International Journal of Neuroscience

doi: 10.1080/00207454.2018.1431005pmid: 29447590

Chen, Jianhuai; Chen, Yun; Gao, Qingqiang; Chen, Guotao; Dai, Yutian; Yao, Zhijian; Lu, Qing

doi: 10.1080/00207454.2017.1387116pmid: 28969487

Aim: Despite increasing understanding of the cerebral functional changes and structural abnormalities in erectile dysfunction, alterations in the topological organization of brain networks underlying psychogenic erectile dysfunction remain unclear.Materials and methods: Here, based on the diffusion tensor image data of 25 patients and 26 healthy controls, we investigated the topological organization of brain structural networks and its correlations with the clinical variables using the graph theoretical analysis.Results: Patients displayed a preserved overall small-world organization and exhibited a less connectivity strength in the left inferior frontal gyrus, amygdale and the right inferior temporal gyrus. Moreover, an abnormal hub pattern was observed in patients, which might disturb the information interactions of the remaining brain network. Additionally, the clustering coefficient of the left hippocampus was positively correlated with the duration of patients and the normalized betweenness centrality of the right anterior cingulate gyrus and the left calcarine fissure were negatively correlated with the sum scores of the 17-item Hamilton Depression Rating Scale.Conclusions: These findings suggested that the damaged white matter and the abnormal hub distribution of the left prefrontal and limbic cortex might contribute to the pathogenesis of psychogenic erectile dysfunction and provided new insights into the understanding of the pathophysiological mechanisms of psychogenic erectile dysfunction.

Jahanshahi, M.; Nikmahzar, E.; Elyasi, L.; Babakordi, F.; Hooshmand, E.

doi: 10.1080/00207454.2017.1389926pmid: 29064725

Objective: Despite the important role of α2-adrenoceptors in pain modulation processes, the impact of administration of α2-adrenoceptor agonist and antagonist on the density of hippocampal α2-adrenoceptor-immunoreactive neurons has not been investigated. Therefore, we aimed to determine the effect of single doses of clonidine and yohimbine on the density of α2-adrenoceptor-immunoreactive neurons in rat hippocampus.Materials and Methods: Adult male Wistar rats received a single dose of clonidine (0.7 mg/kg) alone or 5 min after intraperitoneal (1 mg/kg) and/or intracerebroventricular (5 µg/kg) injection of yohimbine. After histological processing, neurons with α2-adrenoceptor immunoreactivity were identified and counted through immunohistochemical analysis of hippocampal regions.Results: Clonidine slightly increased the number of α2-adrenoceptor-immunoreactive neurons in the hippocampal subregions compared with the normal saline group. Intraperitoneal injection of yohimbine followed by injection of clonidine significantly increased the number of α2-adrenoceptor-immunoreactive neurons in subregions cornu ammonis 1 (CA1) and cornu ammonis 3 (CA3). Intracerebroventricular injection of yohimbine after injection of clonidine significantly reduced the number of α2-adrenoceptor-immunoreactive neurons in all hippocampal subregions.Conclusion: The present study demonstrates that intraperitoneal administration of α2-adrenoceptor agonist clonidine increases the density of α2-adrenoceptor-immunoreactive neurons in rat hippocampus, while intracerebroventricular injection of yohimbine decreases the density of these neurons.

Hara, Takatoshi; Abo, Masahiro; Hara, Hiroyoshi; Kobayashi, Kazushige; Shimamoto, Yusuke; Shibata, Yamato; Sasaki, Nobuyuki; Yamada, Naoki; Niimi, Masachika

doi: 10.1080/00207454.2017.1389927pmid: 28985683

Tezer, F. Irsel; Firat, Aysegul; Tuzun, Erdem; Unal, Isik; Soylemezoglu, Figen; Bilginer, Burcak; Kaymaz, Figen; Oguz, Kader K.; Saygi, Serap

doi: 10.1080/00207454.2017.1389928pmid: 28988523

Purpose: There is evidence that autoimmunity has a specific role in temporal lobe seizures of limbic encephalitis patients. Our aim in this study was to investigate any histopathological clues of autoimmune process in refractory temporal lobe epilepsy (TLE) patients with different pathologically proven hippocampal sclerosis (HS) types.Methods: 22 patients who had undergone epilepsy surgery due to mesial TLE-HS were included. The sera of patients are tested for neuronal antibodies to N-methyl-D-aspartate receptors (NMDAR), leucine-rich, glioma inactivated 1 (LGI1), contactin-associated protein 2 (CASPR2), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), gamma-aminobutyric acid B receptor (GABABR) and glutamic acid decarboxylase (GAD). Pathological and immunohistochemical investigations including neuronal nuclei (NeuN), NMDAR, GAD, glial fibrillary acidic protein (GFAP), CD8+-CD3+ lymphocytes and immunoglobulin G (IgG) were done. Patients were grouped according to type of HS. Clinical features and immunohistochemical changes were defined in these groups.Results: Available sera of 15 patients did not have any neuronal antibodies. Thirteen of 22 patients had HS type 1, three had HS type 2 and two had HS type 3. According to immunohistochemical investigations CD3+ and CD8+ T cell infiltration was more prominent in the hippocampus of patients with classical HS (International League Against Epilepsy (ILAE) Type 1 HS) and there was a significant negative correlation between epilepsy duration and numbers of CD3+-CD8+ lymphocytes in temporal lobe parenchyma.Conclusion: The role of T cell-mediated immunopathology and immunopathological difference in a variety of drug resistant TLE-H2S patients was suggested. These findings can be helpful in understanding the epileptogenicity of HS.

Ke, Zunyu; Zhao, Yu; Wang, Chuanling; Cai, Zhiyou

doi: 10.1080/00207454.2017.1393419pmid: 29034755

Purpose/aim of the study: Various factors are believed to be involved in the etiology of cerebral infarction. Anemia has been shown to deteriorate in association with ischemic stroke. However, the exact clinical association between anemia and ischemic stroke still remains unclear. We evaluated the clinical features of adult anemia patients with acute cerebral infarction and seek a better treatment different from the other causes of cerebral infarction, and to provide a reference for the diagnosis and treatment of these anemia patients with acute cerebral infarction.Methods: Thirty-two adult patients of acute cerebral infarction with anemia were included in this study. A primary discharge diagnosis of acute cerebral infarction with anemia was done, and all subjects were evaluated as retrospective data. The clinical features were analyzed. A chi-square test was used to analyze the associations between different variables. Therapeutic interventions and outcomes were analyzed under t-test, compared between the two groups.Results: The NIHSS score in the patients with the administration of EBV/CA (Expanding blood volume and correcting anemia) more lowed than Non-EBV/CA in 7 days and 14 days after initial hospitalization. The mRS score in the patients with the administration of EBV/CA also more lowed than Non-EBV/CA in 14 days. Moreover, the correlation between Hb-serum-level and NIHSS scores in the time of initial hospitalization is negative significantly.Conclusions: Anemia is associated with increased neuronal damage and deterioration of acute cerebral infarction in the adults. Expanding blood volume and correcting anemia are effective therapeutic measures in the adult patients of acute cerebral infarctions with anemia.

Needle, Alan R.; Baumeister, Jochen; Farquhar, William B.; Greaney, Jody L.; Higginson, Jill S.; Kaminski, Thomas W.; Swanik, C. Buz

doi: 10.1080/00207454.2017.1396219pmid: 29057701

Purpose: Maintaining joint stability is dependent on the ability of the nervous system to sense and react to potentially injurious loads. In attempts to understand the neurophysiologic mechanisms underlying joint stability, this afferent and efferent activity has been quantified separately at the cortical, segmental and peripheral levels using various electrophysiologic techniques in vivo. However, no studies have attempted to quantify sensory and motor activation at multiple levels of the nervous system in a single subset, to understand potential adaptations for optimizing joint stability.Materials and Methods: Muscle spindle afferent activity and sensory cortex event-related desynchronization were quantified during ankle-joint loading; and motor excitability was assessed through transcranial magnetic stimulation and the Hoffmann reflex in a subset of 42 able-bodied individuals. Microneurography and electroencephalography were used to collect the muscle spindle afferent and sensory cortex activation, respectively, as joint load was applied using an ankle arthrometer. Separately, motor-evoked potentials were obtained from the tibialis anterior (TA) and soleus (SOL) using transcranial magnetic stimulation over the motor cortex, and compared to the reflexive responses evoked via sciatic nerve electrical stimulation.Results: Correlation coefficients revealed significant correlations between the motor threshold of the soleus and early muscle spindle afferent activity (r = −0.494) and early cortical event-related desynchronization (r = 0.470), as well as tibialis anterior motor-evoked potential size and late muscle spindle afferent activity (r = 0.499).Conclusions: The results of this study highlight the nervous system's capability to offset motor output based on the volume of sensory input at the segmental and cortical levels.

Sun, Bo; Li, Yifan; Liu, Lizhi; Chen, Zhaohui; Ling, Li; Yang, Fei; Liu, Jiexiao; Liu, Hong; Huang, Xusheng

doi: 10.1080/00207454.2017.1398152pmid: 29077516

Purpose/aim of the study: To date, there are no validated screening scales for small fibre neuropathy. This study investigated the small-fibre neuropathy and the symptom inventory questionnaire as well as the small fibre neuropathy screening list for small fibre neuropathy diagnosis.Methods: Fifty-five patients were divided into small fibre neuropathy and mixed fibre damage groups. Relevant scales, nerve conduction studies and skin biopsies were performed. Relationships between the intraepidermal nerve fibre density and different scales as well as the diagnostic and cut-off values (score at which Youden's index is largest) were determined.Results: Compared with healthy Chinese participants, 20 patients were diagnosed with small fibre neuropathy. Intraepidermal nerve fibre density was moderately and highly correlated with the small fibre neuropathy–symptom inventory questionnaire and small fibre neuropathy screening list, respectively. The diagnostic values were moderate and high for the small fibre neuropathy–symptom inventory questionnaire (cut-off value = 5, sensitivity = 80%, specificity = 81.8%) and small fibre neuropathy screening list (cut-off value = 8, sensitivity = 94.1%, specificity = 90.9%), respectively. There were no significant differences in the visual analogue scale between the small fibre neuropathy group, mixed small and large fibre neuropathy group, pure large fibre neuropathy group and the normal group.Conclusion: Small fibre neuropathy–symptom inventory questionnaire and small fibre neuropathy screening list represent potential small fibre neuropathy screening tools. AbbreviationsEMGelectromyographyENAanti-extractable nuclear antigensESRerythrocyte sedimentation rateIENFDintraepidermal nerve fibre densityIGTimpaired glucose toleranceNCSnerve conduction studiesNDSneuropathy disability scoreOGTToral glucose tolerance testPGPprotein gene productPNperipheral neuropathyROCreceiver operating characteristic curveROC-AUCarea under the ROC curveSFNsmall fibre neuropathySFN–SIQsmall-fibre neuropathy and symptom inventory questionnaireSFNSLsmall fibre neuropathy screening listVASvisual analogue scaleWHOWorld Health Organization

Som Chaudhury, Sutapa; Das Mukhopadhyay, Chitrangada

doi: 10.1080/00207454.2017.1398153pmid: 29076790

Misfolded β-sheet structures of proteins leading to neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) are in the spotlight since long. However, not much was known about the functional amyloids till the last decade. Researchers have become increasingly more concerned with the degree of involvement of these functional amyloids in human physiology. Interestingly, it has been found that the human body is exposed to a tremendous systemic amyloid burden, especially, during aging. Although many findings regarding these functional amyloids come up every day, some questions still remain unanswered like do these functional amyloids directly involve in the fibrillization of amyloid beta (Aβ) 42 peptide or enhance the Aβ42 aggregation rate; whether functional bacterial amyloids (FuBA) co-localize with the senile plaques of AD or not. A detailed review of the latest status regarding the interrelationship between functional amyloids, pathogenic amyloids and misfolded prions and therapeutic assessment of functional amyloids for the treatment of neurodegenerative diseases can help identify an alternative medication for neurodegeneration. A unique mathematical model is proposed here for alteration of Aβ42 aggregation kinetics in AD to carve out the future direction of therapeutic consideration.

Casciato, Sara; D'Aniello, Alfredo; Mascia, Addolorata; Quarato, Pier Paolo; De Risi, Marco; Grammaldo, Liliana G.; Esposito, Vincenzo; Zoccarato, Marco; Di Gennaro, Giancarlo

doi: 10.1080/00207454.2017.1394852pmid: 29053037