Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We administered local botulinum toxin injections on the leg adductors of 12 patients with spastic paraparesis (9 patients with HAM, 2 patients with spinal spastic paraparesis, 1 patient with an identified degenerative disease). Two of them were wheelchair-bound and the other patients could walk with or without help. The patients were assessed by the time to walk 10 m and the spasticity score which was derived from the degree of muscle tone and spasm frequency of leg adductors. After the initial injection, 7 of the 12 patients improved spasticity scores and 8 of the 10 patients could walk 10 m within a shorter time. The time to walk 10 m was markedly shortened in moderate cases. However, one patient complained of leg weakness and the time to walk 10 m was prolonged. Five of the 12 patients received injections 3 to 7 times, and were followed up for a mean of 16.2 months. In 4 of the 5 patients, repeated injections could maintain the improvement of spasticity score and time to walk 10 m. However, injection was discontinued in one patient because of leg weakness. The other side effects were pain and swelling at the injected site and dysarthria. However, these side effects were slight and transient and did not require treatment. No other systemic side effects were observed. In conclusion, the beneficial effects of botulinum injections to spastic paraparesis were (1) improvement of objective symptoms in mild cases, (2) improvement of ADL in moderate cases, and (3) improvement of objective symptoms and ease of nursing care in severe cases. Furthermore, we confirmed the long-term efficacy and safety of botulinum toxin.
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PMID:[Treatment of spastic paraparesis with botulinum toxin with reference to beneficial effects, disease severity and long-term treatment]. 761 46

A 63-year-old woman had suffered from progressive weakness and wasting of the right lower limb for seven years. In the lower limbs, there were profound muscular atrophy and weakness on the right, and mild weakness with spasticity on the left. Muscle strength of the upper limbs was normal. Sensory examination was normal except for paresthesias below the right knee. Anti-HTLV-I antibody titer was raised both in serum and in the CSF. Motor nerve conduction studies of the lower limbs showed small compound muscle action potentials and somewhat slow conduction velocities, more evident in the right side. F-wave was evoked only in the left tibial nerve and its latency was increased. Sensory nerve conduction studies were normal in the lower limbs. Somatosensory evoked potentials (SEPs) after tibial nerve stimulation at the ankles showed increased interpeak latencies between lumbar N20 and scalp P37. Nerve conduction studies in the upper limb were normal. Single fiber electromyography suggested anterior horn involvement not only in the lumbosacral cord but also in the cervical cord. Weakness and spasticity improved after oral administration of prednisolone. The SEPs findings and a favorable response to prednisolone excluded the possibility of amyotrophic lateral sclerosis. This case is a clinical variant of HTLV-I-associated myelopathy presenting profound atrophy of unilateral lower limb.
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PMID:[HTLV-I associated myelopathy presenting with profound atrophy of unilateral lower limb]. 825 34

Human T-cell lymphotropic virus type one (HTLV-1) is associated with tropical spastic paraparesis or HTLV-I--associated myelopathy. We report 2 women with a spastic ataxic illness similar to HTLV-I--associated myelopathy infected solely with HTLV-II. Identification of HTLV-II infection was made serologically, by polymerase chain reaction, and by viral culture (in 1 woman). One woman, treated with 200 mg of danazol orally, three times daily, had pronounced improvement in ambulation, nocturnal spasticity, and nighttime urinary frequency. It appears that infection with HTLV-II may cause an illness similar to HTLV-I--associated myelopathy, but distinguished by the presence of ataxia.
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PMID:Spastic ataxia associated with human T-cell lymphotropic virus type II infection. 848 13

The author disserts on the definition of Tropical Spastic Paraparesis since its first description up to the etiological involvement of HTLV-1 in part of the cases. According to him the basic nucleus of the syndrome consists of a paraparesis with pyramidal signs (spasticity and hyperreflexia) with variable sensory and sphincter symptoms. The retroviral etiology by HTLV-1 is one of the variable elements of the condition. He aims at preventing conceptual distortions in the description of this condition.
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PMID:[Tropical spastic paraparesis: a necessary redefinition]. 873 59

The excitability of the motoneuron (MN) pool in the resting state was compared between normal control subjects and patients with spasticity resulting from HTLV-I-associated myelopathy, using a new parameter, Hslp/Mslp, and the conventional parameters Hmax/Mmax and Hth/Mth. Differences in the excitability of the MN pool between these two groups reached a high degree of statistical significance only when assessed with the new parameter. This suggests the methodological advantage of the Hslp/Mslp over both Hmax/Mmax and Hth/Mth for evaluation of the excitability of the MN pool in the resting state.
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PMID:Evident difference in the excitability of the motoneuron pool between normal subjects and patients with spasticity assessed by a new method using H-reflex and M-response. 883 10

Human T lymphotropic virus type I (HTLV-I)-associated myelopathy/tropical spastic paraperesis (HAM/TSP) is a slowly progressive neurologic disorder following infection with HTLV-I. It is characterized by spasticity and hyper-reflexia of the lower extremities, urinary bladder disturbance, lower extremity muscle weakness, and sensory disturbances. HTLV-I, as an inducer of a strong humoral and cytotoxic response, is a well-known pathogenic factor for the progression of HAM/TSP. Peptides derived from proviral tax and env genes provide epitopes recognized by T cells. We herein report an accumulation of distinct clonotypes of alpha/beta TCR+ peripheral blood T lymphocytes from HAM/TSP patients in comparison with that observed in both asymptomatic carriers and healthy controls, using the reverse-transcriptase PCR/single-strand conformation polymorphism method. We also found that some of the accumulated T cell clones in the peripheral blood and cerebrospinal fluid are HTLV-I Tax(11-19) peptide specific. Such clones were found to expand strongly after being cultured with an HTLV-I Tax(11-19) peptide. Moreover, the cultured samples exhibited a strong MHC class I-restricted cytotoxic activity against HTLV-I Tax(11-19) peptide-expressing targets, and therefore most likely also include the disease-associated T cell clones observed in the patients. This is the first report of a direct assessment of Ag-specific T cell responses in fresh PBL and cerebrospinal fluid.
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PMID:Accumulation of human T lymphotropic virus (HTLV)-I-specific T cell clones in HTLV-I-associated myelopathy/tropical spastic paraparesis patients. 925 72

Fifteen patients with human T-cell lymphotropic virus type-I (HTLV-I)-associated myelopathy (HAM) were treated in an uncontrolled preliminary trial by oral administration of pentoxifylline (PTX). Motor function, neurological evaluation, immunological markers and parameters were evaluated after four weeks. In 13 of the 15 patients, motor disability, especially spasticity, improved substantially. PTX suppressed spontaneous proliferation of peripheral blood mononuclear cells in 14 of the 15 patients at four weeks. No adverse effect was observed. We concluded that PTX may be a safe and beneficial agent for the treatment of HAM.
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PMID:Successful application of pentoxifylline in the treatment of HTLV-I associated myelopathy. 933 18

We report 10 HTLV-I virus seropositive subjects, eight of them with HTLV-I associated myelopathy (HAM), two of them also infected with HIV as well as two asymptomatic HTLV-I+ relatives of two unrelated patients. HTLV-I is endemic in several tropical areas, where it causes different neurological diseases. Only few patients have been reported in our country since 1994. We studied 8 patients, who fulfilled the clinical criteria for chronic spastic paraplegia, and 2 other non-symptomatic HTLV-I seropositive relatives, with electromyography (EMG), motor and sensory conduction velocities (NCV), somatosensory, visual and brainstem auditory evoked potentials (SSEP, VEP and BAEP), Magnetic Resonance Images (MRI) and cerobrospinal fluid (CSF) analysis. The latter was carried out only in seven symptomatic patients. In every case positive ELISA tests for HTLV-I/II were confirmed by Western Blot. The two asymptomatic persons were clinically and electromyographically assessed, one of them was also submitted to SSEPs studies. Three patients were males. Patient's ages ranged from 5 to 65 years old. All symptomatic patients showed muscular weakness, spasticity with pyramidal signs and sphincter disturbances. Five of them had paresthesias and 2 had burning pain on their feet. The EMGs and the NCVs were normal in 7 patients and in the 2 asymptomatic ones. SSEPs, obtained by stimulating the posterior tibial nerves, were impaired in 7 patients and in the asymptomatic person who received the procedure. The 7 symptomatic patients who underwent lumbar puncture had positive tests for HTLV-I in CSF, 3 out of these 7 patients had also high protein levels and 4 had increased number of lymphocytes. In 2 patients intrathecal IgG production could also be demonstrated. MRI were normal in 7 patients and in the 2 asymptomatics, the exception being a female who had bilateral hyperintense lesions in cerebral white matter in T2. In conclusion, tropical spastic paraparesis is apparently a rare disorder in Argentina. However, some cases have been reported recently. Most probably, its prevalence is currently underestimated. Its diagnosis should be considered in every patient with progressive spastic paraplegia.
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PMID:Further studies on HTLV-I associated myelopathy in Argentina. 981 4

The prevalence of HTLV-I reaches 1.8% among blood donors in Salvador, and 40% among chronic myelopathy patients in the state of Bahia, Brazil. The present study shows the epidemiological and clinical picture of patients attending the HAM/TSP Outpatient Unit at the Foundation of Neurology and Neorusurgery (FNN). 114 patients had epidemiologic data collected and 51 of these patients, who had regularly attended the HAM/TSP Unit for at least 1 year, were evaluated for signs, symptoms and disease progression. Most of the 114 patients were female (70%), of African descent, and with a mean age of 51. Sexually transmitted diseases and blood transfusion were the most common risk factors. Paraparesis with spasticity was the predominant sign (85%), bladder dysfunction occurred in 75%, intestinal dysfunction was recorded in 48%. Sensory examination was normal in 50% of the cases studied. The patients' functional status, as measured by the Kurtzke Disability Scale, during the 1 year observation period changed only in early disease. Steroid therapy with prednisone was the most commonly used treatment in this group.
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PMID:HTLV-I associated myelopathy: clinical and epidemiological profile. 1093 95

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


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