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Retrograde degeneration of the corticospinal tract associated with pontine infarction

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Abstract

We report a 40-year-old man with myotonic dystrophy who survived for 5 years after pontine infarction. Serial MRI detected abnormal T2 elongation of the corticospinal tract at the cerebral peduncle 4 years after the infarction. An autopsy confirmed the existence of retrograde degeneration extending from the pons to the internal capsule, evidence that retrograde degeneration in the corticospinal tract occurs above the pontine level. MRI was suggested to be useful for detection of the degenerative process.

Introduction

Retrograde degeneration of the corticospinal tract (RD-CST) of the human central nervous system is considered controversial and exceptional [1], [2], [3], [4]. Of the few cases reported, all were secondary to a lesion in the spinal cord. So rare and inconsistent is this phenomenon, even in experimental settings, that the histological characteristics and pathogenesis of RD-CST remain obscure. This is the first report of a case of RD-CST secondary to a brainstem lesion. It was detected by MRI and confirmed by postmortem examination.

Section snippets

Case report

A 40-year-old man suddenly developed left hemiparesis and was admitted to our hospital. On arrival CT detected a low-density area at the upper pontine basis with right dominance. He had a history of familial progressive muscle weakness from his second decade. Examination showed severe flaccid left hemiparesis and dysarthria. He was bald in front, and his face had the hatchet-like appearance characteristic of myotonic dystrophy. Grip myotonia and percussion myotonia were present. The diagnosis

Discussion

Ours is the first report of RD-CST secondary to a brainstem lesion. This case is characterized by a limited lesion at the pontine basis, the only other event being cardiopulmonary arrest 5 days after pontine infarction. Both T2 high intensity on the MRI and myelin pallor on the histological specimen obscured at the level of the IC (Fig. 1D and G). There was no lesion above this level, including in the primary motor cortices. Serial MRI studies at admission and four and a half years after the

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