Published online Dec 28, 2015. doi: 10.4329/wjr.v7.i12.438
Peer-review started: July 24, 2015
First decision: August 25, 2015
Revised: September 5, 2015
Accepted: October 23, 2015
Article in press: October 27, 2015
Published online: December 28, 2015
Processing time: 158 Days and 10.9 Hours
We describe common and less common diseases that can cause magnetic resonance signal abnormalities of middle cerebellar peduncles (MCP), offering a systematic approach correlating imaging findings with clinical clues and pathologic mechanisms. Myelin abnormalities, different types of edema or neurodegenerative processes, can cause areas of abnormal T2 signal, variable enhancement, and patterns of diffusivity of MCP. Pathologies such as demyelinating disorders or certain neurodegenerative entities (e.g., multiple system atrophy or fragile X-associated tremor-ataxia syndrome) appear to have predilection for MCP. Careful evaluation of concomitant imaging findings in the brain or brainstem; and focused correlation with key clinical findings such as immunosuppression for progressive multifocal leukoencephalopahty; hypertension, post-transplant status or high dose chemotherapy for posterior reversible encephalopathy; electrolyte disorders for myelinolysis or suspected toxic-drug related encephalopathy; would yield an appropriate and accurate differential diagnosis in the majority of cases.
Core tip: Though a few prior reviews have described pathologic processes involving the middle cerebellar peduncles (MCP), our paper offers not only an updated approach to include diffusion tensor imaging but also important correlations of imaging findings with anatomy, pathophysiologic insights and key clinical scenarios. Overall, this concise and comprehensive review is expected to help the readers not only to improve their approach to cases with MCP involvement, but also to increase awareness and understanding of pathologic processes increasingly seen in neuroimaging such as progressive multifocal leukoencephalopahty, posterior reversible encephalopathy and toxic encephalopathies.