deamino-arginine-vasopressin and Demyelinating-Diseases

Topics: Bone Marrow Transplantation; Brain Diseases; Cyclosporine; Deamino Arginine Vasopressin; Demyelinating Diseases; Diabetes Insipidus; Drug Therapy, Combination; Female; Humans; Infant; Leukemia, Promyelocytic, Acute; Magnetic Resonance Imaging; Pons

Topics: Deamino Arginine Vasopressin; Demyelinating Diseases; Humans; Hyponatremia; Magnetic Resonance Imaging; Sodium; Syndrome

There is an increasing and compelling need for early recognition of features of osmotic demyelination syndrome (ODS), and a further attempt at correcting this even where presentation is late.. A 49-year-old male admitted into the emergency department with a complaint of lethargy and severe hyponatremia, with subsequent ODS supervening on initial attempts at correction.. Rapid rise in serum sodium concentration (121 mmol/L in 8 hours from a nadir of 101 mmol/L), concomitant deterioration in patient's conscious level support the diagnosis of ODS.. Concomitant administration of 5% dextrose water with desmopressin with a therapeutic objective of gradual relowering of serum sodium concentration.. Significant improvement in patients' conscious level and motor function with the commencement of sodium relowering therapy. The patient was eventually discharged home.. Regardless of the temporal profile of neurologic sequelae following ODS due to hyponatremia, its worthwhile attempting initial sodium relowering with dextrose 5% and desmopressin and then monitoring of biochemical and neurologic markers.

Topics: Antidiuretic Agents; Brain; Deamino Arginine Vasopressin; Demyelinating Diseases; Drug Therapy, Combination; Glucose; Humans; Hyponatremia; Iatrogenic Disease; Lethargy; Magnetic Resonance Imaging; Male; Middle Aged; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Sweetening Agents; Tomography, X-Ray Computed; Treatment Outcome

Delayed parkinsonism and dystonia are recognized phenomena in osmotic demyelinating syndrome (ODS). Dopamine receptor agonists and levodopa have been reported to benefit select patients.. We report a patient with ODS with severe pseudobulbar deficits, parkinsonism and dystonia, poorly responsive to levodopa, who experienced a remarkable improvement with pramipexole.. A marked response to pramipexole with lack of response to levodopa suggests a pre-synaptic source for his deficits coupled with injuries to non-nigral compensatory structures.. This case highlights a dramatic response of osmotic demyelination-induced parkinsonism/dystonia to pramipexole. A lack of response to levodopa suggests deficits in the pre-synaptic nigral as well as non-nigral compensatory structures.

Topics: Adult; Antiparkinson Agents; Deamino Arginine Vasopressin; Demyelinating Diseases; Dystonia; Epistaxis; Hemostatics; Humans; Hyponatremia; Levodopa; Locked-In Syndrome; Male; Myelinolysis, Central Pontine; Osmotic Pressure; Parkinsonian Disorders; Postoperative Hemorrhage; Pramipexole; Pseudobulbar Palsy; Rhinoplasty; Tetrahydronaphthalenes; Thiophenes; Treatment Failure; Treatment Outcome; von Willebrand Disease, Type 1

Demyelinated lesions in human pons observed after osmotic shifts in serum have been referred to as central pontine myelinolysis (CPM). Astrocytic damage, which is prominent in neuroinflammatory diseases like neuromyelitis optica (NMO) and multiple sclerosis (MS), is considered the primary event during formation of CPM lesions. Although more data on the effects of astrocyte-derived factors on oligodendrocyte precursor cells (OPCs) and remyelination are emerging, still little is known about remyelination of lesions with primary astrocytic loss. In autopsy tissue from patients with CPM as well as in an experimental model, we were able to characterize OPC activation and differentiation. Injections of the thymidine-analogue BrdU traced the maturation of OPCs activated in early astrocyte-depleted lesions. We observed rapid activation of the parenchymal NG2

Topics: Adult; Aged; Animals; Antidiuretic Agents; Astrocytes; Cell Differentiation; Cell Lineage; Deamino Arginine Vasopressin; Demyelinating Diseases; Disease Models, Animal; Female; Humans; Lateral Ventricles; Male; Middle Aged; Myelin Sheath; Myelinolysis, Central Pontine; Neoplasm Proteins; Nestin; Neural Stem Cells; Oligodendrocyte Precursor Cells; Oligodendroglia; Rats; Sodium Chloride

Topics: Deamino Arginine Vasopressin; Demyelinating Diseases; Diabetes Insipidus, Neurogenic; Female; Humans; Hyponatremia; Saline Solution, Hypertonic; Syndrome; Young Adult

Overly rapid correction of chronic hyponatremia can cause osmotic demyelination syndrome (ODS). Minocycline protects ODS associated with overly rapid correction of chronic hyponatremia with hypertonic saline infusion in rats. In clinical practice, inadvertent rapid correction frequently occurs due to water diuresis, when vasopressin action suddenly ceases. In addition, vasopressin receptor antagonists have been applied to treat hyponatremia. Here the susceptibility to and pathology of ODS were evaluated using rat models developed to represent rapid correction of chronic hyponatremia in the clinical setting. The protective effect of minocycline against ODS was assessed. Chronic hyponatremia was rapidly corrected by 1 (T1) or 10 mg/kg (T10) of tolvaptan, removal of desmopressin infusion pumps (RP), or administration of hypertonic saline. The severity of neurological impairment in the T1 group was significantly milder than in other groups and brain hemorrhage was found only in the T10 and desmopressin infusion removal groups. Minocycline inhibited demyelination in the T1 group. Further, immunohistochemistry showed loss of aquaporin-4 (AQP4) in astrocytes before demyelination developed. Interestingly, serum AQP4 levels were associated with neurological impairments. Thus, minocycline can prevent ODS caused by overly rapid correction of hyponatremia due to water diuresis associated with vasopressin action suppression. Increased serum AQP4 levels may be a predictive marker for ODS.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Aquaporin 4; Astrocytes; Behavior, Animal; Benzazepines; Biomarkers; Brain; Chemokines; Cytokines; Cytoprotection; Deamino Arginine Vasopressin; Demyelinating Diseases; Disease Models, Animal; Diuresis; Hyponatremia; Intracranial Hemorrhages; Male; Matrix Metalloproteinases; Minocycline; Neuroprotective Agents; Osmosis; Rats, Sprague-Dawley; Saline Solution, Hypertonic; Sodium; Therapeutics; Time Factors; Tolvaptan; Water-Electrolyte Balance

An alcoholic patient presented with profound hyponatremia (serum sodium concentration, 96 mEq/L) caused by the combined effects of a thiazide diuretic, serotonin reuptake inhibitor, beer potomania, and hypovolemia. A computed tomographic scan of the brain was indistinguishable from one obtained 3 weeks earlier when he was normonatremic. Concurrent administration of 3% saline solution and desmopressin controlled the rate of correction to an average of 6 mEq/L daily and resulted in full neurologic recovery without evidence of osmotic demyelination. This case illustrates the value of controlled correction of profound hyponatremia.

Topics: Alcohol-Related Disorders; Blood Chemical Analysis; Brain Diseases; Deamino Arginine Vasopressin; Demyelinating Diseases; Follow-Up Studies; Humans; Hyponatremia; Male; Middle Aged; Risk Assessment; Saline Solution, Hypertonic; Severity of Illness Index; Sodium; Tomography, X-Ray Computed; Treatment Outcome