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)

Clioquinol is still consumed in India in considerable amounts but no new case reports have appeared since 1977. A review is made for a regional neurotoxicology group of an enquiry that we conducted in Bombay to gather information regarding SMON, spanning the period of 1967 to 1976. Nine patients were diagnosed with a variable degree of confidence as suffering from SMON, two from a retrospective search and seven after a prospective watch for the disease. Myelopathy with predominant more distal dysesthesia was seen more often than the full-blown picture of SMON. The peripheral neuropathy component (N) diagnosed clinically or electrophysiologically was seen only once. Pyramidal tract disturbances and resulting spasticity was as striking as posterior column disorder and sensory ataxia. Subacute myelopathy was seen in six patients, optico-myelopathy in two, and myeloneuropathy only once. It was clear that clioquinol has potential neurotoxicity, but no definitive explanation was forthcoming about the vast difference in the prevalence of SMON as reported from Japan and seen by us in Bombay.
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PMID:SMON as seen from Bombay. 609 94

Percutaneously inserted spinal cord electrical stimulation (PISCES) was carried out in eleven intractable pain cases and in one spastic paraplegic case. The causes of intractable pain constitute subacute myelo-optic neuropathy (SMON) 6 cases, cerebrovascular disease 2 cases, multiple sclerosis (MS) 1 case, Charcot-Marie-Tooth (CMT) 1 case and transverse myelitis (TM) 1 case. The cause of spastic paraplegia was due to the ossification of posterior longitudinal ligament (OPLL). A trial stimulation was performed about two weeks before planning a permanent implantation of PISCES system. For the trial stimulation, epidural electrodes were percutaneously inserted with a guide of fluoroscopy in a X-ray room. The conditions of stimulation were adjusted to give an optimal electric dysesthesia. We employed pulse width 0.1-1.0 msec, pulse rate 1-120 Hz and pulse amplitude 0-10 Volt. If an excellent effect was obtained by trial study, we proceeded to the chronic implantation of PISCES system which were composed of epidural electrodes, a subcutaneous receiver and a surface antenna. The procedure of implantation was carried out in an operating room under local anesthesia. In our series, seven subjects (58%) experienced a rewarding effect by the trial stimulation and three underwent the permanent implantation of PISCES. We summarized the clinical courses of these three cases which were OPLL, CMT and SMON. Compared with the other methods for pain relief, PISCES is most characteristic in its safety and simplicity. To date, PISCES has been applied to various disorders; such as ataxia, spasticity, intractable pain, neurogenic bladder and peripheral vascular disease. But its efficacy has not been established in all these disorders.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Our experiences of PISCES (percutaneously inserted spinal cord electrical stimulation) in SMON and other neurologic disorders]. 661 Nov 63

Proprioceptive loss, paresthesias, and atrophy of the hands can occur with disorders afflicting the upper cervical spinal cord. The diagnosis might be erroneous, because compression in this region might produce signs and symptoms that seem to originate in the lower cervical cord. This article reviews the clinical presentation and radiographic data of a consecutive series of 11 patients who presented between 1992 and 1994 with an extradural lesion above the C4 level. Each patient had a characteristic syndrome of finger and hand dysesthesia, hand atrophy, and occipital or cervical pain. These complaints usually preceded the development of spasticity and gait disturbance. Initial diagnoses included brachial plexopathy, shoulder dysfunction, viral syndrome, and cervical spondylosis at a lower segment. Cervical spondylosis or a herniated disc was the most common pathogenesis. The most commonly involved level was C3-C4. Nine patients underwent a surgical procedure; eight showed significant postoperative improvement (mean time of follow-up examination, 9.7 mo; follow-up range, 1-24 mo). One patient was lost to follow-up. Although the pathophysiology of these findings is unknown, theories include anterior spinal artery ischemia, venous obstruction, and differential decussation of the forelimb and hindlimb fibers of the corticospinal tract. Recognition of this syndrome might prevent inappropriate operative intervention in patients with coexisting pathological conditions of the lower cervical spinal cord.
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PMID:False localizing signs in upper cervical spinal cord compression. 897 49

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

High dose oral anti-spastic medication is effective in the treatment of spasticity but has the disadvantage of frequent systemic side effects such as drowsiness and general weakness. Therefore, neurolytic and chemodenervation procedures are further therapeutic options, especially in cases of local spasticity. Apart from phenol blocks with the risk of persisting painful dysesthesia, botulinum toxin type A (BtxA) appears to be a safe and effective treatment. In 204 patients (mean age, 41.5 years [range 3-91 years]) with acute (n = 29, mean duration of disease 2.9 months [range, 1-6 months]) and chronic (n = 175, mean duration of disease 111 months [range, 7-500 months]) spasticity due to stroke, traumatic brain and spinal injury and other lesions of the upper motor neuron, the effects of single-dose BtxA treatment were studied. An overall dose of 181.2 units [range, 15-600 units] of BtxA (Botox) was injected in a mean of 3.3 [1-14] muscles per patient. Results were assessed using a modified Rating of Response to BtxA (RRB, Brin et al. 1995). The RRB includes a pre- and post BtxA assessment of the severity of spasticity-associated problems (patient's self-assessment), a rating of the current percentage of normal function in the region of the body selected for BtxA and a global rating of changes induced by BtxA. 191 (93.6%) patients demonstrated improvement over a mean of 7.7 weeks [1-36]; no deterioration was observed. Mean overall severity and function improved significantly (p < 0.001). No systemic or severe side effects were registered. Only in 5.9% of the patients were mild (n = 10) or moderate (n = 2) reversible adverse events reported. We conclude that BtxA injections are safe and effective in the treatment of local spasticity.
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PMID:[Safety and tolerance of single-dose botulinum toxin Type A treatment in 204 patients with spasticity and localized associated symptoms. Austrian and German botulinum toxin A spasticity study group]. 1058 88

Lesions of the central nervous system often involve the pyramidal tracts and the sensory pathways to produce spasticity, paresthesias, and dysesthesia. Three patients with intractable spasticity were treated with intrathecal baclofen. Two had an implanted Medtronic SynchroMed pump for long-term delivery of the muscle relaxant. The third patient had undergone a screening trial in which the baclofen was delivered into the intrathecal space through a lumbar catheter. All had excellent relief of spasms on clinical examination, but they reported painful spasms particularly at night. Two of the patients were successfully treated for dysesthesia.
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PMID:Dysesthesia perceived as painful spasticity: A report of 3 cases. 1134 52

We analysed the present state of those SMON patients with severely disturbed visual acuity. In medical screening of SMON Research Group at 1999, 52 out of 1,083 patients and 549 out of 1128 had their histories of complete blindness and complete loss of locomotion ability at the onset of SMON, respectively. Eighty one out of 1,149 patients showed severe visual impairment, including 22 with complete blindness. The number of patients with complete loss of locomotion and that of gait with cane/assistance were 59 and 443, respectively. Then, a large number of SMON patients have been still suffering from sequelae of clioquinol intoxication. Those patients groups with blindness and severe visual acuity yet showed after 30 years more severe disorders in locomotive activity, muscle strength and spasticity of lower extremities, degree of dysesthesia as well as vibratory sensory deficit, and ADL score. Those patients with complete or near complete blindness were profoundly handicapped so that the ratio of patients with a life-long institutionalization was high compared to the groups with less severe visual disturbance. Thus, it seems necessary to make a more extensive and meticulous supports for those SMON patients with blindness as they are in need of more finance and care providers.
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PMID:[Analysis of SMON at 30 years after its outbreak ending: special reference to those patients with blindness]. 1216 96

HTLV-1-associated myelopathy (HAM), also known as tropical spastic paraparesis (TSP), is a chronic progressive demyelinating disease that affects the spinal cord and white matter of the central nervous system. The lifetime incidence of HAM in HTLV-1 carriers is estimated to be less than 5%. Typical time of onset is in the fourth decade of life, with a female-to-male rate of 2:1. Gait disturbance and weakness and stiffness of the lower limbs are common presenting signs and symptoms of HAM. Lower extremities are affected to a much greater degree than upper extremities. Spasticity may be moderate to severe, and lower back pain is common. As the disease progresses, bladder and bowel dysfunction can occur. Sensory involvement is generally mild and can result in a variable degree of sensory loss and dysesthesia. Results of magnetic resonance imaging may be normal, or the scans show atrophy of the spinal cord and nonspecific lesions in the brain. Immunologic evidence suggests that an immune mechanism may play a role in the development of HAM. There is no effective treatment for the myelopathy. Corticosteroids, and INF-gamma may produce transient responses. Danazol, an anabolic steroid, does not improve gait and bladder function. The value of zidovudine (anti-retroviral agent) in the treatment has not been defined yet.
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PMID:[Human T-cell lymphotropic virus type 1(HTLV-1)-associated myelopathy]. 1217 Mar 34

Posttraumatic syringomyelia may result from a variety of inherent conditions and traumatic events, or from some combination of these. Many hypotheses have arisen to explain this complex disorder, but no consensus has emerged. A 28-year-old man presented with progressive lower extremity weakness, spasticity, and decreased sensation below the T4 dermatome five years after an initial trauma. Magnetic resonance imaging (MRI) revealed a large, multi-septate syrinx cavity extending from C5 to L1, with a retropulsed bony fragment of L2. We performed an L2 corpectomy, L1-L3 interbody fusion using a mesh cage and screw fixation, and a wide decompression and release of the ventral portion of the spinal cord with an operating microscope. The patient showed complete resolution of his neurological symptoms, including the bilateral leg weakness and dysesthesia. Postoperative MRI confirmed the collapse of the syrinx and restoration of subarachnoid cerebrospinal fluid (CSF) flow. These findings indicate a good correlation between syrinx collapse and symptomatic improvement. This case showed that syringomyelia may develop through obstruction of the subarachnoid CSF space by a bony fracture and kyphotic deformity. Ventral decompression of the obstructed subarachnoid space, with restoration of spinal alignment, effectively treated the spinal canal encroachment and post-traumatic syringomyelia.
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PMID:Decompressive surgery in a patient with posttraumatic syringomyelia. 2037 79

Selective dorsal rhizotomy (SDR) surgery is a well-established treatment for ambulatory children with bilateral spastic paresis and is performed to eliminate spasticity and improve walking. The objective of this case report is to describe sudden falls as a persistent complication of SDR. The authors report on 3 patients with bilateral spastic paresis, aged 12, 6, and 7 years at the time of surgery. The percentage of transected dorsal rootlets was around 40% at the L2-S1 levels. Sudden falls were reported with a frequency of several a day, continuing for years after SDR. The falls were often triggered by performing dual tasks as well as occurring in the transition from sitting to standing, during running, after strenuous exercise, or following a fright. Patients also had residual hyperesthesia and dysesthesia of the foot sole. The authors hypothesize that the sudden falls are caused by a muscle inhibition reflex of the muscles in the legs, as an abnormal reaction to a sensory stimulus that is perceived with increased intensity by a patient with hyperesthesia. A favorable effect of gabapentin medication supports this hypothesis.
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PMID:Sudden falls as a persistent complication of selective dorsal rhizotomy surgery in children with bilateral spasticity: report of 3 cases. 2710 30


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