The relationship between the interictal epileptiform discharge source connectivity and cortical structural couplings in temporal lobe epilepsy.

Objective: The objective of this study was to explore the relation between interictal epileptiform discharge (IED) source connectivity and cortical structural couplings (SCs) in temporal lobe epilepsy (TLE). Methods: High-resolution 3D-MRI and 32-sensor EEG data from 59 patients with TLE were collected. Principal component analysis was performed on the morphological data on MRI to obtain the cortical SCs. IEDs were labeled from EEG data and averaged. The standard low-resolution electromagnetic tomography analysis was performed to locate the source of the average IEDs. Phase-locked value was used to evaluate the IED source connectivity. Finally, correlation analysis was used to compare the IED source connectivity and the cortical SCs. Results: The features of the cortical morphology in left and right TLE were similar across four cortical SCs, which could be mainly described as the default mode network, limbic regions, connections bilateral medial temporal, and connections through the ipsilateral insula. The IED source connectivity at the regions of interest was negatively correlated with the corresponding cortical SCs. Significance: The cortical SCs were confirmed to be negatively related to IED source connectivity in patients with TLE as detected with MRI and EEG coregistered data. These findings suggest the important role of intervening IEDs in treating TLE.

Characterizing Cerebral Imaging and Electroclinical Features of Five Pseudohypoparathyroidism Cases Presenting with Epileptic Seizures.

Objective: To characterize the cerebral imaging and electroclinical features and investigate their etiological contributions to seizures in pseudoparathyroidism (PHP). Methods: The clinical symptoms, biochemical imaging by magnetic resonance imaging (MRI) and computed tomography (CT) tests, and electroencephalogram (EEG) manifestations of five PHP patients with seizures were retrospectively collected and analyzed. Results: Physical examination showed an average stature in cases 2~4 and short stature in cases 1 and 5. X-ray tests suggested ectopic calcification in four patients. The seizures in four cases were effectively controlled with antiseizure medicines (ASMs). Cerebral CT scans showed extensive brain calcifications in the bilateral basal ganglia (all five cases), cerebellum (cases 1, 3, and 5), thalamus (case 4), and cerebral cortex. Cerebral MRI showed short T1 signals mainly in the basal ganglia. EEG records revealed focal EEG abnormalities, including abnormal slow waves and epileptiform discharges, mainly over the temporal and frontal lobes. The brain areas with focal EEG abnormalities and calcification did not always coincide. Conclusion: The seizures in PHP can be focal to bilateral tonic-clonic. ASMs are effective in epilepsy combined with PHP. Intracranial calcification is not a reliable etiological cause of epilepsy in PHP patients.

Brain structural connectivity sub typing in unilateral temporal lobe epilepsy.

To categorize and clinically characterize subtypes of brain structural connectivity patterns in unilateral temporal lobe epilepsy (TLE). Voxel based morphometry (VBM) and surfaced based morphometry (SBM) analysis were used to detect brain structural alterations associated with TLE from MRI data. Principal component analysis (PCA) was performed to identify subtypes of brain structural connectivity patterns. Correlation analysis was used to explore associations between PC scores and clinical characteristics. A total of 59 patients with TLE and 100 healthy adults were included in this study. Widespread cortical atrophy was shown in both left and right TLE (P < 0.05, FWE corrected). Six principal components (PCs) that explained more than 70% of the variance were extracted for left and right TLE, reflecting patterns of brain structural connectivity. PCs representing perisylvian connectivity were positively correlated with verbal IQ (left TLE: r = 0.696, P < 0.001; right TLE: r = 0.484, P = 0.012) and total IQ (left TLE r = 0.608, P < 0.001) and negatively correlated with disease duration (r = -0.448, P = 0.009). In left TLE, the PC in the ipsilateral mesial temporal region was negatively correlated with age at onset (r = -0.382, P = 0.028). In right TLE, the PC representing the default mode network was negatively correlated with number of antiepileptic drugs (r = -0.407, P = 0.039). This study categorized subtypes of unilateral TLE based on brain structural connectivity patterns. Findings may provide insight into seizure pathways, the pathophysiology of epilepsy, including comorbidities such as cognitive impairment, and help predict treatment outcomes.

Structural brain assessment of temporal lobe epilepsy based on voxel-based and surface-based morphological features.

AIM OF THE STUDY: This study aimed to assess the cerebral voxel-based and surface-based morphological abnormalities of patients with temporal lobe epilepsy (TLE). MATERIALS AND METHODS: A total of 100 healthy adults and 73 patients with TLE were enrolled in this study, and their 3D T1-weighted MRI data were collected. Voxel-based morphology (VBM) and surface-based morphology (SBM) tools were used to compare the morphological differences between healthy adults and patients with TLE. Receiver-operating characteristic (ROC) curves were used to acquire the boundary values for detecting morphological abnormalities in regions of interest from the corrected VBM and SBM analysis. RESULTS: Our results showed that cortical voxels and decreased thickness areas were located in the widespread cortex and subcortical structures in the TLE group. However, after completing the analysis, we found that the left-TLE lesions were limited to the left temporal pole and left hippocampus, while the right-TLE lesions were located in the bilateral medial temporal lobe, including the right hippocampus and bilateral amygdala. ROC-curve results showed that the volume of the left hippocampus at 4,124.45 mm3 and the thickness of the left temporal pole cortex at 3.50 mm could be used as optimal boundary values based on the curves of the left-TLE group. The right-TLE group curves were poor. CONCLUSIONS: Widespread cerebral morphological TLE abnormalities were represented in this study. However, the lesions may be limited after completing a corrected comparison with clinical information. Boundary values of left-TLE group lesions were also obtained.

MiR-21b-3p protects NS2OY cells against oxygen-glucose deprivation/reperfusion-induced injury by down-regulating cyclooxygenase-2.

Recent studies have shown abnormal expression levels of cyclooxygenase-2 (COX-2) and miR-21b-3p in cerebral ischemia-reperfusion (I/R) rat models. Decreased COX-2 expression could reduce brain injury and thus could be a target of miR-21b-3p according to the miRNA databases (miRDB) analysis. However, its functions and underlying mechanisms in I/R injury remain unclear. In our study, we have established an oxygen/glucose deprivation and reperfusion (OGD/R) model by using NS2OY cells. The expression of miR-21b-3p and COX-2 was determined by quantitative real-time PCR or Western blot, and the fluorescence intensities were detected by fluorescence in situ hybridization (FISH) or immunofluorescence. After transfection and OGD/R treatments, the functions of miR-21b-3p and COX-2 on cell viability and apoptosis were detected using cell-counting kit 8, Edu staining, flow cytometry and Hoechst staining, respectively. Finally, dual-luciferase reporter assay was used to explore the relationship between miR-21-b-3p and COX-2. The results have showed that COX-2 mRNA and protein expression were significantly increased; however, the expression of miR-21b-3p was remarkably reduced in NS2OY cells after OGD/R treatment. The changes were most remarkable in OGD 2 h/R24 group. Function analysis has showed that when NS2OY cells were exposed to OGD/R injury, overexpressed miR-21b-3p significantly downregulated COX-2 expression, increased cell viability and decreased apoptosis. In addition, knocking down the expression of COX-2 could also increase cell viability and decrease apoptosis. Dual-luciferase reporter assays showed miR-21b-3p as the target of 3'-UTR of COX-2. Therefore, we concluded that OGD/R-induced injury by down-regulating COX-2.

CT-Guided Chemical Thoracic Sympathectomy versus Botulinum Toxin Type A Injection for Palmar Hyperhidrosis.

BACKGROUND: The present study aimed to evaluate and compare the efficacy of botulinum toxin type A (BTX-A) injection versus thoracic sympathectomy for idiopathic palmar hyperhidrosis. METHODS: Fifty-one patients with idiopathic palmar hyperhidrosis were treated with either BTX-A injection or thoracic sympathectomy between March 2013 and April 2016. The severity of palmar hyperhidrosis was qualitatively measured via the Hyperhidrosis Disease Severity Scale (HDSS). All patients completed a questionnaire that detailed the time taken for the treatment to work, local or systemic adverse effects, and pre- and post-treatment severity of hyperhidrosis. The efficacy and adverse effects of the two treatments were compared and analyzed. RESULTS: Hyperhidrosis-related quality of life improved quickly and significantly in the BTX-A group (26 patients) and the sympathectomy group (25 patients). Compared with pre-treatment, the HDSS score significantly reduced after treatment in both groups (p < 0.05). All patients in the sympathectomy group had cessation of sweating of the hands after treatment, and this curative effect lasted for 12 months. In contrast, the treatment took more time to work in the BTX-A group, and the curative effect lasted for a much shorter period (3 months). The sympathectomy group had a significantly lesser mean HDSS score than the BTX-A group at 1 week, 3 months, 6 months, 9 months, and 12 months after treatment (p < 0.05). The sympathectomy group experienced more complications than the BTX-A group. CONCLUSION: For palmar hyperhidrosis, thoracic sympathectomy is more effective and has a longer lasting curative effect than BTX-A injection, but thoracic sympathectomy has more complications.

Magnetic resonance diffusion tensor imaging following major ozonated autohemotherapy for treatment of acute cerebral infarction.

Major ozonated autohemotherapy has been shown to promote recovery of upper limb motor function in patients with acute cerebral infarction, but whether major ozonated autohemotherapy affects remote injury remains poorly understood. Here, we assumed that major ozonated autohemotherapy contributes to recovery of clinical function, possibly by reducing remote injury after acute cerebral infarction. Sixty acute cerebral infarction patients aged 30-80 years were equally and randomly allocated to ozone treatment and control groups. Patients in the ozone treatment group received medical treatment and major ozonated autohemotherapy (47 mg/L, 100 mL ozone) for 10 ± 2 days. Patients in the control group received medical treatment only. National Institutes of Health Stroke Scale score, modified Rankin scale score, and reduced degree of fractional anisotropy values of brain magnetic resonance diffusion tensor imaging were remarkably decreased, brain function improved, clinical efficiency significantly increased, and no obvious adverse reactions detected in the ozone treatment group compared with the control group. These findings suggest that major ozonated autohemotherapy promotes recovery of neurological function in acute cerebral infarction patients by reducing remote injury, and additionally, exhibits high safety.

Antinociceptive effects of endomorphin-2: suppression of substance P release in the inflammatory pain model rat.

Endomorphin-2 (EM2) and Substance P (SP) exert suppressive and facilitative influences upon nociception, respectively. Although EM2 and SP were often co-expressed in single neurons in dorsal root ganglion (DRG), it is still unknown if and how the nociception-suppressive influences of EM2 might be exerted upon nociception-facilitative effects of SP in the DRG neurons. We examined these issues in the inflammatory pain model rats produced by subcutaneous injection of the complete Freund's adjuvant into the hind paw. The paw withdrawal threshold for mechanical allodynia was measured. Changes of EM2 and SP release were estimated by measuring intrathecal levels of EM2 and SP through in vivo microdialysis analysis of cerebrospinal fluid. The mechanical allodynia was dose-dependently attenuated by intrathecal injection of EM2 or a neurokinin-1 receptor antagonist, and facilitated by intrathecal injection of SP or a mu-opioid receptor (MOR) antagonist. Importantly, intrathecal level of SP was found to be lowered by intrathecal injection of EM2. Morphologically, colocalization of EM2-, MOR- and SP-immunoreactivity in single DRG neurons was observed by immunofluorescent histochemistry, and co-expression of EM2 and SP in large, dense-cored presynaptic vesicles in primary afferents, as well as localization of MOR on pre- and postsynaptic membrane in spinal dorsal horn, was also confirmed electron miscroscopically. Thus, the results indicated that analgesic influences of EM2 upon inflammatory pain might be exerted through suppression of SP release, supporting the assumptions that binding of EM2 to presynaptic MOR might induce such effects.

The relationship between single nucleotide polymorphisms of the NTRK2 gene and sporadic Alzheimer's disease in the Chinese Han population.

Alzheimer's disease (AD) is characterized by the degeneration of basal forebrain cholinergic neurons, whose survival and function are affected by neurotrophins and their receptors. The impaired signaling pathway of brain-derived neurotrophic factor/tropomyosin-related kinase B (BDNF/TrkB) is considered to play an important role in AD pathogenesis. To explore the association of polymorphisms within the NTRK2 gene (encoding TrkB) and sporadic AD (sAD), a case-control study was conducted in a Chinese Han cohort including 216 sAD patients and 244 control participants. Five single nucleotide polymorphisms (SNPs), with four of them within the promoter region and one in intron, were selected and genotyped with a polymerase chain reaction-ligase detection reaction (PCR-LDR) method. No association was revealed between these SNPs or the haplotypes containing four promoter SNPs and the risk of sAD. The results of this study indicate that polymorphisms in the selected regions of the NTRK2 gene are unlikely to confer the susceptibility of sAD in the Chinese Han population.

Diffusion tensor imaging reveals white matter changes associated with cognitive status in patients with Parkinson's disease.

Objective : Cognitive deficit and white matter alteration relationships in Parkinson's disease (PD) were investigated. Methods : Comparison of 64 patients with PD (M:F, 34:30; 64.4 ± 10.4 years) classified as cognitively normal (PD-CogNL, n = 24), mild cognitive impairment (PD-MCI, n = 30), and dementia (PD-D, n = 10) with 21 healthy participants (M:F, 10:11; 60.1 ± 13.6 years) was conducted using white matter fractional anisotropy (FA), region-of-interest analysis, and diffusion tensor imaging. Results : The PD-D and PD-MCI exhibited higher Unified Parkinson's Disease Rating Scale motor scores (P < .001; P < .01) and Hoehn-Yahr stages (P < .001; P < .05) and FA reductions in left frontal/right temporal white matter and bilateral anterior cingulated bundles. Largest FA reductions occurred in PD-D left anterior cingulated bundle and corpus callosum splenium. Disease durations of PD-D = 6.8 ± 6.86, PD-MCI = 5.1 ± 2.9, and PD-CogNL = 4.7 ± 3.4 years, suggesting progressive deterioration. Conclusions : Cerebral white matter deterioration may underlie progressive cognitive impairment in PD.

Major ozonated autohemotherapy promotes the recovery of upper limb motor function in patients with acute cerebral infarction.

Major ozonated autohemotherapy is classically used in treating ischemic disorder of the lower limbs. In the present study, we performed major ozonated autohemotherapy treatment in patients with acute cerebral infarction, and assessed outcomes according to the U.S. National Institutes of Health Stroke Score, Modified Rankin Scale, and transcranial magnetic stimulation motor-evoked potential. Compared with the control group, the clinical total effective rate and the cortical potential rise rate of the upper limbs were significantly higher, the central motor conduction time of upper limb was significantly shorter, and the upper limb motor-evoked potential amplitude was significantly increased, in the ozone group. In the ozone group, the National Institutes of Health Stroke Score was positively correlated with the central motor conduction time and the motor-evoked potential amplitude of the upper limb. Central motor conduction time and motor-evoked potential amplitude of the upper limb may be effective indicators of motor-evoked potentials to assess upper limb motor function in cerebral infarct patients. Furthermore, major ozonated autohemotherapy may promote motor function recovery of the upper limb in patients with acute cerebral infarction.

[Denaturing high-performance liquid chromatography coupled with multiplex PCR for rapid detection of large duplications or deletions in patients with Duchenne muscular dystrophy and spinal muscular atrophy].

OBJECTIVE: To assess the value of multiplex PCR-denaturing high-performance liquid chromatography (PCR-DHPLC) method for screening large duplications or deletions in patients with Duchenne muscular dystrophy (DMD) and spinal muscular atrophy (SMA). METHODS: DNA was extracted from peripheral venous blood samples from 35 DMD and 6 SMA patients. Large duplications or deletions were screened with multiplex PCR coupled with DHPLC method. The results were validated with testing of positive and negative controls. RESULTS: Known duplications or deletions in all controls were reliably detected with multiple PCR coupled with DHPLC. Large duplications or deletions were found in 71.4% of 35 DMD patients, which included 5 large duplications and 20 large deletions. For SMA patients, deletions of SMN1 exon 7 were detected in 16 samples. CONCLUSION: Multiplex PCR coupled with DHPLC method is an effective and reliable method for detecting large genomic duplications or deletions in patients with DMD or SMA.

[Effect of radiofrequency of different temperatures and durations on motor conduction velocity of rat sciatic nerve].

OBJECTIVE: To evaluate the effect of radiofrequency of different temperatures and durations on sciatic nerve motor conduction velocity (MCV). METHODS: The bilateral sciatic nerve of 70 adult SD rats was dissected and exposed to radiofrequency ablation of different temperatures (30, 50, 55, 60, and 70 degrees C) and durations. The nerves were also exposed to increasing ablation temperatures from 30 degrees C to 50 degrees C with an increment of 5 degrees C (60 s at each temperature), and the changes in the MCV parameters were observed. RESULTS: The MCV parameters of rat sciatic nerve underwent significant changes following the radiofrequency exposures (P<0.05) except for the exposure at 55 degrees celsius; for 10 s. Below the temperature of 55 degrees celsius;, the MCV showed no obvious correlation to the exposure time for the group. For the nerves exposed to radiofrequency of 55 degrees celsius;, the latency was not correlated to the exposure time within 30 s, and data could be obtained from 55 s group; with these exceptions, the latency was found to positively while the negative phase wave inversely correlated to the exposure time. With fixed exposure time of 60 s, the MCV parameters were positively correlated to the ablation temperature (below 50 degrees C). Failure of MCV measurement occurred following exposures to 55 degrees celsius; for 50 s (or longer) or to 60 degrees C (or higher) for 10 s. CONCLUSION: Low-temperature radiofrequency (below 50 degrees C) produces definite effects on the MCV of rat sciatic nerve, and the effects are not associated with the exposure time, the mechanism of which remains unclear. At a given temperature, the ablation for sufficiently long durations can result in complete block of the MCV. At higher temperatures, radiofrequency exposure cause obvious nerve conduction block.

[Analgesic effects of chemical lumbar sympathectomy on refractory pain in the lower limbs].

OBJECTIVE: To evaluate the effect of chemical lumbar sympathectomy (CLS) on relieving refractory pain in the lower limbs. METHODS: Twenty-four patients with refractory pain in the lower limbs underwent CLS under X-ray guidance, and 2 ml contrast agent was injected at 1/3 of the second L2 vertebrae (the L2 sympathetic ganglion). Lidocaine was then injected followed by injection of 7% phenol for performing CLS. The visual analog scale was used to assess the pain severity before and after CLS. The effect of CLS on relieving lower limb pain was compared with that of oral pain-relieving medication. RESULTS: The lower limb pain was obviously relieved as shown by significantly decreased VAS scores in these patients after CLS. CLS exhibited a much more potent effect of pain relief in the lower limbs than the oral medication. CONCLUSION: CLS produces significant analgesic effects to relieve refractory pain in the lower limbs.

Inhibiting effect of vagal nerve stimulation to seizures in epileptic process of rats.

OBJECTIVE: Our previous work suggested that sensitivity of hippocampal neurons is changed in process of epileptic activities, and closely parallel to the dynamic characteristic of epileptic activity of the neurons. This study investigated the sensitivity of epileptic brain to vagal nerve stimulation (VNS) in epileptic process. METHODS: Epileptic model was evoked by penicillin. Left vagal nerves were stimulated to inhibit the seizures induced by penicillin. The electrocorticography (ECoG) and electromyography (EMG) were recorded to analyze inhibiting effect of VNS in epileptic process. RESULTS: It was found that VNS could inhibit the seizures caused by penicillin, and the inhibiting effect of VNS to seizures increased as the vagal nerve stimulating time prolonged. It was also found that the inhibiting effect of VNS to seizures decreased in epileptic process. CONCLUSION: The results suggested that the sensitivity of epileptic brain to VNS was different in epileptic process. The inhibiting effect of VNS to seizure decreased as the development of seizures.

[Botulinum toxin type A does not affect spontaneous discharge but blocks sympathetic-sensory coupling in chronically compressed rat dorsal root ganglion neurons].

OBJECTIVE: To study the effect of botulinum toxin type A (BTXA) on spontaneous discharge and sympathetic- sensory coupling in chronically compressed dorsal root ganglion (DRG) neurons in rats. METHODS: In chronically compressed rat DRG, spontaneous activities of the single fibers from DRG neurons were recorded and their changes observed after BTAX application on the damaged DGR. Sympathetic modulation of the spontaneous discharge from the compressed DRG neurons was observed by electric stimulation of the lumbar sympathetic trunk, and the changes in this effect were evaluated after intravenous BTXA injection in the rats. RESULTS: Active spontaneous discharges were recorded in the injured DRG neurons, and 47 injured DRG neurons responded to Ca2+-free artificial cerebrospinal fluid but not to BTXA treatment. Sixty-four percent of the neurons in the injured DRG responded to sympathetic stimulation, and this response was blocked by intravenously injection of BTXA. CONCLUSION: BTXA does not affect spontaneous activities of injured DRG neurons, but blocks sympathetic-sensory coupling in these neurons.