A Rare Imaging Finding in Multiple Sclerosis : Wallerian Degeneration of the Corticospinal Tract

Background: Wallerian degeneration (WD) in central nervous system (CNS) disease is a well known phenomenon, though the process is slower than in the peripheral nervous system. WD has been documented commonly in stroke and rarely in multiple sclerosis (MS). There have been few cases reported of magnetic resonance imaging (MRI) demonstration of WD following a first demyelinating event in patients at risk for MS. Herein, we report two patients with MRI findings of WD of the ipsilateral corticospinal tract after acute demyelinating hemispheric events.

Objectives: To report rare imaging findings in early multiple sclerosis.

Methods: Case series.

Results: Patient 1: A 32-year-old female woke up with a pulling sensation on her left side and left facial droop. Examination showed subtle left sided weakness. MRI of the brain showed 2 periventricular T2 hyperintense lesions, one in right centrum semiovale which showed restricted diffusion and subtle contrast enhancement, and another in right parietal lobe which showed open ring enhancement. Cerebrospinal fluid (CSF) was negative for oligoclonal bands. She was started on Interferon beta-1b. Follow up MRI 7 months after presentation showed new T2 hyperintensities along the right corticospinal tract from the centrum semiovale to the pons. The examination was non-focal at that point. Patient 2: A 46-year-old male with a history of hypertension presented with acute onset right sided weakness and dysarthria. Examination showed dysarthria, right facial droop, and right hemiparesis (arm>leg). MRI of the brain showed 3 large ovoid T2 hyperintense lesions located in the left corona radiata, left occipital-parietal lobe junction and right occipital lobe, all with patchy contrast enhancement. Two of the lesions showed a concentric ring appearance. CSF was negative for oligoclonal bands. His weakness improved after 5 days of high dose intravenous corticosteroids and plasma exchange. Follow-up MRI 9 months later showed one new periventricular lesion without enhancement and T2 hyperintense signal along the left corticospinal tract to the pontomedullary junction.  His examination at follow up was significant for right spastic hemiparesis. 

Conclusions: WD in the corticospinal tract is a rare imaging feature of early MS, presumed to be reflective of axonal degeneration. Although some data suggest that WD is a poor prognostic marker for recovery, our patient-1 has no deficits. Further studies comparing MRI and clinical outcome are indicated to understand this phenomenon.