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)

The histological changes produced in peripheral nerve by topical ethyl alcohol have been infrequently studied in spite of widespread use of this neurotoxic agent in the management of pain and spasticity. In the present study the sciatic nerves of a series of albino mice were exposed to ethanol in concentrations of from 10% to 50% for from 15 to 60 seconds. An immediate physiochemical reaction took place, resulting in splitting of myelin sheaths and swelling of cellular organelles and cytoplasm. Nerves subsequently underwent Wallerian degeneration. A central core of fibers appeared to be normal. The longer exposure times or higher alcohol concentrations increased the extent to which the peripheral rim of altered tissue extended centrally into the nerve. Within altered tissue, all fiber types and sizes were found to be affected to an equal degree. To study the physical properties of alcohol in solution, absolute alcohol was slowly placed at the bottom of a cylinder filled with artificial or normal human spinal fluid and sequential levels of the solution were sampled 30 and 60 seconds after injection. Though hypobaric, alcohol dispersed rapidly so that specimens taken from the bottom of the cylinder were 65% as concentrated as specimens taken from the surface.
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PMID:Dilute ethyl alcohol: effect on the sciatic nerve of the mouse. 17 94

Reciprocal reflex connections were studied in capsular hemiplegia and spastic paresis with spinal cord lesions, using Lloyd's technique. Effects of conditioning stimulation of the tibial or peroneal nerve on the H reflex in the antagonists were examined. Stimulus intensity was controlled with reference to the threshold of the M wave. Weaker stimulation than this threshold was regarded as stimulation of group I afferents. It aroused no subjection sensation in intact subjects. Early and strong inhibition, comparable to Ia inhibition in the cat (Lloyd 1946), was observed from weak stimulation of the tibial nerve on the pre-tibial (flexor) H reflex, but not from the peroneal nerve on the triceps surae (extensor) H reflex in capsular hemiplegia. Alcohol block of extensor motor points resulted in reduction of spasticity without further paralysis in the blocked muscle and a remarkable increase in strength of the antagonist pre-tibial muscles. These results suggest that an extensor spasticity withe flexor weakness, which is common in capsular hemiplegia, may be due to an imbalance of reflex activities via Ia muscle afferents, and that a part of flexor weakness can be restored by "disinhibition' by reduction of Ia inflow from extensor muscles. Ia inhibition was also observed in one third of cases with spinal cord lesions at rest. It returned to normal after recovery from spastic paresis by radical therapy in some cases.
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PMID:Reciprocal Ia inhibition in spastic paralysis in man. 28 52

Spasticity and flexor spasms can be most incapacitating in SCI victims. Muscle relaxants, physiotherapy and elimination of triggering factors must be tried before opting for peripheral surgery or alcohol block. The choice of alcohol block or peripheral surgery depends in whether damage to the spinal cord is complete or incomplete. Results of both the procedures are satisfactory in rightly chosen patients. Alcohol block is a simple, safe and effective method of treating spasticity in the patients of complete paraplegia. The effect is immediate and almost permanent. However, alcohol block is contra-indicated in the patients of incomplete paraplegia where peripheral surgery is a better choice.
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PMID:Treatment of intractable spasticity in spinal cord injured patients. 142 73

Pharmacological interest in the tripeptide thyrotropin-releasing hormone (TRH) is due to the multiple effects it produces. In fact, apart from taking part in regulating the activity of the hypothalamo-pituitary-thyroid axis, TRH produces various neuropharmacological effects which indicate a biological role that is probably more important than that of a releasing hormone. Trials performed in animals have shown, for example, the dose-dependent capacity of TRH to induce analgesia, probably by interacting with the opioid peptide system. Motor activity is affected by TRH. In fact this tripeptide elicits an increase in spontaneous motor and explorative activities by interacting with the dopaminergic neurotransmitter system at the nucleus accumbens level. The neuropharmacological activities of TRH include an interesting arousal effect and an analeptic action on generalized depression of the CNS whether this depression is of natural origin, such as hibernation, or induced pharmacologically (barbiturates, ethanol) or of a traumatic origin (coma). This analeptic action is attributable to stimulation of cholinergic neurons in the septo-hippocampal area and to the presence of terminals containing TRH in the lateral septum and TRH receptors concentrated especially in the medial septum and diagonal band of Broca. It has also been suggested that TRH localized in the pineal gland has a part in activating the neuronal mechanisms of arousal. Associated with the arousal effect and especially evident in variously originated shock conditions are the activating effects of TRH on vegetative functions (body temperature, circulation, the gastrointestinal tract). These stimulatory activities on the CNS were the rationale for therapeutic use of TRH in the initial treatment of coma due to brain trauma and for the treatment of endogenous depression. A most interesting property of TRH is that of counteracting the neurological deficit due to experimental lesion of the spinal cord particularly with regard to spasticity and ataxia. Electrophysiological trials have shown that TRH depolarizes the motoneurons in frog spinal cord thereby increasing the monosynaptic reflex. Furthermore, TRH has recently been shown to have a trophic effect on cultures of rat fetus spinal cord. On this basis TRH has been used successfully for the treatment of amyotropic lateral sclerosis (Charcot's syndrome) and spinocerebellar degeneration. Further support for this therapeutic strategy is given by the demonstration that deafferentiation of rat spinal cord produces an increased density of TRH spinal receptors. Recent studies have also given encouraging results on the possible therapeutic use of TRH for the treatment of Alzheimer's disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pharmacologic profile of protirelin tartrate]. 212 84

Marijuana is reported to decrease spasticity in patients with multiple sclerosis. This is a double blind, placebo controlled, crossover clinical trial of delta-9-THC in 13 subjects with clinical multiple sclerosis and spasticity. Subjects received escalating doses of THC in the range of 2.5-15 mg., five days of THC and five days of placebo in randomized order, divided by a two-day washout period. Subjective ratings of spasticity and side effects were completed and semiquantitative neurological examinations were performed. At doses greater than 7.5 mg there was significant improvement in patient ratings of spasticity compared to placebo. These positive findings in a treatment failure population suggest a role for THC in the treatment of spasticity in multiple sclerosis.
Adv Alcohol Subst Abuse 1987
PMID:Delta-9-THC in the treatment of spasticity associated with multiple sclerosis. 283 1

The formation of tolerance to the hypothermic effect of ethanol was inhibited in rats after intraperitoneal injection of the neurotoxin DSP-4 50 mg/kg. The neurotoxin also significantly suppressed the ethanol withdrawal syndrome; hyperlocomotion, audiogenic seizures and spasticity. These behavioural changes were accompanied by a 52% decrease of the brain norepinephrine (NE) content, with no alterations in the dopamine or serotonin levels. The results indicate that intact NE neurons are necessary for the development of tolerance to ethanol-induced hypothermia and are involved in the expression of the ethanol withdrawal syndrome.
Drug Alcohol Depend 1986 Dec
PMID:Suppression of ethanol tolerance and dependence in rats treated with DSP-4, a noradrenergic neurotoxin. 381 31

Spasticity is partly caused by disinhibition of spinal stretch reflex activity and blocking of the group Ia afferents may improve its clinical symptoms. Since muscle afferent block has been successfully used for treating dystonia, this method may become useful for treating spasticity as well. We injected diluted lidocaine (0.5%, 50 ml/session) and ethanol (5 ml) into thigh adductors (for leg crossing), medial hamstrings (for medial rotation of the leg), quadriceps femoris (for hyperextension of the knee), tibialis posterior and triceps surae muscles (pes equinovarus deformity), biceps brachii and forearm flexors (for flexion deformities of the upper extremity) in 12 patients with spasticity. Although the duration of action was short (< 1 day) at first, it was gradually prolonged to several weeks by repeating the injection every 3-4 days. The final outcome was comparable to that obtained by botulinum toxin injection in the same group of patients. This method may prove its promise as a means of treating spasticity.
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PMID:[Treatment of spasticity with botulinum toxin and muscle afferent block]. 912 98

Spasticity is a velocity-dependent increase in stretch reflex activity. It is one of the forms of muscle overactivity that may affect patients with damage to the central nervous system. Spasticity monitoring is relevant to function because the degree of spasticity may reflect the intensity of other disabling types of muscle overactivity, such as unwanted antagonistic co-contractions, permanent muscle activity in the absence of any stretch or volitional command (spastic dystonia), or inappropriate responses to cutaneous or vegetative inputs. In addition, spasticity, like other muscle overactivity, can cause muscle shortening, which is another significant source of disability. Finally, spasticity is the only form of muscle overactivity easily quantifiable at the bedside. Under the name pharmacological treatments of spasticity, we understand the use of agents designed to reduce all types of muscle overactivity, by reducing excitability of motor pathways, at the level of the central nervous system, the neuromuscular junctions, or the muscle. Pharmacologic treatment should be an adjunct to muscle lengthening and training of antagonists. Localized muscle overactivity of specific muscle groups is often seen in a number of common pathologies, including stroke and traumatic brain injury. In these cases, we favor the use of local treatments in those muscles where overactivity is most disabling, by injection into muscle (neuromuscular block) or close to the nerve supplying the muscle (perineural block). Two types of local agents have been used in addition to the newly emerged botulinum toxin: local anesthetics (lidocaine and congeners), with a fully reversible action of short duration, and alcohols (ethanol and phenol), with a longer duration of action. Local anesthetics block both afferent and efferent messages. The onset of action is within minutes and duration of action varies between one and several hours according to the agent used. Their use requires resuscitation equipment available close by. When a long-lasting blocking agent is being considered, we favor the use of transient blocks with local anesthetics for therapeutic tests or diagnostic procedures to answer the following questions: Can function be improved by the block? What are the roles played by overactivity and contracture in the impairment of function? Which muscle is contributing to pathologic posturing? What is the true level of performance of antagonistic muscles? A short-acting anesthetic can also serve as preparation to casting or as an analgesic for intramuscular injections of other antispastic treatment. Alcohol and phenol provide long-term chemical neurolysis through destruction of peripheral nerve. Experience with ethanol is more developed in children using intramuscular injection, while experience with phenol is greater in adults with perineural injection. In both cases, there are anecdotal reports of efficacy but studies have rarely been controlled. Side effects are numerous and include pain during injection, chronic dysesthesia and chronic pain, and episodes of local or regional vascular complications by vessel toxicity. In the absence of controlled studies, a theoretical comparison of neurolytic agents with botulinum toxin is proposed. Neurolytic agents may be preferred to botulinum toxin on a number of grounds, including earlier onset, potentially longer duration of effect, lower cost, and easier storage. Conversely, pain during injection, tissue destruction with chronic sensory side effects, and lack of selectivity on motor function with neurolytic agents may favor the use of botulinum toxin. Neurolytic agents and botulinum toxin may be used in combination, the former for larger proximal muscles and the latter for selective injection into distal muscles. In the future, neurolytic agents may prove more appropriate in very severely affected patients for whom the purposes of the block are comfort and hygiene. (ABSTRACT TRUNCATED)
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PMID:Traditional pharmacological treatments for spasticity. Part I: Local treatments. 982 83

The use of smoked marijuana as a therapeutic agent is presently a matter of considerable debate in the United States. Many people suffering from a variety of disorders maintain that it is necessary for their adequate treatment. Yet, the evidence to support claims is insufficient for FDA approval. An interim solution is proposed which would allow patients referred by their physicians to participate in a 6-month program of legal marijuana availability, similar to the 'compassionate IND' program of a number of years ago. A technique similar to that used for post-marketing surveillance is proposed for obtaining quantitative data for a limited number of potential indications. These are: (1) nausea and vomiting associated with cancer chemotherapy or other causes, (2) weight loss associated with debilitating illnesses, (3) spasticity secondary to neurological diseases, and (4) chronic pain syndromes.
Drug Alcohol Depend 2000 Feb 01
PMID:An approach to the medical marijuana controversy. 1066 50

Muscle afferent block (MAB) is an intramuscular injection of 0.5% lidocaine and pure ethanol with a volume ratio of 10:1, introduced as an alternative to botulinum toxin injection for focal dystonia and spasticity. As in the case of botulinum toxin injection, the precise localization of target muscles is crucial to obtain the maximal effect from MAB. For this purpose, we performed ultrasonography of cervical muscles (echomyography) in 20 patients with cervical dystonia (11 men, 9 women; mean age 46.1), with ultrasonograph SSD-5500 (Aloca Co. Ltd., Japan) and a 7.5 MHz linear probe. In untreated subjects, the boundaries of muscles could be easily identified, while they tended to become ambiguous after repeated MAB sessions. At rest, there were involuntary worm-like movements of a specific muscle group observed in all patients. Contrary to our expectation, in all but one patient abnormal contraction was limited only in a part of synergists responsible for the abnormal posture. In normal subjects there was no abnormal contraction at rest, and all the synergists were simultaneously activated by the voluntary neck deviation. Normal subjects could not mimick the pattern of muscle activity in dystonic patients. The echo-guided MAB was performed in 16 patients. We could easily observe the diffusion of lidocaine and ethanol into the targeted muscle, and injected portions of the muscle stopped their activities just after MAB. The effect persisted for 3-4 days in at least 5 out of 10 patients who had follow-up examination. On the other hand, the movement stopped only temporarily after the injection of saline or lidocaine only. In 3 out of 16 patients, some of the uninjected synergists were activated as if to substitute for the treated muscle just after the injection. We conclude that cervical echomyography is useful to investigate the pattern of muscle activity in cervical dystonia and to accurately localize the contracting muscles during MAB.
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PMID:[Cervical echomyography in cervical dystonia and its application to the monitoring for muscle afferent block (MAB)]. 1118 6


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