Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Patients with spasmodic torticollis secondary to athetoid cerebral palsy may develop symptomatic degenerative cervical disc disease or spondylosis. In these cases, peri-operative stabilization of the cervical spine is considered to be difficult and recurrence occurs frequently. We reported a case with cervical spondylosis induced by athetoid cerebral palsy. A 44-year-old female with athetoid cerebral palsy had suffered from secondary spasmodic torticollis. 7 years previously, she had been admitted to our hospital for the first time with complaints of gait disturbance, dysesthesia and hypesthesia in all extremities. CT-myelography and MRI showed disc degeneration and spondylosis at the level of C4/5 and C5/6, compressing the spinal cord. She underwent C5 vertebrectomy and C4-6 anterior fusion. However, due to cervical dystonia, it was difficult for her to wear a Philadelphia collar, so she had to under go complete bed rest for postoperative neck stabilization. Her symptoms improved after the operation. 5 years after the first operation, she complained of gait disturbance and sensory disturbance, again. MRI showed compression of the spinal cord at C2-C4, rostral to the level of the previous surgical area. So we planned the second operation. Prior to the operation, we used botulinum A toxin to reduce the athetoid movement of the neck. And we performed C3-6 expansive laminoplasty and partial laminectomy of C2 and C7 laminae. After the second operation, she was able to wear the Philadelphia collar without trouble and her neurological condition improved again. Botulinum A toxin was very effective to control the spasmodic torticollis peri-operatively in this case with cervical dystonia.
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PMID:[Peri-operative treatment with botulinum A toxin prior to posterior cervical decompression in a case with cervical spondylosis caused by spasmodic torticollis secondary to cerebral palsy]. 1451 86

Pain and other nonmotor symptoms in PD are increasingly recognized as a major cause of reduced health-related quality of life. Pain in PD may be categorized into a number of different subtypes, including musculoskeletal, dystonic, radicular neuropathic, and central pain. The onset of pain can vary in relation to motor symptoms, and may precede the appearance of motor symptoms by several years, or occur after the diagnosis of PD has been made. Pain in PD is frequently under-recognized and is often inadequately treated. Levodopa-related dystonia may respond to manipulation of dopaminergic medication. Dopaminergic therapy may also improve musculoskeletal pain related to rigidity and akinesia, as well as akathisia in PD. Botulinum toxin injections can be effective for treatment of painful focal dystonia. Pain and dysesthesia have been reported to improve with DBS, in some cases. Increased understanding of basal ganglia pathways has provided further insights into the pathogenesis of pain in PD, but the exact mechanism of pain processing and modulation remains unclear.
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PMID:Pain in Parkinson's disease. 2195 90

Poststroke central pain (PSCP) can be a debilitating medication-refractory disorder. We report a single case where right unilateral ventral capsule/ventral striatum (VC/VS) deep brain stimulation was used to treat PSCP and inadvertently induced a smile without euphoria. The patient was a 69 year-old woman who had a stroke with resultant dysesthesia and allodynia in her left hemibody and also a painful left hemibody dystonia. In her case, VC/VS stimulation induced a smile phenomenon, but without a euphoric sensation. This phenomenon was different from the typical smile responses we have observed in obsessive-compulsive disorder cases. This difference was considered to be possibly attributable to impairment in the emotional smile pathway.
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PMID:Smile without euphoria induced by deep brain stimulation: a case report. 2536 Jul 66

Hashimoto encephalopathy (HE) is characterized by heterogeneous neurological symptoms. HE is diagnosed based on three criteria-the presence of antithyroid antibodies, neurological symptoms from the cerebrum and/or cerebellum, and a positive response to immunotherapy. We clinically analyzed 18 patients (3 men, 15 women; age range, 38-81years) diagnosed with HE in our hospital from May 2013 to January 2016. Eleven patients showed sensory abnormalities such as strong pain, deep muscle pain, dysesthesia, paresthesia, or neuralgia. Surprisingly, the majority of the pain was distributed in a manner that was not explainable anatomically. Seventeen patients showed motor disturbances, such as weakness, paresis of extremities, or dexterity movement disorder, and eight patients showed give-way weakness, which is disruption of continuous muscle contraction. Other symptoms indicative of brain-related anomalies such as tremor, dystonia, involuntary movements, cerebellar ataxia, parkinsonism, memory loss, and chronic fatigue were also seen. In most patients, such motor, sensory, or higher brain functions were markedly improved with immunosuppressive therapies such as prednisolone, azathioprine, or immunoadsorption therapy. Although give-way weakness and anatomically unexplainable pain are typically considered as being psychogenic in origin, the presence of these symptoms is indicative of HE. HE exhibits diffuse involvement of the entire brain and thus, these symptoms are explainable. We propose that physicians should not diagnose somatoform disorders without first excluding autoimmune encephalopathy.
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PMID:[Clinical Features and Treatment of Hashimoto Encephalopathy]. 2766 88