scholarly journals Osmotic Demyelination: From an Oligodendrocyte to an Astrocyte Perspective

2019 ◽  
Vol 20 (5) ◽  
pp. 1124 ◽  
Author(s):  
Charles Nicaise ◽  
Catherine Marneffe ◽  
Joanna Bouchat ◽  
Jacques Gilloteaux
Keyword(s):  
Glial Cells ◽  
Serum Sodium ◽  
Brain Regions ◽  
Osmotic Demyelination Syndrome ◽  
Brain Areas ◽  
Osmotic Demyelination ◽  
Central Myelin ◽  
Barrier Breakdown ◽  
Blood Brain Barrier Breakdown

Osmotic demyelination syndrome (ODS) is a disorder of the central myelin that is often associated with a precipitous rise of serum sodium. Remarkably, while the myelin and oligodendrocytes of specific brain areas degenerate during the disease, neighboring neurons and axons appear unspoiled, and neuroinflammation appears only once demyelination is well established. In addition to blood‒brain barrier breakdown and microglia activation, astrocyte death is among one of the earliest events during ODS pathology. This review will focus on various aspects of biochemical, molecular and cellular aspects of oligodendrocyte and astrocyte changes in ODS-susceptible brain regions, with an emphasis on the crosstalk between those two glial cells. Emerging evidence pointing to the initiating role of astrocytes in region-specific degeneration are discussed.

Effects of intermittent reperfusion during temporal focal ischemia

1992 ◽  
Vol 77 (6) ◽  
pp. 911-916 ◽  
Author(s):  
Marc S. Goldman ◽  
Robert E. Anderson ◽  
Fredric B. Meyer
Keyword(s):  
Arterial Occlusion ◽  
Vessel Occlusion ◽  
Content Type ◽  
Mca Occlusion ◽  
Ischemic Period ◽  
Occlusion Technique ◽  
Barrier Breakdown ◽  
Aneurysm Repair ◽  
Blood Brain Barrier Breakdown

✓ There is controversy regarding the role of intermittent reperfusion employed as a cerebroprotective measure when temporary arterial occlusion is necessary during repair of difficult aneurysms. The intraluminal suture middle cerebral artery (MCA) occlusion technique was used in 23 Wistar rats under barbiturate anesthesia to induce 60, 90, or 120 minutes of uninterrupted MCA occlusion. The total infarcted areas obtained were compared to those occurring in 27 animals subjected to identical cumulative ischemic periods but with 5 minutes of reperfusion after every 10-minute ischemic period. The mean total infarcted areas in the groups with 60-minute (1.8 ± 0.89 sq mm), 90-minute (1.08 ± 1.02 sq mm), and 120-minute (8.72 ± 5.89 sq mm) intermittent reperfusion were significantly smaller than those occurring in the 60-minute (12.02 ± 3.10 sq mm), 90-minute (11.54 ± 2.68 sq mm), or 120-minute (30.43 ± 6.51 sq mm) control groups, respectively (p < 0.05). Furthermore, there was no difference in the occurrence of blood-brain barrier breakdown, intraparenchymal hemorrhage, hemispheric edema, or seizures between control and intermittent reperfusion groups. The results support the hypothesis that intermittent reperfusion is beneficial if vessel occlusion is required during aneurysm repair.

scholarly journals Isolated Extrapontine Myelinolysis of Osmotic Demyelination Syndrome

2013 ◽  
Vol 114 (1) ◽  
pp. 35-38
Author(s):  
Ömer Yılmaz ◽  
H. H. Armağn ◽  
A. Turan ◽  
M. Duymuş
Keyword(s):  
Serum Sodium ◽  
Rare Case ◽  
Sodium Concentration ◽  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination ◽  
Extracellular Compartment ◽  
Rapid Changes ◽  
The Brain ◽  
Current Report ◽  
Rapid Correction

The osmotic demyelination syndrome (ODS) has been identified as a complication of the rapid correction of hyponatremia for decades (King and Rosner, 2010). However, in recent years, a variety of other medical conditions have been associated with the development of ODS, independent of changes in serum sodium which cause a rapid changes in osmolality of the interstitial (extracellular) compartment of the brain leading to dehydration of energy-depleted cells with subsequent axonal damage that occurs in characteristic areas (King and Rosner, 2010). Slow correction of the serum sodium concentration and additional administration of corticosteroids seems to be a major prevention step in ODS patients. In the current report we aimed to share a rare case which we observed in our clinic.

Osmotic demyelination syndrome following slow correction of hyponatraemia

2021 ◽  
Vol 14 (8) ◽  
pp. e241407
Author(s):  
Isabel Saunders ◽  
David M Williams ◽  
Aliya Mohd Ruslan ◽  
Thinzar Min
Keyword(s):  
Antidiuretic Hormone ◽  
Serum Sodium ◽  
Inflammatory Markers ◽  
Urine Osmolality ◽  
Fluid Restriction ◽  
Osmotic Demyelination Syndrome ◽  
Electrolyte Disturbance ◽  
Osmotic Demyelination ◽  
Sodium Correction ◽  
Hospital Inpatients

Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.

scholarly journals Effects of the alpha-1 antagonist prazosin on KOR agonist-induced reinstatement of alcohol seeking

2019 ◽  
Author(s):  
Douglas Funk ◽  
Kathleen Coen ◽  
Sahar Tamadon ◽  
A D Lê
Keyword(s):  
Stress Responses ◽  
Brain Activation ◽  
Brain Regions ◽  
Stress Disorders ◽  
Kappa Opioid Receptors ◽  
Brain Areas ◽  
Adrenoceptor Antagonist ◽  
Fos Expression ◽  
Alcohol Seeking

Abstract Background Stress is associated with relapse to alcohol seeking during abstinence, but the processes underlying this relationship are poorly understood. Noradrenaline is a key transmitter in stress responses and in stress-induced drug seeking. The alpha-1 adrenoceptor antagonist prazosin has been investigated as a treatment for alcoholism and for chronic stress disorders that are frequently comorbid with alcoholism. In rats, we previously showed that prazosin blocks reinstatement of alcohol seeking induced by footshock and yohimbine stressors, and reduces yohimbine-induced brain activation. The role of alpha-1 adrenoceptors in reinstatement induced by other stressors is not known. Our most recent work is on the role of kappa opioid receptors (KOR) in stress-induced reinstatement of alcohol seeking and have reported that the selective KOR agonist U50,488 induces reinstatement and neuronal activation in stress- and relapse-related brain regions. Here we determine the involvement of alpha-1 receptors in reinstatement and brain activation induced by U50,488. Methods We trained male Long-Evans rats to self-administer alcohol (12% w/v), extinguished alcohol-reinforced responding and then determined the effects of prazosin (1 mg/kg) on U50,488 (2.5 mg/kg)-induced reinstatement and regional Fos expression. Results Prazosin blocked U50,488-induced reinstatement and decreased U50,488-induced Fos expression in the OFC, NAC core, ventral BNST, CeA, BLA and VTA. Conclusions These findings suggest that prazosin may reduce U50,488-induced relapse by inhibiting activity in one or more of these brain areas.

scholarly journals Osmotic Demyelination Syndrome Following Correction of Hyponatremia by ≤10 mEq/L per day

Kidney360 ◽  
2021 ◽  
pp. 10.34067/KID.0004402021
Author(s):  
Srijan Tandukar ◽  
Richard H. Sterns ◽  
Helbert Rondon-Berrios
Keyword(s):  
Risk Factors ◽  
Serum Sodium ◽  
Alcohol Use Disorder ◽  
Neurological Deficits ◽  
Osmotic Demyelination Syndrome ◽  
European Guidelines ◽  
Osmotic Demyelination ◽  
Chronic Hyponatremia ◽  
The Mean ◽  
Sodium Correction

Background: Overly rapid correction of chronic hyponatremia may lead to osmotic demyelination syndrome. European guidelines recommend a correction to ≤10 mEq/L in 24 hours to prevent this complication. However, osmotic demyelination syndrome may occur despite adherence to these guidelines. Methods: We searched the literature for reports of osmotic demyelination syndrome with rates of correction of hyponatremia <10 mEq/L in 24 hours. The reports were reviewed to identify specific risk factors for this complication. Results: We identified 19 publications with a total of 21 patients that were included in our analysis. The mean age was 52 years of which 67% were male. All of the patients had community acquired chronic hyponatremia. Twelve patients had an initial serum sodium <115 mEq/L, of which seven had an initial serum sodium ≤105 mEq/L. Other risk factors identified included alcohol use disorder (n=11), hypokalemia (n=5), liver disease (n=6), and malnutrition (n=11). The maximum rate of correction in patients with serum sodium <115 mEq/L was at least 8 mEq/L in all but 1 patient. In contrast, correction was <8 mEq/L in all but 2 patients with serum sodium >115 mEq/L. Among the latter group, osmotic demyelination syndrome developed before hospital admission or was unrelated to hyponatremia overcorrection. Four patients died (19%), 5 had full recovery (24%) and 9 (42%) had varying degrees of residual neurological deficits. Conclusions: Osmotic demyelination syndrome can occur in patients with chronic hyponatremia with a serum sodium <115 mEq/L despite rates of serum sodium correction <10 mEq/L in 24 hours. In patients with severe hyponatremia and high risk features, especially those with serum sodium <115 mEq/L, we recommend limiting serum sodium correction to <8 mEq/L. Thiamine supplementation is advisable for any hyponatremic patient whose dietary intake has been poor.

scholarly journals Role of Risk Factors in Developing Osmotic Demyelination Syndrome During Correction of Hyponatremia: A Case Study

Cureus ◽  
2020 ◽  
Author(s):  
Tom D.Y. Reijnders ◽  
Wilbert M.T. Janssen ◽  
S.M. Laila Niamut ◽  
Andrea B Kramer
Keyword(s):  
Risk Factors ◽  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination

scholarly journals The Role of Th17 in Neuroimmune Disorders: Target for CAM Therapy. Part II

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Aristo Vojdani ◽  
Jama Lambert
Keyword(s):  
Th17 Cells ◽  
Inflammatory Infiltration ◽  
Blood Brain ◽  
Bacterial Endotoxins ◽  
Pathogenic Factors ◽  
Progressive Neurodegeneration ◽  
Barrier Breakdown ◽  
Blood Brain Barrier Breakdown ◽  
Brain Barriers

Decades of research went into understanding the role that Th1 autoreactive T-cells play in neuroinflammation. Here we describe another effector population, the IL-17-producing T-helper lineage (Th17), which drives the inflammatory process. Through the recruitment of inflammatory infiltration neutrophils and the activation of matrix metalloproteinases, IL-17, a cytokine secreted by Th17 cells, contributes to blood-brain barrier breakdown and the subsequent attraction of macrophages and monocytes into the nervous system. The entry of cells along with the local production of inflammatory cytokines leads to myelin and axonal damage. This activation of the inflammatory response system is induced by different pathogenic factors, such as gut bacterial endotoxins resulting in progressive neurodegeneration by Th17 cells. Through the understanding of the role of bacterial endotoxins and other pathogenic factors in the induction of autoimmune diseases by Th17 cells, CAM practitioners will be able to design CAM therapies targeting IL-17 activity. Targeted therapy can restore the integrity of the intestinal and blood-brain barriers using probiotics,N-acetyl-cysteine,α-lipoic acid, resveratrol and others for their patients with autoimmunities, in particular those with neuroinflammation and neurodegeneration.

scholarly journals Osmotic demyelination syndrome following slow correction of hyponatremia: Possible role of hypokalemia

2013 ◽  
Vol 17 (4) ◽  
pp. 231-233 ◽  
Author(s):  
Mohammed Ashraf ◽  
Parvaiz A. Koul ◽  
Umar Hafiz Khan ◽  
Rafi A. Jan ◽  
Sanaullah Shah ◽  
...  
Keyword(s):  
Osmotic Demyelination Syndrome ◽  
Osmotic Demyelination
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