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)

Encephalitis has been reported to be a rare cause of severe dystonia. We describe five patients with markedly severe dystonia from Japanese encephalitis. These patients with markedly severe dystonia were seen during the past 8 years as a subgroup of 50 patients with Japanese encephalitis. The diagnosis of markedly severe dystonia was based on increasingly frequent episodes of generalized dystonia with bulbar, respiratory, or metabolic derangement or leading to exhaustion or pain. The diagnosis of JE was based on clinicoradiologic features and a fourfold increase of hemagglutination-inhibiting antibody titers in paired serum. The outcome of the patients was defined as a good, partial, or poor recovery on the basis of 1-year clinical status. All the patients were males, and their ages ranged from 6 to 19 years. Movement disorders appeared 1 to 3 weeks after the illness as the level of consciousness started improving. During the next 1 to 4 weeks, patients began to experience markedly severe dystonia. It was associated with marked axial dystonia resulting in opisthotonus and retrocollis in five patients, jaw-opening dystonia in two patients, teeth clenching in one patient, and oculogyric crisis and neck deviation in another patient. The attacks of markedly severe dystonia lasted for 2 to 30 minutes and occurred as many as 20 to 30 times daily. Other developments included fixed limb dystonia in one patient, severe spasticity and rigidity in five patients, and focal muscle wasting in one patient. These patients had only a modest improvement after treatment. Markedly severe dystonia abated by 2 to 6 months in all the patients who were followed up. Cranial magnetic resonance imaging showed bilateral thalamic involvement in all patients, brainstem involvement in three patients, and basal ganglia involvement in two patients. At the 3-month follow-up, all patients had a poor outcome. At 1 year, one patient had a complete recovery; one had a partial recovery; and two were bedridden. It can be concluded that markedly severe dystonia is an important and serious sequela of Japanese encephalitis and may occur as the result of thalamus, midbrain, or basal ganglia involvement in various combinations.
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PMID:Markedly severe dystonia in Japanese encephalitis. 1110 1

The issues presented concern the difficulties facing a family with a spastic child. The aim of the thesis was to define the role of a psychologist in solving difficulties reported by parents of children with spasticity being treated with the help of intrathecal baclofen pump implantation. The research was done using the method of partially structured interviews with the parents of patients after the implantation of the baclofen pump as well as the results of a Questionnaire estimating the effects of treating spastics. The results show that the two main categories of difficulties reported by the parents concern the medical and nurse care, information and communication problems as well as physical and psychological exhaustion. The role and usability of a psychologist in the process of supporting families of spastic children treated with the baclofen pump has been described from a systematic perspective. A psychologist has been indicated as an advantageous support offering benefits to all--the patients, their families as well as the medical personnel--during the whole treatment process.
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PMID:[Psychological aspects of intrathecal baclofen pump implantation in children]. 1795 75

Loss of function, muscle pain and secondary muscoloskeletal complaints are common symptoms of patients with neuromuscular disease. Many patients develop a progressive handicap. Physiotherapeutic treatment is often used in the management of neuromuscular diseases. Different therapeutic strategies are useful depending on the stage and pathophysiology of the disease and with regard to the extent of the patient's handicap. The aims of the physiotherapy and realistic targets should be discussed critically with the patient at the beginning of the treatment. We propose different physiotherapeutic strategies depending on the stage of the underlying disease: 1) Patient is able to walk--active phase: education in self-training with regard to the risks of exhaustion. Manual and physical treatment of mycofascial complaints. 2) Progressive functional loss--assistive phase: support of compensation and daily functioning. 3) Patient in wheelchair or bedbound, loss of most voluntary functions--passive phase. The knowledge of the pathopysiology of the underlying disease is essential for the development of therapeutic strategies. Loss of upper neurons leads to the development of spasticity and muscle hypertonia whereas muscular atrophy and weakness is a prominent feature of lower motor neuron loss. Overtreatment and exhaustive training may lead to secondary muscle damage in primary myopathies. Training in short sessions with intervals between may have protective effects.
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PMID:[Basic principles of non-respiratory physiotherapy for neuromuscular diseases]. 1831 80

The purpose of this investigation was to determine whether changes in surface electromyography (EMG) data during an isometric muscle protocol, in combination with maximal voluntary isometric force, provide information on fatigue occurrence and exercise limitation in children with cerebral palsy. Twelve children with cerebral palsy and 10 age-matched controls completed an assessment of quadriceps muscle fatigue on an isokinetic device with surface EMG measurements, during a sustained isometric contraction at 50% of the maximal voluntary isometric force. The EMG data collected in participants with cerebral palsy suggest that muscle fatigue occurred sooner in children with cerebral palsy relative to the age-matched controls. However, the results demonstrate that no difference was found in time to exhaustion between the able-bodied and participants with cerebral palsy. These contrasting results may be the result of spasticity and co-contraction during maximal testing, which may play an important role in exercise limitation in children with cerebral palsy.
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PMID:Electromyographic (EMG) analysis of quadriceps muscle fatigue in children with cerebral palsy during a sustained isometric contraction. 1979 2

This Review discusses the spinal neuronal changes that occur after a complete spinal cord injury (SCI) in humans. Early after an SCI, neither locomotor nor spinal reflex activity can be evoked. Once spinal shock has resolved, locomotor activity and an early spinal reflex component reappear in response to appropriate peripheral afferent input. In the subsequent 4-8 months, clinical signs of spasticity appear, largely as a result of non-neuronal (for example, muscular) changes, whereas locomotor and spinal reflex activity undergo little change. At 9-12 months, the electromyographic amplitude in the leg muscles during assisted locomotion declines, accompanied by a decrease in the amplitude of the early spinal reflex component and an increase in the amplitude of a late spinal reflex component. This exhaustion of locomotor activity also occurs in nonambulatory patients with incomplete SCI. Neuronal dysfunction is fully established 1 year after the injury without further alterations in subsequent years. In chronic SCI, the absence of input from supraspinal sources has been suggested to lead to degradation of neuronal function below the level of the lesion or, alternatively, a predominance of inhibitory signaling to the locomotor pattern generator. Appropriate training and/or provision of afferent input to spinal neurons might help to prevent neuronal dysfunction in chronic SCI.
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PMID:Behavior of spinal neurons deprived of supraspinal input. 2010 Dec 54

This review describes the changes of spinal neuronal function that occur after a motor complete spinal cord injury (cSCI) in humans. In healthy subjects, polysynaptic spinal reflex (SR) evoked by non-noxious tibial nerve stimulation consists of an early SR component and rarely a late SR component. Soon after a cSCI, SR and locomotor activity are absent. After spinal shock; however, an early SR component re-appears associated with the recovery of locomotor activity in response to appropriate peripheral afferent input. Clinical signs of spasticity take place in the following months, largely as a result of non-neuronal changes. After around 1 year, the locomotor and SR activity undergo fundamental changes, that is, the electromyographic amplitude in the leg muscles during assisted locomotion exhaust rapidly, accompanied by a shift from early to dominant late SR components. The exhaustion of locomotor activity is also observed in non-ambulatory patients with an incomplete spinal cord injury (SCI). At about 1 year after injury, in most cSCI subjects the neuronal dysfunction is fully established and remains more or less stable in the following years. It is assumed that in chronic SCI, the patient's immobility resulting in a reduced input from supraspinal and peripheral sources leads to a predominance of inhibitory drive within spinal neuronal circuitries underlying locomotor pattern and SR generation. Training of spinal interneuronal circuits including the enhancement of an appropriate afferent input might serve as an intervention to prevent neuronal dysfunction after an SCI.
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PMID:Neuronal dysfunction in chronic spinal cord injury. 2106 Mar 14

Hypohidrosis refers to diminished sweating in response to appropriate stimuli. This can cause hyperthermia, heat exhaustion and death. The aetiology of hypohidrosis can be divided into exogenous, dermatological and neurological causes. Exogenous causes act either by systemic neurohormonal inhibition of sweating or localised damage to the skin and sweat glands. Dermatological disorders can result from congenital disorders, wherein other ectodermal tissues may also be affected, or acquired disorders in which manifestations of the primary disease predominate. Neurological disorders should be classified based on an upper motor neuron or lower motor neuron pattern of disease. In the former, there is spasticity and hyperactive reflexes whereas in the latter, flaccidity and hypoactive reflexes predominate. Acquired idiopathic generalised anhidrois refers to isolated anhidrosis with no other detectable abnormalities. When approaching a patient with hypohidrois, exogenous causes should first be excluded. Physical examination, paying attention to mucocutaneous manifestations and neurological signs, will dichotomise if the lesion is dermatological or neurological. In the former, a skin biopsy is the investigation of choice. In the latter, one should consider magnetic resonance imaging of the brain and spinal cord for upper motor neuron lesions, nerve conduction tests for lower motor neuron lesions and autonomic nerve function tests for autonomic dysfunction. Finally, if a diagnosis of acquired idiopathic generalised anhidrosis is suspected, a quantitative sudomotor axon reflex test and serum immunoglobulin-E levels may be performed. Treatment involves addressing the underlying condition and avoidance of aggravating factors. Acquired idiopathic generalised anhidrosis responds well to high dose systemic corticosteroids.
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PMID:Approach to hypohidrosis. 2462 71

There is a significant influence of muscle fatigue on the coupling of antagonistic muscles while patients with post-stroke spasticity are characterized by abnormal antagonistic muscle coactivation activities. This study was designed to verify whether the coupling of antagonistic muscles in patients with post-stroke spasticity is influenced by muscle fatigue. Ten patients with chronic hemipare and spasticity and 12 healthy adults were recruited to participate in this study. Each participant performed a fatiguing isometric elbow flexion of the paretic side or right limb at 30% maximal voluntary contraction (MVC) level until exhaustion while surface electromyographic (sEMG) signals were collected from the biceps brachii (BB) and triceps brachii (TB) muscles during the sustained contraction. sEMG signals were divided into the first (minimal fatigue) and second halves (severe fatigue) of the contraction. The power and coherence between the sEMG signals of the BB and TB in the alpha (8-12 Hz), beta (15-35 Hz), and gamma (35-60 Hz) frequency bands associated with minimal fatigue and severe fatigue were calculated. The coactivation ratio of the antagonistic TB muscle was also determined during the sustained fatiguing contraction. The results demonstrated that there was a significant decrease in maximal torque during the post-fatigue contraction compared to that during the pre-fatigue contraction in both stroke and healthy group. In the stroke group, EMG-EMG coherence between the BB and TB in the alpha and beta frequency bands was significantly increased in severe fatigue compared to minimal fatigue, while coactivation of antagonistic muscle increased progressively during the sustained fatiguing contraction. In the healthy group, coactivation of the antagonistic muscle showed no significant changes during the fatiguing contraction and no significant coherence was found in the alpha, beta and gamma frequency bands between the first and second halves of the contraction. Therefore, the muscle fatigue significantly increases the coupling of antagonistic muscles in patients with post-stroke spasticity, which may be related to the increased common corticospinal drive from motor cortex to the antagonistic muscles. The increase in antagonistic muscle coupling induced by muscle fatigue may provide suggestions for the design of training program for patients with post-stroke spasticity.
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PMID:Muscle Fatigue Enhance Beta Band EMG-EMG Coupling of Antagonistic Muscles in Patients With Post-stroke Spasticity. 3297 23