Clinical Neurology and Neurosurgery 115 (2013) 1164–1166 Contents lists available at SciVerse ScienceDirect Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro Case Report Early corticospinal tract Wallerian degeneration on diffusion-weighted MR imaging after adult stroke: Three cases report Jun Ni a , Ming-li Li b , Ming Yao a , Li-ying Cui a,∗ a b Department of Neurology, Peking Union Medical College Hospital and Chinese Academy of Medical Science, No. 1 Shuai Fu Yuan, Dong Cheng District, Beijing 100730, China Department of Radiology, Peking Union Medical College Hospital and Chinese Academy of Medical Science, No. 1 Shuai Fu Yuan, Dong Cheng District, Beijing 100730, China a r t i c l e i n f o Article history: Received 21 February 2011 Received in revised form 3 March 2012 Accepted 29 September 2012 Available online 2 November 2012 Keywords: Early Wallerian degeneration Stroke Diffusion-weighted imaging Corticospinal tract 1. Introduction Ischemic stroke usually damages supratentorial motor systems which results in hemiparalysis. Both pediatric and adult studies have demonstrated that stroke-induced chronic descending corticospinal tract atrophy on MR imaging is consistent with Wallerian degeneration (WD) and that chronic WD is associated with poor motor outcome [1]. Such findings of WD at chronic phase, however, are of limited clinical significance. Early WD of neonatal and pediatric stroke has been identified on diffusion-weighted MR imaging (DW-MRI) [2]. In terms of early WD on DW-MRI in adult stroke, few case studies have been reported [3–5]. Presented herein are three adult cases of early cerebral peduncle WD secondary to acute hemispheric stroke detected on DW-MRI, which should not be mistaken as separate primary stroke lesions. 2. Cases report 2.1. Patient 1 A 43-year-old woman presented with sudden onset of rightsided weakness for one and a half hours. She was alert, with right facial palsy during examination. Strength was graded as 0 and 3 out of 5 on the right upper and lower extremities, respectively. Right Babinski’s sign was positive. DW-MRI performed two days later ∗ Corresponding author. Tel.: +86 10 65296372. E-mail address: cuiliying2010@yahoo.cn (L.-y. Cui). 0303-8467/$ – see front matter © 2012 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.clineuro.2012.09.027 showed acute infarction in left basal ganglia with hyperintensity on DWI and hypointensity on apparent diffusion coefficient (ADC) map (Fig. A1–2). Imaging of ipsilateral peduncle also demonstrated DWI hyperintensity and ADC hypointensity, which was considered to be early WD (Fig. A3–4). MRA showed right MCA occlusion. Both echocardiography and ECG were normal. She received Atorvastatin Calcium Tablet and Aspirin and had a poor motor outcome with slight improvement of right weakness three months later. 2.2. Patient 2 A 62-year-old man presented with right-sided weakness and slurred speech for one day. He was alert, with partial expressive aphasia during examination. Strength was graded as 4 out of 5 on right upper extremity and normal on the other extremities. Right Babinski’s sign was positive. DW-MRI performed eight days later showed subacute infarction in the left basal ganglia and periventricular white matter and signal abnormalities considered as WD in left peduncle with DWI hyperintensity and hypointensity on ADC map (Fig. B1–4). MRA showed left MCA mild stenosis. Both echocardiography and ECG were normal. He was treated with Aspirin, antihypertensive agent, and glucose control and had improvement of right weakness three months later. 2.3. Patient 3 A 34-year-old man was admitted with three episodes of rightsided weakness for half a month. His weakness relieved after every episode. He was alert, with right facial palsy during examination. J. Ni et al. / Clinical Neurology and Neurosurgery 115 (2013) 1164–1166 1165 Fig. (A1–4 case 1) DW-MRI showed an acute infarction in left basal ganglia (A1) with decreased ADC value (A2). Imaging of the cerebral peduncle demonstrated hyperintensity on DWI (A3) with hypointensity on ADC (A4). (B1–4 case 2) DW-MRI demonstrated an acute infarction in left corona radiate (B1) with decreased ADC value (B2). Imaging of the cerebral peduncle showed hyperintensity on DWI (B3) with hypointensity on ADC (B4). (C1–4 case 3) DW-MRI demonstrated an acute infarction in left basal ganglia (C1) with hypointensity on ADC (C2). DWI hyperintensity (C3) was also seen in left peduncle with hypointensity on ADC (C4). Strength was graded as 5 out of 5 on extremities bilaterally. Brain DW-MRI that was performed ten days after the last onset revealed subacute infarction in the left basal ganglia and hyperintensity in left cerebral peduncle with ADC hypointensity (Fig.C1–4). MRA showed left MCA mild stenosis. Both ECG and transesophageal Echocardiography were normal. He received Atorvastatin Calcium Tablet and Clopidogrel and had a good motor outcome three months later. 3. Discussion A total of three cases are presented on acute or subacute hemispheric stroke with early DW-MRI signal abnormalities (DW hyperintensity and ADC hypointensity) in ipsilateral descending corticospinal tracts (peduncle). It is believed that these lesions located in peduncle are acute WD other than stroke lesions due to the following reasons: (1) the DWI of the patients showed multiple lesions in both anterior and posterior circulations, which might be considered as cardiac embolism. However, ECG and UCG results were normal in all cases and no evidence of cardiac embolism was shown; and (2) the ipsilateral PCA was normal in all cases. As the PCA is the critical vessel for supply of the peduncles this makes additional ischemia in this territory rather unlikely. Findings from these three cases indicate that DWI can detect early injury of corticospinal tracts secondary to WD in adult stroke. Previous reports have shown that acute WD was associated with poor motor outcome. Nevertheless, two of our patients had good motor recovery outcome, which is in conflict with the findings from previous reports. Further studies appear to be necessary. WD is secondary antegrade degeneration of distal axons after injury of the neuronal cell body and/or its proximal axon, which is commonly seen after stroke. Generally, WD cannot be identified up to 4 weeks after stroke using the conventional MRI. The use of DWI for detecting acute WD has recently been reported in neonatal and pediatric stroke patients. However, acute WD after stroke in adults has rarely been reported. This may indicate that neonatal brain might be more susceptible to early corticospinal tracts injury due to the differences in myelin development or water 1166 J. Ni et al. / Clinical Neurology and Neurosurgery 115 (2013) 1164–1166 content between adult and neonate brains. Sometimes lesions detected by DWI may be contaminated by “T2 shine through”, which was expected to be more prominent in adult because of concurrent brain stem small vessel diseases. Nevertheless, the cerebral peduncle lesions reported in the present study were hypointensive in ADC map, which is inconsistent with “T2 shine through”. Up to date, few adult cases have been reported with early corticospinal tract WD after stroke. Uchino [3] and Castillo [4] found early increased corticospinal tract signal on DWI after acute stroke in adults. But these studies were limited in that ADC maps were not generated. Kang [5] reported early WD in two adults after acute stroke with hyperintensity on both DWI and ADC maps. DeVetten and his colleagues found acute corticospinal tract WD on DWI, ADC, and fluid-attenuated inversion recovery imaging, which was associated with stroke outcome [6]. Our three cases, however, appear to show that the WD lesions and the primary stroke lesions share the same imaging features. It has been known that the presumed mechanism of the primary stroke lesions is restricted diffusion due to cytotoxic edema. The precise underlying mechanism remains unclear of these signal changes on DWI and ADC in acute WD lesions. This restricted diffusion possibly results from acute axonal degeneration following damage to a fiber tract or myelin swelling secondary to cytotoxic edema [4]. The potential explanation of observed changes in ADC and DWI of WD lesions may be the cessation of energy-dependent axoplasmic transport processes. According to a recent study [7], the hyperintensity on DWI within acute WD lesions was a transient pathological process of Wallerian degeneration after ischemic stroke. Due to the limited amount of patients that were involved in our study and the findings were only determined from imaging, further patho-radiological study is probably necessary to identify the exact mechanism. More advanced imaging techniques such as diffusion tension imaging (DTI) have been used for detecting early WD and predicting outcome in acute stroke. DTI is more sensitive than the conventional MR imaging in detecting WD. It has also been used as an imaging surrogate marker for motor deficit. Nevertheless, post-processing procedures are needed for DTI, which makes it less applicable to clinical use at this stage. 4. Conclusions The DWI signal abnormality with decreased ADC values along with the ipsilateral corticospinal tracts of a hemispheric infarction should not be mistaken for a second infarction outside the involved vascular territory. 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