Signs of Wallerian Degeneration Occur within Weeks Following Brain Tumor Surgery-Related Ischemic Stroke

Aim: Wallerian degeneration (WD) is characterized by axonal degeneration and demyelination following injury to the CNS. Due to the enlargement of the extracellular space WD results in hyperintense T2 signal changes along the corticospinal tract on MRI and ipsilateral brainstem atrophy. To date not much is known about the time course of such changes in patients with brain tumors.

Methods: We analyzed charts and pre- and post-operative MRI of patients with supra-tentorial brain tumors diagnosed with post-operative WD of the corticospinal tract. Three WD patients were identified who developed hemiparesis consecutive to a surgery-related stroke of the middle cerebral artery territory. MRI was analyzed, searching for typical hyperintense signal changes within the ipsilateral corticospinal tract of the brain stem. We measured the ipsi (ILAT)- and contra (CLAT)- lateral brain stem area on T2-weighted images and calculated an asymmetry index as a measure of hemiatrophy (AI=100*(ILAT-CLAT)/(ILAT+CLAT) [%]). Results were then compared with the extent and time course of contralateral motor weakness. The motor score of the paretic side equals the sum of the proximal and distal upper and lower limb muscle strength (MRC normal motor score: 20, hemiplegia: 0). Control group: six patients not suffering from post-operative WD and hemiparesis.

Results: Pre-operatively no MRI revealed signs of WD and no patient showed any motor deficit. In the post-operative MRI of the WD patients hyperintense signal changes in T2-weighted images within the ipsilateral corticospinal tract descending from the cerebral peduncle through the pons and medulla oblongata together with a hemiatrophy of the brainstem were detected. These changes occurred as early as 1.5 months after surgery and persisted during the whole follow-up period (3.4 to 27.6 months). All WD patients developed contralateral motor deficits with a post-operative decline of the motor score by 8 to 13 points. Neither the imaging changes nor the functional deficits improved over time. In the control group the mean AI was 0.1% (range: -1.81 to 0.97%).

Conclusion: MRI signs of WD develop within a few weeks after stroke due to brain tumor surgery. WD is associated with persisting motor deficit. The hyperintense MRI changes typical for WD must not be confounded with tumor progression or tumor induced edema respectively. Whether corticospinal compression or infiltration by the tumor itself can cause WD is under investigation.