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OBJECTIVE: Electromyographic biofeedback therapy has been widely used in post-stroke muscle rehabilitation training. The purpose of this paper is to systematically evaluate the efficacy of electromyographic biofeedback on treating post-stroke spasticity. METHODS: The randomized controlled trials addressing electromyographic biofeedback in the treatment of post-stroke spasticity were retrieved from PubMed, Cochrane Library, Embase, CNKI, VIP, Chinese BioMedical Literature Database, and WanFang Database. The retrieval time ranged from database inception to June 2021. The risk of bias was evaluated by the Cochrane Collaboration tool and modified Jadad scale. Meta-analysis was performed using RevMan 5.4 software. RESULTS: A total of 15 randomized controlled trials were included, and 878 samples were extracted. The results of Meta-analysis showed that treatment with electromyographic biofeedback ≤ 4 weeks or over 4 weeks showed a significantly lower modified Ashworth scale score [mean difference (MD)=-0.32, 95% confidence interval (CI): -0.45 to -0.19, P < 0.000 01; MD=-0.27, 95% CI: -0.37 to -0.17, P < 0.000 01] and significantly lower clinical spasticity index (MD=-2.05, 95% CI: -2.27 to -1.83, P < 0.000 01) compared with the control group. Compared with the control group, electromyographic biofeedback could significantly improve the motor function (upper limbs ≤ 4 weeks: MD=3.39, 95% CI: 2.02-4.77, P < 0.000 01; upper limbs > 4 weeks: MD=2.53, 95% CI: 2.04-3.02, P < 0.000 01; lower limbs > 4 weeks: MD=3.36, 95% CI: 2.90-3.83, P < 0.000 01; total score ≤ 4 weeks: MD=20.63, 95% CI: 19.38-21.88, P < 0.000 01; total score > 4 weeks: MD=8.08, 95% CI: 3.38-12.78, P=0.000 8), the active range of motion of the ankle joint (≤ 4 weeks: MD=4.87, 95% CI: 1.12-8.62, P=0.01; > 4 weeks: MD=3.69, 95% CI: 3.04-4.34, P < 0.000 01) and electrophysiological parameters (flexor group: MD=-16.80, 95% CI: -24.75 to -8.85, P < 0.000 1; extensor group: MD=17.88, 95% CI: 2.83-32.93, P=0.02) of the hemiplegic limbs. CONCLUSION: Electromyographic biofeedback can effectively improve post-stroke limb spasticity and function. However, more high-quality randomized controlled trials are still needed to further verify its efficacy and safety. [ABSTRACT FROM AUTHOR]

Hereditary spastic paraplegia (HSP) is a group of neurodegenerative disorders with clinical and genetic heterogeneity. The main clinical feature is the progressive spasticity of lower limbs and myasthenia. HSPs are clinically divided into types: simple type and complicated form, the later with additional manifestations of more extensively neurological or non-neurological disorders. In genetics, HSPs are divided into four groups as follows: autosomal dominant, autosomal recessive, X-linked and mitochondrial traits, according to the inheritance modes. About 60 genetic subtypes have been described. With in-depth research on HSP, many new causative genes have been identified. We systematically reviewed the progress of HSPs, mainly including genotype and the corresponding clinical manifestations, for physicians to precisely identify the subtypes of HSP and to diagnose in genetics. [ABSTRACT FROM AUTHOR]

Objective To study the clinical features and diagnostic methods of patients with pure hereditary spastic paraplegia (HSP). Methods Patients diagnosed with pure HSP from October 2006 to February 2013 admitted to Department of Neurology, West China Hospital, Sichuan University were included. The patients were assessed by the Spastic Paraplegia Rating Scale and the clinical features were reviewed. Results Thirty - three HSP patients (21 men and 12 women) were included in the study. Thirteen patients (39.39%) had family history of HSP and the most common genetic mode of the familial cases were autosomal dominant inheritance (11/13). The mean age of onset were (20.35 ± 15.55) years and the mean disease duration were (12.77 ± 9.83) years. All of the included patients presented with signs of impairment of the pyramidal tract such as increased muscular tone, tendon hyperreflexia and positive Babinski's sign of the lower limbs. Impairment of the pyramidal tract also presented in the upper limbs in some patients. Scissors gait appeared in 29 patients and feet deformity in 5 patients. Atrophy of thoracic cord on MRI were presented in 5 patients while 2 patients complicated with peripheral nerve damage. Four patients had a novel exon 10-17 deletion in SPG4 gene. There were no differences in onset age, disease duration and mean score of the Spastic Paraplegia Rating Scale between male and female patients as well as between patients with and without family history (P > 0.05, for all). Conclusion The onset age of pure HSP is variational and males are more common than females. The most common inheritance mode is autosomal dominant and most of the cases are characterized by impairment of the pyramidal tract of the lower limbs and occasionally bladder dysfunction and peripheral nerve damage. Gender and family history do not affect the clinical features. Clinical features, family history and spinal cord MRI will assist the correct diagnosis, and making a definite diagnosis needs genetic tests. [ABSTRACT FROM AUTHOR]