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)

Adult-onset dystonia-parkinsonism is a syndrome in search of a pathology. We therefore reviewed the literature on dystonic manifestations in autopsy-proven cases of multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and idiopathic Parkinson's disease (PD). Only 6 of 140 autopsy reports of MSA remarked on the presence of dystonia in life, but personal observations suggest prominent antecollis may develop at some stage in up to 1/2 of sufferers. Similarly, very few (15/118) clinicopathologic observations on PSP included convincing dystonic manifestations, in contrast to some clinical reports where blepharospasm and early limb dystonia were prominent. Virtually any form of focal and segmental dystonia may sometimes occur with clinically diagnosed PD, with occasional descriptions of hemidystonia-hemiparkinsonism. However, there is pathologic confirmation of this diagnosis in only 1 case. With many patients thought clinically to have PD proving pathologically to have another cause for their parkinsonism, the true frequency and the range of dystonic manifestations acceptable in PD remain unknown.
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PMID:Dystonia in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy. 221 50

Madopar Hydrodynamically Balanced System (HBS), a new sustained-release levodopa preparation, was used to control severe nightly disabilities in 15 outpatients suffering from Parkinson's disease in an advanced state and with long-term levodopa therapy. This medication was given ante noctem in addition to an otherwise unchanged daily regimen of levodopa administration. In 13 patients a considerable diminution in nocturnal akinesia and in the frequency of waking up was reached with a mean dosage of 308 mg of Madopar HBS. Early morning akinesia was only slightly alleviated in four patients. The nocturnal off-period pain disappeared in one patient. Adverse effects consisted of nocturnal dyskinesia in two patients and early morning dystonia in another two patients. The regular use of sleeping pills was clearly reduced after Madopar HBS therapy.
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PMID:Madopar HBS in nocturnal symptoms of Parkinson's disease. 223 93

We studied the clinical characteristics and plasma levodopa (LD) profile of complex, LD-associated dystonia in 33 patients with Parkinson's disease (PD). Generalized, abdominal, respiratory, and myoclonic, but not facial or foot, dystonia could be related to specific phases of the plasma LD cycle. Simultaneous clinical observation and determinations of plasma LD concentrations were often necessary to find the most efficacious dosing schedule for these patients. Maintenance of steady plasma LD concentrations within a dystonia-free window of benefit was the best treatment.
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PMID:Complex dystonia of Parkinson's disease: clinical features and relation to plasma levodopa profile. 232 7

Intermittent treatment with L-dopa over a 2-year period induced abnormal involuntary movements in MPTP-treated squirrel monkeys. Dyskinesias included a choreic and dystonic component. Dose-response curves for chorea and dystonia revealed that the same dose of L-dopa (30 mg/kg) induced the highest score for both dyskinesias: however, the severity was much greater for chorea. Choreic movements were always most prevalent at the time of peak effect, whereas dystonia was apparent at the time of peak effect and at "end-of-dose", and was occasionally observed spontaneously. Our findings indicate that squirrel monkeys treated with MPTP develop L-dopa-induced dyskinesias which closely resemble those observed in Parkinson's disease. This species provides a valuable animal model to develop improved therapeutic agents.
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PMID:Characterisation of dyskinesias induced by L-dopa in MPTP-treated squirrel monkeys. 239 4

We report the clinical spectrum of 3 patients with Parkinson's disease who experienced complex patterns of levodopa-related dystonia. Dystonia was unrelieved by multiple medication regimens but responded well to continuous, duodenal levodopa infusions. Patients were able to remain mobile without severe dystonia despite a very narrow window of benefit between the levodopa concentration necessary to achieve the "on" state and that which caused the onset of dystonic spasms.
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PMID:Continuous levodopa infusions to treat complex dystonia in Parkinson's disease. 247 82

Three patients with clinical and pathological features of corticobasal degeneration are described. They presented with a progressive disease bearing some clinical resemblance to Steele-Richardson-Olszewski syndrome and displaying some pathological features of Pick's disease. Their illness began at the age of 59 to 66 yrs with focal dystonia and myoclonus of an arm, the 'alien hand' sign, or an akinetic-rigid syndrome. They developed a supranuclear gaze palsy, parkinsonian features and mild cerebellar signs. Two patients showed constructional dyspraxia when using the arms. The duration of disease to death was 4 to 6 yrs. Pathological examination showed frontoparietal atrophy with cortical cell loss, gliosis and Pick cells, but there was no significant hippocampal disease or Pick bodies in this region. There was nerve cell loss and gliosis in the thalamus, lentiform nucleus, subthalamic nucleus, red nucleus, midbrain tegmentum, substantia nigra and locus coeruleus. Neuronal inclusions in the substantia nigra, termed corticobasal inclusions, were reminiscent of the globose neurofibrillary tangle of Steele-Richardson-Olszewski syndrome, and other pale inclusions resembled the pale body of Parkinson's disease, but Lewy bodies and neurofibrillary tangles were generally absent. Some nigral inclusions were similar to those in Pick's disease. Despite some pathological similarities to Pick's disease we suggest that the distribution of nerve cell loss and the corticobasal inclusion are unique to corticobasal degeneration.
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PMID:Corticobasal degeneration. 2059 45

We have analyzed magnetic resonance images in 33 patients; 18 patients with Parkinson's disease, 1 patient with diurnally fluctuating progressive dystonia, 1 patient with pure akinesia, 6 patients with multiple system atrophy, 1 patient with flunarizine induced parkinsonism, and 4 patients with unclassified parkinsonism. The MR images were obtained using a 1.5-T GE MR System. A spin-echo pulse sequence was used with a TE of 30 msec and 80 msec and a TR of 2000 msec. No signal abnormalities were seen in any patient with Parkinson's disease but 3 showed slightly decreased signal intensity of the putamen on T2-weighted sequences. Patients with diurnally fluctuating progressive dystonia and pure akinesia evidenced no abnormal findings. All six patients with multiple system atrophy demonstrated decreased signal intensity of the putamen, particularly along their lateral and posterior portions, and an enlarged substantia nigra. Atrophy of the pons and cerebellum was detected in all cases with multiple system atrophy. One case of flunarizine induced parkinsonism showed slightly decreased signal intensity of the putamen. Four cases of unclassified parkinsonism showed decreased signal in the putamen on T2-weighted sequences. Magnetic resonance imaging has the potential to become a useful diagnostic tool in the management of parkinsonism.
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PMID:[Magnetic resonance imaging of parkinsonism]. 258 85

We compared the chronic (2-year) effect of substitution with Sinemet CR with the effect of continued administration of standard Sinemet on motor fluctuations and drug-induced side effects in Parkinson's disease (PD). Twelve patients in each treatment group were pair-matched for age, PD duration, duration of levodopa therapy, dosage of Sinemet, PD disability, and side-effect prevalence at study entry. After 2 years, both groups were more disabled from their PD than at baseline; the disability scores were equivalent for the 2 treatments. The Sinemet CR group had fewer fluctuations and fewer side effects. Compared with the standard Sinemet group, Sinemet CR patients had more "on" time (mean 83% versus 62%, p less than 0.001), and had a lower prevalence of disabling chorea (p less than 0.007), dystonia (p less than 0.003) and sleep disruption (p less than 0.002). Prevalence of hallucinations was equivalent for the 2 groups. These results suggest that Sinemet CR is beneficial in ameliorating and preventing the high frequency of some side effects of standard Sinemet treatment.
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PMID:Development and progression of motor fluctuations and side effects in Parkinson's disease: comparison of Sinemet CR versus carbidopa/levodopa. 258 64

A 12-year-old boy developed occasional attacks of oculogyric crisis after physical exercises or when tired. Following the initial symptom, progressive Parkinsonian features such as bradykinesia, muscular rigidity, hand tremors in posture, mild dysarthria and disorder of postural reflexes developed. There was no marked diurnal fluctuation o symptoms. Serum ceruloplasmin, copper levels, cranial X-ray CT scan and MRI were normal. Measurement of the plasma levels of L-dopa after single oral administration (300 mg) were normal. The treatment with L-dopa improved the Parkinsonian features excluding the attacks of oculogyric crisis in a few weeks. This case is not identical with juvenile Parkinsonism proposed by Yokochi et al for lack of both crural or truncal dystonia and remarkable response to L-dopa. Oculogyric crisis is known in several patients with severe generalized dystonia, and seldom in patients with Parkinson disease or juvenile Parkinsonism. Oculogyric crisis may be one of focal dystonias confined to extraocular muscles.
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PMID:[Oculogyric crisis as an initial symptom of juvenile parkinsonism-like disease]. 260 35

The long term effects of a de novo treatment with levodopa versus bromocriptine were compared in respectively 13 and 15 previously untreated patients with Parkinson's disease in a prospective randomised trial. Thirteen patients were treated with levodopa alone (mean dose 444, SEM 63 mg daily) whereas 15 others received bromocriptine alone (mean dose 50, SEM 6 mg daily) during 37, SEM 4 and 32, SEM 4 months respectively. For a similar decrease in the Columbia rating scale, the nature of long term side effects was different in the two groups: three patients on levodopa developed peak-dose dyskinesias and one other dystonia. With bromocriptine, one patient developed a severe psychosis whereas 3 others suffered from primary lack of efficacy (1 case) or late decrease in efficacy (2 cases). These results demonstrate the potential of D2 dopamine agonists (like bromocriptine) in the de novo treatment of Parkinson's disease; however, their use is limited by their lack of efficacy and/or the occurrence of neuropsychiatric side effects.
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PMID:A randomised controlled study of bromocriptine versus levodopa in previously untreated Parkinsonian patients: a 3 year follow-up. 266 89


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