ObjectiveTo study the differences in body composition between maintenance hemodialysis (MHD) patients with reduced muscle mass and the ones with normal muscle mass by bioelectrical impedance analysis, and explore the influencing factors.MethodsA total of 122 patients undergoing MHD in the hemodialysis center of a general hospital between September 2018 and May 2019 were selected as the research subjects. According to the relative skeletal muscle mass index, they were divided into the muscle loss group and the normal muscle mass group. Their general conditions, post-dialysis body composition, and serum albumin were collected to analyze the differences between the two groups, and a multiple stepwise logistic regression analysis was carried out.ResultsAmong the included subjects, 53 patients had normal muscle mass and 69 patients had muscle mass loss. The post-dialysis body weight, muscle-related indexes, intracellular water, extracellular water (ECW), total body water (TBW), protein, minerals, body cell mass, bone mineral content, body mass index, arm circumference, and arm muscle circumference in the normal muscle mass group were higher than those in the muscle loss group (P<0.05); the percentage of ECW/TBW in the normal muscle mass group was lower than that in the muscle loss group (P<0.05). The multiple stepwise logistic regression analysis showed that the post-dialysis weight [odds ratio (OR)=0.679, 95% confidence interval (CI) (0.535, 0.862), P=0.001] was a protective factor from losing muscle in MHD patients, and the high ECW/TBW [OR=6.926, 95%CI (1.014, 47.280), P=0.048], low body cell mass [OR=57.707, 95%CI (6.927, 480.761), P<0.001], low bone mineral content [OR=9.743, 95%CI (1.220, 77.831, P=0.032], and arm circumference [OR=2.183, 95%CI (1.004, 4.749), P=0.049] were risk factors for muscle loss in MHD patients.ConclusionsMHD patients have a high incidence of muscle loss. It is necessary to monitor the changes of their body composition, especially those who with low post-dialysis body weight, lack of bone minerals and body cells, excessive ECW/TBW, and increased arm circumference after hemodialysis. Both nutritional interventions and exercise interventions should be performed timely and routinely to prevent the occurrence of sarcopenia.
ObjectiveTo explore the clinical features of myasthenia gravis (MG) harboring both acetylcholine receptor antibody (AChRAb) and muscle-specific tyrosine kinase antibody (MuSKAb) positivity.MethodsWe searched PubMed, Web of Science, Embase and China National Knowledge Infrastructure databases (from inception to November 2016), to collect the case reports of MG with both AChRAb and MuSKAb positivity. Along with one case discovered in Department of Neurology, West China Hospital, the clinical data of the cases were retrospectively analyzed.ResultsA total of 13 double-seropositive MG patients were enrolled in this study, demonstrating a marked female predominance (including 1 male and 12 females) and a younger age at onset [(31.07±24.77) years]. During the disease course, 10 of the included patients presented severe bulbar involvement, dyspnea and neck weakness, with myasthenic crisis in 6 individuals. Among the 11 patients with detailed records, abnormal thymus glands comprised 4 thymus hyperplasia and one thymoma. While the response to oral pyridostigmine was unsatisfactory in 11 double-seropositive MG patients, ranging from mild benefit to overt intolerance; the patients treated with plasma exchange (3/3), rituximab (1/1) or corticosteroid (7/12) improved dramatically, with other immumosuppressants and intravenous immunoglobulin partially responsive. Moreover, 5 patients undergoing thymectomy improved markedly or partially.ConclusionsCompared with MG patients with MuSKAb positivity merely, the condition of the double-seropositive MG patients seem to be more severe and further inclined to myasthenic crisis. The incidence of abnormal thymus, such as thymus hyperplasia, is higher. Thymectomy may be an effective treatment for such patients.
Twenty-three patients (28 extremities) suffering secondary ulcer after high ligation and stripping of great saphenous vein were chosen to receive muscle flap formation of potiteal vein. Of which, 21 patients (25 extremities) ulcer scabbed within one week and healed in 2 weeks after operation. The other s were cured in 5 weeks. All patients were followed up 6-12 months with no recurrence and satisfactory results.
our patients with brachial plexus root arulsion, who had undergone various nerve operationswith no functional recovery of the limb, were treated with transfer of sternocledomastoid muscle toreconstruct the function of elbow fleaion. The sternocleidomastoid muscle was datached from itsincertions and was lengthened by fascia lata graft from the thigh , and then , was transferred under theclavicle to the radiai shaft just distal to the radial tuberosity. After the recostruction, The potient...
ObjectiveMitochondrial encephalomyopathy is a series of diseases that drag in central nervous system and generalized muscles. The pathogenesis of the disease is lack of ATP for the dysfunction of mitochondria. The misdiagnosis rate of the disease is high and the purpose of this study is to improve the recognition and diagnosis of mitochondrial encephalomyopathy and thus, clinicians could take rational treatment in time and improve patients' prognosis. MethodsThe clinical data of 11 patients with mitochondrial encephalomyopathy were analyzed including the physical data, clinical presentations, laboratory data, neuroimaging findings, muscle biopsy, genetic testing, treatment and prognosis. Reviewing literature and summarizing the clinical characteristics of mitochondrial encephalomyopathy. ResultsAmong the 11 patients with mitochondrial encephalomyopathy, the mean age was 17 years old. 1 case had family history. 7 cases were misdiagnosed in the first clinic visit. The onset of the 11 cases, 9 were paroxysmal and 2 were hidden. In the course, 10 cases had an epileptic seizure. Among the 9 cases who took the determination of serum lactate, 8 was in high level.9 cases had MRI examination and all found abnormality, 10 patients had EEG examination, and 9 cases found abnormality, 6 cases had muscle biopsy and all found the ragged red fiber(RRF). 6 cases had molecular genetic testing, and all found mutations in mitochondrial DNA. Among the 10 cases who had epileptic seizure, 3 cases can be controlled with single kind of antiepileptic drug. The other 7 cases had a recurrence of epilepsy with single kind of antiepileptic drugs, but can be cotrolled after drug adjusting or drug combination. ConclusionMitochondrial encephalomyopathy is often accompanied by seizure, which is usually found in children, and also often accompanied by systemic muscle symptoms. The clinical manifestations of the disease is not typical, but is complex and varied symptoms, so the clinical misdiagnosis rate is high. Mitochondrial encephalomyopathy mainly involves the main intracranial artery distribution area (parietal lobe, temporal lobe, occipital lobe, etc.) in central nervous system, and can involve more than one part. Patients with mitochondrial myopathy brain are usually detected the elevation of serum lactate levels, but if the lactic acid level is normal, it does not rule out the possibility of the disease, the confirmation of the disease is mainly by muscle biopsy or genetic tests. There is no specific treatment for mitochondrial encephalomyopathy till now, and it still give priority to symptomatic treatment. And the prognosis is poorer.
Objective To observe the delaying effect of neural stem cell (NSC) transplantation on denervated muscle atrophy after peri pheral nerve injury, and to investigate its mechanism. Methods NSCs were separated from the spinal cords of green fluorescent protein (GFP) transgenic rats aged 12-14 days mechanically and were cultured and induced to differentiate in vitro. Thirty-two F344 rats, aged 2 months and weighed (180 ± 20) g, were randomized into two groups (n=16 per group). The animal models of denervated musculus triceps surae were establ ished by transecting right tibial nerve and commom peroneal nerve 1.5 cm above the knee joints. In the experimental and the control group, 5 μL of GFP-NSCsuspension and 5 μL of culture supernatant were injected into the distal stump of the tibial nerve, respectivel. The generalcondition of rats after operation was observed. At 4 and 12 weeks postoperatively, the wet weight of right musculus tricepssurae was measured, the HE staining, the Mallory trichrome staining and the postsynaptic membrane staining were adopted for the histological observation. Meanwhile, the section area of gastrocnemius fiber and the area of postsynaptic membrane were detected by image analysis software and statistical analysis. Results The wounds in both groups of animals healed by first intension, no ulcer occurred in the right hind l imbs. At 4 and 12 weeks postoperatively, the wet weight of right musculus triceps surae was (0.849 ± 0.064) g and (0.596 ± 0.047) g in the experimental group, respectively, and was (0.651 ± 0.040) g and (0.298 ± 0.016) g in the control group, respectively, showing a significant difference (P lt; 0.05). The fiber section area of the gastrocnemius was 72.55% ± 8.12% and 58.96% ± 6.07% in the experimental group, respectively, and was 50.23% ± 4.76% and 33.63% ± 4.41% in the control group, respectively. There were significant differences between them (P lt; 0.05). Mallory trichrome staining of muscle notified that there was more collagen fiber hyperplasia of denervated gastrocnemius in the control group than that in the experimental group at 4 and 12 weeks postoperatively. After 12 weeks of operation, the area of postsynaptic membrane in the experimental group was (137.29 ± 29.14) μm2, which doubled that in the control group as (61.03 ± 11.38) μm2 and was closer to that in normal postsynaptic membrane as (198.63 ± 23.11) μm2, showing significant differences (P lt; 0.05). Conclusion The transplantation in vivo of allogenic embryonic spinal cord NSCs is capable of delaying denervated muscle atrophy and maintaining the normal appearance of postsynaptic membrane, providing a new approach to prevent and treat the denervated muscle atrophy cl inically.
Objective To provide the anatomical basis of contralateral C7 root transfer for the recovery of the forearm flexor function. Methods Thirty sides of adult anti-corrosion specimens were used to measure the length from the end of nerves dominating forearm flexor to the anastomotic stoma of contralateral C7 nerve when contralateral C7 nerve transfer was used for repair of brachial plexus lower trunk and medial cord injuries. The muscle and nerve branches were observed. The length of C7 nerve, C7 anterior division, and C7 posterior division was measured. Results The length of C7 nerve, anterior division, and posterior division was (58.8 ± 4.2), (15.4 ± 6.7), and (8.8 ± 4.4) mm, respectively. The lengths from the anastomotic stoma to the points entering muscle were as follow: (369.4 ± 47.3) mm to palmaris longus, (390.5 ± 38.8) mm (median nerve dominate) and (413.6 ± 47.4) mm (anterior interosseous nerve dominate) to the flexor digitorum superficialis, (346.2 ± 22.3) mm (median nerve dominate) and (408.2 ± 23.9) mm (anterior interosseous nerve dominate) to the flexor digitorum profundus of the index and the middle fingers, (344.2 ± 27.2) mm to the flexor digitorum profundus of the little and the ring fingers, (392.5 ± 29.2) mm (median nerve dominate) and (420.5 ± 37.1) mm (anterior interosseous nerve dominate) to the flexor pollicis longus, and (548.7 ± 30.0) mm to the starting point of the deep branch of ulnar nerve. The branches of the anterior interosseous nerve reached to the flexor hallucis longus, the deep flexor of the index and the middle fingers and the pronator quadratus muscle, but its branches reached to the flexor digitorum superficials in 5 specimens (16.7%). The branches of the median nerve reached to the palmaris longus and the flexor digitorum superficial, but its branches reached to the deep flexor of the index and the middle fingers in 10 specimens (33.3%) and to flexor hallucis longus in 6 specimens (20.0%). Conclusion If sural nerve graft is used, the function of the forearm muscles will can not be restored; shortening of humerus and one nerve anastomosis are good for forearm flexor to recover function in clinical.
Objective To investigate the effect of Ligustrazine on the expressions of FoXO3a, MAFbx, and MuRF1 indenervated skeletal muscle atrophy rats. Methods Fifty-four 8-week-old female Sprague Dawley rats were randomly dividedinto 3 groups: normal control group (group A, n=6), denervated control group (group B, n=24), and Ligustrazine interventiongroup (group C, n=24). After the denervated gastrocnemius models were established in the rats of groups B and C, sal ine andLigustrazine [80 mg/(kg·d)] were given every day by intraperitoneal injection, respectively. However, no treatment was donein group A. At 2, 7, 14, and 28 days after denervation, the wet weight of gastrocnemius was measured to calculate the ratio ofwet weight. The mRNA and protein expression levels of FoXO3a, MAFbx, and MuRF1 were detected by RT-PCR and Westernblot. Results The ratio of gastrocnemius wet weight decreased with time after denervation in groups B and C, showingsignificant differences when compared with that of group A (P lt; 0.05), and group C were significantly higher than that of groupB at 7, 14, and 28 days (P lt; 0.05). The mRNA and protein expressions of FoXO3a, MAFbx, and MuRF1 in groups B and Cwere significantly higher than those in group C at 7, 14, and 28 days (P lt; 0.05), and group C was significantly lower than groupB (P lt; 0.05). Conclusion Ligustrazine may postpone denervated skeletal muscle atrophy by reducing mRNA and proteinexpressions of FoXO3a, MAFbx, and MuRF1.
To evaluate the value of clinical application of examination of fibrillation potential amplitude, 110 patients, 97 males and 13 females, were examined and only the maximum fibrillation potential amplitudes were recorded in 420 muscles. The results showed that there was no significant difference between sexes, ages and sides. However, significant difference was evident between the groups of different frequency (1+ to 4+). The fibrillation potential amplitude was maximum at 3 to 4 months after denervation and still remained at relatively high level for years in certain patients. No significant difference was showed between the time groups in incomplete nerve injuries. Surgery did not affect the course of fibrillation potential amplitude change. It was suggested that the muscle cells sustained their property for years after denervation in some patients, thus it might explain that satisfactory result could be obtained from operative repair in some late cases. The changes of fibrillation potential amplitude might indicate that the changes from muscle denervation was still reversible and might be more accurate than traditional method of examination.
Objective To study the clinical characteristics of mulifocal motor neuropathy. Methods Patients records in China Biological Medicine Database (CBM-disc 1980-2005)and WanFang Database were searched. Demographic data, clinical manifestations, electrophysiology, and laboratory findings on multifocal motor neuropathy were analyzed. Results Of the total 80 patients, 61 cases were males, and 19 were females. A single limb weakness began in all the patients. Weakness was usually accentuated distally(95.3%), accompanied by muscle amyotrophy(76.3%) and fasciculation(46.3%). Reflexes were reduced (96.4%). Sensory impairment and cranial involvement were rare. 92.1% of the patients showed conduction block of motor nerve. Results Of the total 80 patients, 61 cases were males, and 19 were females. A single limb weakness began in all the patients. Weakness was usually accentuated distally(95.3%), accompanied by muscle amyotrophy(76.3%) and fasciculation(46.3%). Reflexes were reduced (96.4%). Sensory impairment and cranial involvement were rare. 92.1% of the patients showed conduction block of motor nerve. Conclusions Clinical features about multifocal motor neuropathy are a single distal limb weakness, muscle amyotrophy, and conduction block of motor nerve. MMN should be differentiated from motor neuron disease and chronic inflammatory demyelinating polyneuropathy.