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

Rigidity in Parkinson patients can be easily quantitated by determining net work required to passively flex and extend the forearm through an arc of 100 degrees. Rigidity thus measured can be subdivided into two very distinct types, resting and activated. Resting rigidity, measured while the patient is relaxed, responds to all effective therapeutic agents and correlates closely to degree of clinical improvement. Activated rigidity, measured during voluntary activity, is not relieved by any presently available medical treatment. It remains unchanged at pre-therapy levels even in patients who may temporarily appear to have dramatic improvement in clinical symptomatology. Longitudinal measurements made in hundreds of parkinson patients over intervals ranging from 5 to 15 years show continuing high levels of activated rigidity through the entire period of study. In marked contrast to our wide experience with parkinson patients is a single, well documented case of Wilson's disease who appears to have recovered completely both by clinical examination and by all of our machine measurements. This patient had high levels of extrapyramidal deficit, repeatedly measured over a period of four months when penicillamine therapy was being investigated. He then suddenly reverted to normal and returned to full time employment. High values of resting rigidity activated rigidity, akinesia and resting tremor all reverted to normal and have remained normal for the past 6 years. The implication of this study is that L-dopa and related treatments only mask the symptomatology of Parkinson's disease and are not retarding the underlying pathological process. Penicillamine, on the other hand, probably does relieve the destructive process in Wilson's disease and may in early cases, permanently relieve the extrapyramidal dysfunction.
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PMID:Failure of L-dopa to relieve activated rigidity in Parkinson's disease. 93 Jul 49

We describe the clinical features of parkinsonism in 25 patients whose age of onset was under 40 years. Among them, 17 patients, whose age of onset was after their 21st birthday, were classified as young onset Parkinson's disease (YOPD), and the remaining 8 whose age of onset was before their 21st birthday were classified as juvenile parkinsonism (JP). Rigidity and akinesia were revealed in all 25 patients. Resting tremor was observed in only 5 patients; 3 in the YOPD group and 2 in the JP group. There were 8 of the 25 patients (32%) who experienced an aching sensation in the leg before or at the onset of the parkinsonian features. In 6 of these 8 cases, the sensory symptoms were on the same side where the clinical manifestations of parkinsonism later developed. In the JP group, 2 patients had right foot dystonia, which improved with levodopa. Diurnal fluctuations in parkinsonian symptoms were found in 9 of the 25 cases. The familial incidence of parkinsonism was higher in the JP group. The parkinsonian disabilities in all 25 cases responded dramatically to levodopa therapy. Unfortunately, 10 cases, 5 in the YOPD group and 5 in the JP group, developed dyskinesia. The longer they took levodopa, the greater the chance of developing dyskinesia. The cumulative percentage of dyskinesia was 100% in the YOPD group and 83% in the JP group by the seventh and fourth year of treatment, respectively. A positive correlation was found between the prevalence of dyskinesia and the duration of treatment in both groups.
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PMID:Early onset parkinsonism in Chinese. 168 78

This report describes a case of cerebrotendinous xanthomatosis (CTX) accompanied by clinical manifestations of parkinsonism, including oily and masked face, marked akinesia, muscle rigidity and resting hand tremor. Magnetic resonance imaging (MRI) of the brain showed high intensity areas on T2 weighted imaging, and slightly low intensity areas on T1 weighted imaging in the right globus pallidus and the left putamen. Cerebral cortical atrophy with slight ventricular dilatation and cerebellar atrophy were present as well. This is a case report of CTX which manifested parkinsonism. Parkinsonism may not be a coincidental manifestation in CTX, but rather represent a symptom of the same underlying diathesis.
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PMID:Parkinsonism in cerebrotendinous xanthomatosis. 186 93

1. Neuroleptic drugs (antipsychotics) produce numerous side effects which include serious extrapyramidal symptoms consisting of akathisia, dystonia, neuroleptic malignant syndrome, parkinsonian reactions such as postural abnormality, tremor, akinesia or bradykinesia, rigidity, and tardive dyskinesia. 2. Among the complications of neuroleptic chemotherapy, the most serious and potentially fatal complication is malignant syndrome, which is characterized by extreme hyperthermia, "lead pipe" skeletal muscle rigidity causing dyspnea, dysphagia, and rhabdomyolysis, autonomic instability, fluctuating consciousness, leukocytosis, and elevated creatine phosphokinase. 3. Neuroleptic malignant syndrome should be differentiated from malignant hyperthermia, lethal catatonia, and other pathological states producing some of these same symptoms. 4. In addition to neuroleptics, malignant syndrome has been caused by thymoleptics (antidepressants), metoclopramide (antiemetic), metoclopramide combined with cimetidine, tetrabenazine, overdosage of benzodiazepine, phenelzine, dothiepin and alcohol, and amphetamine. 5. Factors leading to and/or facilitating the emergence of neuroleptic malignant syndromes are reportedly organic brain syndrome, dehydration, exhaustion, external heat load, excessive sympathetic discharge, use of long acting neuroleptics, high doses of neuroleptics, rapid dose titration with neuroleptics, abrupt discontinuation of antiparkinsonism agents, and concurrent lithium therapy. 6. Although, the pathogenesis of neuroleptic malignant syndrome is not understood completely, a blockade of dopaminergic receptors in the hypothalamus, spinal cord and striatum, an alteration of dopaminergic-serotonergic transmission in the body, an enhanced synthesis and action of prostaglandin E1 and E2, and a modification of calcium-mediated signal transduction in the body have been suggested. 7. The treatment of malignant syndrome includes immediate withdrawal of neuroleptic drugs, i.v. infusion of dantrolene, and oral administration of bromocriptine; or alternatively i.v. infusion of dantrolene and the combination of levodopa-carbidopa. 8. Other measures to enhance the therapeutic effectiveness of the aforementioned regimens are to include the use of anticholinergic drugs such as benztropine to enhance the effectiveness of bromocriptine, of lorazepam if catatonic symptoms persist, or of electroconvulsive therapy (ECT) if psychotic symptoms persist. 9. These treatments, however, must be "active" rather than "passive", in order to avert fatalities and/or unfortunate sequelae from this iatrogenic and incompletely understood disease.
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PMID:Pathogenesis and treatment of neuroleptic malignant syndrome. 197 19

Forty-four Parkinson patients (19 patients of the rigid-akinetic type, 13, of the rigid-akinetic-tremor type, and 12, of the tremor type) were included in a study in order to analyse correlations of the expression of the motor symptoms tremor, rigidity, akinesia, with other clinical parameters, computertomographic aspect of brain atrophy and psychometrically assessed cognitive parameters. Rigidity and akinesia are significantly positively correlated with the severity of motor dysability, stage of the disease, and brain atrophy, as is akinesia with a history of pharmacotoxic psychosis. Tremor is significantly negatively correlated with motor dysability, stage of the disease, and history of pharmacotoxic psychosis. Akinesia is correlated with visuomotor dysfunction (tested with Bender Gestalt Test) and rigidity with the depression score (Zung scale). The tremor type is favorable, the rigid-akinetic type unfavorable with respect to motor disability and psychosis.
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PMID:Prognostic implications of the motor symptoms of Parkinson's disease with respect to clinical, computertomographic and psychometric parameters. 378 47

Recent experimental studies and one clinical case have suggested that grafting tissue from the adrenal medulla into the brain may ameliorate the signs of Parkinson's disease. We describe the treatment of two young patients (35 and 39 years old) with intractable and incapacitating Parkinson's disease, in whom fragments of the adrenal medulla were autotransplanted to the right caudate nucleus. Clinical improvement was noted in both patients at 15 and 6 days (respectively) after implantation and has continued in both. Rigidity and akinesia had virtually disappeared in the first patient at 10 months after surgery, and his tremor was greatly reduced. A similar degree of improvement was present in the second patient at three months. We conclude that autografting of the adrenal medulla to the right caudate nucleus was associated with a marked improvement in the signs of Parkinson's disease in two patients, but our results are preliminary and further work is necessary to see whether this procedure will be applicable over the long term in other types of patients with Parkinson's disease.
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PMID:Open microsurgical autograft of adrenal medulla to the right caudate nucleus in two patients with intractable Parkinson's disease. 382 26

Clinical Neurophysiology brings about 2 major contributions in the study of Parkinson's disease: on the one hand, it makes it possible to measure the motor troubles; on the other, it enables their pathophysiological analysis. The 3 classical signs must be studied separately. Tremor can easily be recorded by electromyography. Moreover, its parkinsonian nature can be specified by studying the resetting of EMG bursts following electrical stimulation of the motor nerve. A pace maker has been demonstrated in the thalamus from where rhythmic messages are first sent to motor cortex and thereafter reverberated to spinal motoneurons. Rigidity can be assessed by sophisticated but not generalized methods. It is easier to evaluate it by long-loop responses evoked by proprioceptive or exteroceptive stimulations. These responses reflect activity in pathways relaying in supraspinal structures. Contrary to spasticity, rigidity is not basically due to dysfunctions in segmentary spinal circuits. It is more likely that it depends on hyperactive and hyperexcitable long loop pathways. This hypothesis is in agreement with well established facts showing that parkinsonian hypertonia vanishes after dorsal root section. Akinesia is complex semeiologically. It is made of various components some of which can be measured. Reaction times and movement times provide interesting data which however are not strictly correlated with the motor handicap. Motor programmes are assembled in normal delays but they are not "called upon" correctly, reflecting a disturbance in the motor planning. A lack of "energetization" of the motor cortex and the pyramidal tract is likely. A functional disconnection between the motor program/plan side and the execution side can be hypothesized to explain the 3 major signs; on the one hand, neural messages are not correctly transferred to the pyramidal system, on the other, spinoencephalospinal loops on the execution side become more active as they escape from the control normally exerted by the plan/program side where basal ganglia play a prominent role.
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PMID:[Clinical neurophysiology in the evaluation and physiopathology of Parkinson's disease]. 383 95

In 15 patients (8 men, 7 women), aged 44-81 years, with idiopathic parkinsonism, the effects of mesulergine (CU 32-085) were observed for up to 3 years. Of these patients, four had been without previous levodopa treatment, five had been on levodopa/decarboxylase inhibitor for 6.4 years and six patients had been on levodopa/decarboxylase inhibitor and bromocriptine for a period of 7.5 years. Mesulergine proved to be effective in all three groups of patients and for each main symptom of the disease. Rigidity and tremor showed a better response than akinesia. A decline in efficacy could be observed after 18 months of treatment. By increasing the levodopa dosage, the worsening of the symptomatology could be reduced again and after 3 years patients were slightly better off than before the introduction of mesulergine. Fine motor performance showed a longer-lasting improvement than walking, which was affected by an increase of freezing. Mesulergine was not fully sufficient when given in monotherapy and the levodopa saving effect was only temporary. Parallel with the decline in the therapeutic response as assessed by the rating scales, there was a worsening in the on/off symptomatology. The on/off symptoms, evaluated by patients themselves, had shown very small or no improvement at the beginning of mesulergine administration, contrasting with the findings reflected in the assessment scales. The most frequent side-effects were hallucinations and dyskinesias. Orthostatic hypotension did not prove a problem. Dyskinesias were not seen during monotherapy with mesulergine in de novo patients.
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PMID:Three-year observation of mesulergine (CU 32-085) in advanced and newly treated parkinsonism. 399 71

1. A reversible disturbance of basal ganglia function was produced in monkeys by the intramuscular administration of reserpine.2. Pallidal discharge was then compared with that recorded in the same animals during movement performance and following passive manipulation of the limbs.3. Akinesia, loss of postural support of the trunk, head and neck and absent postural reflexes were the predominant motor abnormalities produced by reserpine administration.4. Occasionally, postural tremor and catatonia were apparent. Rigidity and resting tremor were absent.5. Recordings made in the pallidum during the presence of akinesia revealed a marked reduction in natural neuronal discharge.6. Some pallidal neurones that remained active were driven in an uncharacteristic manner by peripherally generated afferent inputs from wide territories and by a variety of peripheral stimuli.7. The findings suggest the hypothesis that the akinesia in these animals was due to the diminished pallidal activity, and that pallidal discharge is normally a prerequisite for the performance of spontaneous motor activity. Pallidal neuronal firing may provide a background excitability to motor regions involved in the maintenance and elaboration of natural motor activity.
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PMID:The effects of reserpine on motor activity and pallidal discharge in monkeys: implications for the genesis of akinesia. 741 43


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