SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Punctate keratoderma and spastic paralysis occurred in three generations of a family. Several members had keratoderma of the palms and soles or spastic paralysis or both. The family history was consistent with autosomal-dominant inheritance. The age at onset and the rate of progression of symptoms were variable. The concurrence of these lesions can be interpreted to mean either that the keratoderma and the paraplegia are the pleiotropic effects of the same mutant gene or, less likely, that they are the manifestations of two different autosomal mutations segregating in this family. We are not aware of a similar syndrome having been previously reported.
Fourteen patients with spastic paralysis from various causes (eight with cerebral palsy) who needed minimal two handed activities to assist in self-care and who desired improvement in appearance were treated by proximal row carpectomy. In twelve transfer of flexor carpi ulnaris to extensor carpi radialis brevis was done, and in two the extensors of the wrist were shortened. Various other procedures were done in some patients. Prolonged splinting was carried out. Better extension of the wrist was obtained and supination improved more when the transfer was subcutaneous around the ulnar border than when through the interosseus membrane. Less tendency for the carpus to displace ulnarward was seen when the distal half of the scaphoid was not removed. Strength of grasp and pinch improved, but ability to release objects was diminished due to the more dorsiflexed position of the wrist. Subjective use for two handed activities was improved and the patients were satisfied with the appearance.
OBJECTIVE: To observe clinical therapeutic effect of abdominal acupuncture on spastic paralysis after cerebrovascular disorder. METHODS: Sixty cases of spastic paralysis after cerebrovascular disorder were randomly divided into an abdominal acupuncture group and a body acupuncture group, 30 cases in each group. They all were treated for 5 times each week, for a 3 consecutive weeks, and then the therapeutic effects were observed. RESULTS: The spasm in the abdominal acupuncture group improved significantly, but in the body acupuncture group did not significantly improve. The therapeutic effect in the abdominal acupuncture group was significantly better than that in the body acupuncture group. CONCLUSION: Abdominal acupuncture is a safe and effective therapy for spastic paralysis after cerebrovascular disorder.
Acupuncture and moxibustion have obvious therapeutic effect on spastic paralysis of apoplexy, but there is no common standard for evaluation of therapeutic effects. Available standards for assessment of therapeutic effect of acupuncture and moxibustion on spastic paralysis of apoplexy are not complete. Acupuncture and moxibustion improve clinical symptoms of the patient of spastic paralysis of apoplexy to a considerable degree, a evaluation system for results of clinical symptoms of the patient can be set up, so as to perfect the criteria for evaluation of therapeutic effects of acupuncture and moxibustion on this disease.
OBJECTIVE: To introduce progresses of studies on acupuncture and moxibustion for treatment of spastic paralysis after stroke. METHODS: The literature about acupuncture and moxibustion for treatment of spastic paralysis after stroke in recent ten years were reviewed from the clinical and mechanism studies and so on. CONCLUSION: A great number of clinical and mechanism studies have proved that acupuncture and moxibustion therapy can relieve spastic paralysis after stroke, with better therapeutic effect, no side-effects, flexible selection of acupoints and more methods, but clinical and mechanism studies still need further to be improved and raised.
OBJECTIVE: To evaluate the effectiveness of the Bridle procedure in treatment of foot deformity in children with slight cerebral spastic paralysis. METHODS: From February 1993 to April 1999, 32 cases with 57 deformed feet, due to slight cerebral spastic paralysis, which included 20 males and 12 females, ranging from 4 to 14 years old, were reported after 6 to 74 months' follow-up, averaging 38 months. Bilateral feet were involved in 25 cases and unilateral feet involved in 7 cases. The deformities in all feet, including 26 feet of acroceph-foot deformity in 15 cases, 13 equinovarus deformity in 8 cases and 18 scissors gait deformity in 9 cases, were treated by Bridle procedure, followed by temporal external fixation of long-leg plaster splint for 6 to 8 weeks. RESULTS: Clinical observation revealed complete and permanent correction of deformity in 48 out of all 57 feet (84.2%), reoccurrence of deformity in 7 feet (12.3%), and occurrence of valgus deformity in 2 feet (3.5%). No joint stiffness was observed. CONCLUSION: The Bridle procedure is an easily performed operation and effective in the treatment of foot deformity in children with slight cerebral spastic paralysis.
We studied 15 patients, from 10 families, who presented with severe spastic paralysis with an infantile onset and an ascending progression. Spastic paraplegia began during the first 2 years of life and extended to upper limbs within the next few years. During the first decade of life, the disease progressed to tetraplegia, anarthria, dysphagia, and slow eye movements. Overall, the disease was compatible with long survival. Signs of lower motor-neuron involvement were never observed, whereas motor-evoked potentials and magnetic resonance imaging demonstrated a primitive, pure degeneration of the upper motor neurons. Genotyping and linkage analyses demonstrated that this infantile-onset ascending hereditary spastic paralysis (IAHSP) is allelic to the condition previously reported as juvenile amyotrophic lateral sclerosis at the ALS2 locus on chromosome 2q33-35 (LOD score 6.66 at recombination fraction 0). We analyzed ALS2, recently found mutated in consanguineous Arabic families presenting either an ALS2 phenotype or juvenile-onset primary lateral sclerosis (JPLS), as a candidate gene. In 4 of the 10 families, we found abnormalities: three deletions and one splice-site mutation. All the mutations lead to a truncated alsin protein. In one case, the mutation affected both the short and the long alsin transcript. In the six remaining families, absence of cDNA ALS2 mutations suggests either mutations in regulatory ALS2 regions or genetic heterogeneity, as already reported in JPLS. Alsin mutations are responsible for a primitive, retrograde degeneration of the upper motor neurons of the pyramidal tracts, leading to a clinical continuum from infantile (IAHSP) to juvenile forms with (ALS2) or without (JPLS) lower motor-neuron involvement. Further analyses will determine whether other hereditary disorders with primitive involvement of the central motor pathways, as pure forms of spastic paraplegia, could be due to alsin dysfunction.
Explore the source record for details and available documents.
OBJECTIVE: To report clinical, neuroradiologic, neurophysiologic, and genetic findings on 16 patients from 11 unrelated families with a remarkable uniform phenotype characterized by infantile ascending hereditary spastic paralysis (IAHSP). METHODS: Sixteen patients from 11 families, originating from North Africa and Europe, who presented severe spastic paralysis and ascending progression were studied. RESULTS: Spastic paraplegia started in the first 2 years of life in most patients and extended to the upper limbs by the end of the first decade. The disease progressed to tetraplegia, anarthria, dysphagia, and slow eye movements in the second decade. The clinical course showed a long survival and preservation of intellectual skills. Clinical, neuroradiologic, and neurophysiologic findings were consistent with a relatively selective early involvement of the corticospinal and corticobulbar pathways. No signs of lower motor neuron involvement were observed, whereas motor evoked potentials demonstrated predominant involvement of the upper motor neurons. MRI was normal in young patients but showed brain cortical atrophy in the oldest, predominant in the motor areas, and T2-weighted bilateral hyperintense signals in the posterior arm of the internal capsule. The ALS2 gene, recently found mutated in consanguineous Arabic families with either an ALS2 phenotype or a juvenile-onset primary lateral sclerosis, was analyzed. Alsin mutations were found in only 4 of the 10 families, whereas haplotype analysis excluded the ALS2 locus in one family. CONCLUSIONS: The syndrome of IAHSP is genetically heterogeneous, and no clinical sign can help to distinguish patients with and without Alsin mutations.
A dorsal laminectomy of L-4, L-5, and L-6, followed by resection of the dorsal (afferent) roots of the gastrocnemius muscle (desafferentation) was performed on 3 calves which had spastic paralysis. All signs of the condition disappeared after desafferentation. This suggests an overactive stretch reflex to be the cause of the spastic paralysis.
Explore the source record for details and available documents.
AIMS: In this paper we review the main studies conducted on therapy applied to the bony and soft parts in spastic paralysis of the upper extremity. DEVELOPMENT: Spasticity presents muscular hypertonia and hyperexcitability of the stretch reflex, which are typical of upper motoneuron syndrome. Physiopathologically, spasticity is due to the medullar and supramedullar alteration of the afferent and efferent pathways. Treatment is multidisciplinary and involves the collaboration of rehabilitators, neurophysiologists, neurologists, paediatricians, orthopaedic surgeons and psychologists, who all contribute with their different therapeutic aspects and characteristics (which can be pharmacological, peripheral neurological blockages, surgical, etc.). The characteristic posture of the upper extremities in spastic cerebral palsy is the inward rotation of the shoulder, flexion of the elbow and pronated forearm, and the deformity of the fingers (swan-neck and thumbs-in-palm). The primary objectives in these patients will be to improve communication with their surroundings, perform activities of daily living, increase mobility and walking. CONCLUSIONS: The surgical treatment applied by orthopaedic surgeons in the upper extremities are aimed at achieving an enhanced adaptive functionality rather than morphological normality. Factors to be taken into account include age, voluntary control over muscles and joints, level of severity of the spasticity (Ashworth scale) and stereognostic sensitivity. In general, on soft parts we will use procedures such as dehiscence or lengthening of the flexor muscles of the shoulder and elbow or of the adductor of the thumb; transfer of the pronators in order to adopt the supinating function or of the flexors so as to reinforce the extensors of the forearm, and capsulodesis or tenodesis in the hand. The bony procedures will consist in derotational osteotomies of the humerus and radius and arthrodesis in the wrist or in the metacarpophalangeal joints of the thumb, depending on whether there is greater rigidity or age in the former cases or instability in the latter.
OBJECTIVE: To determine the results of surgical correction of spastic paralysis of the hand due to cerebral palsy. DESIGN: Descriptive. SETTING: Academic Medical Centre, Amsterdam, the Netherlands, and rehabilitation centre De Trappenberg. METHOD: From 1-1-1990 until 1-6-1994 twenty patients with spastic upper limb in cerebral palsy were operated in our hospital. They were all seen preoperatively by our multidisciplinary team, and selected according to the Zancolli classification. Seventeen operations were aimed at improving hand function, the other three were performed for contractures or for cosmetic/hygienic reasons. Surgery was aimed at correcting the muscular imbalance, by weakening spastic muscles via tenotomy or lengthening and by reinforcing paralysed muscles via tendon transfer or rerouting. Often stabilisation of joints by tenodesis, capsulodesis or arthrodesis was necessary as well. RESULTS: Eighteen of the twenty patients were (very) happy with the results. In two patients there was no functional gain. Only once was a postoperative complication seen: pseudarthrosis of the first carpometacarpal joint. This was corrected successfully by rearthrodesis. We found we were able to predict the functional outcome fairly accurately. CONCLUSION: With accurate patient selection, surgical intervention in patients with cerebral palsy may restore hand function adequately and predictably.
Explore the source record for details and available documents.
A case of acute myeloblastic leukemia (AML) with spastic paralysis of the lower extremities caused by a tumor of the spinal cord as the first symptoms of the disease is presented. The tumor consisted of leukaemic cells. A diagnosis of AML type M2, according to FAB classification, was established. A complete remission was achieved after 2 courses of chemotherapy. Patient started to walk after intensive rehabilitation. After 14 months of complete remission, recurrence was observed despite an intensified therapy.
Explore the source record for details and available documents.