Relationship between motor performance and cortical activity of older neurological disorder patients with dyskinesia using fNIRS: A systematic review.

Background: Neurological disorders with dyskinesia would seriously affect older people's daily activities, which is not only associated with the degeneration or injury of the musculoskeletal or the nervous system but also associated with complex linkage between them. This study aims to review the relationship between motor performance and cortical activity of typical older neurological disorder patients with dyskinesia during walking and balance tasks. Methods: Scopus, PubMed, and Web of Science databases were searched. Articles that described gait or balance performance and cortical activity of older Parkinson's disease (PD), multiple sclerosis, and stroke patients using functional near-infrared spectroscopy were screened by the reviewers. A total of 23 full-text articles were included for review, following an initial yield of 377 studies. Results: Participants were mostly PD patients, the prefrontal cortex was the favorite region of interest, and walking was the most popular test motor task, interventional studies were four. Seven studies used statistical methods to interpret the relationship between motor performance and cortical activation. The motor performance and cortical activation were simultaneously affected under difficult walking and balance task conditions. The concurrent changes of motor performance and cortical activation in reviewed studies contained the same direction change and different direction change. Conclusion: Most of the reviewed studies reported poor motor performance and increased cortical activation of PD, stroke and multiple sclerosis older patients. The external motor performance such as step speed were analyzed only. The design and results were not comprehensive and profound. More than 5 weeks walking training or physiotherapy can contribute to motor function promotion as well as cortices activation of PD and stroke patients. Thus, further study is needed for more statistical analysis on the relationship between motor performance and activation of the motor-related cortex. More different type and program sports training intervention studies are needed to perform.

Electroacupuncture brain protection during ischemic stroke: A role for the parasympathetic nervous system.

The demand for using parasympathetic activation for stroke therapy is unmet. In the current study, we investigated whether the neuroprotection provided by electroacupuncture (EA) in an experimental stroke model was associated with activation of the parasympathetic nervous system (PNS). The results showed that parasympathetic dysfunction (PD), performed as unilateral vagotomy combined with peripheral atropine, attenuated both the functional benefits of EA and its effects in improving cerebral perfusion, reducing infarct volume, and hindering apoptosis, neuronal and peripheral inflammation, and oxidative stress. Most importantly, EA rats showed a dramatically less reduction in the mRNA level of choline acetyltransferase, five subtypes of muscarinic receptors and α7nAChR, suggesting the inhibition of the impairment of the central cholinergic system; EA also activated dorsal motor nucleus of the vagus, the largest source of parasympathetic pre-ganglionic neurons in the lower brainstem (detected by c-fos immunohistochemistry), and PD suppressed these changes. These findings indicated EA may serve as an alternative modality of PNS activation for stroke therapy.

Regulating autonomic nervous system homeostasis improves pulmonary function in rabbits with acute lung injury.

BACKGROUND: This study aimed to investigate the effects of regulating autonomic nervous system (ANS) homeostasis by inhibiting sympathetic hyperactivity and/or enhancing parasympathetic activity on pulmonary inflammation and functional disturbance. METHODS: An animal model of acute lung injury (ALI) was established in rabbits by an intratracheal injection of hydrochloric acid (HCl) in rabbits. Animals in control groups were received saline or HCl only, and the others received both HCl and followed treatments: vagus nerve stimulation (VNS), intravenous injection of tetrahydroaminoacridine (THA), or stellate ganglion block (SGB). The effects of different treatments on the changes in autonomic nervous system homeostasis, pulmonary and systemic inflammation, and functional disturbance were detected. RESULTS: Sympathetic nervous activity was higher than parasympathetic nervous activity in rabbits after HCl aspiration, as demonstrated by the significant changes in the discharge frequency of cervical sympathetic/vagus trunk, and heart rate variability. VNS, THA and SGB could significantly alleviate the changes of ANS induced by HCl aspiration and improved the pulmonary function, especially for SGB treatment. CONCLUSIONS: The disturbance of ANS homeostasis is attributed to a predominance of SNS activity. Administration of VNS, THA and SGB are capable to regulate disequilibrium of the ANS in rabbits with HCl-induced ALI and SGB is supposed to be the most effective approach.

The effects of electroacupuncture treatment on the postoperative cognitive function in aged rats with acute myocardial ischemia-reperfusion.

Many literatures have proven that postoperative cognitive dysfunction (POCD) was very common in old patients after the injury of acute myocardial ischemia-reperfusion (AMIR) clinically such as the off-pump coronary artery bypass surgery (OPCAB) without definite mechanism; however, reports on the animal experiments were rarely seen. We hypothesized that AMIR could contribute to cognitive dysfunction, and this severe injury might be impeded by EA via hindering neuroinflammation and oxidative stress response as well as modulating the balance of the autonomic nervous system. The aged male Sprague Dawley rats were randomly assigned into three experimental groups: sham (sham operation), AMIR, and EA (electroacupunture treatment, acupoints GV20 and ST36+AMIR) groups. The survival rate, heart rate variability analysis, examination of pathology within the hippocampal CA1, oxidative stress, systemic inflammation and the behavior testing were evaluated by their corresponding methods. The results showed that the rats subjected to AMIR had lower survival rates, higher malondialdehyde (MDA), decreased superoxide dismutase (SOD) activity, more microglial activation, and presented evidence of severe brain injury and cognitive dysfunction on the 1st, 3rd, 7th days after reperfusion compared to sham-operated controls. Most important of all, the above damages induced by the AMIR were significantly improved by the EA treatment. Our findings indicated that EA treatment could be a neuroprotective therapy for the cognitive dysfunction induced by the AMIR event, which might be attributablefor balancing the autonomic nervous system, inhibiting the neuronic apoptosis, hindering microglial activation, attenuating oxidative stress and restraining the central and peripheral inflammation reactions.

Effects of Dexmedetomidine combined with Dezocine on cognition function and hippocampal microglia activation of rats.

OBJECTIVE: This study aimed to investigate the effects of Dexmedetomidine combined with Dezocine on the cognition and hippocampal microglia activation of rats. METHODS: Laparotomy was successfully performed in 48 rats which were then divided into Dexmedetomidine+Dezocine group and Dezocine group. Rats in Dexmedetomidine+dezocine group were infused with Dexmedetomidine and dezocine via the tail vein after anesthesia; rats in Dezocine group were infused with dezocine via the tail vein. After surgery, rats underwent detection of learning and memory functions at 1, 3, and 7 days after surgery, and the neuroglobin and norepinephrine expression was detected in the hippocampal microglia at the same time points. RESULTS: 1, 3 and 7 days after surgery, the latency to escape in Dexmedetomidine+Dezocine group was significantly shorter than that in Dezocine group, and the number of cells positive for neuroglobin or norepinephrine in the CAL region of hippocampus of Dexmedetomidine+Dezocine group was also markedly higher than that of Dezocine group (P < 0.05). CONCLUSION: Surgery and anesthesia have influence on the cognition of rats to a certain degree, and dexmedetomidine combined with dezocine can effectively improve the impaired cognition due to surgery and anesthesia, which may be attributed to the increase in the protective neuroglobin and norepinephrine in the hippocampus.

Neuroprotective effects of therapeutic hypercapnia on spatial memory and sensorimotor impairment via anti-apoptotic mechanisms after focal cerebral ischemia/reperfusion.

A number of studies have demonstrated that therapeutic hypercapnia ameliorates neurological deficits and attenuates the histological damage of cerebral ischemia-reperfusion injury. However, the effects of therapeutic hypercapnia on impaired spatial memory have not been reported. Here we aimed to investigate the effects and mechanisms of therapeutic hypercapnia on spatial memory in a rat model of focal cerebral ischemia induced by middle cerebral artery occlusion/reperfusion (MCAO/R). Adult male rats were randomly assigned into three experimental groups: sham (sham operation), IR (MCAO/R), and hypercapnia [arterial blood CO2 tension (PaCO2) 80-100 mmHg+IR] groups. Sensorimotor deficits and spatial memory testing were evaluated by an 18-point scoring system and an 8-arm radial maze task, respectively. The hippocampal histological damage and the percentage of apoptotic neurons were evaluated by hematoxylin and eosin (HE) staining as well as flow cytometry. Western blotting was used to investigate the changes of the apoptosis-related Bcl-2 and Bax proteins. The results indicated that hypercapnia treatment significantly improved the abilities of impaired sensorimotor and spatial memory after MCAO/R. Moreover, hypercapnia treatment significantly increased the percentage of surviving neurons and decreased the percentage of apoptotic neurons in the hippocampus after MCAO/R damage. The expressions of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax were significantly increased and decreased in the hypercapnia treated rats, respectively. These findings suggest that therapeutic hypercapnia can attenuate neuronal apoptosis and improve impaired spatial memory and sensorimotor after MCAO/R, which may be attributable to its anti-apoptotic effects through modulation of apoptosis-related protein.

Effects of electro-acupuncture on endothelium-derived endothelin-1 and endothelial nitric oxide synthase of rats with hypoxia-induced pulmonary hypertension.

Pulmonary hypertension (PH) is characterized by elevated pulmonary artery pressure (PAP), pulmonary vascular remodeling and right ventricular hypertrophy, which are mainly due to endothelial dysfunction. Electro-acupuncture has shown beneficial effects on cardiovascular homeostasis, but little evidence has been obtained on pulmonary effects. The goal of the present study was to investigate whether electro-acupuncture on bladder-13 and -15 points can protect against chronic hypoxia-induced PH by regulating endothelium-derived endothelin (ET)-1 and endothelial nitric oxide synthase (eNOS). Male Wistar rats were exposed to hypoxia to induce PH. Hemodynamic analysis revealed that mean PAP was similar under normoxic conditions. Chronic hypoxia increased mean PAP to 37 +/- 3 mmHg, and electro-acupuncture attenuated it to 29 +/- 3 mmHg. Absolute right ventricular weight was ameliorated by electro-acupuncture from 0.288 +/- 0.048 g to 0.228 +/- 0.029 g under hypoxic conditions. Hypoxia-induced right ventricular hypertrophy index decreased from 0.477 +/- 0.069 to 0.378 +/- 0.053 with electro-acupuncture treatment. Histological examination revealed that hypoxic rats showed increased medial pulmonary artery wall thickness as well as muscularization. However, these alternations by chronic hypoxia were attenuated by electro-acupuncture. There was no difference in eNOS or ET-1 between groups under normoxic conditions. Electro-acupuncture treatment significantly improved the circulating eNOS concentration (365.36 +/- 31.51 pg/mL) compared with only hypoxia exposure (247.60 +/- 30.64 pg/mL). In lung homogenate, levels of eNOS under hypoxia increased from 684.96 +/- 117.90 to 869.86 +/- 197.61 pg/mg by electro-acupuncture treatment. Levels of ET-1 changed oppositely to eNOS in response to electro-acupuncture (ET-1 in plasma, 29.44 +/- 2.09 versus 20.70 +/- 2.37 pg/mL; ET-1 in lung homogenate, 120.51 +/- 3.03 versus 110.60 +/- 4.04 pg/mg). In conclusion, these results indicated that treatment with electro-acupuncture can protect against hypoxia-induced PH, possibly by regulating the balance of endothelium-derived vasoconstrictors and vasodilators.

Effects of mixture of lidocaine and ropivacaine at different concentrations on the central nervous system and cardiovascular toxicity in rats.

BACKGROUND: Lidocaine and ropivacaine are often combined in clinical practice to obtain a rapid onset and a prolonged duration of action. However, the systemic toxicity of their mixture at different concentrations is unclear. This study aimed to compare the systemic toxicity of the mixture of ropivacaine and lidocaine at different concentrations when administered intravenously in rats. METHODS: Forty-eight male Wistar rats were randomly divided into 4 groups (n = 12 each): 0.5% ropivacaine (group I); 1.0% ropivacaine and 1.0% lidocaine mixture (group II); 1.0% ropivacaine and 2.0% lidocaine mixture (group III); and 1.0% lidocaine (group IV). Local anesthetics were infused at a constant rate until cardiac arrest. Electrocardiogram, electroencephalogram and arterial blood pressure were continuously monitored. The onset of toxic manifestations (seizure, dysrhythmia, and cardiac arrest) was recorded, and then the doses of local anesthetics were calculated. Arterial blood samples were drawn for the determination of local anesthetics concentrations by high-performance liquid chromatography. RESULTS: The onset of dysrhythmia was later significantly in group IV than in group I, group II, and group III (P < 0.01), but there was no significant difference in these groups (P > 0.05). The onset of seizure, cardiac arrest in group I ((9.2 + or - 1.0) min, (37.0 + or - 3.0) min) was similar to that in group II ((9.1 + or - 0.9) min, (35.0 + or - 4.0) min) (P > 0.05), but both were later in group III ((7.5 + or - 0.7) min, (28.0 + or - 3.0) min) (P < 0.05). The onset of each toxic manifestation was significantly later in group IV than in group I (P < 0.01). The plasma concentrations of the lidocaine-alone group at the onset of dysrhythmia (DYS), cardiac arrest (CA) ((41.2 + or - 6.8) min, (59.0 + or - 9.0) min) were higher than those of the ropivacaine alone group ((20.5 + or - 3.8) min, (38.0 + or - 8.0) min) (P < 0.05). The plasma concentrations of ropivacaine inducing toxic manifestation were not significantly different among groups I, II, and III (P > 0.05). CONCLUSIONS: The systemic toxicity of the mixture of 1.0% ropivacaine and 2.0% lidocaine is the greatest while that of 1.0% lidocaine is the least. However, the systemic toxicity of the mixture of 1.0% ropivacaine and 1.0% lidocaine is similar to that of 0.5% ropivacaine alone.

{µ-6,6'-Dimeth-oxy-2,2'-[propane-1,3-diylbis(nitrilo-methyl-idyne)]diphenolato}trinitratocopper(II)erbium(III) acetone solvate.

In the title complex, [CuEr(C(19)H(20)N(2)O(4))(NO(3))(3)]·CH(3)COCH(3), the Cu(II) ion is coordinated in a square-planar environment by two O atoms and two N atoms of a Schiff base ligand. The Er(III) ion is bis-chelated by three nitrate ligands and coordinated by four O atoms of the Schiff base ligand in a slightly distorted bicapped square-anti-prismatic environment.