Cord and Brain Stem Extensive Wallerian Degeneration: Rare Sequelae of Pontine Hemorrhage
Kajal Patel1, Casandra MacLeod1, Kim Griffin1, Chintan Shah2, Emmanuel Obusez2, Paul Ruggieri2, Jayashree Sundararajan1, Justin Abbatemarco1
1Neurological Institute, Cleveland Clinic, OH, 2Imaging Institute, Cleveland Clinic, OH
Objective:
We describe a case of extensive Wallerian degeneration (WD) as a complication of pontine hemorrhage causing initial diagnostic challenges.
Background:
Wallerian degeneration of the pontocerebellar and corticospinal tracts can be seen post pontine insult. Given this is uncommon, these imaging abnormalities may be misdiagnosed for other neurological conditions such as demyelinating disease.
Design/Methods:
N/A
Results:
A 55-year-old male with a history of poorly controlled hypertension, untreated obstructive sleep apnea, remote lacunar infarct and alcohol use disorder initially presented with sudden-onset right upper extremity weakness. CT brain showed an acute left pontine hemorrhage. Following rehabilitation, the motor symptoms improved significantly with minimal residual deficits. Approximately 3 months from his initial admission, he experienced subacute right-sided weakness in the right upper and lower extremities. MRI Brain and cervical spine with contrast showed FLAIR/T2 hyperintensities involving the bilateral middle cerebellar peduncles. In addition, there were FLAIR/T2 hyperintensities involving the anterior left medulla and upper spinal cord which then decussated into the right lateral corticospinal tract and extended inferiorly to C5 without contrast enhancement. The patient was treated with intravenous methylprednisolone for 5 days with some improvement in symptoms due to concerns for demyelinating disease. After further review of the imaging, findings were thought to be due to WD related to the prior pontine hemorrhage; additional areas of WD were also noted involving the corpus callosum secondary to remote white matter infarcts. This highlights the importance of awareness of different patterns of WD, and not mistaking such imaging findings for alternate etiologies such as a toxic/metabolic process or demyelinating disease.
Conclusions:
While uncommon, this case demonstrates that extensive Wallerian degeneration of the pontocerebellar and corticospinal tracts can be seen as T2 lesions on the MRI post pontine stroke and should not be mistaken for alternate etiologies.
10.1212/WNL.0000000000211578
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