Diffusion-weighted imaging in Wallerian degeneration

doi:10.1016/S0022-510X(00)00373-7

Journal of the Neurological Sciences

Volume 178, Issue 2, 15 September 2000, Pages 167-169

https://doi.org/10.1016/S0022-510X(00)00373-7 Get rights and content

Abstract

We report two patients displaying hyperintensities on diffusion-weighted imaging (DWI) in the area of Wallerian degeneration (WD) at 12 days after stroke. High signal intensities were more conspicuous on DWI than on T2-weighted images. Both patients showed decreased diffusion anisotropy resulting in elevated apparent diffusion coefficient in the area of WD. These patients illustrate that DWI may be useful in the detection of the early stage of WD.

Introduction

Wallerian degeneration (WD) refers to anterograde degeneration of axons and myelin sheath; it results from injury to the proximal portion of the axon or its cell body [1]. Several authors have addressed the temporal relationships of magnetic resonance (MR) imaging of WD and described distinct stages of WD according to abnormalities observed in the MR signal intensities [1], [2].

Diffusion-weighted imaging (DWI) can detect tiny changes in water diffusion, resulting in the early detection of a disturbed cellular homeostasis when cell damage and a fluid-shift from extracellular to intracellular space occur [3]. Early depiction of post-infarction WD with DWI has been recently reported, but the study lacked information about apparent diffusion coefficient (ADC) and diffusion anisotropy [4]. We report two patients with WD at the early subacute stage of ischemic stroke, with the findings of DWI, ADC and diffusion anisotropy.

Section snippets

Subjects and methods

We reviewed two patients (two men; 66 and 72 years) with a large infarction in the territory of the middle cerebral artery (MCA). Both patients were examined on a 1.5 T MR unit (Signa Horizon, Echospeed; General Electric Medical Systems, Milwaukee, WI) with echoplanar imaging (EPI) capability. Fast spin-echo, T2-weighted images (T2WI; TR/TE, 4200/112 ms; field of view, 21×21 cm; matrix, 256×192; and slice thickness, 5 mm with 1.5 mm gap) were obtained. DWI was obtained in the transverse plane

Results

Patient 1 with atrial fibrillation presented with drowsiness, hemiplegia, hemihypesthesia and visual field defect on the left side. T2WI and DWI performed at 1 day after stroke showed hyperintensities in the territory of MCA on the right side. Low signal intensity in the center of the lesion suggested hemorrhagic transformation. At 12 days after onset, the extent of hyperintensities in the MCA territory were more or less attenuated, instead strong high signal intensities appeared along the

Discussion

DWI demonstrated hyperintensities in the area of WD at the early subacute stage of stroke in our patients. High signal intensities along the pyramidal tract in the internal capsule and brainstem in patients with an ischemic stroke could have led to a misdiagnosis of hyperintensities as ischemic lesions. However, lesion distribution involving the midbrain and pons and elevation of ADC values in these areas were compatible with WD rather than ischemic damage.

Various mechanisms have been suggested

Acknowledgements

The authors thank Byung Kee Yoo for his assistance with diffusion-weighted MR data acquisition.

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View full text

Diffusion-weighted imaging in Wallerian degeneration

Abstract

Introduction

Section snippets

Subjects and methods

Results

Discussion

Acknowledgements

Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging

Radiology

MR imaging of Wallerian degeneration in the brainstem: temporal relationships

Am J Neuroradiol

Diffusion-weighted imaging for acute cerebral infarction

Neurol Res

Early abnormalities related to postinfarction Wallerian degeneration: evaluation with MR diffusion-weighted imaging

J Comput Assist Tomogr

Spin diffusion measurements: spin echoes in the presence of a time-dependent field gradient

J Chem Physiol

Wallerian degeneration of the pyramidal tract after a thrombotic stroke

J Neurol Neurosurg Psychiatry