<!-- /* Font Definitions */ @font-face {font-family:SimSun; panose-1:2 1 6 0 3 1 1 1 1 1; mso-font-alt:??; mso-font-charset:134; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 135135232 16 0 262145 0;} @font-face {font-family:"Cambria Math"; panose-1:2 4 5 3 5 4 6 3 2 4; mso-font-charset:0; mso-generic-font-family:roman; mso-font-pitch:variable; mso-font-signature:-1610611985 1107304683 0 0 159 0;} @font-face {font-family:Verdana; panose-1:2 11 6 4 3 5 4 4 2 4; mso-font-charset:0; mso-generic-font-family:swiss; mso-font-pitch:variable; mso-font-signature:536871559 0 0 0 415 0;} @font-face {font-family:"\@SimSun"; panose-1:2 1 6 0 3 1 1 1 1 1; mso-font-charset:134; mso-generic-font-family:auto; mso-font-pitch:variable; mso-font-signature:3 135135232 16 0 262145 0;} /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-unhide:no; mso-style-qformat:yes; mso-style-parent:""; margin:0cm; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:9.0pt; font-family:"Verdana","sans-serif"; mso-fareast-font-family:SimSun; mso-bidi-font-family:"Times New Roman"; mso-ansi-language:FR; mso-fareast-language:ZH-CN;} .MsoChpDefault {mso-style-type:export-only; mso-default-props:yes; font-size:10.0pt; mso-ansi-font-size:10.0pt; mso-bidi-font-size:10.0pt; mso-ascii-font-family:Calibri; mso-fareast-font-family:Calibri; mso-hansi-font-family:Calibri;} @page Section1 {size:612.0pt 792.0pt; margin:70.85pt 3.0cm 70.85pt 3.0cm; mso-header-margin:36.0pt; mso-footer-margin:36.0pt; mso-paper-source:0;} div.Section1 {page:Section1;} --> Background: Central pontine myelinolysis (CPM) in the context of liver transplantation is significant, being the most severe neurological complication in the immediate post-transplant period. Objectives: The absence of identifiable electrolyte abnormalities in these hepatic transplant cases suggests another pathogenic cause of CPM. Our aim was to identify and characterize the phenomenon. Patients and Method: In a series of twenty-seven liver transplant patients between 2005 and 2008, we selected six patients who developed CPM and studied their pre-and post-operative courses. Between post-operative days two and seven, the patients presented with severe hepatic encephalopathy and a predominantly proximal quadriplegia in the absence of electrolyte abnormalities, which was expressed by hyperreflexia and the Babinski sign. Results: In affected patients, MRI images revealed demyelination of the motor pathway in the central area of protuberance. We followed these patients’ motor recovery. We found these changes began in the fingers and hands, followed by forearms, toes, feet, arms and finally legs, defining the somatotopy of the corticospinal pathway at this level. This correlated well with the anatomical distribution of the descending motor fibers within the pons. Conclusions: In this context, we suggest CPM is caused by local entrapment of motor fibers due to the structural rigidity of the central pons, secondary to cytotoxic insults and vasogenic edema on nervous tissue already sensitized by long-standing encephalopathy. This entrapment syndrome preserved axons and injured myelin, but caused no inflammatory reaction, consistent with the classic description of Adams and Victor.