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PubMed1986

The glycine receptor deficiency of the mutant mouse spastic: evidence for normal glycine receptor structure and localization.

Homozygotes of the mutant mouse spastic exhibit reduced binding of 3H-strychnine to homogenates from various regions of the CNS compared with unaffected littermates (White and Heller, 1982). Here we report evidence that the spastic mutation coincides with a reduced concentration and an unaltered structure of the glycine receptor in spinal cord. Scatchard analysis of 3H-strychnine binding revealed a single binding site with a Bmax of 267 +/- 62 fmol/mg protein for spastic and of 864 +/- 220 fmol/mg protein for control mice; no difference was found for the corresponding KD values. Also Ki values of glycine for 3H-strychnine binding and displacement of 3H-strychnine by beta-alanine and taurine were indistinguishable for both preparations. Photoaffinity labeling of synaptic membranes with 3H-strychnine identified an Mr = 48,000 polypeptide in both control and spastic mouse membranes. Tryptic digestion of these membranes produced radiolabeled peptide fragments of identical molecular weights, suggesting that the proteolytic cleavage sites around the antagonist binding site are conserved in the mutant glycine receptor protein. Glycine receptors from both control and mutant mice were purified by affinity chromatography on aminostrychnine agarose. SDS/PAGE revealed three polypeptides of Mr = 48,000, 58,000, and 93,000 in both receptor preparations. Monoclonal antibodies directed against different subunits of the glycine receptor were applied to an enzyme-linked immunosorbent assay. The same pattern of immunoreactivity was obtained for glycine receptor from spinal cord of spastic homozygotes, control mice, and rats, suggesting conservation of the antigenic epitopes in the mutant receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Affinity Labels↗
PubMed1987

Alpha 2-adrenergic receptor levels in obstructive and spastic Raynaud's syndrome.

The present study examines the hypothesis that alterations in the activity of alpha 2-adrenergic receptors (A2R) may underlie the clinical vasospasm seen in patients with Raynaud's syndrome. Platelets were isolated from 13 normal subjects, from 50 patients with vasospastic Raynaud's syndrome, and from 20 patients with obstructive Raynaud's syndrome and A2R levels measured. Binding capacity as determined in femtomoles per milligram of protein (fmol/mg of protein) and affinity were measured by Scatchard plot analysis. In a separate experiment normal human platelets were incubated with either buffer, normal serum, or serum from patients with spastic Raynaud's syndrome and A2R levels were measured. A2R levels in normal subjects averaged 112 +/- 18 fmol/mg; in the patients with spastic Raynaud's syndrome, 191 +/- 14 fmol/mg, p less than 0.01; and in the patients with obstructive Raynaud's syndrome, 164 +/- 31 fmol/mg, p greater than 0.05 (ns). Of the patients with spastic Raynaud's syndrome, 26% had values that were less than the mean value of the normal subjects (69 +/- 7 fmol/mg, p less than 0.05). The A2R levels decreased after incubation with serum from patients who had spastic Raynaud's syndrome by 17.4 +/- 3.1 fmol/mg (p less than 0.05). These results indicate that most patients with vasospastic Raynaud's syndrome have increased platelet A2R levels, which may constitute a primary pathophysiologic abnormality underlying this condition. The presence of subnormal A2R levels in a portion of the patients and the finding of a decrease in measurable A2R levels after incubation in serum from patients with spastic Raynaud's syndrome suggests the possibility of receptor modulation as a mechanism for increased cellular receptor synthesis.

Blood Platelets↗
PubMed1995

[A case of complicated form of hereditary spastic paraplegia associated with hypoplasia of the corpus callosum and cataracta].

Autosomal dominant, autosomal recessive and X-linked recessive varieties of spastic paraplegia have been recognized. Recently, Japanese patients with complicated form of autosomal recessive hereditary spastic paraplegia (HSP) associated with hypoplasia of the corpus callosum have been reported by Iwabuchi et al. We describe a patient with complicated HSP (Iwabuchi type) and cataracta. A 38-year-old man (his parents were a second cousin) was born uneventfully. His motor development was normal. Motor and mental dysfunctions were noticed during the lower classes of an elementary school. He could ride a bicycle at 18 years old but gradually developed galt disturbance and confined to wheelchair since 35 years. He was admitted to our hospital on February 25, 1994. A neurological examination showed mental retardation, dementia, cataracta, cerebellar ataxia, rigidity, spasticity, severe atrophy of the distal muscles of his extremities, paraparesis, hyperreflexia, positive Hoffmann reflexes and Babinski signs, pes cavus and hammer toes. Brain MRI showed thinning of corpus callosum. Clinical and laboratory findings did not support a diagnosis of metabolic disorders showing spastic paraparesis including adrenomyeloneuropathy, Globoid leukodystrophy, metachromatic leukodystrophy, cerebrotendinous xanthomatosis, Arginase deficiency. We considered that our patient was complicated form of HSP (Iwabuchi et al). However, cataract has not been found in Iwabuchi type of HSP. We discussed here other reports showing cataracta with spastic paraparesis.

Adult↗
PubMed2004

Gait analysis of sporadic and hereditary spastic paraplegia.

OBJECTIVES: Sporadic (SSP) and hereditary spastic paraplegias (HSP) are clinically and genetically heterogeneous disorders, which are characterised by a slowly progressive spastic paraparesis. Initial symptoms and the rate of progression are variable even among members of the same family. Spastic paraparesis is the major and most disabling clinical symptom and was assessed with gait analysis using a three-dimensional infrared movement analysis system. METHODS AND RESULTS: 22 patients with clinically and/or genetically confirmed SSP/HSP were compared with age-matched control subjects. Significantly lower values were found for gait velocity, stride length, step height and the range of motion of the knee-angle. The gait pattern is characterised by a severe spasticity of both legs with only mild paresis. The balance-related gait parameters show a broad-based gait without inwardly rotated feet. No correlation was found between disease duration and the severity of the gait disorder and the central motor conduction time to the leg muscles and the abnormal gait parameters. The gait pattern did not differ between the 7 SSP cases and the 15 HSP cases. CONCLUSIONS: We conclude that three-dimensional gait analysis can uncover specific features of such rare gait disorders, and may be used as an objective tool to quantify the impairment of gait parameters in patients with SSP/HSP and thus can be used to monitor disease progression and the effect of therapeutic interventions.

Adult↗
PubMed1988

Chronic progressive spinobulbar spasticity. A rare form of primary lateral sclerosis.

Although it was first described over a century ago (by Charcot in 1865; by Erb in 1875), the concept of primary lateral sclerosis (PLS) is still not universally accepted. Despite this skepticism, several well-documented cases of isolated degeneration with varying degrees of involvement of corticospinal pyramidal pathways have been reported in the literature. The clinical manifestations in these cases can take one of two forms, ie, isolated spasmodic paraplegia or tetraplegia on the one hand or spasmodic tetraplegia associated with a pseudobulbar syndrome featuring severe spastic dysarthria (chronic progressive bilateral spinobulbar spasticity) on the other hand. Obviously, without firm pathologic data, PLS is a hazardous diagnosis for isolated paraplegia or tetraplegia. Conversely, for bilateral spinobulbar spasticity, it would appear to be the only diagnosis possible once investigate findings have eliminated the other possibilities, such as a pyramidal form of amyotrophic lateral sclerosis or a spinal form of multiple sclerosis. To underscore this point, in this report, five cases of chronic progressive bilateral spinobulbar spasticity developed over 5, 10, 12, 10, and 28 years, respectively, for which the only possible diagnosis was PLS. It was concluded that there are three forms of degenerative diseases of the principal motor pathways: one involving both central and peripheral neurons, ie, amyotrophic lateral sclerosis; one involving only peripheral neurons, ie, spinal amyotrophy; and one involving only central motor neurons, ie, PLS.

Bulbar Palsy, Progressive↗
PubMed1995

X-linked pure familial spastic paraparesis. Characterization of a large kindred with magnetic resonance imaging studies.

OBJECTIVE: Families with pure X-linked familial spastic paraparesis are rare. We describe a large kindred with the "pure" form of X-linked familial spastic paraparesis with seven clinically affected males. The current study was designed to identify the presence of nuclear magnetic resonance imaging (MRI) abnormalities in the affected individuals. PATIENTS AND METHODS: Twenty-three individuals were examined, and MRIs of the brain were obtained in all seven affected males and two females. RESULTS: The disease is characterized by spastic gait and increased reflexes without other associated neurologic signs. No male-to-male transmission has been documented in this pedigree. Magnetic resonance images of the brain in affected individuals demonstrate discrete white matter lesions in the periatrial regions, more prominent posteriorly. Similar, although not as extensive, white matter lesions were detected in the brain of the single obligate female carrier studied with MRI. CONCLUSIONS: We report previously undescribed (to our knowledge) findings of MRI in pure X-linked familial spastic paraparesis and discuss the use of MRI in the diagnosis of this disorder and as a possible screening study of potential carriers.

Adolescent↗
PubMed2004

A novel presenilin-1 mutation (Leu85Pro) in early-onset Alzheimer disease with spastic paraparesis.

BACKGROUND: Early-onset familial Alzheimer disease is caused by mutations in the amyloid precursor protein (APP), presenilin-1 (PSEN1), or presenilin-2 (PSEN2) genes. Phenotypic diversity has been reported to be associated with various mutations in PSEN1. Various mutations of PSEN1 have been reported in cases of early-onset Alzheimer disease with spastic paraparesis. OBJECTIVE: To describe a novel mutation in the PSEN1 gene associated with early-onset Alzheimer disease with spastic paraparesis. PATIENT AND METHODS: The patient was a 27-year-old man who developed early-onset dementia with spastic paraparesis. We examined sequences of the PSEN1, PSEN2, and APP genes from the patient and his family. To detect a possible mutation effect on the production of amyloid-beta peptide (Abeta), transfected HEK293 cells were examined for Abeta42 and Abeta40 production. RESULTS: We found a novel mutation (Leu85Pro) in PSEN1. This mutation influenced the production of Abeta, resulting in a 2-fold elevation of Abeta42 production and of the Abeta42/40 ratio. CONCLUSION: To our knowledge, this is the first report of very early-onset Alzheimer disease with spastic paraparesis and with the visual variant form of the disease, which is associated with visuospatial cognitive disorder. The Leu85Pro mutation in PSEN1 was pathogenic.

Adult↗
PubMed2000

Botulinum toxin type A in the treatment of lower limb spasticity in cerebral palsy.

OBJECTIVES: To determine whether botulinum toxin (BtA) is an effective and safe treatment for lower limb spasticity in children with cerebral palsy. Functional outcomes are of particular interest. SEARCH STRATEGY: Studies for inclusion in the review were identified using the Movement Disorders Review Group trials register, the Cochrane Controlled Trials Register, MEDLINE, pharmaceutical company databases, communication with other researchers in the field and reference lists of papers found using above search strategies. SELECTION CRITERIA: Studies were considered eligible for inclusion in the review if they evaluated the efficacy of BtA for the treatment of leg spasticity in children with cerebral palsy. They must have been randomised and include a concurrent control group receiving another intervention. DATA COLLECTION AND ANALYSIS: A paper pro forma was used to collect data from the included studies using double extraction by two independent reviewers. Each trial was assessed for internal validity by each of the two reviewers. Meta-analysis was not possible because results were presented in an incompatable form. A Peto odds ratio was calculated where this was appropriate, otherwise a descriptive summary of the results of the individual studies was compiled. MAIN RESULTS: Three eligible studies were found each with small numbers of subjects. They were short term, used single injection sessions with follow-up of between 4 and 26 weeks. One study (Koman), of twelve ambulant children, compared BtA with injection of a placebo and found non-significant improvements in gait in the BtA group compared to the placebo group. Two studies (Corry, Flett) compared BtA with the use of casts. Each included 20 ambulant children and found improvements in gait, range of ankle movement and muscle tone in both the BtA and cast groups. However there were no significant differences between the groups in either trial. One of these trials (Flett) also assessed motor function using the gross motor function measure (GMFM) (Russell, 1989) and found significant improvements in each group compared to baseline but no significant differences between the groups. The other trial (Corry) performed 3D gait analysis on those children able to co-operate. Maximal plantar flexion and maximal dorsiflexion during walking were both found to be significantly greater in the BtA group compared to the cast group. In all other dimensions there were no significant differences between the groups. REVIEWER'S CONCLUSIONS: This systematic review has not revealed strong controlled evidence to support or refute the use of BtA for the treatment of leg spasticity in cerebral palsy. Ongoing randomised controlled trials are likely to provide useful data on the short term effects of BtA for leg spasticity. Future research should also assess the longer term use of BtA. Ideally studies should be pragmatic in their approach to dose and distribution of toxin to reflect practise. Outcome measures assessing function and disability would give the most useful information.

Botulinum Toxins, Type A↗
PubMed1990

Familial case of May-Hegglin anomaly associated with familial spastic paraplegia.

We report a family with May-Hegglin anomaly associated with familial spastic paraplegia. The propositus was a 39 year old male. His peripheral blood showed a Döhle-like inclusion bodies in WBC, giant platelets, and thrombocytopenia. He had been suffering from progressive gait disturbance of spastic paraplegia since 20 years old. He was in a state of chronic renal failure and showed sensory hearing impairment. His two children showed similar hematological abnormalities and spastic gait. As far as we know, this is the first case of May-Hegglin anomaly associated with familial spastic paraplegia in the literature.

Adolescent↗
PubMed1987

Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases.

Tropical spastic paraparesis (TSP) is a common myeloneuropathy with primary and predominant involvement of the pyramidal tract and minimal sensory loss. The epidemic form of TSP is related to toxic nutritional factors, but the endemic form occurs in clusters in tropical areas, especially in India, Africa, the Seychelles, Colombia, and areas of the Caribbean. We describe the clinical and epidemiological features of 25 TSP patients from Martinique (French West Indies) with serum antibodies to human T-lymphotropic virus type I (HTLV-I). Furthermore, all 11 patients who were seropositive for HTLV-I had specific HTLV-I antibodies in their CSF. All were women. The age of onset varied from 25 to 60 years (mean, 45 years). The main clinical features are spastic paraparesis or paraplegia with spasticity of the upper limbs, minimal sensory loss, and bladder dysfunction. Minimal estimated incidence and prevalence are 1 per 100,000 inhabitants per year and 8 per 100,000, respectively. Seventeen percent of the relatives of patients with HTLV-I-associated TSP have HTLV-I antibodies (1 husband and 7 children). In Martinique, the prevalence of HTLV-I antibodies in the general population is about 2% and reaches 10% for neurological disorders other than TSP. Since our initial report, the association between spastic paraparesis and HTLV-I has been confirmed in Jamaica, Colombia, and Japan, suggesting the neurotropism of this lymphotropic human retrovirus.

Adult↗
PubMed1988

The role of HTLV-I in tropical spastic paraparesis in Jamaica.

We report clinical and laboratory investigations of 47 native-born Jamaican patients with endemic tropical spastic paraparesis and of 1 patient with tropical ataxic neuropathy. Mean age at onset was 40 years, with a female-male preponderance (2.7:1). Neurological features of endemic tropical spastic paraparesis are predominantly those of a spastic paraparesis with variable degrees of proprioceptive and/or superficial sensory impairment. Using enzyme-linked immunoabsorbent assay (ELISA), IgG antibodies to human T-lymphotropic virus type I (HTLV-I) were present in 82% of sera and 77% of cerebrospinal fluids. On Western blot analysis, IgG antibodies detected the p19 and p24 gag-encoded core proteins in both serum and cerebrospinal fluid. Titers were tenfold higher by ELISA in serum than in cerebrospinal fluid, and some oligoclonal bands present in fluid were not seen in serum. Serum-cerebrospinal fluid albumin ratios were normal, and IgG indexes indicated intrathecal IgG synthesis. Histopathological changes showed a chronic inflammatory reaction with mononuclear cell infiltration, perivascular cuffing, and demyelination that was predominant in the lateral columns. In 1 patient, a retrovirus morphologically similar to HTLV-I on electron microscopy was isolated from spinal fluid. Our investigations show that endemic tropical spastic paraparesis in Jamaica is a retrovirus-associated myelopathy and that HTLV-I or an antigenically similar retrovirus is the causal agent.

Adolescent↗
PubMed1989

Tropical spastic paraparesis: a model of virus-induced, cytotoxic T-cell-mediated demyelination?

Tropical spastic paraparesis is a neurological disorder that is most commonly seen in certain tropical (mainly Caribbean) areas and that presents as a progressive spastic paraparesis and urinary dysfunction. Recent studies have revealed an association between tropical spastic paraparesis and human T-cell lymphotropic virus type I (HTLV-I) infection. We report the results of a detailed morphological and immunocytochemical study of a patient with tropical spastic paraparesis. Lesions were restricted to the spinal cord and optic nerve, where demyelination, inflammation, and fiber loss were common features. Lymphocytes were seen closely applied to nerve fibers within which were changes resembling those seen in myelinated central nervous system cultures exposed to cytokines. Immunocytochemically, HTLV-I p19 core protein and a predominance of CD8+ (suppressor/cytotoxic) T cells and expression of class I major histocompatibility antigen were demonstrated in spinal cord lesions. It is postulated that cytotoxic T cells, either directly or via cytokines, induce lysis of the myelin sheath and subsequently the axon, resulting in a mixed picture of demyelination and axonal loss with secondary tractal degeneration. Despite this destruction, extensive remyelination was evident within affected areas of spinal cord.

Female↗
PubMed1993

Spastic paraparesis associated with human T-lymphotropic virus type I: a clinical, serological, and genomic study in Iranian-born Mashhadi Jews.

The Mashhadi-Jewish community originating in Iran is a closed and ethnically segregated population with a unique history and a high rate of intrafamilial marriage among its members. A high risk of infection by human T-lymphotropic virus type I (HTLV-I) and of adult T-cell leukemia associated with such infection was found in this population. HTLV-I is also associated with a syndrome of progressive spastic paraparesis. We therefore evaluated the occurrence of HTLV-I infection and spastic paraparesis in Mashhadi-born Iranian Jews who immigrated to Israel. We examined 83 Mashhadi-born subjects (52 women, 31 men; mean age, 61 +/- 15.5 years) and 73 age-matched non-Mashhadi Iranian-born Jews. Blood samples were tested for HTLV-I antibodies by particle agglutination test. The polymerase chain reaction (PCR) was used to detect HTLV-I proviral DNA sequences from peripheral blood mononuclear cells. Fifteen Mashhadi-born Jews (18%) were both seropositive and PCR-positive for HTLV-I. Four HTLV-I-seronegative subjects were found to be positive for HTLV-I proviral DNA by PCR. Of the 19 HTLV-I-infected subjects (11 women, 8 men; mean age, 59 +/- 16 years), 13 (68%) had spastic paraparesis of varying severity. There were no signs of myelopathy in the Mashhadi-born subjects who were negative for HTLV-I proviral DNA by PCR. None of the non-Mashhadi Iranian Jews was seropositive or PCR-positive for HTLV-I proviral DNA, or had clinical signs of spastic paraparesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Spastic mutant axolotl: identification of a phenocopy pathway with implications for the control of axolotl swimming by the vestibulocerebellum.

The spastic mutant axolotl shows abnormal swimming behavior, which includes a preponderance of "embryonic" swimming elements (coils) versus mature swimming elements (sinusoids) and a failure to entrain sinusoids into a prolonged swimming sequence. The mutant also shows anatomical disorganization in the area acousticolateralis and cerebellar auricle, but it is unclear (1) to what extent the behavioral abnormalities are traceable to the vestibulocerebellar defect or (2) how the vestibulocerebellar pathway modulates swimming behavior in the normal axolotl. We have performed quantitative cine analysis of electric shock-induced swimming bouts in normal axolotls, spastic mutants, and a variety of neurosurgically altered wild-type axolotls. We scored the incidence of coil elements (25% in controls, 70-90% in spastics) versus sinusoid elements, as well as length distributions of coilfree intervals (short to long trains of sinusoidal swimming) and of sinusoidfree intervals (of brief of prolonged coiling). We found that bilateral VIIIth nerve lesions or surgical undercutting of the cerebellar auricle in wild-type axolotls almost exactly reproduced the behavioral deficit seen in spastic (75-81% coils, loss of long sinusoid trains, and appearance of prolonged coiling intervals at least some of which coupled several coils into trains of thrashing behavior). By contrast, neither complete transection of the CNS at low midbrain levels nor section of cranial nerves V, VII, or X (lateral line) resulted in an increased incidence of coil elements beyond 26% nor significantly altered the length distributions of S-intervals and C-intervals. Nor did any of the latter lesions disrupt the spasticlike swimming patterns of axolotls already subjected to auricle or VIIIth nerve lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambystoma↗
PubMed2002

Mutation analysis of the spastin gene (SPG4) in patients in Germany with autosomal dominant hereditary spastic paraplegia.

Hereditary spastic paraplegias (HSP) comprise a genetically and clinically heterogeneous group of neurodegenerative disorders characterized by progressive spasticity and hyperreflexia of the lower limbs. Autosomal dominant hereditary spastic paraplegia 4 linked to chromosome 2p (SPG4) is the most common form of autosomal dominant hereditary spastic paraplegia. It is caused by mutations in the SPG4 gene encoding spastin, a member of the AAA protein family of ATPases. In this study the spastin gene of HSP patients from 161 apparently unrelated families in Germany was analyzed. The authors identified mutations in 27 out of the 161 HSP families; 23 of these mutations have not been described before and only one mutation was found in two families. Among the detected mutations are 14 frameshift, four nonsense, and four missense mutations, one large deletion spanning several exons, as well as four mutations that affect splicing. Most of the novel mutations are located in the conserved AAA cassette-encoding region of the spastin gene. The relative frequency of spastin gene mutations in an unselected group of German HSP patients is approximately 17%. Frameshift mutations account for the majority of SPG4 mutations in this population. The proportion of splice mutations is considerably lower than reported elsewhere.

Adenosine Triphosphatases↗
PubMed2004

Novel mutations in the Atlastin gene (SPG3A) in families with autosomal dominant hereditary spastic paraplegia and evidence for late onset forms of HSP linked to the SPG3A locus.

Hereditary spastic paraplegias (HSP) comprise a genetically and clinically heterogeneous group of neurodegenerative disorders characterised by progressive spasticity and hyperreflexia of the lower limbs. Autosomal dominant hereditary spastic paraplegia linked to the SPG3A locus on chromosome 14q11-21 accounts for approximately 10% of autosomal dominant hereditary spastic paraplegia (ADHSP). It is caused by mutations in the SPG3A gene encoding the protein atlastin. To date, only five disease-causing mutations in the SPG3A gene have been described. We analysed 13 SPG4-negative families for mutations in the SPG3A gene and identified a mutation in 38% (5/13). Two of the mutations are novel, c.481G>C (p.A161P) and c.740A>C (p.H247P). One of the novel mutations was found both in a family with early onset of symptoms and in a late onset family. Furthermore, we report on numerous polymorphisms detected in the SPG3A gene.

Adolescent↗
PubMed2004

Severe resting clonus caused by thyrotoxicosis in a 16-year-old girl with hereditary spastic paraparesis: a case report.

A 16-year-old girl with a history of hereditary spastic paraparesis developed the subacute onset of severe clonus and new upper-extremity spasticity due to thyrotoxicosis. This case demonstrates the ability of hyperthyroid states to worsen symptoms of spasticity in a child with an underlying spastic disorder. It also demonstrates the importance of investigating for common systemic diseases as a cause of movement disorders even in children with underlying known genetic disorders.

Adolescent↗
PubMed2005

Nerve stimulation boosts botulinum toxin action in spasticity.

Spasticity leads to functional and structural changes in nerves and muscles, which alter skeletal muscle function. To evaluate whether short-term electrical nerve stimulation (NS) improves the effect of botulinum toxin in spastic skeletal muscle, we studied changes in the amplitude of the compound muscle action potential (CMAP) recorded from the extensor digitorum brevis (EDB) muscle in response to peroneal nerve stimulation at the ankle after injection of botulinum toxin type A (BTXA) alone or combined with short-term NS. In paraparetic patients, both EDB muscles were injected with BTXA; and NS was applied to one EDB muscle alone. All patients received a 30-minute session of electrical NS once a day for 5 consecutive days after BTXA injection. We used two different stimulation frequencies (low-frequency, 4 Hz; and high-frequency, 25 Hz). EDB-CMAP amplitudes were evaluated before BTXA injection (day 0) and changes in CMAP amplitude, expressed as a percentage (CMAP%), were measured at various time points over a 30-day period after BTXA injection. We compared changes in the CMAP% amplitude on the stimulated and contralateral nonstimulated sides. We also studied the electromyographic activity recorded from EDB muscles over a 30-day period. CMAP% amplitudes measured at all time points after BTXA injections were significantly reduced in both EDB muscles. On days 4, 10, and 15, the CMAP% amplitude reduction was significantly greater for the low-frequency stimulated EDB than for the contralateral nonstimulated EDB. No significant differences in CMAP% were observed for the high-frequency stimulated and nonstimulated EDB. After BTXA injection, spontaneous activity appeared in both EDB muscles; but it appeared earlier and involved larger areas in the stimulated than in the nonstimulated EDB. In conclusion, short-term NS accelerates the effectiveness of intramuscular BTXA injections on the neuromuscular blockade in patients with spastic paraparesis and could induce a rapid and persistent improvement in spasticity. Its action probably arises mainly from low-frequency NS.

Aged↗