Post-hydrocephalus corpus callosum damage

Last revised by Frank Gaillard on 11 Feb 2024

Post-hydrocephalus corpus callosum damage is seen both in the setting of, and following treatment for, long-standing hydrocephalus. The exact pathophysiology remains to be fully elucidated but both compression and rapid decompression with resultant changes in morphology have been implicated.

Two patterns are identified:

  1. thinning of the corpus callosum

  2. swelling evolving to gliosis and distortion following treatment

The term corpus callosum impingement syndrome is encountered in the literature for both patterns 6, although this suggests that the primary etiology is compression which does not appear to be the case in the post-treatment changes encountered (see below).

Affected patients tend to have had a significant hydrocephalus for a protracted period. It is more common in obstructive hydrocephalus (e.g. aqueduct stenosis) 1.

Thinning of the corpus callosum is believed to be caused by impingement of the corpus callosal fibers against the inferior free margin of the falx cerebri due to longstanding and severe hydrocephalus and stretching of the lateral ventricles resulting in axonal loss 7.

The exact mechanisms of the more pronounced scalloping changes seen following decompression, remain to be fully elucidated. Prolonged compression of the corpus callosum against the falx cerebri appears to be necessary, however, it does not appear to be the actual insult that results in eventual damage as pre-decompression the corpus callosum appears thinned but otherwise normal 1-4.

Not only that, but in the acute post-shunting period swelling and increased T2 signal of the corpus callosum have been observed 5 indicating that it is the rapid inferior displacement of the corpus callosum that results from ventricular size reduction that is the likely inciting event.

One postulated mechanism is that protracted superior displacement of the corpus callosum results in the shortening of the perforating branches of the pericallosal artery 2.

When hydrocephalus is subsequently relieved, these tethered perforators are stretched and perhaps occluded resulting in ischemic damage to the corpus callosum 2,5.

Radiographic features will vary depending on when imaging is obtained relative to decompression.

Prior to decompression the corpus callosum will typically appear upwardly bowed with reduced thickness.

Immediately after shunt insertion, no abnormality may be present, if ventricular size has not yet significantly changed. Later, when ventricular size reduces and the corpus callosum descends callosal damage occur. At this time the corpus callosum will appear swollen and edematous.

Over time these acute changes abate resulting in a thinned, gliotic and distorted appearance with characteristic upper-surfface scalloping 1-4.

In the setting of treatment for prior longstanding hydrocephalus, there is essentially no viable differential diagnosis.

The importance of recognizing thes patterns is to differentiate hydrocephalus-related callosal changes from the more serious conditions such as lymphoma, glioblastoma, and demyelinating diseases which can, in the acute and sub-acute period, appear similar.

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