Effect of Melodic Intonation Therapy on Nonfluent Aphasia after Stroke / 中国康复理论与实践

Objective:To observe the effect of melodic intonation therapy combined with speech training on nonfluent aphasia after stroke, and the changes of brain function. Methods:From March, 2017 to August, 2019, 40 patients with nonfluent aphasia after stroke were randomly divided into control group (n = 20) and intensive group (n = 20). Both groups accepted routine speech training, and the intensive group accepted melodic intonation therapy in addition. They were assessed with China Rehabilitation Research Center Chinese Standard Aphasia Examination before and four weeks after treatment. Three patients from each group were examined with resting-state functional magnetic resonance imaging to observe the changes of regional homogeneity (ReHo) of cerebral hemisphere. Results:The scores of comprehension (noun, verb and sentence), repetition (noun and verb), read (noun) and naming (verb) increased in the control group (t > 2.221, P < 0.05), while it increased in comprehension (noun, verb and sentence), repetition (noun, verb and sentence), reading (noun and verb) and naming (noun and verb) in the intensive group (t > 2.179, P < 0.05). The scores of repetition (noun and verb) increased more in the intensive group than in the control group (t > 2.299, P < 0.05)， and the scores of reading (sentence) increased somehow. The ReHo in left cerebellum and temporal occipital area increased and the ReHo in bilateral frontal and temporal cortex decreased after treatment. Conclusion:Melodic intonation therapy based on speech therapy can promote the recovery of speech function for patients with nonfluent aphasia after stroke, especially in sentence reading and words repetition. The changes of the ReHo in resting state may associate with the neurological repairment after brain injury.

Neuroprotective effects of nimodipine and MK-801 on acute infectious brain edema induced by injection of pertussis bacilli to neocortex of rats / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate (NMDA) receptor (MK-801) and antagonist of Ca(2+) channels (nimodipine) on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ([Ca(2+) ](i)) in synaptosomes or content of Evans Blue (EB).</p><p><b>METHODS</b>95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. [Ca(2+) ](i) was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with [(3)H]-MK-801 in the neuronal membrane of cerebral cortex.</p><p><b>RESULTS</b>The levels of water content and EB content of brain tissues, and [Ca(2+) ](i) in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P<0.05). The water content and [Ca(2+) ](i) increased with the duration of infectious brain edema. Nimodipine administered after the injection of PB could significantly decrease the water content, EB and [Ca(2+) ](i) (P<0.05). MK-801 could significantly decrease the water content, EB and [Ca(2+) ](i) in 4 h and 24 h groups (P<0.05). The Kd values were 30.5 nmol/L+/-3.0 nmol/L and 42.1 nmol/L+/-4.2 nmol/L in PB group and NS group respectively (P<0.05), and Bmax were 0.606 pmol/mg.pro+/-0.087 pmol/mg.pro and 0.623 pmol/mg.pro+/-0.082 pmol/mg.pro respectively, without statistical significance (P>0.05).</p><p><b>CONCLUSIONS</b>The changes in the permeability of blood-brain barrier (BBB) and Ca(2+)-overload may participate in the pathogenesis of infectious brain edema. Treatment with nimodipine can dramatically reduce the damage of brain edema and demonstrate neuroprotective effect on brain edema by inhibiting the excess of Ca(2+) influx and reducing the permeability of BBB. MK-801 pretreatment may inhibit the delayed Ca(2+) influx into the neurons. The infectious brain edema is not only cytotoxic brain edema (intracellular edema) but also vasogenic brain edema (extracellular edema) followed by earlier BBB breakdown, so infectious brain edema is complicated with brain edema.</p>

Application of noninvasive cerebral electrical impedance measurement on brain edema in patients with intracerebral hemorrhage / 中华神经科杂志

0.05).②The total positive ratio of PI in ICH was 73.1%.PI was the most sensitive when the position located in the basal ganglia (83.3%) or the volumes of lesions were more than 20 ml (80.0%—88.9%),but was low when the volumes less than 20 ml or the position near the midline.③In the patients with [CH,PI of the hematoma side initially was lower and finally higher than contralateral one.The average transitional time was (19.67? 11.52) h.The ipsilateral PI after the transitional time was much higher than that before the transitional time in the same patients(P