuropeptides. 167 92

Orthostatic dysregulation (OD), originally a German-Scandinavian term partially corresponding to an Anglo-American concept of sympathotonic orthostatic hypotension, is characterised by altered cardiovascular control on standing, and its clinical features include dizziness, palpitation and, occasionally, orthostatic hypotension. The symptomatology suggests presence of cardiovascular adrenoceptor dysfunction, although the aetiology of OD has not been elucidated. The above situation prompted us to investigate autonomic nervous function in OD. The subjects were 8 patients with OD (20 +/- 2 years old; mean +/- SD), all of them fulfilled the diagnostic criteria accepted in Japan, and 6 healthy controls (17 +/- 3 years old). Noradrenaline and isoproterenol infusion tests and conventional haemodynamic functional tests (70 degrees passive head-up tilt, cold pressor test, Valsalva manoeuvre and Aschner's eye-ball pressure test) were carried out upon the subjects under the continuous measurement of blood pressure, pulse rate and respiration. Plasma vasoactive substances (noradrenaline, adrenaline, arginine-vasopressin and renin activity) were also determined in supine position and at 15 minutes after the 70 degrees passive head-up tilt. In noradrenaline infusion test, different doses (0.01 microgram/kg, 0.02 microgram/kg, 0.05 microgram/kg and 0.1 microgram/kg) of noradrenaline were administered by means of intravenous bolus injection, and a degree of subsequent rise in blood pressure was used as an index for the cardiovascular alpha-adrenoceptor sensitivity. In isoproterenol infusion tests cardiovascular beta 1- and beta 2-adrenoceptor sensitivities were assessed, respectively, by a degree of an increase in pulse rate and a degree of a fall in blood pressure following bolus injection of the drug (0.001 microgram/kg, 0.002 microgram/kg, 0.005 microgram/kg and 0.01 microgram/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiovascular alpha- and beta-adrenoceptor sensitivities in orthostatic dysregulation]. 216 87

Patients with transient ischemic attack (TIA) in the vertebrobasilar artery more often complain of disturbance of equilibrium, such as vertigo or dizziness, than of auditory disorders, such as hearing impairment or tinnitus. The author induced TIA in rabbits by injecting adenosine diphosphate (ADP) into the right vertebral artery. Observations of rotatory nystagmus have shown that a peak level of directional preponderance appeared 1 minute after injection of ADP (0.3mg/kg b.w.) and continued for more than 4 minutes. On the other hand, the amplitude of auditory brainstem responses (ABRs) presented no significant changes following the injection of ADP (0.5mg/kg b.w.). However, greater amounts of ADP (1.0 and 2.0 mg/kg b.w.) were found to reduce the amplitude of ABR-waves, although significant reduction was observed for only less than 1 minute. This change was represented by flattening of the later part of the waves, with the first wave much less affected. Electrocochleogram (E. Coch. G.) have also demonstrated a transient reduction in amplitude 10 seconds after injection of ADP (4.0mg/kg b.w.) with correspondingly rapid recovery. In cases of hypertension due to noradrenaline load or trimethaphan-induced hypotension, reduced amplitudes were more profound and continued longer, returning to its normal range within 1 minute. Differences in susceptibility between the equilibrium system and auditory system in TIA of the vertebrobasilar artery are discussed.
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PMID:[Difference in susceptibility between auditory and equilibrium function in rabbits with experimentally-induced transient ischemic attack]. 274 23

A 15-year-old boy with diarrhea, dizziness, dysesthesias, and depression is described. On admission, his blood pressure was 110/84 reclining but less than 40 systolic while standing. Vibratory sensation and nerve conduction velocities were decreased in his lower extremities. CSF protein concentration was normal but sural nerve biopsy demonstrated generalized demyelination. Extensive toxicologic and metabolic screening proved unremarkable. Norepinephrine concentrations in plasma and urine, and CSF concentration of 3-methoxy-4-hydroxy phenylglycol (MHPG) were markedly reduced. The patient demonstrates a combination of autonomic dysfunction, peripheral neuropathy, and affective disorder. This collection of clinical and neurochemical findings represents a previously unreported entity involving a defect of both central and peripheral noradrenergic systems.
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PMID:Autonomic dysfunction, peripheral neuropathy, and depression. 285 34

To determine whether E-643, a new alpha-blocking agent, would reduce the blood pressure, regardless of the posture, a 1 mg dose was given 3 times daily for 7 consecutive days, to 8 male and 7 female inpatients, aged 37--73 years, with essential hypertension. Blood pressure and pulse rate were measured daily in the supine, sitting and standing positions. Before and after the treatment with E-643, plasma levels of noradrenaline, adrenaline, dopamine-beta-hydroxylase, renin and aldosterone were determined, samples being obtained with the subjects recumbent and after standing upright for 60 min. A significant reduction in the systolic and diastolic blood pressures was evident in the supine (172 +/- 31/100 +/- 12 leads to 151 +/- 28/89 +/- 14 mmHg), sitting (158 +/- 22/101 +/- 11 leads to 138 +/- 28/89 +/- 15 mmHg) and standing (153 +/- 32/103 +/- 21 leads to 129 +/- 31/89 +/- 20 mmHg) positions. The reduction in blood pressure remained unchanged throughout the period of administration of E-643. Pulse rate was not affected when the subjects were supine (67 +/- 10 leads to 69 +/- 10 beats/min), but was increased in the sitting (68 +/- 10 leads to 73 +/- 9 beats/min) and standing (73 +/- 10 leads to 81 +/- 11 beats/min) positions. The increased pulse rate tended to decline during continued administration of E-643. Treatment with E-643 produced no significant change in plasma levels of adrenaline, noradrenaline, dopamine-beta-hydroxylase, renin and aldosterone. The antihypertensive effect of treatment was more prominent in the patients with higher levels of plasma catecholamines and dopamine-beta-hydroxylase, and was less prominent in those with higher plasma renin and aldosterone. Two patients had temporary bouts of dizziness and visual disturbances, but there were no subjective complaints during treatment.
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PMID:Antihypertensive effect of E-643, a new alpha-adrenergic blocking agent. 611 9

Diclofensine increases the availability of the three neurotransmitters dopamine, noradrenaline and serotonin by inhibiting their re-uptake into synaptosomes. In a randomized double-blind parallel-group comparative study, a total of 40 patients, some hospitalized (n = 11) and some ambulatory (n = 29), mean age of 39.6 years +/- 12 S.D., with psychoreactive depression were treated for 30 days with 2 X 25 mg/day of diclofensine or with placebo. The assessments of efficacy indicated superiority of diclofensine over placebo. The number of "improved" patients (reduction in the overall depression scores by 50% or better) relative to that of "not improved" patients, was found to be statistically significant (p less than 0.025) on day 10 of treatment. With respect to individual symptoms, anxiety showed a significantly (p less than 0.05) better improvement under diclofensine than under placebo. Side effects were observed in one patient in each group. One patient (diclofensine group) reported a transient slight somnolence, the other (placebo group) reported episodes of transient dizziness. Based on these data it can be concluded that diclofensine is a well tolerated and effective drug for the treatment of symptoms associated with reactive depressions.
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PMID:Therapeutic efficacy and tolerance of diclofensine in psychoreactive depression--a double-blind comparison with placebo. 637 45

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

Parkinsonian patients with orthostatic hypotension and dizziness due to usual antiparkinson therapy have been treated with the precursor amino-acid of noradrenaline, DL-3,4-threo-dihydroxyphenylserine (DL-3,4-threo-DOPS). Oral and intravenous administration improved these side effects significantly. A combined treatment of L-dopa, peripheral decarboxylase inhibitor and DL-3,4-threo-DOPS seems to be of benefit with respect to akinesia and orthostatic hypotension.
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PMID:DL-3,4-threo-DOPS in Parkinson's disease: effects on orthostatic hypotension and dizziness. 642 May 17


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