Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-seven patients with muscle spasticity secondary to central nervous system pathology were treated with dantrolene sodium for periods of up to two years. The drug was effective in reducing muscle spasms, clonus, muscle tone, and the force of muscle contraction elicited by Achilles tendon tap and tibial nerve stimulation, but improvement of function was seen less often. The incidence of side-effects was considerable, and poses a problem regarding patient acceptance of drug treatment.
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PMID:Dantrolene sodium: long-term effects in patients with muscle spasticity. 77 22

The reflex EMG responses from a tendon tap or an imposed, medium amplitude (30 degrees), stretch at a range of stretch velocities have been recorded from the triceps and biceps muscles of normal human subjects and in both the affected and "unaffected" arms of hemiparetic patients under relaxed conditions. In the hemiparetic arm, exaggerated tendon jerks were, as expected, observed in both muscles. The response of the biceps to elbow extension was also exaggerated compared with normal values and displayed both an additional earlier component and a much reduced velocity threshold. The triceps, in contrast, showed depressed responses to elbow flexion, with a much higher velocity threshold than normal subjects. Furthermore, on the supposedly "unaffected" side of the hemiparetic subjects, the reciprocal pattern was seen, with depression of the biceps response and a raising of its threshold, along with considerably exaggerated responses in the triceps including earlier components not seen in the normal subjects. The increased excitability of the flexor musculature on the spastic side may be paralleled by increases in activity in the segmental pathways responsible for modulation of agonist/antagonist activity in the ipsi and contralateral limb, leading to an inhibition of the ipsilateral extensors and contralateral flexors and excitatory input to the contralateral extensors. Thus the "good" side of hemiparetic patients also receives pathological changes, and studies of the mechanisms of spasticity should avoid the use of the "unaffected" side of hemiparetic subjects as a control for monitoring pathological reflexes.
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PMID:Pathological stretch reflexes on the "good" side of hemiparetic patients. 232 53

The local application of cold has been used to decrease spasticity and facilitate neuromuscular function, but previous attempts to identify its effect on the stretch reflex have not been entirely successful. We examined the effects of cold on the Hoffmann (H) reflex and on the tendon tap (T) reflex in 16 subjects. A series of H/M recruitment curves and T-reflexes were recorded via surface EMG electrodes before and during cooling of the triceps surae. Skin and intramuscular temperatures were recorded with average decreases of 18.4C and 12.1C, respectively. Peak-to-peak amplitude of the M, H, and T compound action potentials (CAPs) was measured. In all cases, the amplitude of the maximal M-wave decreased (p less than 0.001) in response to cooling. These changes in the recording of CAPs should be considered when cooling experiments result in alterations in H or T waveforms. When using the M-wave as a covariant in our analysis, there were no significant changes in the H-reflex amplitude; the height of CAPs elicited by T decreased (p = 0.025). Our findings do not support earlier claims that simple cooling facilitates the excitatory alpha motoneuron pool as measured by the H-reflex; we do confirm that muscle spindle activity, as measured by the T-reflex, is decreased by muscle cooling.
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PMID:Effect of cooling on H- and T-reflexes in normal subjects. 361 11

We present here thirteen patients (5 men and 8 women, aged 31 to 73, mean 55 years) with spastic paraparesis who showed clinical features similar to those of HTLV-1 associated myelopathy without HTLV-1 antibody, but with positive antibody to hepatitis B virus (HBV). All of these patients showed slowly progressive difficulty in walking. Five patients had previous histories of blood transfusion, of these one with history of B hepatitis. Neurologically, muscle weakness, spasticity and exaggerated deep tendon reflexes in the lower extremities were common to all the patients. Seven patients showed Babinski's reflex. Disturbance of micturition was noted in 3 patients. None showed organic changes of the spine on magnetic resonance image (MRI). None was serologically positive for syphilis and had cryoglobulin and hypergammaglobulinemia. Elevated levels of the liver enzymes were noted in two patients. All patients were positive for hepatitis B surface antibody (HBs-Ab) (EIA) but negative for hepatitis B surface antigen (HBs-Ag) (EIA). Five patients were seropositive for hepatitis C virus (HCV) (PHA). In 3 of them, reverse transcriptase polymerase chain reaction was performed but failed to detect HCV-RNA. All patients underwent spinal tap, and showed normal cell count and protein concentration in their cerebrospinal fluid (CSF). Atypical cells were not observed in all the patients. The CSFs from three patients were tested for HBs-Ag and HBs-Ab. HBs-Ag was negative in all three patients, but HBs-Ab was positive in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hepatitis B virus antibody positive spastic paraparesis]. 795 26

This article will review those electrophysiological investigations which have addressed the neuronal mechanisms underlying impaired gait. The aims of the review are to provide further insights to the underlying pathophysiology of impaired gait and also towards the selection of an appropriate treatment. From the patients' point of view the first indication of a central motor system lesion is an impairment of movement, most notably locomotion. These symptoms are characteristic in cases of spasticity, cerebellar lesion or Parkinson's disease. Clinical examination reveals typical changes in tendon tap reflexes and muscle tone which were believed to account for the movement disorder presented. However, we now know that there is only a weak relationship between the physical symptoms observed during clinical examination under passive motor conditions and the altered neuronal mechanisms underlying the impairment during active motion. By recording and analysing electrophysiological and biomechanical parameters during functional movements such as locomotion, the significance of impaired reflex behaviour or the pathophysiology of muscle tone and its contribution to the movement disorder can be reliably assessed. Consequently, the treatment should not be cosmetic, i.e. the correction of an isolated clinical parameter, but should be based on the pathophysiology and significance of those mechanisms underlying the impairment of the patients' movements. Data from electrophysiological and biomechanical investigations of locomotion of patients with spasticity, cerebellar disorder or Parkinson's disease are discussed in this review. The neuronal mechanisms, which are essentially central programs and afferent input, involved in disorders of gait are evaluated on the basis of their function in healthy subjects. The impact of this analysis in deciding an appropriate treatment are discussed with respect to the pathophysiology underlying the gait disorder (spasticity, cerebellar disorder or Parkinson's disease). At the present time we have only a basic understanding of the essential receptor systems, such as leg extensor load receptors, and their interaction with other systems involved in postural control. In the future, the knowledge gained from gait analysis may help in the selection of the appropriate pharmacological and physical treatment required even though the patient may only be at an early stage of motor impairment.
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PMID:Neurophysiology of gait disorders: present and future applications. 930 81

Remitting hemiplegic spasticity in apoplexy (HSA) is an important problem in today's clinical study. Through teaching and clinical practice, the authors summed up the effective acupuncture methods for remitting HSA: puncture deeply the acupoints on the superior-spasm side (SSS) by filiform needles so as to obtain the intensive needling sensations in the deep tissues (ISDT) until the superior spasm is immediately remitted; tap the skin on the inferior-spasm side (ISS) by skin needles until the corresponding muscle contracts. The methods have showed a significant immediate and long-term therapeutic effect.
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PMID:Acupuncture methods for hemiplegic spasm. 1043 14

Whether or not a lesion confined to the pyramidal tract produces spasticity in humans remains an unresolved controversy. We have studied a patient with an ischemic lesion of the right medullary pyramid, using objective measures of hyper-reflexia, spasticity, and weakness. Electromyographic activity (EMG) of the biceps muscles was recorded under the following conditions: (1) in response to a tendon tap with an instrumental reflex hammer, (2) in response to imposed quick stretch with motion analysis, and (3) during an isometric holding task. Hyper-reflexia of the involved arm in response to tendon tap was shown to be due primarily to an increase in the gain of the reflex arc. No velocity-dependent increase in the response to quick stretch of the involved arm was present. This was consistent with the absence of detectable spasticity on the clinical exam. These findings suggest that a lesion confined to the medullary pyramid can give rise to weakness and hyper-reflexia without causing spasticity. Moreover, these findings suggest that different anatomical substrates may underlie the clinical phenomena of hyper-reflexia and spasticity.
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PMID:Hyper-reflexia without spasticity after unilateral infarct of the medullary pyramid. 1083 76

This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of first, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the first symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap reflexes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the significance of, for example, impaired reflex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and significance of the mechanisms underlying the disorder of functional movement which impairs the patient.
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PMID:Spastic movement disorder. 1096 97

In the belief that changes in the adductor reflex (AR) may be helpful in evaluating lumbar root and plexus lesions, expression of the AR was studied in 43 healthy human subjects. ARs elicited with an electronic reflex hammer were recorded from the inner side of the proximal thigh using needle and surface electrodes, and patellar reflexes (PRs) were recorded simultaneously. These reflexes were obtained by tapping the ipsilateral medial aspect of the knee, the contralateral patellar tendon, the ipsilateral and contralateral anterior superior iliac spines, and the Achilles tendon. The H reflex of the obturator nerve was also evaluated in 17 cases. ARs were evoked consistently by tapping the ipsilateral medial aspect of the knee and by contralateral patellar tap, and by tapping ipsilateral and contralateral anterior superior iliac spines when a needle recording electrode was used. Sometimes an Achilles tendon tap also elicited the AR ipsilaterally. By contrast, the PR could only be elicited by a tap to the ipsilateral patellar tendon. ARs have somewhat different features than other well-known tendon reflexes such as the PR and are recorded consistently when a needle electrode is used, being elicited from both distal and proximal areas of the legs by tapping the Achilles tendon or anterior superior iliac spines unilaterally or bilaterally. Their role in evaluating lumbar root disease and monitoring adductor spasticity merits investigation.
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PMID:Adductor T and H reflexes in humans. 1694 59

The central nervous system (CNS) is, after the peripheral nervous system, the second most frequently affected organ in mitochondrial disorders (MCDs). CNS involvement in MCDs is clinically heterogeneous, manifesting as epilepsy, stroke-like episodes, migraine, ataxia, spasticity, extrapyramidal abnormalities, bulbar dysfunction, psychiatric abnormalities, neuropsychological deficits, or hypophysial abnormalities. CNS involvement is found in syndromic and non-syndromic MCDs. Syndromic MCDs with CNS involvement include mitochondrial encephalomyopathy, lactacidosis, stroke-like episodes syndrome, myoclonic epilepsy and ragged red fibers syndrome, mitochondrial neuro-gastrointestinal encephalomyopathy syndrome, neurogenic muscle weakness, ataxia, and retinitis pigmentosa syndrome, mitochondrial depletion syndrome, Kearns-Sayre syndrome, and Leigh syndrome, Leber's hereditary optic neuropathy, Friedreich's ataxia, and multiple systemic lipomatosis. As CNS involvement is often subclinical, the CNS including the spinal cord should be investigated even in the absence of overt clinical CNS manifestations. CNS investigations comprise the history, clinical neurological examination, neuropsychological tests, electroencephalogram, cerebral computed tomography scan, and magnetic resonance imaging. A spinal tap is indicated if there is episodic or permanent impaired consciousness or in case of cognitive decline. More sophisticated methods are required if the CNS is solely affected. Treatment of CNS manifestations in MCDs is symptomatic and focused on epilepsy, headache, lactacidosis, impaired consciousness, confusion, spasticity, extrapyramidal abnormalities, or depression. Valproate, carbamazepine, corticosteroids, acetyl salicylic acid, local and volatile anesthetics should be applied with caution. Avoiding certain drugs is often more beneficial than application of established, apparently indicated drugs.
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PMID:Central nervous system manifestations of mitochondrial disorders. 1694 41


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