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)

The aim of the present study was to find out whether a blockade of adenosine A2A receptors by the selective antagonist, SCH 58261, potentiates the attenuating effect of L-DOPA, the well-known antiparkinsonian drug, on parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic method, which simultaneously measured muscle resistance of a rat hindfoot to passive extension and flexion in the ankle joint and the electromyographic (EMG) activity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was produced by reserpine (5 mg/kg ip) injected in combination with alpha-methyl-p-tyrosine (alpha-MT, 250 mg/kg ip). L-DOPA (25 mg/kg ip) or SCH 58261 (0.1 mg/kg ip) administered separately, slightly influenced the reserpine + alpha-MT-induced muscle rigidity. However, only ankle joint extension was affected significantly while the effect on flexion of the rat hindfoot was not significant. Neither L-DOPA nor SCH 58261 given separately modified the reserpine-enhanced tonic or reflex EMG activities in both muscles examined. However, when L-DOPA (25 mg/kg) was given together with SCH 58261 (0.1 mg/kg), a clear synergistic effect was seen on both examined movements and muscles. The present results show that the blockade of adenosine A2A receptors potentiates the antiparkinsonian effect of L-DOPA. Since such an effect was seen in different animal models of Parkinson's disease (PD), it seems that co-administration of SCH 58261 may allow for the lowering of the doses of L-DOPA in clinical practice, which indicates a potential therapeutic value of this compound in the treatment of PD.
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PMID:Synergistic effect of SCH 58261, an adenosine A2A receptor antagonist, and L-DOPA on the reserpine-induced muscle rigidity in rats. 1292 42

A 64-year-old male with treated Parkinson's disease underwent mechanical valve replacement for aortic valve regurgitation. The antiparkinsonian drugs for internal use were interrupted on the morning of the operative day. After the operation, the patient developed fervescence, muscle rigidity, hidropoiesis and a rise in creatine kinase. The patient was diagnosed as neuroleptic malignant syndrome and given medication dantrolene sodium and antiparkinsonian drugs on the 5th postoperative day. The symptom of neuroleptic malignant syndrome disappeared on 12 postoperative days. As the stress of open heart surgery with extracorporeal circulation trigger off neuroleptic malignant syndrome, the patient with Parkinson's disease need early beginning of antiparkinsonian drugs on account of prevention of neuroleptic malignant syndrome after operation.
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PMID:[Neuroleptic malignant syndrome after aortic valve replacement; report of a case]. 1367 24

An 80-year-old man was admitted to our hospital because of bradykinesia, muscle rigidity and respiratory dysfunction during sleep. Concerning bradykinesia and muscle rigidity, we diagnosed him as the early/moderate stage of Parkinson's disease without autonomic dysfunction. Polysomnography (PSG) showed a series of obstructive hypopneas and apneas. After administration of antiparkinsonian drugs, rigidity of the neck and trunk was diminished along with a drastic decrease in hypopnea on PSG. We consider that sleep hypopnea in this patient is caused by involvement of the striated musculature surrounding the upper-airway and/or rigidity in the trunk. These conditions are treatable with antiparkinsonian drugs.
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PMID:Improvement of sleep hypopnea by antiparkinsonian drugs in a patient with Parkinson's disease: a polysomnographic study. 1468 57

The efficacy of the majority of drugs currently used for treatment of Parkinson's disease is insufficient. Moreover, such therapeutics are not devoid of serious side effects. Multiple studies on animal models of parkinsonism have shown that new class of drugs, acting selectively on metabotropic glutamate receptors (mGluRs) might be very promising for the future therapy of Parkinson's disease. This review briefly describes changes in glutamatergic transmission in the neuronal circuitry of the extrapyramidal system that occur in parkinsonian patients, contains background information on structure, function and distribution of mGluRs throughout the basal ganglia and concentrates on discussion of the results obtained from numerous animal model studies aimed to establish potential antiparkinsonian properties of various mGluR ligands. The reviewed literature data indicate that among these compounds group I mGluR antagonists and group II mGluR agonists might be beneficial to the treatment of parkinsonian akinesia and muscle rigidity.
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PMID:Role of metabotropic glutamate receptors in animal models of Parkinson's disease. 1473 87

Patients with Parkinson's disease develop gait disturbances. Although the use of walkers is very effective for maintaining locomotive ability, patients who have symptoms such as frozen gait (FG) and festinating gait may fall even with a walker equipped with a brake as they cannot use the brake well in an emergency and fail to follow the accelerating walker. None of the studies on walking aids to date have addressed real-time detection of FG or the use of this information for the control of the walking aid, monitoring of the state of improvement in the ambulatory function, or evaluation of the effect of the use of a walker. In this study, we evaluated whether the state called FG, a characteristic symptom of Parkinson's disease, can be detected by the use of a sensor-controlled walker with heel-to-toe pressure sensors. The following two measurements were carried out in one male healthy and a one male patient with stage 3 Parkinson's disease by the Hoehn-Yahr scale showing mild muscle rigidity, hypokinesia, and FG. In the healthy subject, the heel-to-toe pressure showed smooth heel-to-toe shifts during the standing phase. In the patient with Parkinson's disease, the heel-to-toe response time was about 2.4 times longer than in the healthy subject at the beginning of walking, and FG could be recorded as the difficulty in lifting the foot by the toes. Also, when FG was observed during walking, the pressure waves recorded by the same sensors showed two peaks occurring at short interval, indicating double landings.
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PMID:Real-time measurement of frozen gait in patient with parkinsonism using a sensor-controlled walker. 1500 Feb 64

Rigidity in Parkinson's disease (PD) is defined as an increased resistance to passive movement of a joint. The plastic-type rigidity is uniform and constant throughout the entire range of motion, whereas the cogwheel-type rigidity is accompanied by tremor. Rigidity in PD has been understudied. Thus, its pathophysiological basis remains unclear. The purpose of the study is to examine neuromuscular/biomechanical properties of PD rigidity and to provide its physiological characteristics. We hypothesize that PD rigidity presents as a flattened trace of joint torque vs. angular position (torque-angle relation) of the wrist, because the forces generated by lengthening muscles are offset by activation of the antagonist, i.e. show "shortening reaction" (SR). Experiments were conducted on six PD subjects medication OFF and ON. PD severity was assessed based on the unified Parkinson's disease rating scale. Each subject sat on a chair and was instructed to relax, with the wrist coupled to the device. The servomotor applied constant velocity displacement to create wrist flexion/extension. Electromyographic (EMG) responses were monitored from wrist muscles, along with position, velocity and torque. EMG magnitudes were computed over the movement period. Slopes were derived from the torque-angle trace. Results showed that SRs were routinely recorded OFF medication, but substantially reduced ON medication. Due to the interaction of SR, torque-angle relation was flatter OFF medication and became steeper ON medication. Correlation analyses showed that a strong correlation (R=0.65) existed between SR and torque-angle slope OFF medication, exclusively. We suggest that SR may play an important role in mediating the mechanical features of PD rigidity.
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PMID:The role of shortening reaction in mediating rigidity in Parkinson's disease. 1512 73

The neurodegenerative death of dopaminergic neurons of the pars compacta of the substantia nigra leads to the classical triad of resting tremor, muscle rigidity, and bradykinesia of Parkinson's disease. Parkinson's disease is a common disease of elderly patients requiring perioperative anaesthesia. Particular anaesthetic problems are neurological, respiratory, and cardiovascular. The clinical features and the interaction of common anaesthetics with the drug therapy of the patient present an anaesthetic challenge and directly influence perioperative morbidity and mortality.
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PMID:[Anaesthesia in patients with Parkinson's disease]. 1577 5

We report a 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty in eye-lid opening, and marked pseudo-bulbar palsy. He felt difficulty of it, hand movement at 59 years old. When he was 60 years old, monotonous speech and slowness of movement appeared. He visited a neurologist who noted vertical gaze palsy, neck rigidity, and bradykinesia. He was diagnosed as progressive supranuclear palsy (PSP) and given 300 mg L-Dopa/Benserazide by the neurologist. This medication improved his rigidity and bradykinesia. At 62 years of the age, his eye-lids closed involuntary and it was difficult to open. In addition, he began to complain of wearing-off, autonomic symptoms, and dysphagia. Anti-parkinsonian drugs were increased, but his bradykinesia progressed. At 64 years of the age, he was admitted to the Neurology Service of Juntendo Hospital. On admission, he was alert and not demented. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, upward and downward gaze were markedly restricted. His face was hypomimic and seborrhoic. It was difficult to swallow liquid or solid for him. No weakness was noted, but he walked in small steps with freezing and falling tendency to backward. Rigidity was noted on his extremities and stronger on his left side than right. Tremor was absent. Bradykinesia of his body and extremities was marked. No cerebellar ataxia was noted. Deep tendon reflexes were within normal range. Planter response was flexor bilaterally. Myerson's sign was noted. Sensory and autonomic function were normal. He was treated with L-Dopa, Pergolide, and Bromocriptine. However, these medications improved his bradykinesia and gait disturbance only slightly, dysphagia became progressively worse. He developed aspiration pneumonia when he was 65 years old and admitted to Juntendo Hospital. A large amount of sputum was aspirated from his trachea. Two days after from admission, he was found dead on his bed. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had progressive supranuclear palsy (PSP). Other differential diagnoses included Parkinson's disease, pallido-nigroluysian atrophy (PNLA), multiple system atrophy (MSA), and corticobasal degeneration(CBD). Many participants considered that PSP or PNLA was most likely. Post-mortem exmination revealed marked nigral neuronal loss and gliosis. The globus pallidus and the luysian body changed mildly. However, the frontal cortex was relatively spared, there were many ballooned neurons in the cortical layer. Other parts were spared. With sliver (Bodian and Gallyas-Braak) and anti-phsphorylated tau stain, abundant astrocytic plaques, neurofibrillary tangles, and argyrophilic threads on the frontal cortex, striatum, and substantia nigra were seen. There was no tufted astrocyte which was hallmark of diagnosis of PSP. In addition, several Lewy bodies were seen in the brainstem. Because astrocyte plaque was considered specific for pathology of CBD, the pathologist revealed that the pathological diagnosis of this patient was CBD. Nevertheless, discussion was focused on the relatively mild degeneration of the frontal cortex for CBD.
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PMID:[A 65-year-old man with rigid-bradykinetic parkinsonism, vertical gaze palsy, difficulty of eye-lid opening, and marked pseudo-bulbar palsy]. 1578 4

Parkinson's disease (PD) is a neurodegenerative disorder characterised by motor symptoms (resting tremor, brady- or akinesia and muscle rigidity), and also by postural problems gait disorder and fatigue as well as behavioural and autonomic symptoms, including thermoregulatory impairment. These symptoms are strikingly similar with some motor phenomena, evoked by the whole body cooling, though the primary cause of PD and cold-induced symptoms are apparently different. The review is focused on the hypothesis that thermoregulatory mechanisms are involved in pathophysiology of motor disorders in PD. The comparative analysis provides some examples of analogy between PD and the state of cooling in respect with tremor, muscle hypertonus, postural reactions and impairment of gross and fine muscle performance. This analogy cannot be considered as specific, because in some normal conditions the motor system utilises identical strategy to compensate for motor deterioration, e.g. at fatigue and ageing. However, such motor phenomena, as neuroleptic malignant syndrome and paired discharges of motor units indicate that the "thermoregulation-dependent component" exists in the pathophysiology of PD. Data on the influence of the whole body cooling and heating on muscle performance, rigidity and tremor in PD patients also provide evidence for the involvement of thermoregulatory mechanisms in PD.
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PMID:"Thermoregulation-dependent component" in pathophysiology of motor disorders in Parkinson's disease? 1583 63

Idiopathic parkinsonism (IP) is a common disorder, conventionally regarded as neurodegenerative. Its cardinal features, poverty and slowness of movement, muscle rigidity, postural abnormality and a characteristic tremor, are associated with loss of dopaminergic neurones in the substantia nigra of the brain. Genetic factors explain only a minority of cases, and a common toxic environmental insult remains elusive. We propose that IP is a systemic disorder resulting from a ubiquitous peripheral infection, and that only the tip of the iceberg comes to diagnosis. There is evidence for inflammatory/immune activation peripherally and in the brain. We have used statistical modelling to explore links with non-specific and specific systemic markers of inflammation/infection in IP probands, and explore whether their partners and siblings have a frank or pre-presentation parkinsonian state. Critical to this approach is continuous objective measures of the facets of IP. Hypotheses on causality and mechanism are based on the statistical models. There is pathological and clinical evidence for direct involvement of the gastrointestinal tract in IP. The candidacy of Helicobacter pylori infection as a trigger event or driving infection is relatively high. We have found that eliminating infection in late parkinsonism with cachexia, a stage usually considered intractable, can result in a U-turn. However, eradication therapy may not provide a complete solution. Persistence of antibody against cytotoxin-associated antigen (CagA), increases the predicted probability of being labelled as having parkinsonism. Evidence for autoimmunity and immunocompromise is used to build schemes for the natural history. We conclude that current classifications of neuropsychiatric disease may not prove the best with respect to defining sub-clinical disease, prophylaxis or halting progression.
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PMID:Role of inflammation in gastrointestinal tract in aetiology and pathogenesis of idiopathic parkinsonism. 1586 6


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