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PubMed1990

Treatment of spasticity with botulinum toxin: a double-blind study.

We studied the effect of botulinum-A toxin on spasticity of the leg adductors in 9 patients who were either chair-bound or bed-bound with chronic stable multiple sclerosis. We injected botulinum toxin (400 mouse units) or placebo into the adductor muscles in a randomized, crossover, double-blind design. Two physicians, who were unaware of the treatment order, used an objective rating scale and independently assessed the patients; interobserver correlation was excellent (r = 0.93-0.81). We found that botulinum toxin produced a significant reduction in spasticity (p = 0.009) and a significant improvement in the ease of nursing care (p = 0.009). There were no adverse effects during this short-term trial. This is the first demonstration of the beneficial effect of botulinum toxin on focal spastic muscle contractions.

Adult↗
PubMed1993

Spastic ataxia associated with human T-cell lymphotropic virus type II infection.

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.

Antibodies, Monoclonal↗
PubMed2005

Distinct novel mutations affecting the same base in the NIPA1 gene cause autosomal dominant hereditary spastic paraplegia in two Chinese families.

Hereditary spastic paraplegia (HSP) is a neurodegenerative disease characterized by lower-limb spasticity, hyperreflexia, progressive spastic gait abnormalities, and an extensor-plantar response. It is genetically very heterogeneous, with 28 Human Genome Organisation (HUGO)-approved IDs in the database (last search: August 8, 2004). Following the identification of the SPG6 gene, NIPA1, we have identified two novel mutations, c.316G>C and c.316G>A, in two independent Chinese families linked to the SPG6 locus. These two mutations would cause a p.G106R substitution, and cosegregated with the disease. Structural predictions suggest that p.G106 is located in the third transmembrane domain of the protein, and that the mutant p.G106R disrupts this structure, causing the intramembrane loop to descend into the cytoplasm. Our results identify two novel mutations responsible for HSP and suggest that c.316 of theNIPA1 gene may be a mutational hotspot.

Adult↗
PubMed2006

Clinical and genetic study of a Brazilian family with spastic paraplegia (SPG6 locus).

We describe a Brazilian family in which inheritance of a G106R mutation in the SPG6 gene (also know as NIPA1) resulted in an autosomal dominant form of hereditary spastic paraplegia (ADHSP). Clinical investigations indicated that this family has a pure form of spastic paraplegia. All patients presented with gait difficulty in their twenties, progressing to frank spastic paraplegia during the next decade. Our report further supports evidence that mutations in SPG6 cause ADHSP.

Adult↗
PubMed1983

Partial selective denervation in spastic palsies (hyponeurotization).

Treating spastic palsies is a difficult problem. Hyponeurotization is a technique in which peripheral nerves are partially and selectively denervated to diminish spasm in muscles, hence reducing spasticity and tenseness so inimical to movement. Hyponeurotization can be performed in all spastic patients who are capable of cooperating. It should be avoided in cases of athetosis and brain impairment. Partial denervation is employed to reduce spasm; tenotomies, tendon lengthening, and myoectomy are employed to increase length in retracted muscles. Secondary surgery is usually required to further correct the spasm after the "adoption" phenomenon is complete. The results with hyponeurotization have been good in a high percentage of cases in which the surgery strictly adhered to basic principles.

Humans↗
PubMed2005

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes.

Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

Contracture↗
PubMed2005

Excitatory synaptic potentials in spastic human motoneurons have a short rise-time.

This study assessed whether changes in size or time-course of excitatory postsynaptic potentials (EPSPs) in motoneurons innervating spastic muscle could induce a greater synaptic response, and thereby contribute to reflex hyperexcitability. We compared motor unit (MU) firing patterns elicited by tendon taps applied to both spastic and contralateral (nonspastic) biceps brachii muscle in hemiparetic stroke subjects. Based on recordings of 115 MUs, significantly shortened EPSP rise times were present on the spastic side, but with no significant differences in estimated EPSP amplitude. These changes may contribute to hyperexcitable reflex responses at short latency, but the EPSP amplitude changes appear insufficient to account for global differences in reflex excitability.

Excitatory Postsynaptic Potentials↗
PubMed1993

Voiding dysfunction in patients with spastic paraplegia: urodynamic evaluation and response to continuous intrathecal baclofen.

Patients with hereditary spastic paraplegia (HSP), a degenerative central nervous system disorder characterized by progressive lower extremity spasticity, frequently experience symptoms of voiding dysfunction. Urodynamic evaluation of patients with HSP has not been reported, and the etiology of voiding dysfunction remains unexplained. We present our evaluation of three men (ages 42-62 years) with this rare syndrome. Urgency of urination was a uniform and dominant complaint, and two patients regularly experienced urge incontinence. Other symptoms included frequency (n = 3), nocturia (n = 3), and diminished force of stream (n = 1). Postvoid residual volumes were less than 25 ml in all patients. On urodynamic evaluation the two patients with urge incontinence displayed cystometric evidence of involuntary detrusor contractions. Pelvic floor EMG recordings suggested detrusor-sphincter dyssynergia (DSD). In addition, one patient exhibited markedly diminished bladder compliance (1.0 ml/cm H2O) and capacity (50 ml). All patients reported marked symptomatic improvement when treated with continuous intrathecal baclofen. Evaluation during baclofen treatment revealed increases in bladder compliance and capacity, with apparent resolution of DSD in one patient. Voiding symptoms in these patients most likely arise from a neurogenic etiology; however, a contributory role for chronic outlet obstruction from striated muscle spasticity may also exist.

Adult↗
PubMed2003

The role of neurosurgical interventions for control of spasticity in neurorehabilitation: new findings on functional microanatomy of the tibial nerve.

Harmful spasticity after cerebral or spinal damage disturbs functional recovery in neurorehabilitation, but neurosurgical interventions for relief of spasticity are not widely performed, at least in Asian countries including Japan. We have been performing various types of neurosurgical treatment for spasticity such as selective peripheral neurotomy, selective dorsal rhizotomy, microsurgical DREZotomy, and intrathecal baclofen administration. We deal with both children and adults. From our experience of tibial neurotomy, in particular, we describe functional microsurgical anatomy of the tibial nerve in the popliteal fossa. This is the first report on this regional functional anatomy.

Electric Stimulation↗
PubMed1995

A neurophysiological method for the evaluation of motor performance in spastic walking patients.

Intrathecal baclofen is at present the best treatment for severe spasticity of various etiologies. In walking patients affected by severe spasticity a careful evaluation of the motor performance is needed for a correct indication for this treatment. The examination should focus on the delicate balance between spasticity and voluntary muscle activation which is crucial for an improvement of motor performance during gait. Seven patients have been neurophysiologically evaluated by the use of a Cibex apparatus measuring torque and movement velocity of the lower limbs simultaneously with static and dynamic recordings of the EMG.

Adult↗
PubMed1988

Hypomanic behaviour associated with familial spastic paraplegia.

Psychiatric manifestations of familial spastic paraplegia are rare and have been described only infrequently. A 35-year-old male is reported, who presented both hypomanic behaviour and gait disturbances as features of a previously undiagnosed familial spastic paraplegia. This association implies that the CNS manifestations of familial spastic paraplegia may overlap with the neurochemical or neuroanatomic substrata regulating mood.

Adult↗
PubMed1992

Local botulinum toxin in the treatment of spastic drop foot.

Ten patients with spastic drop foot were treated by local injections of botulinum toxin A (botulinum toxin A haemagglutinin complex). The purpose was to improve stance and gait and/or to facilitate physiotherapy and patient care. Various calf muscles were injected using EMG guidance. The average dose used was 23 ng. Prior to and 4 weeks after treatment, positions of the upper and lower ankle joint at rest and the corresponding end positions of passive and active movement were determined. In addition, changes of spasticity and pain, the transmission phenomenon and stance and gait were evaluated. Most patients showed improvement of some aspects of the spastic drop foot. Positions of the upper and lower ankle joint were improved in most of the patients, as were the other parameters examined. Except for weakness of the injected muscles no side-effects were observed. The results appear promising and may be optimized in further trials by using higher doses of the toxin.

Adolescent↗
PubMed1996

Impaired stretch reflex and joint torque modulation during spastic gait in multiple sclerosis patients.

The modulation of the short latency stretch reflex of the soleus muscle during walking was investigated in seven spastic multiple sclerosis (MS) patients and nine healthy control subjects. Ankle joint stretches were applied by a system which can rotate that ankle joint in any phase of the step cycle during treadmill walking. The torque related to the muscle fibres contracting prior to the stretch and the passive tissues around the ankle joint were measured as the "non-reflex torque". At the same time the short latency stretch reflex-mediated EMG response was measured. The findings show that the stretch reflex modulation was impaired in spastic patients during walking. The stretch reflex modulation was quantified by a modulation index of an average 50% (range -5 to 100%) in the patients and 93% (78-100%) in the control subjects (P < 0.05). The passive stiffness of the ankle joint was at the same time increased in the patients (P < 0.05). It is proposed that the impaired modulation of the stretch reflex along with increased ankle joint stiffness contribute to the impaired walking ability in spastic MS patients.

Adult↗
PubMed1979

Percutaneous epidural neurostimulation in modulation of paraplegic spasticity. Six case reports.

Six cases of paraplegic, post-traumatic spasticity, alleviated by percutaneous epidural neurostimulation with temporary or permanent implanted neuroelectrodes from the L1 to L4 intervertebral levels are presented. Modulation of this spasticity and secondary beneficial physiological effects were achieved, including regulation of bowel regimens, production of sweating and piloerection below the level of the lesion, and morning erections. The main advantages of percutaneous epidural neurostimulation in modulating spasticity are the avoidance of destructive neurosurgical procedures, the regulation of secondary physiological and autonomic responses, the avoidance of antispasticity medications, and the reversibility of the neurostimulation procedure.

Adolescent↗
PubMed1985

Hindered muscle relaxation in spasticity: experimental evidence suggesting a possible pathophysiological mechanism.

In ten spastic patients and in an equal number of healthy controls, the relaxation phase occurring at the end of an isotonic voluntary contraction has been studied on soleus muscle using EMG and H-reflex methods. In the spastic group, the duration of motor unit-decruitment was consistently prolonged (from two to six times the control values). Moreover, the decrease in the excitability of the H-reflex arc, which normally accompanies the end of muscle contraction was delayed in time, reduced in amplitude or in some cases even absent. As a rule, patients in whom such release-associated inhibition (RAI) was lacking or severely reduced exhibited the longest motor unit-decruitment times, due to the interference of sustained clonic sequences. It is proposed that a lowered effectiveness of RAI might explain the clonic activity which frequently hinders voluntary muscle relaxation in spasticity.

Adult↗
PubMed2002

[Treatment of hip adductor spasticity with botulinum toxin type B].

For the treatment of focal spasticity using botulinum toxin, only studies using type A have been published. Botulinum toxin type B (Neurobloc) is registered for cervical dystonia, but there is increasing interest in ist effectiveness for treating other diseases. Four patients, each with seriously disabling hip adductor spasticity of different origins, were treated with botulinum toxin type B following the failure of other therapeutic options. Total doses of 10,000 IU to 22,000 IU were injected bilaterally into the hip adductor muscles. A reduction in muscle tone or painful spasms was observed in all patients within 2 weeks, leading to an improvement in gait and increased ease of nursing care. Therefore, botulinum toxin type B may be a more cost-effective treatment for hip adductor spasticity than botulinum toxin type A.

Adult↗
PubMed2005

Spinal cord magnetic resonance imaging in autosomal dominant hereditary spastic paraplegia.

Hereditary spastic paraplegia (HSP) is a genetically heterogeneous group of neurodegenerative disorders characterized by progressive lower extremity weakness and spasticity. HSP pathology involves axonal degeneration that is most pronounced in the terminal segments of the longest descending (pyramidal) and ascending (dorsal columns) tracts. In this study, we compared spinal cord magnetic resonance imaging (MRI) in 13 HSP patients with four different types of autosomal dominant hereditary spastic paraplegia (SPG3A, SPG4, SPG6, and SPG8) with age-matched control subjects. The cross-section area of HSP subjects at cervical level C2 was 59.42 +/- 12.57 mm2 and at thoracic level T9 was 28.58 +/- 5.25 mm2. Both of these values were less than in the healthy controls (p < 0.001). The degree of cord atrophy was more prominent in patients with SPG6 and SPG8 who had signs of severe cord atrophy (47.60 +/- 6.58 mm2 at C2, 21.40 +/- 2.4 mm2 at T9) than in subjects with SPG3 and SPG4 (66.0 +/- 8.94 mm2 at C2, p < 0.02; 31.75 +/- 2.76 mm2 at T9, p < 0.001). These observations indicate that spinal cord atrophy is a common finding in the four genetic types of HSP. Spinal cord atrophy was more severe in SPG6 and SPG8 HSP subjects than in other types of HSP we studied. This may suggest a different disease mechanism with more prominent axonal degeneration in these two types of HSP when compared with HSP due to spastin and atlastin mutations.

Adult↗
PubMed2006

Cerebral metabolic and structural alterations in hereditary spastic paraplegia with thin corpus callosum assessed by MRS and DTI.

INTRODUCTION: Hereditary spastic paraplegia with thin corpus callosum (HSP-TCC) is a complicated form of autosomal-recessive hereditary spastic paraplegia. Characteristic clinical features comprise progressive spastic gait, cognitive impairment, and ataxia. Diagnostic MRI findings include thinning of the corpus callosum and non-progressive white matter (WM) alterations. METHODS: To study the extent of axonal involvement, we performed localized proton magnetic resonance spectroscopy (MRS) of the cerebral WM and cortical grey matter (GM) in a patient with HSP-TCC at 20 and 25 years of age. The second investigation included diffusion tensor imaging (DTI). RESULTS: While MRS of the GM was normal, affected WM was characterized by major metabolic alterations such as reduced concentrations of N-acetylaspartate and N-acetylaspartyl-glutamate, creatine and phosphocreatine, and choline-containing compounds as well as elevated levels of myo-inositol. These abnormalities showed progression over a period of 5 years. DTI revealed increased mean diffusivity as well as reduced fractional anisotropy in periventricular WM. The metabolic and structural findings are consistent with progressive neuroaxonal loss in the WM accompanied by astrocytic proliferation-histopathological changes known to occur in HSP-TCC. CONCLUSION: Our results are in agreement with the hypothesis that the primary pathological process in HSP-TCC affects the axon, possibly due to impaired axonal trafficking.

Adult↗