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)

The health condition of female cash register operators in relation to their working conditions was investigated. A questionnaire study revealed that cash register operators more frequently complained of general fatigue, headache, sleeplessness, and low back pain than female office machine operators or other female workers. Dullness and pain in the shoulder, arm, hand, and fingers especially on the right side were characteristic of cash register operators. Physical examinations in 1973 showed that 31.3% of 371 cash register operators suffered from muscle rigidity or tenderness; 13 were severely afficted and, 69 operators had to be either laid off, reassigned to other jobs, or given shorter working hours. Occupational cervicobrachial disorders were suggested to have been caused by repetitive upper limb motions combined with static load, an unfavorable working environment, and mental stress. Implementation of some improvements including shorter operation time, worker rotation, and adoption of electronic registers proved effective in reducing the number of sufferers of cervicobrachial disorders found during the 1975 physical examinations. But the improvements were not effective enough to alleviate fatigue of the neck, shoulder, and back due presumably to sustaining upper limbs while operating the keyboard.
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PMID:Health hazard among cash register operators and the effect of improved working conditions. 102 12

Intracellular free Mg2+ concentration ([Mg2+]i) was measured in isolated single fibres of Xenopus muscle using the fluorescent Mg2+ indicator furaptra. In resting muscle the [Mg2+]i was 1.7 mM in a Mg(2+)-free Ringer solution. There was no significant change in [Mg2+]i over 2 h in Mg(2+)-free Ringer solution. Elevating extracellular [Mg2+] to 40 mM for 5 min caused a small rise (0.13 mM) in [Mg2+]i. There was no detectable rise in [Mg2+]i after 5 min in Na(+)-free Ringer solution. These results suggest that the membrane is relatively impermeable to Mg2+ and that there was no detectable Na(+)-Mg2+ exchange over 5 min. When muscle fibres were fatigued by repeated tetani continued until force declined to about 40% of control, [Mg2+]i showed characteristic changes. During the early period of fatigue when force first showed a small decline and then became almost stable, [Mg2+]i was unchanged; during the final period of fatigue when force declined more rapidly, [Mg2+]i increased by 0.8 mM. Recovery of [Mg2+]i took about 30 min. Recovery of force was complex: tetanic force first declined (post-contractile depression) and then slowly recovered to control. Since the minimum force occurred at about the time when [Mg2+]i had recovered, it seems unlikely that post-contractile depression is caused by elevated [Mg2+]i. Rigor, produced by inhibiting oxidative phosphorylation and glycolysis, was associated with a larger increase (1.6 mM) in [Mg2+]i than fatigue. The rise in [Mg2+]i during fatigue and metabolic blockade could be explained as release of Mg2+ normally bound to ATP. A model of the metabolic changes and the resulting increase in [Mg2+]i explains our results reasonably well.
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PMID:Myoplasmic Mg2+ concentration in Xenopus muscle fibres at rest, during fatigue and during metabolic blockade. 141 55

Symptoms of Parkinsonism, most likely induced by an oral contraceptive, were greatly reduced by combined therapy of nicergoline and bromocriptine. A 38-year-old housewife had taken an oral contraceptive, which contained .05 mg of ethinyl estradiol and .5mg of norgestrel per tablet, for 7 years, when she presented took the following symptoms: she stumbled easily, took short, quick dancing/skating steps without arm movement, and found it increasingly difficult to keep slippers on while walking. In the afternoons she experienced extreme fatigue and rigidity in her lower limbs. After a while, languor spread to other parts of her body as well, and she was examined on April 5, 1991. The patient's face was mask-like, and her body was bent forward with her forearms flexed. She showed frozen gait and lowered initiation in her movement. Muscle rigidity was found in both upper and lower extremities, and especially on the right side. A brain MRI showed lacunar infraction with small patches of high signal intensities in the white matter of the bilateral frontal lobes and high signal intensities in the left periventricular white matter. Urine was normal; blood cholesterol and iron were slightly raised. Hormonal examinations showed lowered LH, FSH, progesterone and 24-hr 17-KGS. CT was normal. She was ordered to stop taking pills and to take nicergoline and bromocriptine, which greatly reduced these symptoms except during the first menstruation following the treatment. When mask-like facial expressions, demarche a petit pas, and languor in her lower extremities did not recur during the next menstruation, bromocriptine treatment was discontinued. Four months later nicergoline therapy was also discontinued.
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PMID:[A case of parkinsonism induced by an oral contraceptive]. 156 36

Patients with Parkinson's disease may have more difficulty performing repetitive motor acts than single motor acts because of bradykinesia and skeletal muscle rigidity. We thought that repetitive ventilatory tasks might be similarly limited and that this dysfunction would likely contribute to respiratory muscle fatigue. We studied 9 patients with Parkinson's disease who had no evidence of restrictive or obstructive lung disease and 5 normal age-matched control subjects who performed repetitive, forced inspiratory resistive-loaded tasks. The time a given mean airway opening pressure could be sustained, the incremental oxygen cost of breathing, and the work rate of breathing (W) were measured. Although maximal static inspiratory pressures were comparable in both groups, 8 of the 9 patients could not sustain as high a W in the resistive-loaded tasks as could the normal control subjects (41.0 +/- 23.0 versus 67.7 +/- 29.1 J/min; mean +/- SD, p less than 0.01) and the efficiency of breathing was reduced (2.0 +/- 0.8 versus 3.8 +/- 1.4%; p less than 0.01). These findings are similar to derangements of task performance by peripheral skeletal muscle groups in Parkinson's disease.
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PMID:Respiratory muscle dysfunction in Parkinson's disease. 319 26

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

Multiple sclerosis (MS) is the most common cause of progressive neurological disability in young adults. In addition to spasticity, tremors, weakness, sensory disturbances, depression, cognitive problems, and bladder or bowel dysfunction, sexual dysfunction (SD) is also a prevalent and destructive manifestation of the disease that severely affects quality of life. Evaluation of this disorder requires insight into the primary (changes that directly affect libido, sexual response and orgasm due to direct damage to the nervous system), secondary (complaints which are related to the physical disability of MS, such as fatigue, muscle rigidity, weakness and spasms), and tertiary (emotional, social and cultural aspects of MS) components of MS-associated SD. Given the complexity and multifactorial nature of SD, a multidisciplinary approach is necessary when treating patients with MS. The aim of this Review is to provide a holistic approach to the evaluation and management of SD in patients with MS, incorporating the latest data from the fields of urology, neurology, nursing, social work, and psychology. What is currently known regarding the evaluation and management of SD in patients with MS will be presented from the perspective of these specialties.
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PMID:Sexual dysfunction in patients with multiple sclerosis: a multidisciplinary approach to evaluation and management. 1919 23

Parkinson's disease (PD) is characterized by a progressive loss of nigrostriatal dopaminergic neurons associated with intracellular Lewy inclusion bodies. The result is poverty of movement, increased muscle rigidity, and tremor at rest and on posture. Midbrain/nigral structural abnormalities can be demonstrated in vivo with both transcranial sonography (TCS) and diffusion tensor magnetic resonance imaging (DTI) while positron emission tomography (PET) and single photon emission computed tomography (SPECT) ligands exist to demonstrate dopamine terminal dysfunction. These radiotracers are markers of dopamine storage capacity, vesicular monoamine and dopamine transporter availability. While loss of putamen dopaminergic function leads to motor disability, Lewy bodies not only target dopamine neurons but have also been observed in serotoninergic, noradrenergic, and cholinergic neurons. As a consequence, non-dopaminergic neurotransmission is also impaired resulting in non-motor symptoms including sleep disturbance, fatigue, depression, dementia, and autonomic dysfunction. PET and SPECT ligands exist to interrogate the function of monoaminergic and cholinergic neurons. Cortical and limbic Lewy body disease is seen in more advanced PD and this can be detected with FDG PET as abnormal covariance between levels of resting brain metabolism in these regions. Additionally, widespread microglial activation can be detected in PD with PET. This review discusses the role of structural and functional imaging for understanding parkinsonian syndromes and aiding in their diagnosis and management.
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PMID:Imaging biomarkers in Parkinson's disease. 2189 6

While statins target many of the pathways to neuroprogression in schizophrenia, the safety and efficacy of statins for treating schizophrenia has never been examined. This is an 8-week randomized double blind controlled clinical trial examining the efficacy and safety of adjunctive lovastatin (20 mg/day) treatment or placebo for people with schizophrenia. The baseline characteristics of the two groups were not different. Endpoint changes in Positive and Negative Syndrome Scale (PANSS) total and subscale scores did not differ between the two groups. However there was a significant difference between the doses of risperidone used in the two groups. The mean dose in the lovastatin and placebo groups were 4.8(1.8) and 3.4(1.4) mg/day, respectively (P<.03). No serious adverse events were reported. Slowness of movements, muscle rigidity, increased appetite, and decreased energy were the most common adverse effects, and these rates did not differ between the two groups. This study failed to demonstrate a benefit of lovastatin on symptoms of schizophrenia. This combination was well tolerated. However, a higher dosage of risperidone was used for treating the disorder in those taking concomitant lovastatin compared to placebo.
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PMID:Lovastatin for the adjunctive treatment of schizophrenia: a preliminary randomized double-blind placebo-controlled trial. 2501 14

Fibromyalgia syndrome (FM), the most common central sensitivity syndrome (CSS) affecting over 5% of the population, is a disorder of chronic widespread pain accompanied by numerous other symptoms that causes significant functional impairment. The core FM symptom domains can be recalled using the FIBRO mnemonic and include Fatigue and Fog (cognitive dysfunction), Insomnia (difficulties with all aspects of sleep including initiation, maintenance and restorative), Blues (depression and anxiety), Rigidity (stiffness in muscles and joints) and Ow! (widespread pain and tenderness). While typically presenting in middle-aged women, FM can affect both sexes at any age. FM is a syndrome of abnormal central pain processing and increased central sensitivity caused by neurobiological changes that cause dysregulation of mechanisms that normally regulate pain sensation. There are currently three different methods for diagnosing FM; the 1990, 2010 and modified 2010 American College of Rheumatology (ACR) criteria. While disabling, FM symptoms can be managed with a regimen of pharmacologic and nonpharmacologic treatments. Medication types with benefit in treating FM include anticonvulsants, antidepressants, anti-inflammatories, muscle relaxers, tramadol, and stimulants. Beneficial nonpharmacologic therapies include aerobic and resistance exercise, stretching, cognitive behavioral therapy, and education. Effective management requires formulation of an individualized regimen since patients differ widely in symptoms and treatments they find beneficial. Such an individualized regimen should be based on a systematic assessment of problematic symptoms conducted at baseline and each follow-up with treatments modified over time. While challenging, FM symptoms can be effectively managed and patients can lead full, productive lives.
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PMID:Fibromyalgia: the prototypical central sensitivity syndrome. 2608 13

Parkinson's disease (PD) is a neurodegenerative multisystem disorder characterized by progressive motor symptoms such as bradykinesia, tremor and muscle rigidity. Over the course of the disease, numerous non-motor symptoms, sometimes preceding the onset of motor symptoms, significantly impair patients' quality of life. The significance of non-motor symptoms may outweigh the burden through progressive motor incapacity, especially in later stages of the disease. The advanced stage of the disease is characterized by motor complications such as fluctuations and dyskinesias induced by the long-term application of levodopa therapy. In recent years, it became evident that various non-motor symptoms such as psychiatric symptoms, fatigue and pain also show fluctuations after chronic levodopa therapy (named non-motor fluctuations or NMFs). Although NMFs have moved into the focus of interest, current national guidelines on the treatment of PD may refer to non-motor symptoms and their management, but do not mention NMF, and do not contain recommendations on their management. The present article summarizes major issues related to NMF including clinical phenomenology and pathophysiology, and outlines a number of open issues and topics for future research.
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PMID:Nonmotor fluctuations: phenotypes, pathophysiology, management, and open issues. 2870 50


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