Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026837 (muscle rigidity)
 1,077 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In an open study, 60 Parkinson patients with varying aetiology were submitted to a treatment with the long-acting antiparkinsonian drug dexetimide and L-Dopa. Rigor, tremor and akinesia were favourably influenced. An advantage over other antiparkinsonian agents is its long duration of action and the possibility of a simple dosage. Further investigations concerning its long-term effect and elucidation of its interactions with different drugs commonly administered in parkinsonian disorders seem desirable.
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PMID:Treatment of Parkinsonian syndrome with dexetimide. 55 48

A study of the catecholamine excretion, their precursor DOPA and final metabolites--Homovaniline and vanilylphenylglycolic acid in torsion dystonia, detected certain changes which were different in patients with various clinical forms of the disease. On the basis of clinical and biochemical data 3 forms of torsion dystonia were distinguished: 1) with a prevalence in the clinical picture of muscle rigidity, leading to the development of pathological postures; 2) hyperkinetic forms and 3) mixed forms. In patients of the first group there was a decreased excretion of all catecholamines. On the basis of obtained data the conclusion is made that there is a drop in the intensity of the process of dophamine synthesis and an increase of its catabolism. In the hyperkinetic form, on the contrary, there is a tendency to an increase of dophamine synthesis. It is assumed that there is a drop in the intensity of the process of adrenaline synthesis and an increase of its catabolism. On the basis of biochemical heterogeneity of torsion dystonia the authors recommended different approaches in treating different forms of this disease. In a prevalent muscular rigidity the functions of the dophaminergic systems should be intensified: on the one hand, by administering precursors of dophamine L-DOPA, on the other--by inhibiting antagonistic activity with the aid of different cholinolytic preparations. In a hyperkinetic form a favorable effect is attained by preparations, inhibiting the dophaminergic activity (mainly preparations of the phenothiazine and butyrophenon series).
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PMID:[Pathogenesis and treatment of torsion dystonia]. 69 99

The experiments on rats have shown that bilateral administration of kainic acid (0.1-0.15 microgram) into the rostral parts of caudate nuclei led to the development of hypokinesia and rigidity. An increase in the electrical activity--the formation of the generator of pathologically increased excitement (GPIE) was noted in a zone of kainic acid injection. Rigidity and hypokinesia were attenuated and the GPIE activity was depressed after cyclodol (1-10 mg/kg) or L-DOPA (100-200 mg/kg) administration. Combined administration of cyclodol (2 mg/kg) and L-DOPA (50 mg/kg) induced potentiated antiparkinsonian effect. Dopamine microinjections into the GPIE area depressed its activity and abolished rigidity and hypokinesia. These data suggest that the Parkinson syndrome develops under the influence of GPIE induced by kainic acid administration into caudate nuclei.
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PMID:[Modelling of the parkinsonian syndrome by the administration of kainic acid into the caudate nucleus]. 359 43

We analyzed patients with Parkinson's disease from various aspects such as clinical findings, the degree of independence in daily life, care environment, quality of life (QOL) and treatment at home. The subjects were 104 in- and outpatients (47 males and 57 females) seen at our hospital. The mean age was 69.85 years in the males and 70.35 years in the females. The disease most frequently developed at the age of 60-69 years and the disease duration was 5 years or more in 52 patients. Rigidity was the most common symptom (91 patients), followed by gait disturbance (n = 87) and tremor (n = 86). Levodopa/carbidopa was the drug most frequently used (77 patients). The number of patients treated by combination drug therapy increased with the duration of disease. Concerning the degree of independence in daily life, assistance was often necessary in bathing, dressing and undressing, toileting and walking. In particular, total assistance was necessary in patients with Hoehn-Yahr stage-IV and V disease. The comprehensive QOL was the lowest in terms of social activities, hobbies and leisure activities, followed in order by work and subjective QOL. QOL decreased in each item with the severity of the disease. Treatment at home was performed for 19 patients, of whom 11 are still being treated by our staff. Treatment at home combined with persons who care for the patient and in cooperation with other welfare resources may improve the patient's QOL. In diseases that require long-term care such as Parkinson's disease, a comprehensive care management system should be established from the aspect of the patient's QOL.
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PMID:Clinical findings, status of care, comprehensive quality of life, daily life therapy and treatment at home in patients with Parkinson's disease. 938 6

The aim of the present study was to find out whether the classic neuroleptic fluphenazine is a good model compound for inducing parkinsonian-like muscle rigidity in rats. The muscle tone was measured as resistance developed by the rat's hind foot to passive flexion and extension. Fluphenazine in doses of 0.4-3.0 mg/kg i.p. induced a dose-dependent increase in the hind foot resistance to passive movements. The muscle rigidity induced by fluphenazine 1.5 mg/kg i.p.) was counteracted in a dose-dependent manner by the main antiparkinsonian drug L-DOPA (25-75 mg/kg i.p.). The present results suggest that the fluphenazine-induced muscle rigidity may be a useful model of parkinsonian rigidity.
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PMID:Muscle rigidity induced by fluphenazine in rats is antagonized by L-DOPA, an antiparkinsonian drug. 967 Jan 14

We describe an autopsy case of parkinsonism with bradykinesia, muscle rigidity, and dementia as major symptoms. The patient had developed bradykinesia at the age of 62, and then muscle rigidity, a parkinsonian posture, bradylalia, and dementia gradually appeared. Neurological examination revealed rigidity in the neck and limbs, with motion and speech being generally slow. He lacked involuntary movements including alien hand, tremor, chorea, and dystonia. Vertical gaze palsy, both upward and downward was noted, but other cranial nerves were intact. He was diagnosed as suffering from PSP clinically based on vertical gaze palsy, bradykinesia, instability on standing and gait, and dementia. Levodopa was only transiently effective. Within three years he became bed-ridden and in a state of akinetic mutism. At age 65 he died from pneumonia. Neuropathology revealed severe neuronal degeneration and gliosis in the substantia nigra. Because atrophy of the tegmentum of brainstem, dentate nuclei, inferior olivary nuclei was very mild and Alzheimer neurofibrillary tangles in the brainstem were relatively few, PSP was ruled out. Cortical neuronal degeneration was not apparent, but in the deep layer of cingulate gyrus, frontal lobe, and insula, there were several ballooned neurons. Gallyas-Braak silver staining showed no tuft-shaped astrocytes, specific for PSP, but it disclosed astrocytic plaques in the basal ganglia and the cerebral cortex. At present, astrocytic plaques are recognized as a hallmark of corticobasal degeneration (CBD), along with ballooned neurons in the cerebral cortex. The present case thus illustrates that CBD has a wide spectrum and may include cases in which degeneration of cerebral cortex is very mild.
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PMID:[An autopsy case of corticobasal degeneration without prominent cortical pathology--an imitator of progressive supranuclear palsy]. 1096 56

GAIT ARRESTS: They affect the evolution of the disease. This freezing phenomenon which induces falls sometimes constitutes an initial sign. Like the gait initiation failure, freezing can be controlled by sensory stimulation, notably visual inputs, but also by more sustained attention. FALLS ARE MAINLY CONNECTED WITH BOTH POSTURAL INSTABILITY AND RIGIDITY: They are poorly influenced by dopaminergic therapies. The progressive decrease of step width represents a main factor in their occurrence. PRECOCITY OF GAIT DISORDERS IS UNUSUAL IN PARKINSON'S DISEASE: Other parkinsonian syndromes such as progressive supranuclear palsy, multiple system atrophy and vascular parkinsonian syndrome must then be evoked. Their association with a cognitive impairment and abnormal sphincter behaviour infers a diagnosis of normal pressure hydrocephalus. GAIT IMPROVES WITH L-DOPA THERAPY: Speed, step length and duration of the swing phase are increased without change of cadence. Progressive loss of L-dopa efficiency on gait and postural stability contrasts with the persistent effect on tremor, rigidity and bradykinesia; a functional abnormality of nondopaminergic systems can explain these symptoms. In the following stages, gait troubles increased by motor fluctuations and abnormal involuntary movements are less controlled by L-dopa therapy. PHYSICAL THERAPY PLAYS A MAJOR ROLE IN THERAPEUTIC MANAGEMENT: An individual or collective rehabilitation project must be established according to the stage of evolution; the exercises aim to protect postural control and coordination. Visual or sound rhythmic inputs can be employed in the case of gait initiation failure. THE EFFECTS OF FUNCTIONAL NEUROSURGERY ARE IN THE COURSE OF EVALUATION: Thermolesion and chronic electrical stimulation of deep brain structures have opposite effects on gait troubles. Bilateral thalamotomy or pallidotomy are sometimes a source of disequilibrium. Chronic thalamic stimulation does not induce either benefits or adverse effects. On the other hand, stimulation of the internal pallidum improves gait kinematic parameters; improved postural adjustments have also been reported. The effect of subthalamic nucleus stimulation is comparable to that of L-dopa, however the long-term effect remains to be evaluated.
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PMID:[Gait disorders in Parkinson disease. Gait freezing and falls: therapeutic management]. 1128 86

The aim of the present study was to find out whether blockade of adenosine A(2A) receptors by a selective antagonist, SCH 58261, influenced parkinsonian-like muscle rigidity. Muscle tone was examined using a combined mechano- and electromyographic method which simultaneously measured muscle resistance (MMG) of a rat hindfoot to passive extension and flexion in the ankle joint and electromyographic activity (EMG) of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity produced by reserpine (5 mg/kg + alpha-methyl-p-tyrosine, 250 mg/kg) was antagonized by SCH 58261 (0.1-5 mg/kg). SCH 58261 (5 mg/kg) also reduced reserpine-enhanced tonic and reflex EMG activities in both the gastrocnemius and the tibialis muscles. Moreover, SCH 58261 in doses of 1 and 5 mg/kg abolished muscle resistance induced by haloperidol (0.5 mg/kg). However, only the highest dose of SCH 58261 (5 mg/kg) decreased tonic EMG activity enhanced by haloperidol. Administration of L-DOPA (75 and 100 mg/kg) dose-dependently decreased the muscle resistance as well as tonic EMG activity evoked by haloperidol. Combined administration of SCH 58261 (0.1 mg/kg) and L-DOPA (50 mg/kg) in doses which did not affect the haloperidol-induced muscle rigidity produced a pronounced synergistic effect. The ability of SCH 58261 to diminish the parkinsonian-like muscle rigidity and to potentiate the effect of L-DOPA in this model seems to indicate a therapeutic value of this compound in the treatment of Parkinson's disease.
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PMID:SCH 58261, an A(2A) adenosine receptor antagonist, counteracts parkinsonian-like muscle rigidity in rats. 1140 Jan 82

We reported a 74-year-old male case of progressive supranuclear palsy (PSP) who responded to tandospirone citrate, a serotonin receptor (5-HT1A) agonist. The patient manifested postural instability and gait disturbance at 71 years. Additionally, he showed vertical gaze paresis, regidity of the neck, extremities and trunk, bradykinesia and mild cognitive impairment. A brain MRI revealed moderate atrophy of bilateral frontal/temporal lobes and of midbrain tegmentum one year after the onset. The patient had been diagnosed as PSP and treated with L-DOPA. However, L-DOPA therapy showed only transient response for a few months. His symptoms deteriorated gradually, and he became unable to sit, stand up or walk by himself. Tandospirone citrate was additionally administered at 30 mg/day. Rigidity and bradykinesia were remarkably improved in two weeks after the start of tandospirone treatment. He became able to stand up and walk a short distance with supports in four weeks. Cognitive disturbance was also slightly improved. Tandospirone citrate was effective on our case of PSP, especially on rigidity. Our findings suggest that combination of levodopa and tandospirone citrate is a useful therapy for PSP.
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PMID:[A case of progressive supranuclear palsy improved with tandospirone citrate]. 1148 61

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


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