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)

We studied various forms of dystonia associated with Parkinson's disease (PD) in 207 patients who were on levodopa therapy for more than 1 year. Dystonia, sometimes more than one type, occurred in 63 (30%). In five patients, dystonia preceded initiation of treatment. Fifteen patients had peak-dose dystonia, 33 had early-morning dystonia, and 20 had "off-period" dystonia. The different clinical features of the dystonias are presented and compared. Findings indicate that dystonia is a frequent feature of levodopa-treated PD patients.
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PMID:Forms of dystonia in patients with Parkinson's disease. 358 17

Thirty-five patients with early mild Parkinson's disease were treated from the outset with small doses of L-dopa (mean dose, 396 to 454 mg daily) and a peripheral decarboxylase inhibitor, for a mean of 6 years. Overall mortality ratio was 1.2:1, worse for women than for men. After 6 years of treatment, only one-third of patients were better, and drug-related complications were common (peak-dose dyskinesias in 54% of patients, off-period dystonia 20%, wearing-off effects 52%, on-off oscillations 6%, visual hallucinations and toxic confusional states 17%). We found no evidence that long-term results were markedly improved with low-dose regimens.
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PMID:Low-dose L-dopa therapy in Parkinson's disease: a 6-year follow-up study. 376 73

15 years' experience with Parkinson's disease treated with levodopa was compared to the 15 years before the advent of levodopa. Progression to severe disability and death was prolonged, at each stage of severity, by 3 to 5 years. At each duration of illness, the percentage of patients with severe disability was reduced significantly. There was some indication that independence was prolonged by early treatment. Life expectancy was increased to approximately that of the unaffected population. However, especially with patients with onset of disease before the age of 50, fluctuations of therapeutic response and severe abnormal involuntary movements interfered with satisfactory therapeutic results. Supplemental bromocriptine produced a smoother therapeutic response and decreased "off" period dystonia and leg pains in over 70% of patients. At dosages below 20 mg daily, it was not particularly effective in severely affected disabled patients. Adverse reactions prevented the use of bromocriptine in less than 20% of patients.
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PMID:Result of chronic levodopa therapy and its modification by bromocriptine in Parkinson's disease. 398 85

Although trihexyphenidyl has been used effectively for many years in the treatment of Parkinson's disease, little is known about its pharmacokinetics. Using a sensitive radioreceptor assay for anticholinergic drugs, we assayed trihexyphenidyl in human serum and studied its pharmacokinetics following short-term and long-term administration to patients with dystonia. Previously untreated patients had a biphasic semilogarithmic plot of serum concentration-time consisting of an initial rapid distribution phase and a later slower elimination phase. Patients on long-term treatment showed only the slower elimination phase. Elimination followed first-order kinetics and was rapid, with a half-life of 3.7 +/- 0.4 (SEM) hours. There was no relationship between half-life and peak serum level, age, duration of therapy, or etiology or severity of dystonia. Although acute anticholinergic side effects paralleled the rise and fall of serum anticholinergic levels, the response of dystonia did not.
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PMID:Pharmacokinetics of trihexyphenidyl after short-term and long-term administration to dystonic patients. 403 49

The gait of normal subjects was examined electromyographically and the pattern was altered during preferential blockade of large nerve fibres to alternating activity in flexor and extensor muscles.The EMG activity was disrupted more in flexor than extensor muscles by preferential ischaemic blockade. Normal gait was associated with flexor contraction only when the foot was lifted and placed on the ground, whereas during ischaemic blockade flexor contraction continued during the interval between foot lifting and foot placement.The `freezing' or `blocking' gait in Parkinson's disease was found to be associated with coactivation of flexor and extensor muscles and this phenomenon occurred only in patients with features of flexion dystonia in the electromyographic recordings of their tonic stretch reflexes. Eight of nine patients with evidence of flexion dystonia showed a deterioration in their response to l-dopa therapy over a two year period, whereas four patients without flexion dystonia maintained their clinical improvement.
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PMID:Influence of dystonia on the response to long-term L-dopa therapy in Parkinson's disease. 473 32

Most classifications of movement disorders emphasize their differential diagnosis and epidemiology according to clinical history and neurological examination. This review of movement disorders is organized according to the hypothesis of basal ganglia neurotransmitter imbalance in order to emphasize current research based on the pharmacology of these disorders. Specifically, dopamine (DA) excess and acetylcholine (ACh) deficiency may characterize part of the pathology of several hyperkinetic movement disorders including tardive dyskinesia, Huntington disease, Gilles de la Tourette syndrome, l-dopa dyskinesias, tardive Tourette syndrome, and toxic Tourette syndrome. The mirror image of this paradigm, namely DA deficiency and ACh excess, may characterize several rigid-dystonic movement disorders including Parkinson disease, drug-induced dystonias, and dystonia musculorum deformans. Finally, the unique combination of DA excess with ACh excess may characterize idiopathic orofacial dyskinesia (also known as Meige dystonia, Brueghel syndrome, and blepharospasm-oromandibular dystonia). Evidence supporting this formulation of movement disorders is reviewed, the limitations of this hypothesis are discussed, and new data from our own studies are presented.
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PMID:The neuropharmacology of tardive dyskinesia, spontaneous dyskinesia, and other dystonias. 612 51

We measured the kinetic constants for the unidirectional influx of L-DOPA into red blood cells of patients with Parkinson's disease (seven patients), Huntington's disease (seven patients), and other extrapyramidal diseases (11 patients), and in five controls. Influx consisted of two components with low affinity and high exchange capacity. In individual subjects, the L-DOPA concentration giving half-maximal influx (Km) varied between 0.04 and 2.19 mM, and the maximum velocity (Vmax) of the saturable transport component was between 20 and 578 mumol/l cell water/h, which is compatible with the neutral amino acids of low affinity for the transport system. The range of Kd (the first-order rate constant for the unsaturable component) was between 0.11 and 0.36 hour-1. There was no gross deficit of the L-DOPA uptake process in patients with Parkinson's disease, Huntington's disease, dystonia, or other extrapyramidal diseases.
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PMID:Normal erythrocyte uptake of L-DOPA in Parkinson's, Huntington's, and related diseases. 622 Dec 1

Blink rate, a putative noninvasive marker of central dopamine activity, was assessed in medication-free patients with Parkinson's disease, progressive supranuclear palsy, Huntington's disease, and dystonia. The normal control rate of 24 blinks per minute was significantly higher than the rate of 12 and 4 blinks per minute recorded for patients with Parkinson's disease and progressive supranuclear palsy, respectively. The rates for patients with Huntington's disease and dystonia did not differ significantly from those of controls (36 and 26 blinks per minute, respectively).
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PMID:Blink rates and disorders of movement. 623 89

The cerebrospinal fluid concentration of hydroxylase cofactor has been measured in patients with Parkinson's disease, the Shy-Drager and Steele-Richardson syndromes, adult onset focal dystonia, essential tremor, Huntington's disease and presenile dementia. The results were compared with age matched controls and low values were demonstrated for all disease groups studied except for focal dystonia.
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PMID:CFS hydroxylase cofactor levels in some neurological diseases. 644 17

Immunoreactive vasoactive intestinal peptide (VIP) was measured in lumbar and ventricular cerebrospinal fluid (CSF) from patients with various neurological disorders and in 2 hour aliquots of cisternal fluid removed continuously from rhesus monkeys. Although most of the VIP in concentrated pools of human ventricular fluid and of monkey cisternal fluid co-eluted with synthetic porcine VIP28 on a column of Sephadex G-25 superfine, there was evidence that smaller immunoreactive fragments were also present. A circadian pattern of CSF VIP concentration was observed in 2 of the 3 monkeys studied, with highest levels occurring at night and lowest during the day. Ventricular fluid VIP levels were highest in hydrocephalic children and lowest in patients with multiple sclerosis or epilepsy, while VIP was not detectable in ventricular fluid from patients in coma following a severe head injury. There were no significant differences in VIP concentrations in CSF from patients with dystonia. Parkinson's disease, or Alzheimer's disease, suggesting that VIP containing neurons are not affected in these disorders. Lumbar fluid VIP levels were low in patients undergoing aneurysm surgery. Since VIP is a potent vasodilator, these findings may have important implications in relation to the development of vasospasm following subarachnoid hemorrhage.
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PMID:Vasoactive intestinal peptide in cerebrospinal fluid. 647 66


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