The Effect of Saddle-Assistive Device on Improving the Gait Parameters of Patients with the Lower Limbs Weakness:A Pilot Study

To help walking,using assistive devices can be considered to reduce the loads caused by weight and to effectively decrease the propulsive forces.In this study,a mobility Saddle-Assistive Device(S-AD)supporting body weight while walking was evaluated on two healthy volunteers.This device is based on the support of body weight against gravity with the help of a saddle,which is not used in other passive mobility assistive devices.To prove the efficiency of this device,the experimental results obtained while walking with this device were compared with those related to walking without the assistive device.The results showed that this device could significantly reduce the forces and torque of the lower and upper limbs when walking.By distributing the load on the saddle,the vertical force and the propulsive force in the best conditions were decreased to 46.7%and were increased to 13.7%in body weight,respectively.Using a S-AD can help patients with lower limbs weakness and elderly people to walk.

Early-onset ophthalmoplegia,cervical dyskinesia,and lower extremity weakness due to partial deletion of chromosome 16:A case report

BACKGROUND We explored the genotype-phenotype correlation of the novel deletion 16p13.2p12.3 in an 8-year-old child with progressive total ophthalmoplegia,cervical dyskinesia,and lower limb weakness by comparing the patient’s clinical features with previously reported data on adjacent copy number variation(CNV)regions.CASE SUMMARY Specifically,we first performed whole-exome sequencing,CNV-sequencing,and mitochondrial genome sequencing on the patient and his parents,then applied“MitoExome”(the entire mitochondrial genome and exons of nuclear genes encoding the mitochondrial proteome)analysis to screen for genetic mitochondrial diseases.We identified a de novo 7.23 Mb deletion,covering 16p13.2p12.3,by both whole-exome sequencing and CNV sequencing.We also detected 16p13.11 in the deleted region,which is the recurrent distinct region associated with neurodevelopmental disorder.However,the patient only displayed features of progressive total ophthalmoplegia,cervical dyskinesia,and weakness in his lower limbs without neurodevelopmental disorder.The“MitoExome”sequencing was negative.Brain magnetic resonance imaging revealed non-specific sporadic changes in the occipital parietal lobe and basal ganglia.CONCLUSION Taken together,these results indicated that 16p13.2p12.3 deletion causes a syndrome with the phenotype of early-onset total ophthalmoplegia.The“MitoExome”analysis is powerful for the differential diagnosis of mitochondrial diseases.We report a novel copy number variant in this case,but further confirmation is required.

Asymmetric limb weakness in Guillain-Barre syndrome:Three case reports

BACKGROUND Guillain-Barrésyndrome(GBS)is an autoimmune-mediated peripheral neuropathy characterized by symmetric weakness.Asymmetric weakness in GBS is uncommon and may be easily confused with other differential diagnoses.We herein present three cases of asymmetric GBS and review the literature on this atypical subtype of GBS in order to describe the characteristics of asymmetric GBS and to provide experience for clinicians.CASE SUMMARY Different from patients in the previous reports,our patients showed persistent asymmetric limb weakness from the onset to recovery phase.All three patients were serologically positive for antecedent infections.Two of the three cases had IgG antibodies against ganglioside GM1.Two patients received immunotherapy including intravenous immunoglobulin and plasma exchange,while one patient received only supportive treatment.Autoantibodies against gangliosides,asymmetry of congenital development of blood-nerve barrier and limb use may contribute to the development of asymmetric limb weakness in GBS.CONCLUSION Asymmetric GBS may be a rare clinical variant and should be considered when a patient develops acute and progressive asymmetric limb weakness.The differences in clinical features and prognosis between asymmetric GBS and classic GBS deserve further investigation in a large study.

Effect of Sijunzi Decoction on the Myonuclear Domain of Rat Soleus in Spleen Qi Deficiency

Objective: To study the mechanism of Sijunzi decoction treating limb weakness in spleen Qi deficiency (SQD) based on the myonuclear domain (MND) theory. Methods: 40 male Sprague-Dawley rats were randomly divided into the normal group, SQD model group (model group), SQD+ still water group (SW group) and SQD+ Sijunzi decoction group (CM group), 10 rats each group;Grip-Strength Meter was used to measure limb grip strength;transmission electron microscope was employed to observe the ultrastructural changes of the myofibers, Image Pro 6.0 was used to measure the myonuclear numbers, cross-section area (CSA) and then their ratios (the MND sizes) were calculated, immunofluorescence assay was chosen to test the expressions of paired box gene 7 (Pax7) and myogenic differentiation antigen (MyoD). Results: Compared with those in the normal group, limb grip strength was decreased, sarcomeres were abnormal, and all the myonuclear numbers, CSA and MND sizes were reduced, but the Pax7+ cell numbers were increased, significantly, in the model and SW groups;Compared with those in the model and SW groups, limb grip strength was increased, sarcomeres were basically normal, the myonuclear number and CSA were both greater, and the Pax7+ and MyoD+ cell numbers were both increased, significantly, in the CM group. Conclusion: Sijunzi decoction might increase the myonuclear number by activating the MSCs to treat limb weakness in SQD.

Symptom experience and symptom burden of patients following first-ever stroke within 1 year： a cross-sectional study

Symptoms that are multidimensional and concurrent should be assessed from different dimensions and managed together. Few studies have evaluated concurrent and multidimensional symptoms in patients with stroke. Most studies of stroke focused on dysfunctions and complications. We hypothesize that patients with stroke have a heavy symptom burden within 1 year. This study aimed to describe multidimensional and concurrent symptoms within 1 year after stroke. This study recruited 230 patients with stroke from the Rehabilitation Department of Xuhui District Center Hospital of Shanghai and the Shanghai Sunshine Rehabilitation Center in China from March to September 2017. The patients＇ multidimensional symptom experience and symptom burden were analyzed using a self-made structured questionnaire and the influential factors for symptom burden were identified. The mean number of symptoms in patients with stroke was 11.7 ± 3.5. More than two thirds of the participants suffered from at least 10 co-occurring symptoms. Unilateral limb weakness had the highest prevalence and frequency. Participation restriction had the highest symptom dimensions of severity and distress. Lack of self-care ability（severity）, memory deterioration（frequency）, imbalance of body（distress）, moodiness（distress）, being unable to move limbs at will（distress）, shoulder pain（distress）, and slower response（frequency） were independent factors of the total symptom burden score. These findings can provide essential information for efficient symptom management of patients with stroke.

Cortical infarction of the right parietal lobe and neurogenic heart disease A report of three cases

Three male patients were diagnosed with new cortical infarctions of the right parietal lobe on the basis of head magnetic resonance imaging; high-intensity signals indicating lesions in the right parietal lobe were noted on diffusion-weighted images at admission. Two of them presented with left hand weakness, and one exhibited left upper limb weakness. Treatment for improving blood supply to the brain was administered. One patient died suddenly because of ventricular fibrillation 3 days after admission. The other two patients had increased troponin levels and abnormal electrocardiograms, and were diagnosed with acute myocardial infarction half a month after admission. When lesions exist in field 7 of the parietal cortex （resulting in paralysis of the contralateral hand）, the sympathetic center of the posterior lateral nucleus of the hypothalamus demonstrates compensatory excitement, which easily causes tachyarrhythmia and sudden death. Our experimental findings indicate that close electrocardiograph monitoring and cerebral infarction treatment should be standard procedures to predict and help prevent heart disease in patients with cerebral infarction in the right parietal lobe and left upper limb weakness as the main complaint.

Gitelman syndrome:A case report

BACKGROUND Gitelman syndrome(GS)is an autosomal recessive salt-losing renal tubulopathy arising from mutations in the thiazide-sensitive Na-Cl cotransporter gene.Due to its low incidence and lack of awareness,GS can be easily misdiagnosed or missed in diagnosis.CASE SUMMARY A 24-year-old male presented with>4 years of repeated limb weakness without any treatment.The previous day,the patient was bitten by ants and showed weakness of the lower limbs.The patient had hypokalemia(1.66-2.83 mmol/L),hypomagnesemia(0.4 mmol/L),hypocalciuria(1.51-2.46 mmol/d),metabolic alkalosis(7.47-7.54),normal blood pressure,and increased activity of aldosterone and plasma renin activity(PRA)(PRA 6.4 and 16.45 ng/mL/h and aldosterone 330.64 and 756.82 pg/mL in the supine and upright position,respectively).In addition,SLCI2A3 gene mutation with GS was diagnosed.Oral and intravenous supplementation with potassium and magnesium was initiated.Serum magnesium returned to 0.48 mmol/L and serum potassium returned to 3.08 mmol/L,alleviating the patient’s fatigue symptoms.CONCLUSION GS should be considered in patients with hypokalemia complicated with hypomagnesemia.Genetic testing is essential to confirm the diagnosis.