Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
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PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58

Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to dogs produces clinical, pathological and neurological features in dog resembling human Parkinson's disease. Using this animal model, we studied the changes in diurnal rhythms of urine volume, creatinine in urine, and vasopressin, aldosterone and renin activity in plasma. Before MPTP treatment, urine volume showed a peak between 17.00 and 1.00 and plasma vasopressin concentration also showed a clear circadian rhythm with a peak at 13.00 and a minimum level at 5.00. Two weeks after MPTP treatment (2.5 mg/kg i.v.), the rhythm of urine volume disappeared and that of vasopressin became less clear. Plasma renin activity increased 2 and 4 weeks after MPTP treatment. The increase was, however, not enough to change the concentration of plasma aldosterone. We examined the effect of L-3,4-dihydroxyphenylalanine (levodopa), on the circadian pattern of urine volume and vasopressin attenuated by MPTP. Levodopa (4 mg/kg/day) was administered orally every day from the first week after MPTP treatment. The circadian rhythms of urine volume and vasopressin reappeared within one week after the start of levodopa administration.
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PMID:Disappearance of circadian rhythms in Parkinson's disease model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in dogs. 150 21

This paper gives a review on the clinical features of autonomic failure which occur in idiopathic Parkinson's disease (PD), mainly based on the recent publications, especially from Japan. In 1817, James Parkinson already mentioned bowel and bladder dysfunctions in his original article. Since then, a number of clinical studies have disclosed the occurrence of autonomic failure in this disease. It is known that relatively minor degrees of orthostatic hypotension are not rare, but other features of autonomic failure are rather uncommon, generally mild in severity and nonprogressive. Orthostatic hypotension is suggested as a possible side effect of L-dopa. Postprandial hypotension is occasionally found, and vasopressin is proven to prevent it remarkably. There is low electrocardiographic R-R interval variability which indicates impaired parasympathetic activity. Thermoregulatory sweating is nearly normal, but its center is functionally impaired. Resting skin temperature is slightly lower. Both salivation and lacrymation are quantitatively within normal limits. Little is known on sexual function in PD.
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PMID:Autonomic nervous system disorders in Parkinson's disease. 185 22

1. The application of in situ hybridization histochemistry to the study of neuropeptide gene expression in human brain postmortem tissues is reviewed. We focus on neuropeptides preferentially expressed in hypothalamus and basal ganglia. 32P-labeled oligonucleotides were used as hybridization probes. 2. Autoradiography combined with computerized image analysis was used to visualize and quantify the hybridization signal. 3. Several criteria were considered in order to ascertain the specificity of the signal, including Northern analysis, use of heterologous probes, competition assays, and thermal stability of the hybrids. 4. In control human striatum high levels of hybridization signal were observed for somatostatin, neuropeptide Y, and preproenkephalin A mRNAs. In contrast, no detectable signal was observed with the cholecystokinin, arginine-vasopressin, and oxytocin probes in this area. In the hypothalamus high levels of oxytocin and arginine-vasopressin mRNAs were visualized in several nuclei. Preproenkephalin A and somatostatin mRNAs were also observed in this region, while cholecystokinin mRNA was not detected. 5. No significant correlations were found between the density of the hybridization signal and parameters such as postmortem delay, age, and gender in the population studied. 6. Finally, alterations of mRNA levels for some of these peptides were found in Parkinson's disease and Huntington's chorea striatal tissues. 7. These results show that in situ hybridization histochemistry can be used to examine at the microscopic level neuropeptide gene expression in postmortem materials.
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PMID:The use of in situ hybridization histochemistry for the study of neuropeptide gene expression in the human brain. 233 44

A possible etiology considered in a case of inappropriate antidiuretic hormone secretion syndrome in a patient with Parkinson's disease treated with levodopa was an organic or functional dysregulation due to Parkinson's disease or its treatment. An unusual feature in this case was the long duration of the syndrome.
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PMID:[Parkinson's disease and inappropriate antidiuretic hormone secretion syndrome]. 307 Jun 89

In Huntington's disease, there is a decrease of the neuropeptides, substance P, enkephalins, and cholecystokinin in the striatonigral system, whereas in Parkinson's disease an increase of substance P is found in the substantia nigra. Several neuropeptides should be involved in Alzheimer's disease: substance P, endorphins, vasopressin, ACTH, somatostatin, vasoactive intestinal peptide, cholecystokinin, neurotensin, delta sleep-inducing peptide. Alterations of substance P, vasoactive intestinal peptide, cholecystokinin, somatostatin, and endorphins may be related to the pathophysiology of schizophrenia. Delta sleep-inducing peptide may interfere in addiction pathology.
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PMID:Putative peptide neurotransmitters in human neuropathology: a review of topography and clinical implications. 618 57

Vasopressin immunoreactivity was measured post-mortem in the locus coeruleus and substantia nigra of 16 cases of Parkinson's disease and multisystem atrophy, 10 cases of Huntington's chorea and 28 normal controls. Amounts of vasopressin did not differ significantly (P greater than 0.05) between the 3 groups. Immunohistochemistry demonstrated vasopressin within nerve terminals. These data are consistent with an extrinsic vasopressin system in the human locus coeruleus and substantia nigra.
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PMID:Extrahypothalamic vasopressin is unchanged in Parkinson's disease and Huntington's disease. 621 62

A double-blind crossover pilot study was carried out in six patients with Parkinson's disease in order to test the possible therapeutic effect of L-vasopressin after treatment for 1 month with 30 I.U. intranasally daily. The investigation was completed in five cases. No effects was noticed after LVP treatment.
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PMID:Vasopressin therapy in Parkinson's disease. 721 Nov 72

We determined the number of immunocytochemically identified oxytocin (OXT) and vasopressin (AVP) neurons in the paraventricular nucleus (PVN) of the human hypothalamus of six Parkinson's disease (PD) patients ranging from 59 to 83 years of age. Six subjects without a primary neurologic or psychiatric disease, ranging from 69 to 88 years of age, served as controls. The OXT-immunoreactive cell number in the PVN of the PD patients was 22% lower than that of the control subjects. Although Lewy bodies were present in the nucleus basalis of Meynert, there were no Lewy bodies in the PVN of these patients. Doubt is raised about the presumed direct relationship between the presence of Lewy bodies and neuronal degeneration in PD. The AVP-immunoreactive cell number in the PD patients showed a similar decreasing trend, but the 18% reduction failed to reach statistical significance. The presence of tyrosine hydroxylase-positive neurons in the PVN was not affected in PD patients, supporting the notion that dopaminergic neurons of the mesencephalon, but not of the hypothalamus, are affected in PD. The decreased number of OXT-containing neurons in the PVN suggests that dopamine may be important for the function of these neurons and may provide a neural basis for some autonomic and endocrine disturbances in PD.
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PMID:Decreased number of oxytocin-immunoreactive neurons in the paraventricular nucleus of the hypothalamus in Parkinson's disease. 790 35

Central autonomic dysfunctions can be due to primary (degenerative) or secondary disorders. Autonomic failure (AF) may be a major manifestation of multiple system atrophy (MSA) and idiopathic Parkinson's disease (IPD). In both MSA and IPD, AF is almost invariably associated with neuronal loss in the intermediolateral cell columns. Dysautonomia in MSA is early, severe, and progressive, including marked orthostatic hypotension and urinary incontinence and is complicated by respiratory disturbances, such as laryngeal stridor and sleep apnea. MSA/AF can be differentiated from primary (or pure) autonomic failure (PAF) without central nervous system involvement. PAF is mainly a disorder of the postganglionic neurons. In contrast to PAF, MSA/AF has preserved basal sympathetic activity, decreased cerebrospinal fluid (CSF) neurotransmitter markers, impaired vasopressin response to hypotension, and impaired adrenocorticotrophic hormone/beta endorphin response to hypoglycemia. AF in IPD is generally less severe than in MSA. Poor response to L-Dopa, abnormal urethral sphincter electromyography, and CSF markers may distinguish MSA from IPD. Secondary autonomic disorders may result from traumatic, vascular, inflammatory, demyelinating, or neoplastic lesions involving corticolimbic, hypothalamic, brainstem, or spinal autonomic network. These disorders can cause AF or autonomic hyperactivity, such as arrhythmia, hypertension, and hyperthermia. However, many disorders may only produce subclinical abnormalities.
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PMID:Central autonomic disorders. 845 95


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