Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.
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PMID:Action of dantrolene sodium in spasticity with low dependence on fusimotor drive. 13 20

A rare case of mesenchymal chondrosarcoma originating from the thoracic spinal dura was reported. A 10-year-old girl complained of paresis of the right leg in June 1977. Then she became unable to walk early in August, and a complete paraparesis developed on August 18. She was admitted to our department on August 22. On admission she had complete paraparesis, bilateral ankle clonus, upward plantar reflexes, sensory disturbance below T7, shincter disturbance and neck stiffness. Plain thoracic X-ray revealed bilateral decalcification of pedicles of T6. Myodil myelography showed a complete block between T6 and lower end of T7 vertebrae. Bilateral laminectomy from T3 to T8 was performed. A tumor originating from the spinal dura was located in the right dorsal extradural space. The tumor was totally removed together with a small area of the affected dura. Light microscopy showed mesenchymal chondrosarcoma. Her recovery from neurological deficiencies was excellent and now she can run 14 months after surgery. Metastasis or recurrence has not yet been seen.
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PMID:[A case of mesenchymal chondrosarcoma originating from the spinal dura (author's transl)]. 49 58

Immediately after a patient with myoclonus epilepsy smoked a nicotine-containing cigarette, tetraparesis and hyperreflexia with ankle clonus developed, but disappeared within several minutes. During paresis, the H-reflex size of the soleus muscle increased, EEG showed more slow waves than before smoking, and the cerebral perfusion increased around the motor cortex as shown by single photon emission CT. A similar effect occurred when the patient chewed nicotine gum, and smoking a cigarette with a high nicotine content induced severe positive and negative myoclonus after the development of tetraparesis. Administration of the C6-type nicotinic antagonist mecamylamine not only countered the smoking effect, but ameliorated the spontaneous positive and negative myoclonus. Mecamylamine may prove useful for the treatment of positive and negative myoclonus in myoclonus epilepsy.
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PMID:Nicotine-sensitive paresis. 173 70

The effects of cyproheptadine, a serotonergic antagonist, were studied in seven patients with spastic paresis of spinal origin. Six patients were included in a double blind crossover trial (maximal dose 24 mg/day). The patients were evaluated on both their spasticity and locomotor function. Four of the patients also participated in an open trial in which cyproheptadine was administered for a minimum of six months at optimal dose. Patients walked on a treadmill at full weight bearing when possible, or with 40% of their body weight externally supported, as required, by an overhead harness system. Cyproheptadine considerably decreased the sustained ankle clonus and episodes of spontaneous spasms observed in all the patients who previously presented these manifestations of spasticity. Two patients who required body weight support (BWS) during locomotion could walk at full weight bearing during cyproheptadine therapy. A more normal timing of EMG patterns in these patients during cyproheptadine therapy was associated with temporal distance changes and marked improvement of joint angular displacement. In contrast, the other patients showed marginal changes in the EMG and the kinematic pattern but eventually managed to walk at a higher speed. These preliminary results suggest that cyproheptadine can reduce spasticity and enhance locomotor function in spinal cord injured patients.
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PMID:The effects of cyproheptadine on locomotion and on spasticity in patients with spinal cord injuries. 224 57

Is characterized by several various signs. One of these, spasticity, involves a velocity dependent increase in muscle stiffness during stretch and by hyperactive tendon jerks. When intense, spasticity impedes residual strength in antagonistic muscles and interferes with attempts to move, especially if complicated by clonus and/or spasms. Assessment of spasticity is multifactorial and implies clinical as well as instrumental methods. The pathophysiological mechanisms responsive for the hyperexcitability of the myotatic reflex can be studied by methods of clinical neurophysiology. It appears that there are various factors involved at the spinal level, involving reduction in both pre- and post-synaptic inhibitions. Although spasticity is not responsible for the major part of the disability imposed by upper motor neurone syndrome, it should be reduced. The therapeutic methods are medical, surgical or from physical medicine. In many cases, the results have been validated by blind studies. As paresis is the most disabling effect, it would be worthwhile to develop drugs able to reduce spasticity and increase muscle strength at the same time. Recent trials suggest than TRH-T may be effective in this regard.
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PMID:[Pyramidal syndrome: its physiopathology and treatment]. 269 2

The effects of cyproheptadine were studied in two patients with spastic paresis. The study consisted of two phases: a control phase (no medication) and a cyproheptadine phase (8 mg t.i.d.). The effects were evaluated from electromyographic (EMG) and kinematic analysis of treadmill walking with a portion of body weight supported, and from clinical examination and subjective assessments. Episodes of spontaneous spasms and elicited clonus were reduced with cyproheptadine. Improvement in locomotor function was evidenced by a decreased cycle duration, more regular foot-floor contact, functional joint excursions, and increased walking speed. In addition, a tonic EMG activity pattern was replaced by phasic muscle activation in the proximal extensors especially. Selective proximal movements were unmasked (hip flexion) and certain functional activities (transfers, dressing) were facilitated. The results support the role of cyproheptadine as an antispastic medication. Study of the short-term and long-term benefits of cyproheptadine is continuing.
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PMID:Quantitative assessment of the effect of cyproheptadine on spastic paretic gait: a preliminary study. 377 12

A right-handed woman of 90, taking aspirin 160 mg daily, suffered acute neck pain radiating to the shoulders, with right side hemiparesis and numbness occurring minutes thereafter. On admission 2.5 hrs later, examination showed paresis and hyporeflexia of the right limbs accompanied by neck stiffness and vertebral tenderness in level C7. Acute stroke was the initial working diagnosis. Cerebral CT was normal. Symptoms progressed with left arm numbness and left ancle clonus, and eight hours after symptom onset there was bilateral plantar inversion, reduced skin prick sensibility below C4, bladder paresis and anal sphincter hypotonia. CT myelography revealed an intraspinal mass extending from C2 to C6. 14 hours after symptom onset, a spinal epidural haematoma was removed by spinal laminectomy. Recovery and functional outcome was good. Symptoms, work-up and treatment are discussed with reference to previous publications.
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PMID:[A 90-year-old woman with acute hemiparesis]. 1693 75

Among the three main factors of motor impairment that emerge in chronological order following a lesion to central motor pathways, the last two antagonize movement: 1) stretch-sensitive paresis, a reduction of agonist motor unit recruitment upon voluntary command, worsened by antagonist stretch; 2) soft tissue contracture, and 3) muscle overactivity. Types of muscle overactivity include 1) spasticity, an increase in the velocity-dependent response to muscle stretch, measured at rest; 2) spastic dystonia, i.e., chronic tonic muscle activity at rest, sensitive to stretch of the dystonic muscle and 3) spastic co-contraction, an inappropriate degree of antagonistic contraction during voluntary agonist command, sensitive to stretch of the co-contracting muscle. A five-step clinical assessment may closely parallel this phenomenology, in which the first four steps aim at quantifying the antagonistic potential of each muscle group. Step-1 measures passive range of motion, i.e., the angle of arrest upon slow stretch of the muscle group assessed (minimizing spastic dystonia), which provides insight on soft tissue length and extensibility. Step-2 measures the angle of catch or clonus upon fast passive stretch of the muscle group assessed, which provides insight on stretch reflex excitability. Step-3 measures the range of active motion against the muscle group assessed, a net result of agonist recruitment minus the combined resistance from passive soft tissue stiffness and spastic co-contraction in the muscle group assessed. Step-4 measures the maximal frequency of rapid alternating movements along the maximal active range of motion, evaluating Step-3 performance repeatability. Step-5 evaluates active function, using for example a walking test (10 m or 2 min) for lower limb and the Modified Frenchay Scale for upper limb assessment, and perceived function through patient global subjective assessment.
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PMID:Five-step clinical assessment in spastic paresis. 2092 7

Spasticity is a term commonly used to describe a collection of muscle overactivity patterns associated with the upper motor neuron syndrome including actual spasticity, clonus, dystonia, co-contraction, associated reactions, and flexor or extensor spasms. Gait dysfunction in the upper motor neuron syndrome can be due to a combination of paresis, impaired coordination and balance, and muscle overactivity and contracture. Treatment options include physiotherapy, assistive devices, orthotic devices, oral and intrathecal medications, intramuscular chemodenervation, neurolysis, and/or neuro-orthopaedic surgical procedures. The objective evaluation of walking and its underlying muscle activation patterns can be performed by the simultaneous collection of joint kinematics, kinetics, and dynamic electromyography (EMG) data that serve as an extension of the physical examination to better discern primary gait deviations from compensatory gait deviations as well as underlying muscle overactivity from contracture. Despite the science behind instrumented three-dimensional gait analysis, its specific contribution to clinical and surgical decision-making is not well utilized because of its associated cost, the incorrect view by some insurance companies of gait analysis being a research technique, the dearth of qualified clinical gait and motion analysis laboratories accessible to adult patients, and limited access to orthopaedic surgeons who have experience in the treatment of neurological disorders for this patient population.
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PMID:Instrumented Gait Analysis: A Tool in the Treatment of Spastic Gait Dysfunction. 2748 23

Adult T cell lymphoma (ATL), is a peripheral T cell neoplasm associated with infection by human T-lymphotropic virus (HTLV). This is a case of a 28-year-old lady who presented with back pain for the past month and recent onset weakness in her lower extremities bilaterally. She has a history of T-cell lymphoma secondary to HTLV-1 under remission since 2014 and systemic lupus erythematosus complicated by lupus nephritis. On physical examination patient had hyper-reflexia in both knees, ankle clonus bilaterally and spasticity in both her lower extremities. She also had a diffuse, scaly, macular rash in her upper and lower extremities and ulcer-like lesions on the plantar surface of both feet. Her lumbar puncture showed lymphocyte predominance. The Western Blot test was positive for HTLV antibodies in the CSF. The patient was started on IV Methylprednisone which considerably improved her symptoms. The biopsy of her skin lesions showed an immunophenotype of T-cells similar to the cells in the bone marrow at the time of diagnosis of the lymphoma. HTLV infection is an etiologic agent for ATL as well as for tropical spastic paresis. One should have a high degree of suspicion for tropical spastic paresis in patients with HTLV-1 infection as it can easily go undiagnosed. Indolent forms of ATL can also present in the form of skin lesions in later stages. It is also important to distinguish between skin manifestations of ATL and cutaneous T cell lymphomas, and the importance of skin biopsies for the same cannot be undermined.
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PMID:A case of HTLV-1 associated adult T-cell lymphoma presenting with cutaneous lesions and tropical spastic paresis. 2955 50


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