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

Flunarizine hydrochloride (FZ), a calcium entry blockade, has been used nationwide in Japan as a cerebral active vasodilator since October, 1984. The present paper reports 31 cases of FZ-induced Parkinsonism, depression and akathisia, referred to our hospital between October 1986 and September 1988. Out of the 31 patients, four including two with Parkinson's disease and one each with progressive supranuclear palsy and olivopontocerebellar atrophy showed worsening of their parkinsonian symptoms within a few months after FZ administration. The remaining 27 patients (7 males and 20 females) newly developed Parkinsonism after treatment with FZ. Symptoms appeared one week to two years (mean: 6.1 months) after starting FZ of a daily dose of 10 mg. FZ had been used in 6 patients for cerebrovascular episodes confirmed by clinical history or brain CT, and in the remainder, for dizziness, light-headedness, hypertension, amnesia or hypochondric neurotic complaints. Akinesia and bradykinesia progressed rather rapidly after onset, and patients became unambulatory within several months. Symptoms had worsened, and L-dopa, anticholinergic drugs, and bromocriptine had been ineffective until FZ was discontinued. Their Parkinsonism was characterized by marked akinesia, bradykinesia, and moderate rigidity. Masked face was seen in most of them. Tremor was absent at rest, and induced in 12 patients by posture and/or action. Sixteen patients were accompanied by depression, and five, by akathisia. Improvement began several weeks after withdrawal of FZ, and most patients recovered almost completely within a few months although mild rigidity and bradykinesia remained in some.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Parkinsonism, depression and akathisia induced by flunarizine, a calcium entry blockade--report of 31 cases]. 258 81

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

In order to evaluate sympathetic functions in Parkinson's disease (PD), thermal sweating was examined with colorimetric method in 50 cases of PD (22 males & 28 females, mean age at examination: 58 +/- 9.6 ys, mean duration of illness: 5.3 +/- 3.6 years, Hoehn and Yahr's stage: II-IV, patients without drugs: 15), and following results were obtained; normal sweating in 20 (A), possible generalized hyperhidrosis in 5 (B), localized hyperhidrosis in 4 (C), unilateral hypohidrosis in 7 (D), hypohidrosis over the trunk and legs in 7 (E), and anhidrosis over the trunk and lower extremities in 7 (F). In group F, acetylcholine- or pilocarpine-sweating was also defective, suggesting that postganglionic sympathetic fibers were also impaired. The results were analyzed with respect to age, duration and severity of illness, predominant somatic symptoms, postural changes of blood pressure or subjective dysuria. Abnormal sweating appeared to be related to higher age, severity of PD, and to rigid akinesia as the predominant symptoms. Group B appeared to involve relatively young patients without orthostatic hypotension or dysuria. Group B and C included 5 tremor-dominant patients. But, these features were not statistically significant. Patients in group F had rigid akinesia as the predominant feature (p less than 0.01), and showed higher incidence of dysuria (p less than 0.05). They appeared to have severe PD symptoms in spite of relatively shorter duration of the disease. An administration of drugs including anticholinergics had no significant influence upon the present results. It has been reported by several authors that the rapid progression of PD symptoms and early deterioration of mental status are related to rigid akinesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Thermal sudomotor deficits in Parkinson's disease]. 258 86

N-isopropyl-p[123I]iodoamphetamine (123I-IMP) SPECT and regional cerebral blood flow (rCBF) studies were performed in 20 patients with Parkinson's disease (PD) and 8 normal subjects. RCBF was measured by the arterial blood sampling method which used the microsphere model. We analyzed seven factors which might be related to the rCBF in PD, i.e., age, stage, duration of the disease, cerebral atrophy, severity of dementia, laterality of symptoms and motor disability score (MDS; the degree of akinesia, rigidity, tremor, gait disturbance, freezing and pulsion sign). Compared with normal subjects, global CBF (supratentorial mean rCBF) was reduced 21.8% in PD. In particular, rCBF in the basal ganglia and that of frontal cortex were reduced 25.3%, 24.8%, respectively. Distribution patterns of rCBF in PD were almost as same as those in normals except for cerebellum. The reduction of both rCBFs in the basal ganglia and parietal cortex significantly correlated with MDS (p less than 0.05, respectively). Especially, akinesia was closely correlated to the reduction of rCBF in the parietal cortex (p less than 0.02). Moreover, we observed a significant relationship between cerebral atrophy and reduction of rCBF in each region except for cerebellum. However, there was no significant correlation between the severity of dementia and reduction of rCBF, even in the frontal cortex or parietal cortex. These data show that the severity of dementia in PD may be connected with other factors except for rCBF. 123I-IMP SPECT study is a useful method for clinical evaluation of PD.
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PMID:[Clinical evaluation of Parkinson's disease using 123I-IMP SPECT]. 261 27

Dopamine (DA) is degraded in part by MAO, an intraneuronal and glial enzyme localized at the outer mitochondrial membrane. DA is a good substrate for MAO-B and selegiline enhances DA-transmission and improves akinesia of Parkinson's disease (PD) by selective MAO-B blockade. Immunocytochemistry (ICC) and histochemistry (HC) demonstrate that neurons of substantia nigra (SN) lack MAO near totally (but see Moll et al 1988). Consequently, inhibition of MAO-B in this brain area occurs mainly in glial cells. Therefore an increase of DA in glia seems to be of long-lasting therapeutic benefit in PD. In addition, synthesis of hydrogen peroxide generated via MAO-B is blocked by selegiline. By this toxicity by endogenous free radicals is diminished. Furthermore, exogenous neurotoxicity by MAO-B substrates can be prevented by inhibition of MAO-B, while such MAO-A substrates are metabolized at the level of the MAO-A containing endothelium of capillaries. As conclusion, selegiline is a safe inhibitor of MAO-B that reduces neurotoxicity possibly triggering PD. (Table: see text).
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PMID:Neurochemical perspectives to the function of monoamine oxidase. 261 92

Although rigidity and akinesia are two of the cardinal features of Parkinson's disease, their exact pathophysiology remains uncertain. Mechanisms which may contribute to rigidity include accentuation of the long-latency component of the stretch reflex and enhanced fusimotor drive causing increased sensitivity of muscle spindles. Current evidence concerning the role of these factors in rigidity is reviewed. The relationship between akinesia, prolonged reaction times, and delay in initiation of internally generated movements in parkinsonian patients is discussed.
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PMID:Pathophysiology of rigidity and akinesia in Parkinson's disease. 265 33

For the stereotactic treatment of Parkinson's disease, the target is usually located in the thalamus; this point is related to nearby structures (third ventricle). Then the position is controlled by electrophysiological recordings. The lesion of the target results in permanent suppression of the contralateral tremor and/or rigidity but it changes neither the course of the disease nor the akinesia. Owing to the risk of dysarthria with bilateral procedures, the main indication for surgery is parkinsonism with unilateral tremor or rigidity. Particularly interesting for the future are the possibilities of stimulation through implanted chronic electrodes.
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PMID:[Stereotaxic treatment in Parkinson's disease]. 265 87

This open trial is a study of the effect of adding bromocriptine (BC) to the treatment of patients who had taken a dopa-containing preparation (LD) for many years. Sixty-five patients entered the trial at an average age of 66.6 years. The mean duration of Parkinson's disease was 12.74 years and LD had been taken by one-half of them for more than 10 years and by an additional 27% for longer than 5 years. The duration of treatment with BC exceeded 2 years in 45% of cases and the average dose of BC was 19.27 mg/day. On the Hoehn and Yahr scale 70.8% of patients were classified as between stages II and IV, 24.6% were in stage I and 4.6% were in stage V. Dopa-induced involuntary movements were observed in 60% of patients at the beginning of the trial but were present in only 25% at the completion, due to the dopa-sparing effect of BC allowing a reduction of the dose of LD by an average of 34%. End-of-dose failure was reduced only slightly and on-off oscillations were not influenced by the addition of BC to LD. Tremor, rigidity, akinesia and dysarthria improved in 22% of all patients but BC offered no beneficial effect on the various gait disorders of Parkinson's disease. The conclusion of the study is that 47.7% of patients felt that the addition of BC to LD had reduced their involuntary movements and the disabilities of their disease.
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PMID:The addition of bromocriptine to long-term dopa therapy in Parkinson's disease. 270 77

In order to investigate the neuronal basis of cognitive disorders in Parkinson's disease, the neuropsychological performance of 120 patients with idiopathic Parkinson's disease was analysed in relation to motor symptoms as a function of their response to levodopa. Cognitive impairment was poorly correlated with akinesia and rigidity, symptoms which respond well to levodopa treatment, and was not correlated at all with that part of the patients' motor score that could be improved by the drug. In contrast, strong correlations were found between all neuropsychological test scores and axial symptoms such as gait disorder and dysarthria, which respond little if at all to levodopa treatment. The neuropsychological test scores were also strongly correlated with the motor score of patients estimated when clinical improvement was maximal under levodopa treatment. This score is assumed to represent residual non-dopaminergic motor dysfunctions. The correlations suggest that much of the cognitive impairment in Parkinson's disease results from the dysfunction of non-dopaminergic neuronal systems.
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PMID:Does cognitive impairment in Parkinson's disease result from non-dopaminergic lesions? 270 38

The frequency of shoulder disturbances, particularly frozen shoulder, has not been assessed previously in Parkinson's disease. In a survey of 150 patients compared with 60 matched control subjects a significantly higher incidence of both a history of shoulder complaints (43% vs. 23%) and frozen shoulder (12.7% vs. 1.7%) was found in the Parkinson's disease population. Those developing a frozen shoulder had initial disease symptoms indicative of akinesia twice as frequently as tremor while the ratio was reversed in those without frozen shoulder. In at least 8% of the patients frozen shoulder was the first symptom of disease, occurring 0-2 years prior to the onset of more commonly recognised features. Parkinson's disease should be added to the list of causes of frozen shoulder, and clinicians must be aware that the latter is often the presenting symptom of Parkinson's disease.
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PMID:Frozen shoulder and other shoulder disturbances in Parkinson's disease. 270 37


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