Analysis of a case of corticobasal degeneration started with primary progressive aphasia / 中华神经科杂志

Objective:Through a typical case of corticobasal degeneration (CBD) with primary progressive aphasia (PPA) to analyze the clinical characteristics of CBD and the special manifestations of aphasia with that disease.Methods:Retrospective analysis was performed on a patient with PPA based CBD who was admitted to the First Affiliated Hospital, Sun Yat-sen University in July 2020 to summarize the clinical features and diagnostic thinking of CBD.Results:The patient was a 59-year-old male, manifested rapidly progressive dysfunction of language and memory function. The aphasia was mainly featured as slow speech, reduced content and grammatical errors, and diagnosed as PPA, non-fluent grammatical variation. The imaging results showed the atrophy of the left frontal lobe, parietal lobe, basal ganglia and thalamus, coupled with the reduction in 18F-fluorodeoxyglucose radioactive uptake. The patient was finally diagnosed as possible CBD. Conclusions:PPA as the initial manifestation of CBD is very rare in clinical practice. The high non-specificity of clinical features and the lack of typical motor symptoms result in the difficulty of correct diagnosis of CBD. Timely functional imaging in nuclear medicine and reliable biomarkers help to facilitate early diagnosis of atypical CBD.

Neurofibrillary tangle-predominant dementia / 中华老年医学杂志

Neurofibrillary tangle-predominant dementia(NFTPD)is one type of late-onset dementia, with memory disorders as the main clinical manifestation.The pathological feature is the presence of a large number of neurofibrillary tangle(NFT)in the hippocampus with no or little amyloid deposition in the brain.In recent years, primary age-related tauopathy(PART)has been proposed as a new pathological term, which means that NFT appears in the medial temporal lobe with aging, but no amyloid deposits, and NFTPD is one type of dementia associated with the progression of PART.

A case of unilateral hypertrophic olivary degeneration following bilateral medial medullary infarction / 中华神经科杂志

Bilateral medial medullary infarction is a rare type of stroke. Hypertrophic olivary degeneration (HOD) is usually secondary to the lesion involving the Guillain-Mollaret triangle with vacuolar degeneration of inferior olivary nucleus neurons and enlargement of inferior olivary nucleus. The primary lesions involving the Guillain-Mollaret triangle are usually located in midbrain, pons and cerebellum. A case of unilateral HOD secondary to bilateral medial medullary infarction is reported and the clinical characteristics, diagnosis and treatment are analyzed in order to improve the understanding of HOD.

Neurofibriilary tangle-predominant dementia / 中华老年医学杂志

Neurofibrillary tangle-predominant dementia (NFTPD)is one type of late-onset dementia,with memory disorders as the main clinical manifestation.The pathological feature is the presence of a large number of neurofibrillary tangle(NFT)in the hippocampus with no or little amyloid deposition in the brain.In recent years,primary age-related tauopathy(PART)has been proposed as a new pathological term,which means that NFT appears in the medial temporal lobe with aging,but no amyloid deposits,and NFTPD is one type of dementia associated with the progression of PART.

Efecto de la oxitocina en los niveles de malondialdehído, óxido nítrico y proteína s100b en el recién nacido / Effect of oxytocin on the levels of malondialdehyde, nitric oxide, and s100b protein in newborns

RESUMEN Objetivos. Evaluar los efectos de la administración de oxitocina en la conducción del parto en los niveles de malondialdehído (MDA), óxido nítrico (ON) y proteína S100B en el recién nacido. Material y Métodos. Se seleccionó a 80 gestantes a término sin patología obstétrica y fetal, formando dos grupos: Gestantes con parto normal y conducidas con oxitocina. Se extrajo sangre inmediatamente después del parto de la vena de cordón umbilical para medir MDA, ON y de la arteria para la proteína S100B. Se cuantificó la concentración de MDA y ON por métodos espectroscópicos y la proteína S100B por ELISA. Resultados. Se tuvo valores de 3,4 uMol/L y 3,6 uMol/L de MDA y 1,4 uMol/Ly 1,8 uMol/L de ON en el grupo conducido con oxitocina y control respectivamente sin diferencia significativa, los niveles de S100B fueron mayores en el grupo conducido con oxitocina, con una mediana de 1,36 μg/L comparado con el grupo de parto normal 1,11 μg/L (p=0,03). No hubo relación entre la dosis de oxitocina administrada y los niveles de MDA, ON y S100B. Conclusiones. No hay diferencia entre los niveles de MDA y ON entre las gestantes con parto normal y conducidas. Hay diferencia significativa en los niveles de proteína S100B en recién nacidos de parto con oxitocina. No hay relación entre la dosis de oxitocina y los niveles de estrés oxidativo y proteína S100B.

ABSTRACT Objectives. To assess the effects of the administration of oxytocin during labor management on the levels of malondialdehyde (MDA), nitric oxide (NO), and S100B protein in newborns. Materials and Methods. We selected 80 term pregnant women without obstetric and fetal pathology, forming two groups: pregnant women with normal delivery and pregnant women conducted with oxytocin. Blood was collected immediately after delivery from the umbilical cord vein to measure MDA, ON and from the artery for protein S100B. The concentration of MDA and ON was quantified by spectroscopic methods and the protein S100B by ELISA. Results. Values of 3.4 uMol/L and 3.6 uMol/L of MDA and 1.4 uMol/L and 1.8 uMol/L of NO were obtained in the oxytocin and control group, respectively, without significant difference; S100B levels were higher in the oxytocin managed group, with a median of 1.36 μg/L compared to the normal delivery group 1.11 μg/L (p=0.03). There was no relationship between the dose of oxytocin administered and the levels of MDA, ON, and S100B. Conclusions. There is no difference between MDA and NO levels between pregnant women undergoing a normal or managed birth. There is a significant difference in S100B protein levels in newborns born via an oxytocin-managed delivery. There is no relationship between oxytocin dose and levels of oxidative stress and S100B protein

Characteristics of cerebral glucose metabolism in patients with corticobasal degeneration / 中华核医学与分子影像杂志

Objective To identify abnormal cerebral glucose metabolism characteristics in patients with corticobasal degeneration (CBD) using 18 F-fluorodeoxyglucose (FDG) PET imaging. Methods From January 2014 to January 2017, resting-state brain 18 F-FDG PET imaging was performed in 10 CBD patients (5 males, 5 females; average age: (63.4±6.2) years) and 20 age-matched healthy subjects (8 males, 12 female; average age: (63.6±6.2) years). Voxel-based statistical parametric mapping (SPM) was used to analyze images to obtain the CBD-related brain metabolic characteristics. The regional cerebral metabolic rate of glucose (rCMRglc) was compared between 2 groups by two-sample t test. Results Compared with healthy controls, CBD group demonstrated asymmetrically decreased glucose metabolism mainly in the cere-bral hemisphere opposite to the more clinically affected body side, including the superior, middle and inferi-or frontal gyrus, the precentral gyrus, the superior and inferior parietal lobule, the angular gyrus, the supra-marginal gyrus, the precuneus, the middle occipital gyrus, the middle and inferior temporal gyrus, Heschl gyrus, the fusiform gyrus, the insula and the thalamus. And relatively increased glucose metabolism was present in ipsilateral precentral and postcentral gyrus, hippocampus, insula and putamen, bilateral cerebel-lum, paracentral lobules and pontine. The rCMRglc in those regions was significantly different between CBD patients and healthy controls (t values: 4.236-9.044, all P<0.01). Conclusion The asymmetric cerebral glucose metabolism features in CBD based on 18 F-FDG PET imaging contribute to the differential diagnosis between CBD patients and healthy subjects.

Axonal injury and repair mechanism after ischemic stroke / 国际脑血管病杂志

The process of axonal injury after ischemic stroke can be roughly divided into three stages. Each stage has its different temporal and spatial pattern, as well as unique molecular cascade reactions. The process of axonal injury is also related to ischemic stroke subtype, and the treatment must be adjusted accordingly. Axon-glial intercellular neurotransmitter-energy metabolism coupling disorder and Ca2 + overload-mediated apoptosis-like degeneration are the main mechanisms of early axonal injury after stroke. Axonal regeneration and remyelination of damaged axons after stroke play an important role for the recovery of neurological function. Elucidating the axonal injury and repair mechanism after stroke can provide a new strategy for stroke treatment.

Imaging of secondary damage in remote regions after focal cerebral infarction / 国际脑血管病杂志

After ischemic stroke, secondary damages such as neuron loss, gliosis, and axonal degeneration occur in the nonischemic remote brain regions that have synaptic connections with the primary infarction site.These secondary damages in the remote brain regions may affect the recovery of neurological function.Several advanced neuroimaging techniques have been used to detect these secondary damages.This article reviews the research progress in this field.

Dynamic changes of cathepsin B expression in the ipsilateral thalamus after cerebral cortical infarction in rats / 国际脑血管病杂志

ObjectiveTo investigate the expression change of cathepsin B (CathB) in the ventroposterior nucleus (VPN) of the ipsilateral thalamus after cortical infarction in rats.MethodsThe adult male Sprague-Dawley rats were randomly divided into either a sham operation group or a model group.The latter was further divided into postoperative 1-, 2-, 3-, 4-, and 8-week groups.A model of cerebral cortical infarction was induced by electrocoagulation the cortical branch of middle cerebral artery.Immunohistochemical staining and immunofluorescence were used to detect the protein expression and cellular localization of CathB in the VPN at each time point.ResultsThe expression level of VPN CathB in thalamus increased gradually after cerebral cortical infarction.It reached the peak at 4 weeks, and decreased at 8 weeks, however it was still higher than the control group (all P<0.05).The release of CathB from the lysosomes into the cytoplasm were found.In addition, the expression level of CathB in the activated astrocytes was significantly increased at 3 weeks after cerebral cortical infarction.ConclusionsDuring 1-8 week after cerebral cortex infarction, CathB in the VPN of the ipsilateral thalamus maintained higher expression level, suggesting that it might play a certain role in secondary degeneration in the thalamus after cerebral cortical infarction.

Neural Ablation and Regeneration in Pain Practice

A nerve block is an effective tool for diagnostic and therapeutic methods. If a diagnostic nerve block is successful for pain relief and the subsequent therapeutic nerve block is effective for only a limited duration, the next step that should be considered is a nerve ablation or modulation. The nerve ablation causes iatrogenic neural degeneration aiming only for sensory or sympathetic denervation without motor deficits. Nerve ablation produces the interruption of axonal continuity, degeneration of nerve fibers distal to the lesion (Wallerian degeneration), and the eventual death of axotomized neurons. The nerve ablation methods currently available for resection/removal of innervation are performed by either chemical or thermal ablation. Meanwhile, the nerve modulation method for interruption of innervation is performed using an electromagnetic field of pulsed radiofrequency. According to Sunderland's classification, it is first and foremost suggested that current neural ablations produce third degree peripheral nerve injury (PNI) to the myelin, axon, and endoneurium without any disruption of the fascicular arrangement, perineurium, and epineurium. The merit of Sunderland's third degree PNI is to produce a reversible injury. However, its shortcoming is the recurrence of pain and the necessity of repeated ablative procedures. The molecular mechanisms related to axonal regeneration after injury include cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules, and their receptors. It is essential to establish a safe, long-standing denervation method without any complications in future practices based on the mechanisms of nerve degeneration as well as following regeneration.

The impaired activity of sensory afferent nerves in diabetes mellitus of rats in acute myocardial ischemia and reperfusion / 临床麻醉学杂志

Objective The aim of the study was to investigate the diabetic neuro-degeneration and its changes in neuroreaction to myocardial ischemia and reperfusion,by evaluation of the altera-tion of noxious thermal threshold and expression of substance P (SP),calcitonin gene related peptide (CGRP)in dorsal root ganglia in upper thoracic segments (T1-5 )in diabetic rats.Methods Thirty two male Sprague-Dawley rats,weighing 180-200g,were randomly divided into control group (group C)and diabetic group (group DM),1 6 rats in each group.rats in DM group were fed with high sug-ar-fat diet for 14 weeks and were given streptozotocin (STZ,35 mg/mg,i.p.)at the end of the 4 th week,to set up diabetes experimental model.The animals in control group were fed with standard la-boratory diet.Tail flick latency to thermal stimulation was measured weekly.At the end of 10 weeks after administration of STZ,diabetic rats (and rats in control group)were further divided into myo-cardial ischemia-reperfusion group (group IR)and sham operation group (group Sham).The left an-terior descending branch of coronary artery was occluded for 30 min followed by reperfusion for 120 min,establishing myocardial ischemia-reperfusion.The histological immunofluorescence assay and Enzyme-linked immunosorbent assay (ELISA)were carried out to evaluate the changes of the expres-sions of CGRP and SP in the dorsal root ganglia.Results The tail flick latency was significantly in-creased in group DM,compared to the group C (P < 0.01).The immunoreactive materials for CGRP and SP in the sensory neurons in dorsal root ganglia of upper thoracic segments (T1-5 )were markedly declined in group DM (P <0.01 or P < 0.05).Furthermore,levels of SP and CGRP were signifi-cantly lower in the DRG of the group IR after myocardial ischemia-reperfusion,compared to that in the group sham (P <0.01).Conclusion Diabetes causes sensory denervation and obvious reduction of expression of SP and CGRP in the sensory neuron innervating heart during myocardial ischemia-reper-fusion,indicating impairment of adaptive reactivity of neuro-endocrine function of cardiac sensory nerves.

Neural complications and physical disabilities in leprosy in a capital of northeastern Brazil with high endemicity / Complicações neurais e incapacidades em hanseníase em capital do nordeste brasileiro com alta endemicidade

INTRODUCTION: Leprosy is an infectious disease whose etiologic agent is Mycobacterium leprae, manifested by dermatological and neurological signs and symptoms. OBJECTIVE: To investigate neural changes and the degree of physical disability in the eyes, hands and feet before and after treatment, as well as sociodemographic and clinical profile of patients affected by leprosy. METHOD: A longitudinal epidemiological study comprising 155 patients with leprosy, from a spontaneous demand, diagnosed between March 2010 and February 2011, and treated with multidrug therapy (MDT) between March 2010 and July 2012 in a program for leprosy eradication in São Luis (MA), Brazil. RESULTS: Before treatment, 46.5% of patients were considered as borderline, 51.6% had some alteration in the eyes and 52.3% in the feet, and the radial nerve (18.7%) was the most affected. There was a statistically significant difference between the changes in the radial nerve at the beginning of and after treatment. CONCLUSIONS: The analysis points to late diagnosis, as some patients have had abnormal neural and physical disabilities before treatment. .

INTRODUÇÃO: A hanseníase é uma doença infectocontagiosa cujo agente etiológico é o Mycobacterium leprae, que se manifesta por sinais e sintomas dermatoneurológicos. OBJETIVO: investigar as complicações neurais e o grau de incapacidades físicas nos olhos, mãos e pés antes e após o tratamento, bem como o perfil sociodemográfico e clínico dos pacientes acometidos pela hanseníase. MÉTODO: Estudo epidemiológico do tipo longitudinal constituído por 155 pacientes com hanseníase, a partir da demanda espontânea, diagnosticados no período de março de 2010 a fevereiro de 2011 e tratados com poliquimioterapia (PQT) entre março de 2010 a julho de 2012, em um programa de eliminação da hanseníase, no município de São Luís (MA). RESULTADOS: Antes do tratamento, 46,5% dos pacientes apresentaram forma dimorfa, 51,6% possuíam alguma alteração nos olhos e 52,3% nos pés, sendo o nervo radial (18,7%) o mais acometido. Houve diferença estatisticamente significante entre as complicações do nervo radial no inicio e após o tratamento. CONCLUSÕES: Evidenciou-se a presença do diagnóstico tardio, posto que alguns pacientes já apresentavam complicações neurais e incapacidades físicas antes do tratamento. .

Therapeutic applications of umbilical cord mesenchymal stem cells in Parkinson’s disease / 中国组织工程研究

BACKGROUND:Animal experiments have repeatedly verified that umbilical cord stem celltransplantation can improve the rotational behavior of rats with Parkinson’s disease, with lower immune rejection response. OBJECTIVE:To evaluate the therapeutic effects of human umbilical cord mesenchymal stem celltransplantation in the treatment of Parkinson’s disease using the Unified Parkinson’s Disease Rating Scale. METHODS:Fifteen patients with Parkinson’s disease were enrol ed, including 8 males and 7 females, aged 52-76 years. Hoehn&Yahr staging was 3-5. After informed consent was obtained from puerperae and the procedure was approved by the hospital ethics committee, ful-term maternal umbilical cord was aseptical y col ected, to culture umbilical cord mesenchymal stem cells. Al patients were hospitalized, and treated with human umbilical cord mesenchymal stem celltransplantation via carotid artery puncture. Neurological function of patients was assessed using a comprehensive rating scale for Parkinson’s disease before and 1 month after cells transplantation. Higher score indicated more severe neurological deficits. RESULTS AND CONCLUSION:Fifteen patients entered the result analysis. Compared with before transplantation, 15 patients showed significantly lowered scores on the Unified Parkinson’s Disease Rating Scale at 1 month after transplantation (P<0.05). The improvement was mainly concentrated in the tremor and rigidity, but bradykinesia and unstable position were not improved. Graft versus host disease did not occur in al 15 cases. These findings indicate that umbilical cord blood mesenchymal stem celltransplantation for treating Parkinson’s disease has obvious curative effects and significantly improves neurological functions.

Microtubule-Targeting Agents Enter the Central Nervous System (CNS): Double-edged Swords for Treating CNS Injury and Disease / 대한배뇨장애요실금학회지

Microtubules have been among the most successful targets in anticancer therapy and a large number of microtubule-targeting agents (MTAs) are in various stages of clinical development for the treatment of several malignancies. Given that injury and diseases in the central nervous system (CNS) are accompanied by acute or chronic disruption of the structural integrity of neurons and that microtubules provide structural support for the nervous system at cellular and intracellular levels, microtubules are emerging as potential therapeutic targets for treating CNS disorders. It has been postulated that exogenous application of MTAs might prevent the breakdown or degradation of microtubules after injury or during neurodegeneration, which will thereby aid in preserving the structural integrity and function of the nervous system. Here we review recent evidence that supports this notion and also discuss potential risks of targeting microtubules as a therapy for treating nerve injury and neurodegenerative diseases.

Análisis comparativo de marcadores de lesión en modelos de isquemia cerebral focal y global en ratas / Injury markers in two models of cerebral ischemia

Introducción. Los indicadores espacio-temporales de lesión son esenciales en el estudio neuropatológico y terapéutico de la isquemia cerebral. Objetivo. Optimizar la técnica de dos modelos de isquemia cerebral (focal y global) y hacer un análisis comparativo de la progresión del daño cerebral, mediante marcadores de neurodegeneración. Materiales y métodos. Se sometieron ratas Wistar a oclusión temporal de la arteria cerebral media o a oclusión de cuatro vasos, y se evaluaron comparativamente el tiempo quirúrgico, la tasa de supervivencia y la recuperación neurológica. Se utilizó trifenilo de tetrazolio para establecer la distribución del infarto y tinción con Fluoro - Jade B ® como marcador de neurodegeneración. La inmunorreacción de la astroglía se evaluó con el anticuerpo contra la proteína acídica fibrilar de la glía ( Glial Fibrillary Acidic Protein, GFAP) y el anticuerpo AT-8 contra la proteína tau hiperfosforilada, 24, 48 y 72 horas después de la isquemia. Resultados. Los modelos de isquemia utilizados requirieron menor tiempo quirúrgico y hubo menor riesgo de muerte, respecto a estudios previos. En el modelo focal, las células positivas con Fluoro - Jade B ® y los astrocitos reactivos, se evidenciaron en corteza e hipocampo a las 24 horas después de la isquemia. En el modelo global, se observó tinción Fluoro - Jade B ® positiva a las 24 horas, aumentando significativamente la reacción de la GFAP a las 72 horas en corteza y a las 48 horas en el hipocampo. La reacción contra la proteína tau hiperfosforilada aumentó progresivamente y fue máxima a las 72 horas en ambos modelos. Conclusiones. Los dos modelos de isquemia cerebral, oclusión temporal de la arteria cerebral media y oclusión de cuatro vasos, fueron optimizados. En estos modelos, los marcadores la tinción Fluoro - Jade B ® y la GFAP permitieron detectar procesos de neurodegeneración 24 horas después de la isquemia, en tanto el marcador de proteína tau hiperfosforilada (AT-8) incrementó progresivamente su reacción hasta las 72 horas, lo cual sugiere la propagación de la excitotoxicidad y la alteración de enzimas implicadas en la fosforilación de proteínas del citoesqueleto.

Introduction: Spatio-temporal indicators of injury are essential for the study of neuropathological processes and for developing therapeutic approaches for stroke. Objective: This study sought to optimize the techniques of two cerebral ischemia models (focal and global) and to comparatively evaluate the progression of brain damage by analyzing markers of neurodegeneration. Materials and methods: Wistar rats were subjected to temporary occlusion of the middle cerebral artery (t-MCAO) or four-vessel occlusion (4-VO), and surgical time, survival rate and neurological recovery were comparatively evaluated. Triphenyl tetrazolium was used to determine the distribution of the infarction, and Fluoro-Jade B was used as a marker of neurodegeneration. Astroglial immunoreactivity was assessed with an anti-glial fibrillary acidic protein (GFAP) antibody, and an anti-AT-8 antibody was used to detect hyperphosphorylated tau protein at 24, 48 and 72 hours post-ischemia. Results: The cerebral ischemia models employed (t-MCAO and 4-VO) required less surgical time and presented less of a death risk compared to those in previous studies. In the focal model, Fluoro-Jadepositive cells and reactive astrocytes were observed in the cerebral cortex and the hippocampus at 24 hours post-ischemia. In the global model, we observed Fluoro-Jade-positive cells at 24 hours, and a significant increase in the reactivity of GFAP was observed at 72 hours in the cortex and at 48 hours in the hippocampus. The immunoreactivity of hyperphosphorylated tau protein increased progressively, reaching a maximum at 72 hours post-ischemia in both models. Conclusions: These results suggest that in the t-MCAO and 4-VO ischemia models, the expression of Fluoro-Jade and GFAP indicates early neurodegeneration at 24 hours post-insult. In contrast, the immunoreactivity of the hyperphosphorylated tau protein marker (AT-8) progressively increases until 72 hours post-insult, which suggests that the progression of excitotoxicity and alteration of enzymes involves the phosphorylation of cytoskeletal proteins.

Ultrastructural transneuronal degeneration study of axonal elements within the paratrigeminal nucleus in sinoaortic deafferented rats / Estudo ultraestrutural de degeneração transneuronal dos elementos axonais do núcleo paratrigeminal de ratos com desnervação sino-aórtica

Objective: Morphological study that searched to authenticate the presence of sinoaortic baroreceptor inputs within the dorsolateral medullary nucleus under electron microscopy analysis. Methods: After a 5-day survival period, 9 baroreceptor-denervated rats deeply anaesthetized with equithesin were transcardially perfused and their brains were histologically processed. Results: The neuronal cytoarchitecture of the paratrigeminal nucleus comprehends afferent projections from other nuclei that have a distributive character regarding visceral and nociceptive functions in the cardiovascular reflex integration response. Conclusion: The medial portion of the nucleus receives afferent projections of the rostral ventrolateral medulla, as shown by retrograde neurotracing studies. The present results show that the medial extent of the paratrigeminal nucleus contains degenerated axoplasmic cellular components in sinoaortic deafferented rats. The number of degenerated axonal fibers was also larger in this area of the nucleus.

Objetivo: Estudo morfológico que buscou verificar, por meio de microscopia eletrônica, a presença de aferências de receptores sino-aórticos em núcleo localizado na região dorso-lateral bulbar. Métodos: Após 5 dias de sobrevida, 9 ratos com desnervação sinoaórtica anestesiados com equitesina foram submetidos à perfusão transcardíaca, e o encéfalo de cada um deles foi processado histologicamente. Resultados: A citoarquitetura neuronal do núcleo paratrigeminal compreende projeções aferentes de outros núcleos que apresentam uma característica distributiva em relação às funções viscerais e nociceptivas na integração do reflexo cardiovascular. Conclusão: A porção medial do núcleo recebe projeções aferentes da região rostro-ventrolateral do troncoencefálico, confirmadas por meio de estudos com rastreadores neuronais. Os resultados indicam que a região medial do núcleo paratrigeminal contém o maior número de fibras axonais degeneradas.

Double-Peak Response in Orthodromic Sensory Nerve Conduction of the Median Nerve

OBJECTIVE: To understand the neural generator of double-peak potentials and the change of latency and amplitude of double peaks with aging. METHOD: In 50 healthy subjects made up of groups of 10 people per decade from the age of 20 to 60, orthodromic sensory nerve conduction studies were performed on the median nerves using submaximal stimulation. Various stimulus durations and interstimulation distances were used to obtain each double peak in the different age groups. The latency and amplitude of the second peak were measured. Statistical analyses included one-way ANOVA and correlation tests. p-values<0.05 were considered significant. RESULTS: When the cathode moved in a proximal direction, the interpeak intervals increased. Second peak amplitudes decreased, and second peak latencies were delayed with aging (p<0.05). In some older people, second peaks were not obtained. CONCLUSION: Our experiments indicate that the double-peak response represented the two stimulation sites under the cathode and anode. The delayed latency and decreased amplitude of the second peak that occurs with aging represented peripheral nerve degeneration in aging, which starts at the distal nerve.

The clinic manifestations and the changes of electromyogram in patients with chronic N2hexane intoxication / 中国基层医药

Objective To investigate the characteristics of the clinic manifestations and the electromyogram changes in patients with chronic N2hexane intoxication. Methods The clinic manifestations, the electromyography and nerve conduction velocities were analyzed in 9 patients with N2hexane intoxi2 cation. Results The main clinical manifestations of the disease were acroparesthesia and asthenia, especially in legs. The abnormality rate of electromyography in patients with N2hexane intoxication was 100%. The conduction velocity of the sensory nerve and the motor nerve decreased at a rate of 33.33% and 88.89% respectively. The distal latencies were prolonged( 100% ). The denervated electromyogram was 33.33%. Conclusion The main clinical manifestations of the disease were Peripheral neuropathy. The chronic N2hexane intoxication mainly led to the imparement, especially in the distal region of the motor nerve in legs,and the damages of the nerve could be related to the duration of exposure to N2hexane.

Sensory involvement in the SOD1-G93A mouse model of amyotrophic lateral sclerosis

A subset of patients of amyotrophic lateral sclerosis (ALS) present with mutation of Cu/Zn superoxide dismutase 1 (SOD1), and such mutants caused an ALS-like disorder when expressed in rodents. These findings implicated SOD1 in ALS pathogenesis and made the transgenic animals a widely used ALS model. However, previous studies of these animals have focused largely on motor neuron damage. We report herein that the spinal cords of mice expressing a human SOD1 mutant (hSOD1-G93A), besides showing typical destruction of motor neurons and axons, exhibit significant damage in the sensory system, including Wallerian-like degeneration in axons of dorsal root and dorsal funiculus, and mitochondrial damage in dorsal root ganglia neurons. Thus, hSOD1-G93A mutation causes both motor and sensory neuropathies, and as such the disease developed in the transgenic mice very closely resembles human ALS.

Novos conceitos em retinopatia diabética: dano neurológico versus dano vascular / New concepts on diabetic retinopathy: neural versus vascular damage

A retinopatia diabética é a principal causa de cegueira legal irreversível em adultos na idade produtiva. Estima-se que o número de pessoas com risco de desenvolver perda de visão decorrente do diabetes dobre nos próximos 30 anos. Alguns estudos sugerem que alterações neurodegenerativas ocorram antes do comprometimento vascular. Essas alterações incluem aumento da apoptose neural, reatividade de células gliais, ativação microglial e metabolismo alterado do glutamato, e podem explicar algumas das deficiências funcionais que ocorrem logo após o início do diabetes, como alterações precoces no eletrorretinograma. O presente artigo de revisão visa apresentar evidências atuais que apontem a neurodegeneração como possível evento inicial da retinopatia diabética.

Diabetic retinopathy is the leading cause of irreversible legal blindness in working-age adults. The number of people worldwide at risk of developing vision loss from diabetes is predicted to double over the next 30 years. Some elements suggest that neurodegenerative changes occur beyond vascular damage. These changes include increased apoptosis, glial cell reactivity, microglial activation, and altered glutamate metabolism, and could explain some of the functional abnormalities that begin soon after the onset of diabetes, as early changes in electroretinogram. This review article will present some evidences that point out neurodegeneration as a possible initial event in diabetic retinopathy.