UNASSIGNED: Current guidelines recommend limiting the rate of correction in patients with severe hyponatremia to avoid severe neurologic complications such as osmotic demyelination syndrome (ODS). However, published data have been conflicting. We aimed to evaluate the association between rapid sodium correction and ODS in patients with severe hyponatremia.
UNASSIGNED: We searched PubMed, Embase, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials from inception to November 2023. The primary outcome was ODS and the secondary outcomes were in-hospital mortality and length of hospital stay.
UNASSIGNED: We identified 7 cohort studies involving 6,032 adult patients with severe hyponatremia. Twenty-nine patients developed ODS, resulting in an incidence rate of 0.48%. Seventeen patients (61%) had a rapid correction of serum sodium in the first or any 24-hour period of admission. Compared with a limited rate of sodium correction, a rapid rate of sodium correction was associated with an increased risk of ODS (RR, 3.91 [95% CI, 1.17 to 13.04]; I2 = 44.47%; p = 0.03). However, a rapid rate of sodium correction reduced the risk of in-hospital mortality by approximately 50% (RR, 0.51 [95% CI, 0.39 to 0.66]; I2 = 0.11%; p < 0.001) and the length of stay by 1.3 days (Mean difference, -1.32 [95% CI, -2.54 to -0.10]; I2 = 71.47%; p = 0.03).
UNASSIGNED: Rapid correction of serum sodium may increase the risk of ODS among patients hospitalized with severe hyponatremia. However, ODS may occur in patients regardless of the rate of serum sodium correction.

Signs and symptoms of hypernatremia largely indicate central nervous system dysfunction. Acute hypernatremia can cause demyelinating lesions similar to that observed in osmotic demyelination syndrome (ODS). We have previously demonstrated that microglia accumulate in ODS lesions and minocycline protects against ODS by inhibiting microglial activation. However, the direct effect of rapid rise in the sodium concentrations on microglia is largely unknown. In addition, the effect of chronic hypernatremia on microglia also remains elusive. Here, we investigated the effects of acute (6 or 24 h) and chronic (the extracellular sodium concentration was increased gradually for at least 7 days) high sodium concentrations on microglia using the microglial cell line, BV-2. We found that both acute and chronic high sodium concentrations increase NOS2 expression and nitric oxide (NO) production. We also demonstrated that the expression of nuclear factor of activated T-cells-5 (NFAT5) is increased by high sodium concentrations. Furthermore, NFAT5 knockdown suppressed NOS2 expression and NO production. We also demonstrated that high sodium concentrations decreased intracellular Ca2+ concentration and an inhibitor of Na+/Ca2+ exchanger, NCX, suppressed a decrease in intracellular Ca2+ concentrations and NOS2 expression and NO production induced by high sodium concentrations. Furthermore, minocycline inhibited NOS2 expression and NO production induced by high sodium concentrations. These in vitro data suggest that microglial activity in response to high sodium concentrations is regulated by NFAT5 and Ca2+ efflux through NCX and is suppressed by minocycline.

Osmotic Demyelination Syndrome (ODS) is one of the primary cause of demyelination in alcoholics and malnourished resulting in various kind of clinical manifestations in pontine symptoms, neuro-behavioural symptoms movement disorders as well as speech and language and swallowing difficulties. The study was done to introspect the prognosis of swallowing therapy in a patient with ODS using MASA (Mann Assessment of Swallowing Ability). A 36 years old male with a history of regular alcohol intake and hypertensiom reported in our healthcare centre with hypoaklemia and speech, language and swallowing difficulty. Magnetic resonance imaging of the brain showed bilateral symmetrical T2 and T2 FLAIR (fluid attenuated inversion recovery) hyperintensity lesion in the bilateral basal ganglia involving the caudate nuclei, putaminal region and bilateral thalami with similar lesion along the mid brain. There were no areas of acute restriction in diffusion study. The findings suggested of Osmotic Demyelination Syndrome (ODS).When accessed with N-DAT, WAB and MASA; patient was diagnosed with Spastic Dysarthria, Transcortical Motor Aphasia and Moderate Dysphagia. Intervention was provided using speech and swallowing therapy and when introspected with MASA scores, improvement was seen within 5 days and statistically 97% of variance was seen inferring the progressing trend in the MASA scores. This study concludes that MASA can be an effective tool in introspecting the prognosis of Dysphagia in ODS and early intervention in the management of dysphasia shows positive results.

UNASSIGNED: Hyponatremia, defined as a serum sodium concentration <135 mmol/l, is a frequent electrolyte disorder in patients presenting to an emergency department (ED). In this context, appropriate diagnostic and therapeutic management is rarely performed and challenging due to complex pathophysiologic mechanisms and a variety of underlying diseases.
UNASSIGNED: To implement a feasible pathway of central diagnostic and therapeutic steps in the setting of an ED.
UNASSIGNED: We conducted a narrative review of the literature, considering current practice guidelines on diagnosis and treatment of hyponatremia. Underlying pathophysiologic mechanisms and management of adverse treatment effects are outlined. We also report four cases observed in our ED.
UNASSIGNED: Symptoms associated with hyponatremia may appear unspecific and range from mild cognitive deficits to seizures and coma. The severity of hyponatremia-induced neurological manifestation and the risk of poor outcome is mainly driven by the rapidity of serum sodium decrease. Therefore, emergency treatment of hyponatremia should be guided by symptom severity and the assumed onset of hyponatremia development, distinguishing acute (<48 hours) versus chronic hyponatremia (>48 hours).
UNASSIGNED: Especially in moderately or severely symptomatic patients presenting to an ED, the application of a standard management approach appears to be critical to improve overall outcome. Furthermore, an adequate work-up in the ED enables further diagnostic and therapeutic evaluation during hospitalization.

Osmotic demyelination syndrome (ODS) is a disorder characterised by the widespread development of demyelination in both pontine and extrapontine regions. It has been recognised as a complication arising from the rapid correction of hyponatraemia. This study presents the case of a 20-year-old Thai female patient at 10 weeks gestation, exhibiting an initial presentation of catatonia - an uncommon manifestation of ODS. The patient developed symptoms following the rapid correction of hyponatraemia in the context of hyperemesis gravidarum. Magnetic resonance imaging (MRI) of the brain revealed a trident or bat-wing-shaped pattern in T2-weighted and fluid-attenuated inversion recovery (FLAIR) sequences at the central pons. The patient underwent five cycles of plasmapheresis and received rehabilitation, leading to clinical improvement.
CONCLUSIONS: Osmotic demyelination syndrome (ODS) is a rare but potentially devastating neurological complication, such as catatonia, resulting from the correction of hyponatraemia.Pregnancies complicated by hyperemesis gravidarum tend to exhibit hyponatraemia and hypokalaemia, which serve as contributing risk factors for ODS.Plasmapheresis is considered as an option in the treatment of ODS for the removal of inflammatory substances.

BACKGROUND: Osmotic demyelinating syndrome, commonly recognized as a consequence of the rapid correction of hyponatremia, has been known to cause motor, neuropsychiatric, or extrapyramidal symptoms. We reported a patient with an unusual presentation involving bilateral hand weakness, and pseudobulbar affect. The imaging was compatible with osmotic demyelinating syndrome with bilateral hand knob lesions, despite no history of overcorrection of hyponatremia.
METHODS: A 44-year-old female presented with three weeks of emotional lability, spastic dysarthria, and bilateral hand weakness following ankle surgery and a mild head injury. Physical examination revealed weakness in the intrinsic hand muscles, leading to a claw-like deformity of the hands, although sensation remained unimpaired. Magnetic resonance imaging (MRI) of the brain revealed several hyperintensities on fluid-attenuated inversion recovery imaging involving various areas, including the hand knob area of the bilateral precentral gyri, caudate, lentiform nuclei, and pons, suggestive of osmotic demyelinating syndrome. Clinical improvement was observed following a trial of intravenous pulse methylprednisolone and plasmapheresis.
CONCLUSIONS: Bilateral hand weakness is an unusual manifestation of osmotic demyelinating syndrome. The precentral gyrus, specifically in the hand knob area, is the vulnerable region that can result from osmotic demyelinating syndrome.

Hyponatremia is a disorder of water homeostasis. Water balance is maintained by the collaboration of renal function and cerebral structures, which regulate thirst mechanisms and secretion of the antidiuretic hormone. Measurement of serum-osmolality, urine osmolality and urine-sodium concentration help to diagnose the different reasons for hyponatremia. Hyponatremia induces cerebral edema and might lead to severe neurological symptoms, which need acute therapy. Also, mild forms of hyponatremia should be treated causally, or at least symptomatically. An inadequate fast increase of the serum sodium level should be avoided, because it raises the risk of cerebral osmotic demyelination. Basic pathophysiological knowledge is necessary to identify the different reasons for hyponatremia which need different therapeutic procedures.
UNASSIGNED: Die Hyponatriämie ist eine Störung des Wasserhaushaltes. Die Wasserhomöostase wird durch das Zusammenspiel von Nierenfunktion und den zerebralen Strukturen des Durstempfindens und der Produktion des antidiuretischen Hormons aufrechterhalten. Durch die Messung der Serum-Osmolalität, Harn-Osmolalität und Harn- Natriumkonzentration können die meisten Ursachen der Hyponatriämie identifiziert werden. Hyponatriämien führen zu einem Hirnödem und können damit schwere neurologische Symptome verursachen, welche eine akute Therapie benötigen. Aber auch milde Formen der Hyponatriämie bedürfen einer, wenn möglich kausalen, oder zumindest symptomatischen Behandlung. Eine inadäquat rasche Korrektur der Hyponatriämie sollte vermieden werden, da diese das Risiko für ein zerebrale osmotische Demyelinisierung erhöht. Da die Art der Therapie eng mit der Ursache der Hyponatriämie zusammenhängt, ist eine Grundkenntnis der pathophysiologischen Prozesse für eine optimale Behandlung notwendig.

Hyponatremia is a common electrolyte disorder requiring careful management to prevent severe complications. Osmotic demyelination syndrome (ODS) is a serious neurological disorder that can develop from rapid correction of hyponatremia. Herein, is a description of the case of a 61-year-old man with multiple risk factors, including alcoholism, hypokalemia, malnutrition, and alcoholic liver cirrhosis, who developed ODS despite adherence to the recommended correction rate for hyponatremia. The patient presented to the emergency department with generalized weakness, gait disturbance, and decreased muscle strength. Initial laboratory investigations revealed severe hyponatremia, hypokalemia, and dehydration. The patient was treated with cautious correction of the hyponatremia below 8 mmol/L per day. However, on the seventh hospital day, he developed tremors, rigidity, and decreased consciousness and was diagnosed with osmotic demyelination syndrome. Despite receiving general supportive care, desmopressin, and dextrose 5% in water to reduce the serum sodium levels, the patient did not show significant improvement and was transferred to a nursing home for long-term conservative care on day 35 of hospitalization. This case report highlights the challenges associated with the diagnosis and management of osmotic demyelination syndrome and the importance of identifying patients at high risk of developing this neurological disorder.

A murine osmotic demyelinating syndrome (ODS) model was developed through chronic hyponatremia, induced by desmopressin subcutaneous implants, followed by precipitous sodium restoration. The thalamic ventral posterolateral (VPL) and ventral posteromedial (VPM) relay nuclei were the most demyelinated regions where neuroglial damage could be evidenced without immune response. This report showed that following chronic hyponatremia, 12 h and 48 h time lapses after rebalancing osmolarity, amid the ODS-degraded outskirts, some resilient neuronal cell bodies built up primary cilium and axon hillock regions that extended into axon initial segments (AIS) where ADP-ribosylation factor-like protein 13B (ARL13B)-immunolabeled rod-like shape content was revealed. These AIS-labeled shaft lengths appeared proportional with the distance of neuronal cell bodies away from the ODS damaged epicenter and time lapses after correction of hyponatremia. Fine structure examination verified these neuron abundant transcriptions and translation regions marked by the ARL13B labeling associated with cell neurotubules and their complex cytoskeletal macromolecular architecture. This necessitated energetic transport to organize and restore those AIS away from the damaged ODS core demyelinated zone in the murine model. These labeled structures could substantiate how thalamic neuron resilience occurred as possible steps of a healing course out of ODS.

OBJECTIVE: Osmotic demyelination syndrome is usually caused by rapid correction of hyponatremia but sometimes develops from acute severe hypernatremia. Studies suggested that serum sodium increasing at the rate of less than 6~8 mmol/L in 24 hours has a low risk of osmotic demyelination syndrome, but sometimes exceptions present. Aside from the classical sites of involvement, such as pons and basal ganglia, internal capsules are rarely affected. We report a case with acute paraparesis caused by acute hypernatremia-induced extrapontine myelinolysis involving the posterior limbs of bilateral internal capsules.
METHODS: A 54-year-old man was admitted for aseptic encephalitis and moved to the intensive care unit due to poor consciousness and respiratory failure. Although cerebrospinal fluid pleocytosis was improved later, acute hypernatremia due to partial diabetes insipidus developed. He presented acute paraplegia two days later with a negative result on the whole spine MRI. Although the increasing rate of serum sodium did not exceed the recommended safety range, the extrapontine myelinolysis involving posterior limbs of the bilateral internal capsule, as long as the corpus callosum, still developed. The patient regained partial walking ability after one year.
CONCLUSIONS: This case report extends the spectrum of classical osmotic demyelination in clinical manifestations, image findings, and the causal range of electrolyte derangements.