Background： Wallerian degeneration （WD） of bilateral middle cerebellar its characteristics have not yet been clarified because of the low incidence peduncles （MCPs） can occur following pontine infarction, but Thus, the present study discussed the clinical and radiological features to improve the awareness of this disease. Methods： Clinical and radiological information from consecutive individuals diagnosed with WD of bilateral MCPs following pontine infarction in three hospitals over the past 4 years between October 2012 and October 2016 were retrospectively investigated and compared with a control group （patients with pontine infarction had no secondary WD）. Results： This study involved 30 patients with WD of MCPs, with a detection rate of only 4.9%. The primary infarctions （χ2 -24.791, P = 0.001, vs. control group） were located in the paramedian pons in 21 cases （70.0%）, and ventrolateral pons in nine cases （30.0%）. WD of the MCPs was detected 8-24 weeks after pons infarction using conventional magnetic resonance imaging （M RI）; all secondary WDs were asymptomatic and detected incidentally. All WD lesions exhibited bilateral, symmetrical, and boundary blurring on MRI. The signal features were hypointense on Tl-weighted imaging, hyperintense on T2-weighted imaging and fluid-attenuated inversion recovery, and slightly hyperintense or isointense on diffusion-weighted imaging and apparent diffusion coefficient maps. Secondary brainstem atrophy was found in six （20.0%） cases. A Modified Rankin Scale score 0-2 was found in 10 （33.3%） cases and score 〉2 in 20 （66.7%） cases at 90 days after discharge, and the short-term prognosis was worse than that in control group （χ2 =12.814, P - 0.001 ）. Conclusions： Despite the rarity of bilateral and symmetrical lesions of MCPs, secondary WD should be highly suspected if these lesions occur within 6 months after pontine infarction, particularly parainedian ports. Conventional MRI appears to be a relatively sensitive method f
Zhi-Yong ZhangZhi-Qin LiuWei QinYa-Wen ChenZun-Jing Liu
Dural arteriovenouscommunications betweenfistulas （DAVFs） are directthe intracranial arterial andvenous systems without an intervening nidus. Clini-cians sometimes fail to give a correct diagnosis ofDAVF. Given the similarity of their clinical andmagnetic resonance imaging （MRI） manifestations,diagnostic confusion may arise between DAVF andcerebral venous sinus thrombosis （CVST） （Simonet al., 2009）.
Li-li SUNWen-xiong TANGLei LIUWei WANGSi-xun ZHANGZun-jing LIU
To the Editor： A 38-yearoold man was admitted to our hospital with transient aphasia and weakness of the right extremities. As a habitual smoker, he had been diagnosed with hypertension and hyperlipidemia 3 and 10 years prior, respectively. With regard to family history, he stated that his father had suffered cerebral infarction.
Zhi-Yong ZhangShoichiro SatoZhao-Hui TianWen-Xiong TangZun-Jing Liu
Willed-movement training has been demonstrated to be a promising approach to increase motor per- formance and neural plasticity in ischemic rats. However, little is known regarding the molecular signals that are in- volved in neural plasticity following willed-movement training. To investigate the potential signals related to neural plasticity following willed-movement training, littermate rats were randomly assigned into three groups： middle cerebral artery occlusion, environmental modification, and willed-movement training. The infarct volume was measured 18 d after occlusion of the right middle cerebral artery. Reverse transcription-polymerase chain reaction （PCR） and im- munofluorescence staining were used to detect the changes in the signal transducer and activator of transcription 3 （STAT3） mRNA and protein, respectively. A chromatin immunoprecipitation was used to investigate whether STAT3 bound to plasticity-related genes, such as brain-derived neurotrophic factor （BDNF）, synaptophysin, and protein in- teracting with C kinase 1 （PICK1）. In this study, we demonstrated that STAT3 mRNA and protein were markedly increased following 15-d willed-movement training in the ischemic hemispheres of the treated rats. STAT3 bound to BDNF, PICK1, and synaptophysin promoters in the neocortical cells of rats. These data suggest that the increased STAT3 levels after willed-movement training might play critical roles in the neural plasticity by directly regulating plasticity-related genes.
