摘要Objectives: To explore the main etiological factors of central pontine myelinolysis (CPM) and of the “osmotic demyelination syndrome(ODS)”that occurs after hepatic transplantation, to explore the differential diagnosing the manifestation consisting of dysarthria, dysphagia and quadriplegia presented after vomiting for a number of times, and to explore which fraction to be mainly involved by the “ODS”, what to be the pathological mechanism of the “ODS”, and how to prevent the “ODS”.Methods: Physiopathological principles are applied on the base of the clinical certificates, the diagnostic results differring from those in the case reports (that have been analyzed again by us).Results and Conclusions: It could be suggested that (1) CPM based mainly on alcoholism should result mainly from beriberi, as was mentioned by HUANG Ke-wei, the well-known Chinese neurologist, before or in 1960; (2) The coma secondary to hepatic transplantation could be often caused by Wernicke encephalopathy(WE, one of beriberi), which could be asscociated with the postoperative elevated corticosteroid or/and high-starch food for liver cirrhosis, which complicated by hepatic encephalopathy; (3)The case that was in 1995 reported by Kabeer et al, of possiblity of the earliest reported CPM due to cyclosporine, appeared to be the bilateral type of pontine lower paracentral hematal syndrome, a bilateral uncomplete Foville syndrome. It should be considerable whether an epileptic attack related to both cyclosporine and corticosteroid could result from reverible posterior leukoencephalopath syndrome with negative MRI owing to the effect of corticosteroid; (4) It is cerebral cortex that could be mainly involved by the “ODS” following a number of times of vomiting, of which one of evidences has been the 2 cases reported by Tomlinson et al in 1976.The kind of “ODS” following the encephalopathy of alkalosis yet without hypoxemic hypoxia, is possibly preventable not only if the correction of hypokalemia is firstly comsidered and also if corticosteroid(for 3 days or shorter) is preventivly applied before correction of hyponatremia(0.9%NaCl, via digestive tract).Dose -filled vitamin B1 (i.m.), however, ought to be given so as not to induce beriberi including CPM before corticosteroid is used; (5) The hypokalemia caused by vomiting and alkalosis thereof, can maybe account for dysarthria, dysphagia and quadriplegia, when there is not obvious difference between the severity of bulbar paralysis and that of quadriplegia ; and quadriceps reflex often plays down in patient with hypokalemic non-periodic paralysis(HNP).Thereby, each of some reported cases with (clinical)CPM, including several of 22 ones reported by Heng, et al(2007), the one by Shintani, et al(2005) and the one by B?hr, et al(1990), has shown itself rather as sub-clinical CPM (with HNP) than clinical CPM (without HNP) suggested only by MRI.(6)It is supposed that why for CPM to involve the pyramidal tract inside pone, could be based on that the pontine paracentral branch of basilar artery had tended to “degeneration”in a limited degree since the cerebellar branches and posterior cerebral branch precedently developed following the evolution of the zoogenetic cerebellum and occipital lobe towards human brain, therefore, the pathologic mechanism of a beriberi CPM could be similar to the compensatory process of the bilateral type of the “chronic medipontine paracentral hematal syndrome” assumed by us. The whole essay including the aforementioned things has been published in No.1 of Vol.2012 of Academy Journal of Medical College of Henan University of China in Chinese language in March, 2012[1].