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 authors report the case of a young man who suffered multiple injuries in a motor vehicle accident, the most significant of which arose in the brain, creating an unusual clinical syndrome. After experiencing an initial coma for several days, the patient was found to have a right-sided homonymous hemianopsia and a right hemiparesis, which was more marked at the shoulder and was accompanied by preservation of finger movement. Dystonic movements appeared 2 months later and progressed, along with increased spasticity on volition, to severe uncontrolled arm movements at 2 years postinjury. This motor disorder continued to worsen during the following 6 years prior to the patient's death. At autopsy, the left side of the brain was observed to have marked atrophy of the optic tract, a partial lesion of the posterior portion of the medial segment of the globus pallidus (GP), and a reduction in the size of the internal capsule at the level of the GP, suggesting impaired circulation to these areas at the time of injury. The isolated lesion of the internal segment of the GP was the presumed cause of the dystonia, acting through an alteration in thalamic inhibition. The atrophic subthalamic nucleus was the probable cause of the hemiballismus. The authors speculate that this and other delayed and progressive features of this case were the result of an active, but disordered, adaptive process that failed to compensate and, instead, caused even greater problems than the original injury.
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PMID:Delayed onset of hemidystonia and hemiballismus following head injury: a clinicopathological correlation. Case report. 1121 70

Patients surviving severe traumatic brain injury (TBI) often suffer from residual impairments in motor control, communication skills, cognition and social behaviour. These distinctly hamper their capability to return to their 'pre-trauma' activity. Comprehensive and integrated rehabilitation programmes initiate, during the acute phase, a prolonged treatment process which starts at the most sophisticated medical systems. There is no clear end point for the treatment of these patients, since the recovery process and the rehabilitation activity may continue for years, even after patients return home to live with their families. The inherent inability to make a firm early prediction regarding outcome of patients and the late appearance of additional symptoms stress the need for a comprehensive close long-term follow-up. The following presentation concerns the description of the treatment strategy and long-term improvement of a 22-year-old male who suffered from very severe TBI. On admission to the emergency room, he was in the decerebrated position and his Glasgow Coma Scale (GCS) was at the lowest (3). The focus of this presentation is on the recovery of motor function. The initial motor disabilities included weakness in all four limbs, in particular left hemiplegia, and right hemiparesis with severe bilateral ataxic elements and a marked tremor of the right arm. Range of motion was limited in hips, and he suffered from stiff trunk and neck. Goals of physiotherapy were directed towards improving range of motion (ROM) and active movement. Casting, use of orthoses, biofeedback, hydrotherapy, hippotherapy, medication and nerve blocks for reducing spasticity were timely applied during the process. The motor improvement in this very severe TBI patient who is now over 3 years post-injury still continues and has a functional meaning. He has succeeded in being able to stand up by himself from a chair and is able to walk unaided and without orthoses for very short distances--up to five steps. He is able to drink soup without assistance and play a few notes on the piano. Marked cognitive improvement occurred as well. It is concluded that motor improvement may be evident over long periods of time and various timely interventions may assist in the process.
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PMID:Combined motor disturbances following severe traumatic brain injury: an integrative long-term treatment approach. 1142 91

This review evaluates research investigating spasticity, weakness, stiffness and central nervous system plasticity following cerebrovascular accident. The term spasticity is frequently applied to a variety of movement impairments exhibited by stroke patients, impairments which may actually represent weakness or alterations in mechanical properties of muscle. Experimental research indicates spasticity occurs in response to stretch of relaxed hemiparetic muscle. In actively contracting muscle of stroke patients, research findings have shown reduced EMG activity and weakness of muscles of both affected and unaffected sides of the body. Additionally, in actively contracting hemiparetic muscle, evidence has revealed non-reflex mediated stiffness which can be attributed in part to changes in connective tissue arising from disuse secondary to hemiparesis. Clinical implications of these scientific findings are presented for the physiotherapy management of cerebrovascular accident.
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PMID:The pathophysiological and clinical implications of neuro-muscular changes following cerebrovascular accident. 1167 45

This study investigated the role of paresis, excessive antagonist coactivation, increased muscle-tendon passive stiffness and spasticity in the reduced stance phase plantarflexor moment (Mmax) and swing phase dorsiflexion during gait (DFmax) in subjects with a recent (<6 months post-stroke) hemiparesis (patients). The gait pattern of the paretic and non-paretic sides was evaluated in 30 patients (aged 57.8+/-10.8 years), whereas only one side was evaluated in 15 healthy controls (aged 59.1+/-9.8 years) while walking at natural and very slow speeds. Peak plantarflexor moment (Mmax) and peak medial gastrocnemius (MG) activation during the stance phase, as well as peak dorsiflexion angle (Dfmax) and peak tibialis anterior (TA) activation during the swing phase, were retained for analysis. In addition, a coactivation index and a plantarflexor spasticity index were calculated for both the stance and the swing phase, and plantarflexor passive stiffness was evaluated on an isokinetic dynamometer. The results showed that Mmax on the paretic and non-paretic sides were both reduced compared with control values at natural speed. This reduction was combined to a low MG activation (paresis) on the paretic side. On the non-paretic side, the reduced plantarflexor moment was related to excessive coactivation levels. The swing phase Dfmax tended to be reduced (not significantly) on the paretic side of the patients compared with control values. This reduction was neither associated with excessive antagonist coactivation nor to plantarflexor hyperactive stretch reflexes, but rather to an increased plantarflexor passive stiffness. In some of the patients, however, an increased TA activation that overcame the plantarflexor passive stiffness allowed for normal DFmax values. The functional consequences of the disturbed mechanisms of motor control observed in both the paretic and non-paretic sides are discussed.
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PMID:Mechanisms of disturbed motor control in ankle weakness during gait after stroke. 1198 99

A new therapeutic method for the rehabilitation of central paresis of the upper extremity, especially of fine skilled finger movements, is presented. The therapeutic concept is the activation of reorganization processes in the CNS. These processes are elicited by the induction of proprioceptive input to the CNS which corresponds physiologically to the lost input during active movements. The input is generated by repetitive peripheral magnetic stimulation (RPMS) at the innervation zone of the paretic muscles. The stimulation leads to a motion of the activated muscles. The proprioceptive input is generated by two mechanisms: adequately by activation of mechanoreceptors of the stimulated muscles during the induced contractions and relaxations and inadequately by direct activation of the involved sensorimotor afferents. The method has been applied to 52 patients suffering from spastic paresis of the upper extremity. A simple clinical quantification using the Ashworth scale revealed that spasticity could be remarkably (1-2 points) reduced already by one session of RPMS lasting 15 minutes. In order to get an objective insight into the improvement of active motor performances, a neurophysiological investigation of active finger extensions was performed in eight patients suffering from a central hemiparesis. Following RPMS of the paretic finger extensors, the patients could perform rapid finger extensions with larger displacement and velocity at diminished amounts of EMG activity.
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PMID:Facilitation of skilled finger movements by repetitive peripheral magnetic stimulation (RPMS) - a new approach in central paresis. 1271 22

We studied how different patterns of muscle tone disorders depend upon lesion site using CT. 111 patients not earlier 3 months after hemispheric stroke were studied. We showed the degree of spasticity to be determined by depth of hemispheric damage in relation to posterior limb of capsula intema. It also correlates with the degree of corticoreticular pathway damage. Even or irregular damage to this pathway which accompany pyramidal tract stipulates different patterns of spasticity, distribution and its interaction with structure of hemiparesis. Degree and structure of post-stroke muscle tone disorders after 3 months from the onset of stroke is depend on hemispheric damage but do not depend on the duration of recreative or residual period of the disease. It can be applied in medical expertise that pattern and prominence of post-stroke muscle tone disorders 3 months after stroke onset depend on lesion location, but not on the length of recovery period or period of residual changes.
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PMID:[Pathological aspects of post-stroke muscle tone disorder: clinical-neuro-visual study]. 1283 May 42

The origins of impaired finger and hand function were examined in 10 stroke survivors with chronic spastic hemiparesis, with the intent of assessing whether mechanical restraint or altered neurophysiological control mechanisms are responsible for the well-known impairment of finger extension. Simultaneous extension of all four metacarpophalangeal (MCP) joints of the impaired hand was either externally imposed using a rotary actuator or attempted voluntarily by the subject. Trials were conducted both before and after administration of a local anesthetic, blocking the median and ulnar nerves at the elbow. The anesthetic was administered to reduce the activity of the muscles flexing the MCP joints, in order to distinguish mechanical from neuronal resistance to imposed MCP rotation. We found that the nerve blockade resulted in a reduction in velocity-dependent torque (P = 0.01), thereby indicating significant joint impedance due to spasticity. Blockade also produced a posture-dependent reduction in static torque in declaratively relaxed subjects (P = 0.04), suggesting some tonic flexor activity for specific hand postures. No change in either extensor isometric (P = 0.33) or isokinetic (0.53) torque was apparent, but 3 of the 10 subjects did exhibit substantial (>10 degrees ) improvement in voluntary MCP extension following the blockade. This improvement seemed largely due to a decrease in inappropriate flexor activity during the movement, rather than an increase in extensor activity. We argue that persistent and inappropriate flexor activation plays a role in limiting voluntary finger extension, and that this activation is potentially a reflection of altered supraspinal control of key spinal pathways. In all cases, this inappropriate activation was compounded by weakness, apparent in both the extensor and flexor muscles.
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PMID:Relative contributions of neural mechanisms versus muscle mechanics in promoting finger extension deficits following stroke. 1292 90

Leber hereditary optic neuropathy (LHON)/pediatric onset dystonia is associated with a G to A transition at nucleotide position (np) 14459, within the mitochondrial DNA (mtDNA)-encoded ND6 gene. This mutation has been reported in families presenting with LHON alone, LHON plus dystonia, or pediatric dystonia with typical age of onset less than 5 years. The mutation changes a moderately conserved alanine to a valine at amino acid residue 72, which is within the most evolutionarily conserved region of the ND6 protein. Pediatric onset disease is associated with basal ganglia dysfunction, spasticity, and encephalopathy. We report a family with G14459A mtDNA mutation and a broad spectrum of clinical manifestation. The proband was a 3-year-old girl with anarthria, dystonia, spasticity, and mild encephalopathy. MRI of the brain demonstrated bilateral, symmetric basal ganglia lucencies associated with cerebral and systemic lactic acidosis. Her maternal first cousin presented with a new onset limp and mild hemiparesis along with similar MRI findings with a much milder phenotype. Additional investigation of the family members with the mutation has revealed both asymptomatic and symptomatic individuals with variable clinical and laboratory features of mitochondrial disease. This study re-emphasizes the heterogeneous clinical manifestation of homoplasmic G14459A mtDNA mutation even within the same family, and supports the hypothesis that nuclear genes may play a role in modifying the clinical expression of mitochondrial disease. Published 2003 Wiley-Liss, Inc.
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PMID:Variable clinical manifestation of homoplasmic G14459A mitochondrial DNA mutation. 1473 85

We compared the electroclinical features and evolution of patients with two different types of abnormal cortical organization: unilateral closed-lip schizencephaly (SCHZ) and unilateral polymicrogyria (PMG). Between February 1990 and June 2002, 51 children with either unilateral PMG or closed-lip SCHZ were selected through neuroradiological analysis for investigation at our service. We evaluated the frequency of epilepsy, electroclinical features and evolution. The mean time of follow-up was 7 years (range 1-12 years). All patients underwent neurological examination, computed tomography scan and magnetic resonance imaging, serial electroencephalographic (EEG) recordings and neuropsychological assessment. Thirty-six of the 51 patients had unilateral PMG. All patients had hemiparesis with mild spasticity. Mental retardation was mild in 20 and moderate in 14. In two patients IQ was normal. Partial motor seizures were recorded in 28 patients, with secondary generalization in 20. The median age at onset of seizures was 2 years (range 4 months-7 years). Interictal EEGs showed unilateral spikes in all patients. In 21 patients epilepsy worsened between the ages of 4 and 8 (mean 5.6 years) with frequent atonic seizures, atypical absences, epileptic negative myoclonus and gait difficulties. EEGs showed continuous spike-wave activity or bilateral high-frequency spike discharges during slow-wave sleep. Frequent relapses of atonic and myoclonic seizures were seen in nine patients. At present, 16 patients are seizure-free. Fifteen patients with unilateral SCHZ were included in the study. Focal motor seizures were registered in seven cases, in three of them with secondary generalization. The median age at onset of epilepsy was 2.5 years (range 1-4 years). Interictal EEGs showed unilateral spikes in these seven cases. All patients except one presented mild spastic hemiparesis. Mental retardation was mild in ten children, moderate in two and IQ was normal in three. Although the underlying mechanisms leading to PMG and SCHZ are probably similar, the electroclinical phenomenon of secondary bilateral synchrony with frequent negative myoclonus was not present in our cases with unilateral closed-lip SCHZ.
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PMID:Unilateral closed-lip schizencephaly and epilepsy: a comparison with cases of unilateral polymicrogyria. 1503 Sep 2

Hemiparesis is common after stroke and often severely disabling. Until very recently, the only therapeutic option for motor recovery was physiotherapeutic training. Experimental animal studies have shown that when applied in addition to exercises pharmacological interventions that affect the norepinephrine system can enhance the rate of functional motor recovery. These effects were observed when an increase in norepinephrine concentration in the CNS was pharmacologically induced. We recently showed that 3 weeks of single daily doses of 100 mg L-dopa, which is metabolized into norepinephrine in the brain, increase the efficacy of physiotherapy in hemiparetic stroke patients. Two additional randomized controlled trials with stroke patients also demonstrated the clinical relevance of this approach for motor recovery and independence in activities of daily living. Modifying effects of other frequently occurring clinical symptoms such as spasticity, neglect, and attention were also investigated. Thus, in view of its minimal side effects, L-dopa can be recommended in conjunction with exercise therapy to improve the functional outcome in stroke rehabilitation.
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PMID:Advances in adjuvant pharmacotherapy for motor rehabilitation: effects of levodopa. 1550 79


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