Clinical and imaging features of bilateral Wallerian degeneration of the middle cerebellar peduncles secondary to isolated pontine infarction / 国际脑血管病杂志

Objective:To investigate the clinical and imaging features of bilateral Wallerian degeneration of the middle cerebellar peduncles secondary to isolated pontine infarction.Methods:Patients diagnosed as bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction admitted to the Second Affiliated Hospital of Zhengzhou University from June 2017 to December 2021 were retrospectively included. Patients with bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction reported between January 2001 and December 2021 were collected by searching Chinese and English databases, and their clinical and imaging characteristics were summarized.Results:A total of 48 patients with bilateral Wallerian degeneration of cerebellar middle peduncle after isolated pontine infarction were included, including 14 patients admitted to the Second Affiliated Hospital of Zhengzhou University, and 34 patients collected by searching the Chinese and English databases. Thirty-three patients were males (68.75%) and 15 were females (31.25%). Their age was 65.8±10.7 years old (range, 37-88 years). Most patients had vascular risk factors, and hypertension was the most common. Dysarthria and limb weakness were the main clinical symptoms at admission. The infarct sites of all 48 patients were located in the blood supply area of paramedian pontine arteries, of which 37 (77.08%) were unilateral (18 on the left and 19 on the right), 6 (12.50%) were bilateral sides, and 5 (10.42%) had incomplete data. When Wallerian degeneration was diagnosed, 8 patients (16.67%) had dizziness or ataxia, 6 (12.50%) had aggravated original symptoms, and the remaining 34 (70.83%) had no new symptoms or aggravated original symptoms. All patients showed symmetrical abnormal signals in bilateral middle cerebellar peduncles, with obvious hyperintensity on T 2 or diffusion-weighted imaging (DWI). One patient showed T 2 hyperintensity in bilateral middle cerebellar peduncle on the next day after the onset of the infarction, which was the earliest case to find secondary Wallerian degeneration after isolated pontine infarction. Conclusions:Wallerian degeneration should be considered when symmetrical lesions of bilateral middle cerebellar peduncles occur after isolated pontine infarction. Wallerian degeneration may occur early after isolated pontine infarction. Most cases have no new symptoms or aggravated original symptoms. Conventional MRI can identify it early.

Research progress on dental pulp stem cells in the repair of peripheral nerve injury / 口腔疾病防治

@#Peripheral nerve injury (PNI) is a common disease in the oral cavity that can easily lead to loss of function and abnormal appearance. The application of dental pulp stem cells (DPSCs) combined with tissue engineering in the repair of PNI is a research hotspot. DPSCs have the advantages of abundant sources, simple extraction, low immunogenicity and a high proliferation rate in vitro. They can differentiate into Schwann cells (SCs). SCs can induce autophagy and secrete key neurotrophic factors, such as nerve growth factor, brain-derived neurotrophic factor, ciliary neurotrophic factor and glial cell-derived neurotrophic factor. SCs are beneficial for the repair of nerve injury. DPSCs in different periods have differences in immune regulation, anti-inflammatory effects, expression of neural markers, angiogenesis and so on, which provide more diversified choices for nerve repair. At present, the introduction of tissue engineering provides a more controllable and improved microenvironment for DPSCs, which is conducive to the application and development of DPSCs in regenerative medicine and tissue engineering. However, there are still many problems to be solved, such as the selection of stem cells, functional link recovery, uncontrollable direction of axon regeneration, regulation of the peripheral nervous system and mechanism of repair.

Claudin 14/15 play important roles in early wallerian degeneration after rat sciatic nerve injury / 中华创伤杂志(英文版)

PURPOSE@#Wallerian degeneration (WD) is an antegrade degenerative process distal to peripheral nerve injury. Numerous genes are differentially regulated in response to the process. However, the underlying mechanism is unclear, especially the early response. We aimed at investigating the effects of sciatic nerve injury on WD via CLDN 14/15 interactions in vivo and in vitro.@*METHODS@#Using the methods of molecular biology and bioinformatics analysis, we investigated the molecular mechanism by which claudin 14/15 participate in WD. Our previous study showed that claudins 14 and 15 trigger the early signal flow and pathway in damaged sciatic nerves. Here, we report the effects of the interaction between claudin 14 and claudin 15 on nerve degeneration and regeneration during early WD.@*RESULTS@#It was found that claudin 14/15 were upregulated in the sciatic nerve in WD. Claudin 14/15 promoted Schwann cell proliferation, migration and anti-apoptosis in vitro. PKCα, NT3, NF2, and bFGF were significantly upregulated in transfected Schwann cells. Moreover, the expression levels of the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK signaling pathways were also significantly altered.@*CONCLUSION@#Claudin 14/15 affect Schwann cell proliferation, migration, and anti-apoptosis via the β-catenin, p-AKT/AKT, p-c-jun/c-jun, and p-ERK/ERK pathways in vitro and in vivo. The results of this study may help elucidate the molecular mechanisms of the tight junction signaling pathway underlying peripheral nerve degeneration.

3-methyladenine improves the efficiency of sciatic nerve allograft in mice / 中国组织工程研究

BACKGROUND: Recent studies have shown that the occurrence of Wallerian degeneration is closely related to autophagy in Schwann cells. The regulation of autophagy in Schwann cells can significantly affect the occurrence and development of Wallerian degeneration, subsequently altering axon regeneration and myelination. OBJECTIVE: To clarify whether sciatic nerve allograft can achieve higher efficiency when the cell autophagy is inhibited by 3-methyladenine. METHODS: We harvested 16 sciatic nerve segments from 8 female C57BL/6J mice that were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. in China. All the segments were equally divided into experimental and control groups and cultured in 3-methyladenine culture medium and normal culture medium for 72 hours, respectively. Another 16 female C57BL/6J mice were taken to make animal models of left sciatic nerve defects. After modeling, the sciatic nerve segments were grafted to repair sciatic nerve defect through microsurgery: 3-methyladenine-treated nerve segments in the experimental group and normally treated nerve segments in the control group. Sciatic nerve index in each mouse was recorded at 2, 4, 6, and 8 weeks after modeling. At 8 weeks after modeling, the regenerated nerve segments were histologically analyzed using hematoxylin-eosin staining, immunofluorescent staining, toluidine blue staining, and transmission electron. The animal experiment was approved by the Animal Ethics Committee of Peking Union Medical College. RESULTS AND CONCLUSION: There were no differences in the sciatic nerve index between the two groups (P > 0.05) except at 8 weeks after modeling (P < 0.05). Hematoxylin-eosin staining revealed an intact nerve structure in the experimental group but a large area of voids in the control group. Immunofluorescent staining indicated that there were nerve tracts with more complete structures in the experimental group than the control group. Toluidine blue staining revealed some myelinated and unmyelinated nerve fibers regenerated in the experimental group and only a few of myelinated nerve fibers and unmyelinated axons newly formed in the control group. Under the transmission electron microscope, myelin sheath thickness and myelinated fiber diameter were significantly higher in the experimental group than the control group (P < 0.05). Therefore, 3-methyladenine-treated nerve allografts could inhibit autophagy in Schwann cells, maintain the myelin sheath structure of the allograft, and promote axonal regeneration and functional recovery.

Clinical and Radiological Features of Wallerian Degeneration of the Middle Cerebellar Peduncles Secondary to Pontine Infarction / 中华医学杂志(英文版)

<p><b>Background</b>Wallerian degeneration (WD) of bilateral middle cerebellar peduncles (MCPs) can occur following pontine infarction, but its characteristics have not yet been clarified because of the low incidence. Thus, the present study discussed the clinical and radiological features to improve the awareness of this disease.</p><p><b>Methods</b>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).</p><p><b>Results:</b>This study involved 30 patients with WD of MCPs, with a detection rate of only 4.9%. The primary infarctions (χ =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 (MRI); 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 T1-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 (χ =12.814, P = 0.001).</p><p><b>Conclusions</b>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 paramedian pons. Conventional MRI appears to be a relatively sensitive method for detecting WD of MCPs, which might affect the short-term prognosis.</p>

Célula de Büngner / Büngner cell

Las lesiones del nervio periférico constituyen una condición clínica frecuente; por ello, entender su fisiopatología y los avances en el campo de la regeneración nerviosa es fundamental para brindar el mejor tratamiento a los pacientes. En los últimos años se ha venido dando cada vez mayor importancia a los eventos regenerativos después de la lesión, donde interviene en gran medida una expresión fenotípica única en este proceso, derivada de células ya presentes, fenómeno clave para la recuperación de la función del nervio lesionado. Este artículo revisó la literatura disponible con el objetivo de entender mejor este evento regenerativo y se encontraron procesos celulares y moleculares que suceden en los axones.

Peripheral nerve injuries are a common clinical condición for which the understanding of the pathophysiology and advances in the fteld of nerve regeneration are important to provide the best treatment for patients. In recent years, it has been giving increasing importance to the regenerative events after injury, where it operares largely unique phenotypic expression in this process, derived from cells already present, kev event for the recoven- of nerve function injured. A review of the literature is done with the aim of a better understanding of this regenerative event, fínding a series of cellular and molecular processes that go on axonal level.

Effect of lipopolysaccharide on Wallerian degeneration after peripheral nerve injury in rats / 中国实验动物学报

Objective To investigate the effects of lipopolysaccharide(LPS) on myelin phagocytosis during Wallerian degeneration after early peripheral nerve injury in rats.Methods Fifty male Wistar rats were recruited and randomly divided into LPS group(n=20),model group(n=20) and sham group(n=10).The right sciatic nerves of rats in the LPS and model groups were cut and sutured end-to-end,while the sciatic nerve of sham group rats were only exposed.Immediately after surgery,the rats in LPS group were given microinjections of LPS(2 g/L) into the surgical site in a final volume of 1 μL,and the rats in other two groups were injected with the same volume of saline.The sciatic nerves were taken at 1.5 h,24 h and 7d after surgery.Real-time quantitative PCR(qRT-PCR) was applied to detect the dynamic expressions of IL-1β mRNA and MCP-1 mRNA.Immunofluorescence staining was used to test the expression of CD68+ macrophages in sciatic nerves.HE staining was used to observe the pathological alterations of sciatic nerves tissue.ORO staining was used to observe sciatic nerves demyelination.LFB staining was used to detect the sciatic nerves myelin.Sciatic function index was used to evaluate the recovery of motor function in rats.Results Compared with the model group,qRT-PCR indicated that the expression of IL-1β and MCP-1 from LPS group were increased at 1.5 h and 24 h after surgery(P<0.001, P<0.001),respectively.Compared with the model group,the expression of CD68+ cells was increased significantly at 7th day after surgery(P<0.05).Histological examination showed that compared with the model group,a lot of inflammatory cells and Schwann cells were found at sciatic nerve stump in the LPS group at 7th day after operation.ORO staining showed that the degree of demyelination in the LPS group was higher than that in the model group.LFB staining showed that the sciatic nerve stump demyelination appeared in both model group and the LPS group at 7th day after operation,but compared with the model group,myelin debris clearance in the LPS group was significantly accelerated(P<0.05).Finally,compared with the model group,the SFI in the LPS group was increased significantly at 20 d after surgery(P<0.05).Conclusions The results confirm that LPS is possible to manipulate the innate immune response to accelerate myelin clearance during Wallerian degeneration after early peripheral nerve injury in rats.

Imaging of secondary damage in remote regions after focal cerebral infarction / 国际脑血管病杂志

After ischemic stroke, secondary damages such as neuron loss, gliosis, and axonal degeneration occur in the nonischemic remote brain regions that have synaptic connections with the primary infarction site.These secondary damages in the remote brain regions may affect the recovery of neurological function.Several advanced neuroimaging techniques have been used to detect these secondary damages.This article reviews the research progress in this field.

Neural Ablation and Regeneration in Pain Practice

A nerve block is an effective tool for diagnostic and therapeutic methods. If a diagnostic nerve block is successful for pain relief and the subsequent therapeutic nerve block is effective for only a limited duration, the next step that should be considered is a nerve ablation or modulation. The nerve ablation causes iatrogenic neural degeneration aiming only for sensory or sympathetic denervation without motor deficits. Nerve ablation produces the interruption of axonal continuity, degeneration of nerve fibers distal to the lesion (Wallerian degeneration), and the eventual death of axotomized neurons. The nerve ablation methods currently available for resection/removal of innervation are performed by either chemical or thermal ablation. Meanwhile, the nerve modulation method for interruption of innervation is performed using an electromagnetic field of pulsed radiofrequency. According to Sunderland's classification, it is first and foremost suggested that current neural ablations produce third degree peripheral nerve injury (PNI) to the myelin, axon, and endoneurium without any disruption of the fascicular arrangement, perineurium, and epineurium. The merit of Sunderland's third degree PNI is to produce a reversible injury. However, its shortcoming is the recurrence of pain and the necessity of repeated ablative procedures. The molecular mechanisms related to axonal regeneration after injury include cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules, and their receptors. It is essential to establish a safe, long-standing denervation method without any complications in future practices based on the mechanisms of nerve degeneration as well as following regeneration.

MRI findings of Wallerian degeneration in pyramidal tract after cerebral injury / 中国基层医药

Objective To analyze the MRI findings of Wallerian degeneration in pyramidal tract after cere-bral injury for improving the diagnosis accuracy.Methods The MRI findings of Wallerian degeneration in pyramidal tract in 25 cases were analyzed in association with the primary cerebral injury.Results All the primary diseases were above the tentorium of cerebellum in 25 cases,MRI in 2 cases demonstrated a continuous thin band -like long T1 or isometric T1 and long T2 abnormal changes in pyramidal tract,hyperintensify on FLAIR and DWI.2 cases showed hypointensify on T1 WI,hyperintensify on T2 WI and FLAIR,isointensity on DWI.21 cases showed hypointensify on T1 WI,hyperintensify on T2 WI and FLAIR,isointensity or hypointensify on DWI with brainstem atrophy.Conclusion MRI is valuable in the diagnosis of Wallerian degeneration in pyramidal tract after cerebral injury.

Hydrogen proton magnetic resonance spectroscopy study on early Wallerian degeneration of the pyramidal tract after cerebral infarction / 实用放射学杂志

Objective To investigate the feasibility of hydrogen proton magnetic resonance spectroscopy (1 H-MRS)for detection of Wallerian degeneration of the pyramidal tract after cerebral infarction.Methods Multiple metabolic indices including NAA,Cho, Cr of the bilateral cerebral peduncle were detected by using 1 H-MRS in 1 5 patients with unilateral middle cerebral artery infarction and 1 5 age-matched healthy volunteers,NAA/Cr,Cho/Cr were also calculated.Comparing the difference between cerebral infarction group and the control group ,the ROC curve was analyzed.Results The values of NAA/Cr in the ipsilateral cerebral peduncle of cerebral infarction patients were significantly lower than that of the contralateral,and there were significant differences between the two groups(P 0.05),the Cho/Cr values of the ipsilateral and the contralateral cerebral peduncle had no significant difference compared with the control group (P >0.05).Conclusion 1 H-MRS can detect Wallerian degeneration of the pyramidal tract after cerebral infarction.

Treating Peripheral Nerve Injuries / The Japanese Journal of Rehabilitation Medicine

Peripheral nerve injuries are usually caused by trauma and are different from peripheral neuropathy. Clinical signs include flaccid paralysis, sensory loss and rapid muscle atrophy. Peripheral nerve lacerations are best treated by early microsurgical repair. There are several defining characteristics of peripheral nerve laceration and regeneration, namely, the degeneration of distal axons (Wallerian degeneration), the misdirection of regenerating axons, slow axonal regeneration and rapid muscle atrophy. Following nerve laceration, distal axons fall into axonal degeneration and leave empty Schwann tubes. Afterwards, several regenerating axons sprout from each proximal axon and they then regenerate into distal Schwann tubes in an almost random fashion. When sprouting axons migrate into different Schwann tubes other than their original tubes, misdirection occurs and functional recovery will not occur. The speed of axonal regeneration is usually from 1 to 2 mm a day. Denervated muscle atrophy progresses rapidly and becomes irreversible after one year. Therefore, muscles more than 36 cm distal to the nerve laceration site, for example, the hand muscles after a brachial plexus injury or the foot muscles after a sciatic nerve injury will not recover even after perfect nerve repair is accomplished. So far, neither Wallerian degeneration nor axonal misdirection can be prevented via pharmacological means. At present, the best functional recovery can be obtained by microsurgical nerve repair with correct funicular matching in order to prevent joint contracture and muscle atrophy, which can be prevented to a certain degree with stretching and electro-stimulation of the affected muscles. Additionally, sensory re-education can be used to improve object recognition.

Relation between fractional anisotropy in the cerebral peduncles and changes in motor evoked potential after acute middle cerebral artery territory infarction / 国际脑血管病杂志

Objective To investigate the changing characteristics of the fractional anisotropy (FA) in cerebral peduncles and its relation with motor evoked potential (MEP) after acute cerebral infarction and to clear the clinical sigiificance of the low limit value of the FA in cerebral peduncles. Methods The low limit value of the FA in normal cerebral peduncles was determined based on mean - 1. 64 standard deviation. The patients with acute cerebral infarction (n = 58) were divided into MEP positive group and MEP negative group according to the absence and presence of MEP, in which the patients in the MEP positive group were redivided into the FA in cerebral peduncles ＜ the low limit value and≥ the low limit value groups according to the FA in cerebral peduncles on the affected sides. Results The low limit value of the FA in normal cerebral peduncles was 0. 36. There was significant difference in the FA in cerebral peduncles on the affected sides between the MEP negtive and MEP positive groups. The MEP negative group was the lowest (P=0. 000). The FA in cerebral peduncles on the affected sides in the positive group was significantly lower than that on the unaffected sides (P=0. 000), and the latency on the affected sides was longer than that on the normal sides (P=0. 000). The FA in cerebral peduncles on the affected sides was negatively correlated with the MEP latency (r=-0.332,P=0. 042). The MEP latency in the FA＜the low limit value group was significantly longer than that in the FA ≥ low limit value group (P=0. 002). There were no significant differences in the FA in cerebral peduncles on the normal sides and the MEP latency among an groups. The detection rate of the FA in cerebral peduncle＜0. 36 on the affected sides was the highest (50%). Conclusions In the evaluation of the prognosis of the patients, the changes of the FA in cerebral peduncles on the affected sides in patients with acute cerebral infarction had correlation,consistency, and complementarity with MEP.The detection rate of the low limit value of the FA in normal cerebral peduncles was the highest in the MEP negative patients. When the FA in cerebral peduncles was＜0.36 on the affected sides, particularly when MET was negative, it might predict that the prognosis was poor.

Secondary damage remote from middle cerebral artery territory infarction / 国际脑血管病杂志

The research of the secondary damage remote from middle cerebral artery territory infarction has made significant progress in recent years.More animal experiments from the cellular,biochemical and molecular levels have been performed for in-depth and detailed research on remote site damage. The injury mechanisms such as oxidative damage and β amyloid deposition have been found.The new imaging detection technologies,such as magnetic resonance diffusion tensor imaging(DTI),have gradually been applied to the diagnosis of remote site damage.

Transient lysosomal activation is essential for p75 nerve growth factor receptor expression in myelinated Schwann cells during Wallerian degeneration / 대한해부학회지

Myelinated Schwann cells in the peripheral nervous system express the p75 nerve growth factor receptor (p75NGFR) as a consequence of Schwann cell dedifferentiation during Wallerian degeneration. p75NGFR has been implicated in the remyelination of regenerating nerves. Although many studies have shown various mechanisms underlying Schwann cell dedifferentiation, the molecular mechanism contributing to the re-expression of p75NGFR in differentiated Schwann cells is largely unknown. In the present study, we found that lysosomes were transiently activated in Schwann cells after nerve injury and that the inhibition of lysosomal activation by chloroquine or lysosomal acidification inhibitors prevented p75NGFR expression at the mRNA transcriptional level in an ex vivo Wallerian degeneration model. Lysosomal acidification inhibitors suppressed demyelination, but not axonal degeneration, thereby suggesting that demyelination mediated by lysosomes may be an important signal for inducing p75NGFR expression. Tumor necrosis factor-alpha (TNF-alpha) has been suggested to be involved in regulating p75NGFR expression in Schwann cells. In this study, we found that removing TNF-alpha in vivo did not significantly suppress the induction of both lysosomes and p75NGFR. Thus, these findings suggest that lysosomal activation is tightly correlated with the induction of p75NGFR in demyelinating Schwann cells during Wallerian degeneration.

Analysis of a case of Wallerian degeneration after stroke / 中华神经科杂志

Objective To study the process and mechanism underlying Wallerian degeneration of the central nervous system after stroke.Methods A case suspected of stroke with bilateral symmetrical lesions in middle cerebellar peduncles (MCPs) was described.The etiology of bilateral MCP abnormal signals on MR was analyzed according to the clinical process and neuroanatomy.Results Unilateral paramedian pontine infarction,covering the crossing area of pontocerebellar fibers, would cause bilateral secondary degeneration of MCPs,with hyperintense signals on T2-,Flair and diffusion-weighted images.Conclusions Wallerian degeneration of projecting system is a common sequel after stroke and should not be misdiagnosed as other diseases.

The Role of Axonopathy in Parkinson's Disease

New genetic and environmental studies of Parkinson's disease have revealed early problems in synaptic function and connectivity indicating that axonal impairment may be an important hallmark in this disorder. Since many studies suggest that axonal dysfunction precedes cell body loss, it is critical to target axons with treatments aimed at preserving "connectivity" as well as to develop and verify "biomarkers" with which to assess disease progression and drug efficacy.

Wallerian degeneration of the corticospinal tracts on diffusion tensor imaging after stroke and its relationship with impaired motor function / 国际脑血管病杂志

Wallerian degeneration of the corticospinal tracts is the anterograde degener-ation of distal axons and myelin caused by the upper motor neuron injury or axonal injury.Stroke is the most common cause of Wallerian degeneration of the corticospinal tracts. Conventional magnetic resonance imaging (MRI) of Wallerian degeneration of the corticospinal tracts is a linear abnormal signal that connects the original lesion along the corticospinal tracts, but the conventional MRI signal does not reveal Wallerian degeneration until 4 weeks after stroke. Diffusion tensor imaging (DTI) detects early Wallerian degeneration of the corticospinal tracts, and dynamically observes the process of pathological changes from early subacute stage to chronic stage. 1his article reviews Wallerian degeneration of the corticospinal tracts on DTI after stroke, especially the effect in early Wallerian degeneration, as well as the values in predicting prognosis and late rehabilitation in patients with stroke.

Diffusion tensor imaging in detection of Wallerian degeneration of pyramidal tract after cerebral infarction / 中华神经科杂志

Objective To investigate the evolution of diffusion indices in the pyramidal tract with Wallerian degeneration(WD)due to cerebral infarction using diffusion tensor imaging(DTI),and to study the relationship between early changes of diffusion indices and motor deficit.Methods Fifteen patients (13 males and 2 females)with acute cerebral infarction(within 7 days)were recruited from the Neurology Department from Mar 2006 to Jan 2007.A11 patients were assessed with DTI.National Institutes of Health Stroke Scale(NIHSS),Bathel Index(BI),modified Rankin Scale(mRS)and Motricity Index(MI)within 7 days from onset,and at the second week.DTI was performed with SIEMENS Trio 3.0 T MR scanner.The placement of region of interest(ROI),measurement of diffusion indices were performed by DTI Studio software.The mean diffusivity(MD),the fractional anisotropy(FA),the first eigenvalue (λ1),the second eigenvalue(λ2),and the third eigenvalue(λ3)were computed.Results At the second week.NIHSS was 6.93±3.39.BI 45.33±26.01,mRS 4.33±0.90.and MI 69.47± 60.71.At the second week from onset.MD of the pyramidal tract at the levels of the middle slice of pons and the superior slice of medulla oblongata showed no significant differences between both the two sides at second week from onset. Other ROI showed significant differences between both sides.MD.FA and λ1 of affected side were lower than the unaffected side.λ2 and λ3 of the affected side were higher than the unaffected side.Positive correlations were found between FA and BI(r=0.530,P=0.042),FA and MI(r=0.543,P=0.036)at the second week.Negative correlations were found between FA and NIHSS(r=-0.613,P=0.015)at the second week.Conclusions DTI can detect the changes in the pyramidal tract due to WD within 7-14 days after ischemic stroke.including a decrease of the fractional anisotropy.the first eigenvalue and increased the second and the third eigenvalues.The fractional anisotropy of the second week from onset is related to the outcome of the motor function.

Advance in Correlation between Post-stroke Wallerian Degeneration and Rehabilitation Outcome (review) / 中国康复理论与实践

@# Various central nerve system lesions involved cerebral hemisphere and nerve fiber tract such as cerebral infarction and hemorrhage can cause Wallerian degeneration,which is similar to the pathological change of peripheral nerve cut.There is a clear correlation between the degree of recovery and the degree of Wallerian degeneration.This article reviews the advances in feature of poststroke Wallerian degeneration and the correlation between post-stroke Wallerian degeneration and rehabilitation outcome.