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)

Of 23 children with hereditary spastic paraplegia (HSP), spasticity was the only neurological abnormality in eight patients (pure form). Additional neurological abnormalities in the 15 with complicated HSP included cognitive impairment, pseudo-bulbar palsy, cerebellar dysfunction and polyneuropathy. 19 children presented with abnormal gait, recognised at a mean age of three years in the pure form and five years in the complicated form. These forms were distinguished at a mean age of 11 years. Early non-motor developmental delay or rapidly ascending paraparesis, with spread of spasticity to the arms and with involvement of bulbar structures, predicted development of the complicated form. The pure form was inherited in an autosomal dominant manner in five patients. The autosomal recessive form was commonly associated with additional neurological abnormalities and a more rapid rate of progression.
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PMID:'Pure' and 'complicated' forms of hereditary spastic paraplegia presenting in childhood. 204 52

Computerized analysis of gait was performed in six patients with hydrocephalus (mean age, 75.7 years), for comparison with other elderly patients with gait problems and age-matched controls. A decrease in velocity and stride, an increase in sway, and the proportion of time spent in double-limb stance were nonspecific features correlated with declining performance. Certain features appeared to characterize hydrocephalic gait when compared among groups; cadence was diminished, and there was a reduction of step height and a decreased counterrotation of the shoulders relative to the pelvis. An abnormal tendency toward cocontraction in antagonist muscle groups was observed in electromyographic data from the leg muscles, suggesting that the normal phased activation of muscle groups is disturbed. Although data are not conclusive, we believe that the gait disorder in normal-pressure hydrocephalus reflects a subcortical motor control disorder rather than a phenomenon of spasticity or apraxia.
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PMID:Gait disorder in late-life hydrocephalus. 382 77

We report a Caucasian family in which four males out of a total of seven siblings are mentally retarded. Three of the affected individuals have spasticity in the lower limbs (spastic paraplegia), pes cavus deformity of both feet and an abnormal gait. In addition, they show palmar and plantar hyperkeratosis. The other male sibling does not have spasticity, but his lower limb reflexes are abnormally brisk and he has slight pes cavus deformity. He also shows hyperkeratosis of his palms and soles and is less mentally retarded that his brothers. The mother of the affected boys has normal intelligence, but has plantar hyperkeratosis and a strong facial resemblance to her retarded sons. Her three daughters are normal. The pedigree information is compatible with a sex-linked mode of inheritance and no specific biochemical or cytogenetic abnormality has been found in the affected individuals. There have been no previous reports of hyperkeratosis palmaris et plantaris in other inherited spastic syndromes.
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PMID:Four brothers with mental retardation, spastic paraplegia and palmoplantar hyperkeratosis. A new syndrome? 622 37

Sixty-five cases of clinically diagnosed multiple lacunar state have been analysed. The clinical course of multiple lacunar state is usually progressive in nature, simulating degenerative diseases, in contrast with the mode of acute onset seen in the other vascular diseases. Average age at the initial visit was 63.8 year-old, and sex ratio showed marked male preponderance, being 12 for males and 1 for females. Gait disturbance and speech disturbance are the most frequent initial symptoms, followed by slow motion, emotional lability and swallowing difficulty. Neurological manifestations are dysarthria, short-stepped and apraxic gait, hyperreflexia, positive Babinski and Chaddock reflexes, minimal spasticity, dementia, positive palmo-mental reflex, emotional lability, fixed face, rigidity, bradykinesia, foot grasping, dysphagia, positive Myerson's sign and tremor, in the order described. The important point is that the rigidity is paratonic and the tremor is action or postural, not the cogwheel rigidity or resting tremor like Parkinson's disease. The appearance of pathological reflexes (Babinski and Chaddock reflexes) are quite important, especially Chaddock reflex, which can frequently become positive despite negative or equivocal Babinski reflex. Hypertension, especially longstanding in nature, is the major contributing factor in this disorder. CT scan showed the presence of one or more lacunes in 52 out of 65 cases (80.0%). The detection of lacune can be influenced by the quality of CT scan, and the high resolution CT scanner is greatly useful for that purpose. It is stressed that the detailed neurological and computed tomographic evaluations will make it possible to reach the clinical diagnosis and appropriate treatment of multiple lacunar state.
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PMID:[Clinical studies on multiple lacunar state]. 674 15

Gait abnormalities in children with cerebral palsy are the consequence of contractures across joints, muscle spasticity, and phasically inappropriate muscle action. Though abnormalities involving one of the major joints of the lower extremity will usually have consequences on the function of the other joints, it is possible to recognize certain primary disorders at each joint. The most common gait abnormalities of the knee in patients with cerebral palsy occur in the sagittal plane. Based on the experience gained from performing gait analysis on more than 588 patients with cerebral palsy, four primary gait abnormalities of the knee have been identified: jump knee, crouch knee, stiff knee, and recurvatum knee. In this review, each abnormality is described by its motion analysis laboratory profile (physical examination, motion parameters, electromyography [EMG] data, and force plate data). The most common etiologies and the consequences for gait of each disorder are also considered. Appreciation of the most common pathologic patterns of gait should facilitate accurate and detailed analysis of the individual patient with gait abnormalities.
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PMID:Common gait abnormalities of the knee in cerebral palsy. 845 27

To study the clinical picture of lathyrism in Unnao, India and compare it with that reported from other endemic areas, 41 patients from Unnao were studied. Their mean age was 42.9 years (range 22-85) and the mean duration of the illness was 17.1 years (range 2-30). They had been regularly consuming Lathyrus Sativus (LS). The patients complained of walking difficulty due to weakness and leg stiffness (32 each), and of frequency of micturition (4). Gait abnormalities included spastic gait (24), toe walking (18) and the necessary use of walking sticks (13). Weakness was mild to moderate, and was less prominent than was spasticity. In 8 patients the physical signs were asymmetrical. Peripheral neuropathy was present in only one patient, but muscle atrophy and widespread fasciculations were not found. A higher frequency of peripheral neuropathy and lower motor neuron involvement has been reported from Bangladesh and Israel. Severe spasticity in the absence of prominent weakness in lathyrism may be due to the involvement of certain specific groups of corticospinal fibres.
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PMID:Clinical aspects of neurolathyrism in Unnao, India. 849 40

This article will review those electrophysiological investigations which have addressed the neuronal mechanisms underlying impaired gait. The aims of the review are to provide further insights to the underlying pathophysiology of impaired gait and also towards the selection of an appropriate treatment. From the patients' point of view the first indication of a central motor system lesion is an impairment of movement, most notably locomotion. These symptoms are characteristic in cases of spasticity, cerebellar lesion or Parkinson's disease. Clinical examination reveals typical changes in tendon tap reflexes and muscle tone which were believed to account for the movement disorder presented. However, we now know that there is only a weak relationship between the physical symptoms observed during clinical examination under passive motor conditions and the altered neuronal mechanisms underlying the impairment during active motion. By recording and analysing electrophysiological and biomechanical parameters during functional movements such as locomotion, the significance of impaired reflex behaviour or the pathophysiology of muscle tone and its contribution to the movement disorder can be reliably assessed. Consequently, the treatment should not be cosmetic, i.e. the correction of an isolated clinical parameter, but should be based on the pathophysiology and significance of those mechanisms underlying the impairment of the patients' movements. Data from electrophysiological and biomechanical investigations of locomotion of patients with spasticity, cerebellar disorder or Parkinson's disease are discussed in this review. The neuronal mechanisms, which are essentially central programs and afferent input, involved in disorders of gait are evaluated on the basis of their function in healthy subjects. The impact of this analysis in deciding an appropriate treatment are discussed with respect to the pathophysiology underlying the gait disorder (spasticity, cerebellar disorder or Parkinson's disease). At the present time we have only a basic understanding of the essential receptor systems, such as leg extensor load receptors, and their interaction with other systems involved in postural control. In the future, the knowledge gained from gait analysis may help in the selection of the appropriate pharmacological and physical treatment required even though the patient may only be at an early stage of motor impairment.
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PMID:Neurophysiology of gait disorders: present and future applications. 930 81

Lower extremity symptoms are caused by lesions at any level of the neuraxis, from cortex to muscle. HIV affects virtually every level of the nervous system, either directly or indirectly. The presence of pathology at multiple levels and by multiple processes further complicates the bedside diagnosis of a patient with AIDS and neurologic symptoms. Many neuropathies and other conditions that affect the lower extremities can be identified with careful history and physical examination, confirmed with limited testing, and can be treated successfully. Distal symmetric polyneuropathy is the most common lower extremity disorder, but it must be distinguished from similar-appearing neuropathies caused by medications, B12 deficiency, or vasculitis. Diffuse infiltrative lymphocytosis syndrome also causes a painful peripheral neuropathy that must be distinguished from distal symmetric polyneuropathy. Inflammatory demyelinating polyneuropathies are characterized by muscle weakness. They occur in early, asymptomatic HIV infection and respond to plasmapheresis or steroids. Mononeuropathies in patients with CD4 counts more than 200 often resolve on their own. Multiple mononeuropathies, which occur in patients with CD4 counts less than 50, are often associated with cytomegalovirus infection and may follow a rapidly progressive course unless treated promptly and aggressively. Progressive polyradiculopathy occurs late in the course of AIDS, is often caused by cytomegalovirus, is rapidly progressive, and generally is fatal unless recognized and treated promptly. Muscle weakness, myalgia, and fatigue are common in HIV and have multiple causes. Lower extremity spasticity may be caused by treatable etiologies such as spinal cord abscess, tumor, disc compression, B12 deficiency, or ischemia. Gait disturbances are common but nonspecific and may be caused by treatable neurologic disorders at any level of the neuraxis.
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PMID:Neurologic problems of the lower extremity associated with HIV and AIDS. 957 54

Spastic paretic stiff-legged gait is a frequently encountered gait problem in patients with traumatic brain injury, as well as in many other patients with upper motor neuron disease. Formerly, spasticity of the quadriceps was considered to be the sole cause of stiff-legged gait. Quantitative gait analysis, however, may implicate hip flexor weakness or poor ankle mechanics as the cause of stiff-legged gait. We discuss the use of an algorithm to evaluate stiff-legged gait in traumatic brain injury using a quantitative gait analysis system such that the specific etiology of stiff-legged gait can be identified and can serve as the basis of a treatment plan.
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PMID:An algorithm to assess stiff-legged gait in traumatic brain injury. 1019 72

Using criteria of the classification recently described by Nutt et al., we examined gait disorder in five patients with normal pressure hydrocephalus (NPH). Their cerebrospinal fluid (CSF) pressures were in the normal range, and trials of CSF removal produced temporary improvement of symptoms. Surgical procedures to relieve hydrocephalus improved gait disorders in all patients. No patient showed spasticity, sensory ataxia, cerebellar ataxia, extrapyramidal signs, or limb apraxia. All walked slowly with a wide base and a short stride. The arm swing normally associated with walking was preserved. In standing, patients were unsteady and fell easily when pushed. Four patients showed hesitation in initiating walking and in turning. These clinical features fit Nutt's criteria for frontal gait disorder and frontal disequilibrium. Unlike findings in Parkinson's disease, where similar gait disorders may occur, other extrapyramidal signs, Myerson's sign, and upper limb dysfunction were absent in NPH, and arm swing while walking was preserved. We suspect that ventricular dilatation disturbs neuronal connections between the supplementary motor area and the globus pallidus in NPH patients.
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PMID:Gait disturbance in patients with low pressure hydrocephalus. 1174 14


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