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Query: UMLS:C0026838 (spasticity)
6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present work developed an animal model of hindlimb spasticity by analyzing the electrophysiological and behavioral consequences of L5 spinal cord lesions in cats. In chronically lesioned animals (1 to 6 months), the L7-S1 dorsal roots were stimulated and evoked potentials were recorded from hindlimb flexor and extensor motor nerves. Following lateral hemisection, the monosynaptic responses were 2-5 times larger (for voltage-time integral and for amplitude) on the ipsilateral side than those from the contralateral side or from control animals. Half-widths, rise-times, and latencies of the monosynaptic responses were the same on both sides. Behavioral signs of spasticity, including hypertonia and increased deep tendon reflexes, were displayed from the ipsilateral hindlimb following lateral hemisection. With lateral hemisection or with extensive dorsal quadrant lesions, hopping and proprioceptive placing reflexes were abolished; these behavioral observations impart functional significance to physiological and anatomical studies of a mid-lumbar center considered to be important for movement control. The present model represents the first demonstration of a statistically significant correlation between electrophysiological and behavioral observations of spasticity for animals with a lateral hemisection. These correlations demonstrate the utility of behavioral screening of animals for subsequent neurophysiological analyses. This facilitates the investigation of cellular events underlying spasticity and of strategies for its relief with tissue repair techniques affecting local circuitry involved in spasticity.
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PMID:Correlative electrophysiological and behavioral evaluation following L5 lesions in the cat: a model of spasticity. 174 95

Sites of action of centrally active muscle relaxant drugs are not well defined. Clinical experience with such drugs suggests that the spinal cord may be one of the important regions from which pathologically increased muscle tone may be relieved. Supraspinal centers that may also be involved in the expression of muscle relaxant action have not yet been defined. We report here that microinjections of therapeutically relevant muscle relaxants into the midbrain tegmentum of genetically spastic rats decrease muscle tone. The substantia nigra is the region from which midazolam, baclofen, and tizanidine (drugs used clinically in the treatment of spasticity), or gamma-vinyl-GABA, (-)-2-amino-7-phosphonoheptanoate, and [D-pro2-D-phe7-D-trp9]-substance P (experimental drugs active in animal models of spasticity), reduce muscle tone in genetically spastic rats and Hoffmann reflexes in normal rats. The effects of muscle relaxant drugs are topographically restricted to the substantia nigra pars reticulata and are receptor specific. These observations disclose a previously unknown function of the substantia nigra in mediating muscle relaxation.
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PMID:Substantia nigra: a site of action of muscle relaxant drugs. 197 34

Clinical trial. The effects of protirelin tartrate (TRH-T) administration on chronic post-stroke spasticity were studied in a multicentre trial (study on the treatment of chronic post-stroke spasticity--11 centres involved). Patient evaluation included the quantification of muscular strength examined in proximal and distal areas, muscular tone according to the Ashworth scale, reflex intensities (using a 5 graded scale); daily autonomy was also considered according to the Parkside Behaviour Rating Scale (PBRS). Patients were administered 2 mg of TRH-T twice daily by intramuscular route. The most interesting finding emerging from the trial was that TRH-T administration elicited, at the same time, a reduction of spasticity, hypertonia and hyperreflexia together with an increase in muscular strength and improvement of daily activities. The therapeutic profile of TRH-T therefore seems to be based on its unusual capacity of acting simultaneously on deficiency symptoms (hyposthenia, loss of dexterity) and positive symptoms (hypertonia, hyperreflexia), both of which are present in cases of post-stroke spasticity. Electrophysiological findings. By means of coded electrophysiological tests it is possible to explore specific compartments of the motorial and spinal network and consequently obtain activity profiles for each single substance capable of modifying its reactivity. The H/M ratio, reciprocal Ia inhibition and the activities of the Renshaw circuit were not changed following TRH-T administration. Opposite findings were recorded with regard to the F wave according to whether the flector or extensor nucleus was explored; the consequent hypothesis of TRH-T activity at the interneuron level was supported by the inhibition of the short head biceps reflex following administration of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of TRH-T for the symptomatic treatment of the pathology of the upper motoneurons and electrophysiologic evaluation of its efficacy]. 212 88

Baclofen, the most effective drug for treating spasticity, is a specific agonist of gamma-aminobutyric acid-B receptors, and is very abundant in the superficial layers of the spinal cord. Given orally, baclofen does not easily penetrate the blood-brain barrier, and is distributed equally to the brain and spinal cord. Direct intrathecal administration was given in order to change the distribution of the drug by preferentially perfusing the spinal cord. Eighteen patients presenting a severe spastic syndrome were treated with chronic intrathecal infusion of baclofen in the lumbar cerebrospinal fluid. After clinical preselection, 38 patients were implanted with a lumbar access port allowing long-term trials in order to determine the efficacy of baclofen therapy and the effective 12-hour dose. The 18 patients selected for chronic administration were implanted with a programmable pump. The pathology in these cases was: multiple sclerosis (6 cases), posttrauma spastic syndrome (eight cases), and (one case each) cerebral palsy, ischemic cerebral lesion, spinal ischemia, and transverse myelitis. The mean follow-up period was 18 months (range 4 to 43 months). The clinical results were evaluated according to muscular hypertony on Ashworth's scale (changed for occurrence of painful spasms) and functional improvement. Results were better for spastic syndrome secondary to traumatic medullary lesion than for demyelinating disease. Hypertonia was improved in all cases as confirmed by the registration of the Hoffman (H) reflex. Painful muscular spasms disappeared in 14 of the 16 affected patients. Significant functional improvement was noted in nine patients and was considerable in three. The risk of side effects secondary to overdose (such as excessive hypotonia or central depression) and the absence of a specific baclofen antagonist stresses the necessity for accurate determination of the efficient dose. After an initial titration period and adjustment of the therapeutic dose, the individual doses were from 21 to 500 micrograms/24 hrs (mean 160 micrograms/24 hrs). This new conservative method is very effective, perfectly reversible, and safe when administered in conditions favorable to its use.
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PMID:Chronic intrathecal baclofen administration for control of severe spasticity. 230 74

Even in patients with complete loss of sensation and paraplegia after cervical spinal trauma, abdominal operations usually require general or spinal anesthesia due to spasms and increased muscle tone. Both anesthetic types have serious drawbacks under these circumstances, e.g. hyperkalemia induced by relaxation or the impossibility of adequate monitoring of the level of spinal blockade. After an onset time of 1-2 h the intrathecal injection of approx. 100 micrograms baclofen, a spinally acting GABAB-agonist, led to complete and long-lasting suppression of surgically induced spasticity. This could be demonstrated by neurological examination (spasticity scores: Ashworth score, spasm score, clonus score) during 5 neurosurgical operations in 3 patients with paraplegia. Except for slight sedation, the patients had no discomfort during operation. Intrathecal baclofen was also effective against autonomic hyperreflexia, i.e. vegetative dysregulation such as bradycardia or hypertension, provoked by catheterization or bladder surgery.
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PMID:[Intraoperative suppression of spasticity using intrathecal baclofen]. 230 48

The first part of the paper exposes the basic characteristics of the human spasticity which should be modeled: No hypertonia at rest; velocity-dependent myotatic responses, and fatigability. To model a syndrome including these signs is a related but different problem. Results and limits of the clinical neurophysiology concerning the spasticity are briefly quoted. Animal models would better assist the human neurophysiology when having their neuroanatomy closer to the human one. The second part confirms that a local unilateral excision of the ad hoc sensorimotor cerebral cortice of the Baboon induces a permanent palsy of the contralateral foot and leg, and after delay signs of spasticity in the Sol. Neither clasp-knife phenomenon nor fatigability is observed. There is no sign of motoneuron hyper-excitability. A GABA-related pharmacology suggests a significant defect in the presynaptic inhibition of the reflexogenic IA in-put, and possibly a defect in a post-synaptique gabaergic inhibition. Finally the monkey is considered as a valuable support for modeling the human spasticity, symptom and possibly syndrome.
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PMID:[Animal modeling and experimental pharmacology of human spasticity]. 236 13

The effects of conditioning stimulation of a mixed nerve in the leg, the common peroneal nerve (CPN), on the ipsilateral soleus H-reflex were compared with the effects of stimulating its cutaneous branch, the superficial peroneal nerve (SPN), in two groups of subjects--normals and patients with spinal spasticity subsequent to a clinically complete transection of the spinal cord. Condition-test delays of 20 msec to 2 sec, measured from the end of the 20 msec train (3 pulses at 100 Hz), were investigated. In normal subjects, CPN stimulation at 1.4 X MT profoundly depressed the soleus H-reflex. There was an initial depression (peak 40-90 msec) followed by a slow recovery which was incomplete at condition-test delays of 2 sec. One-half of the subjects showed a late facilitation, or disinhibition, peaking at 170-190 msec. The inhibitory effects were attributed to activation of low threshold, groups I and II, muscle afferents because stimulation of the SPN, at 1.5 X threshold for a compound action potential recorded from the CPN, had only facilitatory effects on the soleus H-reflex. Facilitation occurred at condition-test delays of 30-190 msec. The cutaneous stimulation was presumed to activate the largest, A beta, cutaneous afferents as it elicited a weak paraesthesia on the dorsum of the foot. The results suggested that cutaneous afferents may have contributed to the late facilitation seen with CPN conditioning stimulation. In spinal cord-lesioned subjects, CPN stimulation depressed the soleus H-reflex but the decrease was less and the recovery was faster and more complete than in normals. The magnitude of the initial depression at 20-100 msec varied with the severity of the spasticity, subjects with mild spasticity showing less of a depression. Weak cutaneous conditioning stimulation either had no effect or produced a slight depression of the soleus H-reflex, providing clear evidence that transmission in the pathways mediating the facilitatory effects of cutaneous afferents onto extensor motoneuronal pools is depressed in spinal spasticity. This may shift the balance of activity toward the flexor motoneurones, thus favouring the development of, for example, flexor spasms and flexor hypertonia. Since inhibitory effects from cutaneous stimulation are associated with activation of higher threshold afferents in normal man, the present results may reflect a decrease in the threshold for flexor withdrawal reflexes commonly associated with spasticity of spinal origin.
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PMID:Inhibitory and facilitatory effects from the peroneal nerve onto the soleus H-reflex in normal and spinal man. 244 16

Cerebral palsy, suffered as a result of an anoxic episode during the perinatal period, is the most common physical disability in childhood. Spastic cerebral palsy is characterized by increased muscle tone and decreased range of motion resulting in impaired motor function. Application of an old neurosurgical procedure, the selective posterior rhizotomy, is a new alternative for treatment of spasticity which interferes with a child's motor ability. A detailed evaluation process is necessary to identify suitable candidates. The procedure involves selective surgical severing of L2 to S2 rootlets following electrophysiological stimulation and identification of abnormal responses. An overview of the surgical procedure, as well as nursing implications for the pre- and postoperative and rehabilitative periods will be discussed.
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PMID:Selective posterior rhizotomy in the pediatric cerebral palsy population: implications for nursing practice. 252 27

Reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in a group of 16 patients with writer's and other occupational cramps. The early disynaptic phase of reciprocal inhibition was normal. However, there was a reduction in the amount of later, presynaptic inhibition, when compared with age-matched normal subjects. Similar findings were seen in 2 patients with symptomatic hemidystonia in whom structural brain lesions were present. However, this reduction in presynaptic inhibition was not specific to patients with dystonia. In a further group of 13 patients with hemiparesis or hemiplegia due to stroke, abnormalities of both early and later phases of reciprocal inhibition were found. The patients with spasticity exhibited less disynaptic inhibition than those with normal tone or flaccid limbs. The changes in the presynaptic phase of reciprocal inhibition did not correlate with the clinical signs of spasticity and increased muscle tone. These results provide objective evidence of a physiological basis for the action or task-specific focal dystonias such as writer's cramp.
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PMID:Reciprocal inhibition between forearm muscles in patients with writer's cramp and other occupational cramps, symptomatic hemidystonia and hemiparesis due to stroke. 273 Oct 27

Six patients with long-lasting spasticity resistant to different drug therapies including oral baclofen received a bolus injection of lumbar intrathecal baclofen. Electromyographic (EMG) reactions of leg muscles (soleus, tibialis anterior, quadriceps, and hamstrings) to standard stimuli and during attempts at voluntary activation were recorded before the drug injection and up to 3 h after the injection. Responses to joint movements, H-reflexes, ankle clonus, and defensive reactions were noticeably suppressed within 30-45 min after the injection and had practically disappeared after 2 h. Ankle clonus was seen only in patients with H-reflexes, and clonus disappeared when the reflex responses to the n. tibialis stimuli were absent. A decrease in clonus EMG burst amplitudes was accompanied by a decrease in the clonus frequency. These observations favor the autooscillation hypothesis of clonus. Baclofen injection led to improvement in selective voluntary activation of leg muscles in patients with residual motor control. These results suggest that execution of voluntary motor commands in the patients suffered from functionally abnormal spinal circuitry rather than from changes in the descending motor commands. Intrathecal baclofen appears to be an effective way of eliminating increased muscle tone and spasms which can allow for voluntary motor function when it is present.
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PMID:Short-term effects of intrathecal baclofen in spasticity. 291 60


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