The osmotic demyelination syndrome: the resilience of thalamic neurons is verified with transmission electron microscopy

A primary cilium in oligodendrocytes: a fine structure signal of repairs in thalamic Osmotic Demyelination Syndrome (ODS)

“…8,20 Consequently, one would consider that myelination could also undergo some restitution in the ODS-susceptible regions of the CNS after myelinolysis where loss of axon parts along with macroglial damages have been recognized. [15][16][17][18] This report again analyzes the same groups of mice that have revealed ODS extrapontine tissue's changes in [15][16][17][18] and further comforts all those data of this murine model of osmotic demyelinating syndrome (ODS) where the relay ventral posterolateral (VPL) and ventral posteromedial (VPM) thalamic nuclei have been shown susceptible toward osmotic-induced demyelination. 19 It adds information about ongoing ODS oligodendrocyte changes and repairs.…”

“…Those changes were revealed along with astrogliosis as well as with clasmatodendrosis (cell body swelling with fragmentation of distal processes 16,17,42 ). They were linked to other myelin repression or damages of molecular markers and losses [15][16][17]43 accompanied by a local, restricted microglial cell's reactivity, [15][16][17][18][19] verified by ultrastructure. [15][16][17] In ODS, the delimited CNS EPM cytotoxic events of the thalamic injuries do not involve irreversible damages in the CNS neurons, demonstrating resilience in the same demyelinated regions.…”

“…ODS induction was based on the correction of a chronic hyponatremia, adapted protocol from, 36 as described in. [15][16][17][18] Briefly, an osmotic minipump (Model 1004, Alzet, Cupertino, CA) was filled with desmopressin acetate (2 µg/ml; Minirin, Ferring, Saint-Prex, Switzerland) and inserted subcutaneously under anesthesia into the back of animals at day 0. Standard pellets and water were switched to a low-sodium liquid diet (AIN76A, MP Biomedicals, Santa Ana, CA), given ad libitum for the whole duration of hyponatremia.…”

“…[15][16][17] In ODS, the delimited CNS EPM cytotoxic events of the thalamic injuries do not involve irreversible damages in the CNS neurons, demonstrating resilience in the same demyelinated regions. 18 Others have observed LIF (Leukemia Inhibitory Factor), secreted at ODS48h by both astrocytes and microglial cells, 8 as stimulating myelination can suggest healing out of ODS. Moreover, clinical ODS cases can heal after a proper rebalancing osmolarity.…”

“…[1][2][3][4][5][6][7][8] The ODS neuropathologic syndrome is caused by a hastily adjustment of a temporary or chronic deficiency of the homeostatic sodium gradient as it can be pertinent to diverse homeostatic hormonal sodic perturbations such as those afflicted by exaggerated body fluid losses and emergently treated for alcoholism, diabetes as well as to defective dialysis. [1][2][3][9][10][11][12][13][14] A large reference list of ODS literature was recently cited [15][16][17][18][19] and it appeared that EPM lesions can appear before any CPM ones [19][20][21][22][23][24][25] and ODS in human EPM cases would be more frequent than CPM ones. 23 There, ODS can frequently appear clinically in the elderly, hospitalized population.…”