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)

Dantrolene sodium was effective in controlling spasticity and improving function in 11 of 13 patients taking part in a 14-week double-blind crossover study. Clonus and lower-extremity tendon jerks were reduced in almost all patients (10 and 11 respectively) during dantrolene sodium therapy at 200 to 400 mg/day. Activities of daily living showed marked improvement in 3 cases and moderate improvement in 8. All 13 patients reported decreases in the frequency of intermittent painful spasm. Side effects were minimal and consisted mainly of an initial 3- to 4-day period of weakness and lightheadedness.
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PMID:Efficacy of dantrolene sodium in the treatment of spasticity. 1789 68

Clinical signs and symptoms of spasticity include hypertonia, involuntary movements (spasms, clonus), decreased range of motion, contractures, and often spasm-related pain. When spasticity is refractory to medical management, patients may be referred for intrathecal baclofen (ITB) pump placement. We reviewed a cohort of amyotrophic lateral sclerosis (ALS) patients with intractable spasticity requiring ITB to further define the impact of ITB on pain relief in this patient population. From 2003 to 2005, eight patients (mean age 43.8 years; 5 men, 3 women) with ALS received ITB for pain associated with intractable spasticity at our institution. Mean disease duration preoperatively was 47.4 months, mean follow-up was 9.8 months, and pain was evaluated using a 0-10 scoring system. All patients experienced spasticity relief in response to a preoperative bolus test injection of ITB (25-50 microg) via lumbar puncture. Following ITB pump placement, the average reduction of pain was 54% (P = 0.0082). Six patients (75%) experienced pain score reduction, three of whom had complete pain relief. Postoperative pain reduction was predicted by the degree of pain reduction following preoperative ITB test injection. These results support ITB as a treatment modality for pain associated with spasticity in ALS.
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PMID:Intrathecal baclofen for spasticity-related pain in amyotrophic lateral sclerosis: efficacy and factors associated with pain relief. 1789 58

Action tremor has been described in cerebellar, task-specific, dystonic, or Holmes tremor. We report 2 patients who developed unilateral kinetic or isometric action tremor of the upper extremity, following cervical spondylotic myelopathy and capsular ischemic stroke. Slight motor weakness and spasticity with exaggerated tendon jerks and passive stretch-induced clonus were present on the same limb. The central motor pathways lesions might have been responsible for a hyperexcitability of the stretch-reflex arc and an enhancement of the coactivation of skeletal muscles through a loss of the descending or segmental control of the spinal reflexes. The unusual topography of the symptoms, their occurrence during motion, and the similar frequency of the passive clonus and the action tremor, led us to hypothesize that both patients had prolonged action-induced clonus, mimicking action tremor. Lesions of the central motor pathways lesions might be responsible for action tremor under certain conditions.
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PMID:Action-induced clonus mimicking tremor. 1799 33

There is still a debate whether primary lateral sclerosis (PLS) is a distinct pathological entity or whether it represents one end of a continuous spectrum of motor neuron disease (MND). In this report we present four PLS patients who have been observed from the time of symptom onset (1990-1999) through January 2007. All of them have had only upper motor neuron (UMN) signs and slow clinical progression. Three patients have been presented with spastic paraparesis. Spasticity was the main clinical feature in demonstrated cases with hyperactive deep tendon reflexes, clonus, and Babinski signs. One patient was presented with spastic dysarthria at the disease onset. Mean disease duration, measured from symptom onset to the present, was 11.5 years in our reported series. All four PLS patients had not developed lower motor neuron (LMN) signs during this time of observation. This prospective analysis of our PLS series is in agreement with data from other studies suggesting that pure PLS cases have a prolonged course of disease with a high level of independence when compared to other MND.
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PMID:Pure primary lateral sclerosis--Case reports. 1826 42

Hyperekplexia (MIM #149400) is a rare neurological disorder characterized by an exaggerated startle response, infantile hypertonia and hyperreflexia without spasticity, a hesitant gait that usually improves by 3 years of age, and nocturnal myoclonus. Familial hyperekplexia is usually autosomal dominant resulting from mutations in the inhibitory glycine receptor subunit alpha 1 (GLRA1) gene on chromosome 5q. We identified a 3-generation family with progressively severe phenotypes of hyperekplexia. All affected family members were found to be heterozygous for a novel arginine271proline mutation in GLRA1. Long-term follow-up of the affected members of the third generation, now aged 6 and 7 years, reveals enhanced startle responses and persistent hypertonia of the extremities without clonus or a catch, tight heel cords and abnormal toe-walking gait, and plantar flexor reflexes. The 7-year-old child recently reponded well to a benzodiazepine. Future studies are warranted to examine whether this new missense mutation is solely responsible for this atypical phenotype.
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PMID:A novel GLRA1 mutation associated with an atypical hyperekplexia phenotype. 1907 49

Intrathecal baclofen (ITB) is increasingly being used to reduce spasticity among children with cerebral palsy, dystonia, and spinal cord injuries. However, complications such as withdrawal, which is a potentially life-threatening condition, can occur. Intrathecal baclofen withdrawal should be differentiated with autonomic dysreflexia, malignant hyperthermia, neuroleptic malignant syndrome, and serotonin syndrome. We report a case of ITB withdrawal secondary to low residual volume in the pump reservoir and resembling serotonin syndrome in an adolescent with cerebral palsy. He presented with agitation, diaphoresis, increasing spasticity, rigidity, jitteriness, hyperreflexia, clonus, tachycardia, hypertension, and rhabdomyolysis. Treatment consisted of emergent refilling of the pump, intravenous diazepam, and oral cyproheptadine. We also emphasize the importance of prompt recognition of ITB withdrawal among high-risk patients.
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PMID:Intrathecal baclofen withdrawal resembling serotonin syndrome in an adolescent boy with cerebral palsy. 1924 Jun 73

Among the three main factors of motor impairment that emerge in chronological order following a lesion to central motor pathways, the last two antagonize movement: 1) stretch-sensitive paresis, a reduction of agonist motor unit recruitment upon voluntary command, worsened by antagonist stretch; 2) soft tissue contracture, and 3) muscle overactivity. Types of muscle overactivity include 1) spasticity, an increase in the velocity-dependent response to muscle stretch, measured at rest; 2) spastic dystonia, i.e., chronic tonic muscle activity at rest, sensitive to stretch of the dystonic muscle and 3) spastic co-contraction, an inappropriate degree of antagonistic contraction during voluntary agonist command, sensitive to stretch of the co-contracting muscle. A five-step clinical assessment may closely parallel this phenomenology, in which the first four steps aim at quantifying the antagonistic potential of each muscle group. Step-1 measures passive range of motion, i.e., the angle of arrest upon slow stretch of the muscle group assessed (minimizing spastic dystonia), which provides insight on soft tissue length and extensibility. Step-2 measures the angle of catch or clonus upon fast passive stretch of the muscle group assessed, which provides insight on stretch reflex excitability. Step-3 measures the range of active motion against the muscle group assessed, a net result of agonist recruitment minus the combined resistance from passive soft tissue stiffness and spastic co-contraction in the muscle group assessed. Step-4 measures the maximal frequency of rapid alternating movements along the maximal active range of motion, evaluating Step-3 performance repeatability. Step-5 evaluates active function, using for example a walking test (10 m or 2 min) for lower limb and the Modified Frenchay Scale for upper limb assessment, and perceived function through patient global subjective assessment.
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PMID:Five-step clinical assessment in spastic paresis. 2092 7

Spasticity, a classical clinical manifestation of an upper motor neuron lesion, has been traditionally and physiologically defined as a velocity dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex. Clinically spasticity manifests as an increased resistance offered by muscles to passive stretching (lengthening) and is often associated with other commonly observed phenomenon like clasp-knife phenomenon, increased tendon reflexes, clonus, and flexor and extensor spasms. The key to the increased excitability of the muscle stretch reflex (muscle tone) is the abnormal activity of muscle spindles which have an intricate relation with the innervations of the extrafusal muscle fibers at the spinal level (feed-back and feed-forward circuits) which are under influence of the supraspinal pathways (inhibitory and facilitatory). The reflex hyperexcitability develops over variable period of time following the primary lesion (brain or spinal cord) and involves adaptation in spinal neuronal circuitries caudal to the lesion. It is highly likely that in humans, reduction of spinal inhibitory mechanisms (in particular that of disynaptic reciprocal inhibition) is involved. While simply speaking the increased muscle stretch reflex may be assumed to be due to an altered balance between the innervations of intra and extrafusal fibers in a muscle caused by loss of inhibitory supraspinal control, the delayed onset after lesion and the frequent reduction in reflex excitability over time, suggest plastic changes in the central nervous system following brain or spinal lesion. It seems highly likely that multiple mechanisms are operative in causation of human spasticity, many of which still remain to be fully elucidated. This will be apparent from the variable mechanisms of actions of anti-spasticity agents used in clinical practice.
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PMID:Spasticity mechanisms - for the clinician. 2120 67

The serotonin toxicity (ST) is a potentially life-threatening adverse drug reaction results from therapeutic drug use, intentional self-poisoning, or inadvertent interactions between drugs. ST can be caused by a single or a combination of drugs with serotonergic activity due to excessive serotonergic agonism on central nervous system and peripheral serotonergic receptors (monoamine oxidase inhibitors, tricyclic antidepressants, SSRIs, opiate analgesics, over-the-counter cough medicines, antibiotics, weight-reduction agents, antiemetics, antimigraine agents, drugs of abuse, H2-antagonist and herbal products). The serotonin toxicity is often described as a clinical triad of mental-status changes (agitation and excitement with confusion), autonomic hyperactivity (diaphoresis, fever, tachycardia, and tachypnea), neuromuscular abnormalities (tremor, clonus, myoclonus, and hyperreflexia) and, in the advanced stage, spasticity; not all of these findings are consistently present. In this article, we describe two cases of ST due to interaction between Citalopram and two CYP2D6 inhibitors: Cimetidine and Topiramate and their clinical resolution after treatment discontinuation.
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PMID:Serotonin toxicity: a short review of the literature and two case reports involving citalopram. 2149 Oct 99

We report the case of a previously healthy 4 year-old African American female who presented to the emergency department with acute onset of unilateral abducens nerve palsy and torticollis. Within 12 h of presentation, the patient's symptoms progressed to include ipsilateral facial nerve palsy and gait ataxia. On exam, the patient demonstrated right cranial nerve VI and VII palsies, ataxic gait with left lateropulsion, spasticity of bilateral lower extremities with clonus, and the presence of bilateral Babinski sign. MRI of the brain and spinal cord revealed severe Chiari I malformation with associated extensive holochord syringomyelia and syringobulbia. The patient underwent successful surgical decompression 72 h after initial presentation. We review the literature on Chiari malformations and syringomyelia, including epidemiology, presentation and neurological manifestations, and treatment recommendations. As our patient had a very acute presentation, we additionally review the previously reported cases of acute and atypical presentation of patients with Chiari I malformation and syringomyelia. The aim of this report is to make practitioners aware of the acuteness with which children with Chiari malformation type I with syringomyelia and syringobulbia can present.
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PMID:Acute VI nerve palsy in a 4 year-old girl with Chiari I malformation and pontomedullary extension of syringomyelia: case report and review of the literature. 2156 92


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