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.

Osmotic demyelination syndrome (ODS) is a neurological disorder usually after rapid correction of hyponatremia. Only few cases of ODS with hypernatremia and diabetes insipidus (DI) in postpartum state is reported. Postpartum hypernatremia is described as severe hypernatremia in postpartum period and presents as an encephalopathy with rhabdomyolysis with diffuse white matter hyperintensities suggestive of osmotic demyelination.
UNASSIGNED: The authors present a case of 29-year-old female who presented with chief complaint of altered sensorium and quadriparesis. Two days prior to onset of symptoms, she underwent caesarean section, was kept on nil per oral and free fluid restriction, after which she had confusion, altered sensorium, and weakness in all four limbs. Sodium level was 170 mEq/l. Urine osmolality and plasma osmolality was 150 and 410 mOsm/kg of water, respectively. MRI showed high signal intensity lesion in pons suggestive of demyelination. She was diagnosed ODS with transient DI and quadriparesis, in postpartum period due to further rise in sodium after free fluid restriction and nil per oral. She was treated with desmopressin, 5% dextrose and 0.9% normal saline, her quadriparesis recovered and desmopressin was tapered and stopped over 45 days and discharged at stable state.
UNASSIGNED: ODS can rarely be associated with hypernatremia in postpartum female presenting as quadriparesis and altered sensorium.
UNASSIGNED: Clinicians should be familiar of ODS with hypernatremia with transient DI in postpartum period, which is reversible and can be managed by desmopressin and fluid replacement.

Osmotic demyelination syndrome (ODS) as a result of the hyperosmolar hyperglycemic state is rare and can present with variable neurological manifestation due to lysis of myelin sheath.
UNASSIGNED: A 44-year diabetic male presented with complaints of sudden onset, progressive bilateral weakness in lower limbs, and slurring of speech for the past 1.5 months. Cerebellar examination showed a bilaterally impaired finger nose test, dysdiadochokinesia, impaired heel shin test, and an impaired tandem gait. MRI brain (T2 and fluid-attenuated inversion recovery sequences) showed high signal intensity in the central pons and bilateral cerebellum. With a diagnosis of ODS with poorly controlled diabetes, he was treated with insulin, metformin, and supportive measures following which his symptoms subsided gradually.
UNASSIGNED: A rapid correction of hyponatremia is considered the most common cause of ODS. Variations in plasma glucose levels, a rare cause of ODS, can cause an abrupt osmolality change causing pontine and extrapontine myelinolysis. Prevention of rapid correction of hyponatremia and rapid changes in plasma osmolality in vulnerable patients is the mainstay of treatment.
UNASSIGNED: Clinical features, imaging studies, and monitoring of serum osmolality, serum glucose, and electrolytes aid in diagnosis and favorable outcomes for the patient.

Rapid correction of hyponatremia is the most frequent predisposing factor for the development of central pontine myelinolysis (CPM). Alcoholism, cirrhosis, malnutrition, and severe burns are associated conditions that often present in combination with a rapid rise in serum sodium concentration. However, its association with hyperglycemia has not been as well established. There have been recent reports of acute to subacute presentation of CPM with hyperglycemia. We report an unusual case of a 48-year-old Caucasian male who presented with pseudobulbar palsy, ataxia, and quadriplegia with worsening pontine hyperintensities and was diagnosed with CPM in the setting of persistent hyperglycemia with normal serum sodium.

Hypernatremia (serum sodium>160 meq/L) present with diverse neurological manifestations, ranging from flaccid paralysis to impaired cognition, encephalopathy, and even deep coma. Osmotic demyelination refers to changes in brain cells because of an acute change in plasma osmolality. It is further divided into two types, i.e., central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM). Patients with EPM, besides spasticity, may also present with other movement disorders such as catatonia, parkinsonism, and dystonia. We present a case of a postpartum woman bought to the emergency department by her relatives in an unconscious state. In view of poor sensorium (Glasgow coma scale < 7), she was intubated and received mechanical ventilatory support. On admission, computed tomography ofthebrain was normal, and the patient was transferred to the intensive care unit (ICU) for further management. The preliminary work-up in the ICU showed hypernatremia (serum sodium of 182 mEq/L) with hyper-osmolality (359 mOsm/kgH2O). She was managed as per the ICU protocol for hypernatremia. During her ICU stay, her sensorium improved, but she developed flaccid paralysis and was quadriplegic. Thus, a tracheostomy was performed, and she was weaned from the ventilator. After ventilator weaning, she was transferred to the ward for further rehabilitation. During rehabilitation, the patient was able to sit and takefoodorally.To date, only a few cases are reported in postpartum women with acute severe hypernatremia caused by high-grade fever and loss of body fluids leading to extra-pontine demyelination and flaccid paralysis. This case highlightsthat prompt recognition and appropriate intervention can improve the outcomes in these patients.

A 6-year-old castrated male Chihuahua dog was presented with hindlimb paresis and ataxia. The dog had hyponatremia and was diagnosed as hypoadrenocorticism 10 days before its visit, and the neurologic signs including generalized tonic seizures and hindlimb paresis occurred 3 days after correction of hyponatremia at a referral hospital. Based on history and clinical findings, osmotic demyelination syndrome (ODS) secondary to rapid correction of hyponatremia was highly suspected. After administration of anti-convulsant and supplements, seizures did not occur, and gait was normalized within 2 weeks. Phenobarbital was tapered and finally discontinued after 3 months, and seizure did not recur. The neurologic signs were completely resolved and the dog continued to be free of neurologic or additional clinical signs over the 19-month follow-up period. ODS should be included among the differential diagnoses in case of any acute neurological dysfunction that occurs with episodes of rapid correction of hyponatremia. To the author\'s knowledge, this is the rare case report of a dog with hypoadrenocorticism and presumed ODS after rapid correction of hyponatremia leading to neurologic signs including seizures and ataxia.

Central pontine myelinolysis is a non-inflammatory neurologic deficit and can have a wide array of clinical features, predisposing risk factors as well as different patterns of onset along with a big difference in prognosis ranging from asymptomatic cases to encephalopathy and also mortality. Apart from the common risk factors like hyponatremia and sudden correction of electrolyte imbalances, sometimes, the least prevalent risk factors such as pregnancy seem to link with the central pontine myelinolysis. Mostly its onset is sudden after the inciting factors. However, it is also likely to have cases of central pontine myelinolysis with gradual onset of clinical features. The purpose of the case report is to highlight the link between pregnancy and central pontine myelinolysis. The slow onset of clinical features in pregnancy-linked central pontine myelinolysis can also be considered. The patient in the case report presented with gradual onset clinical features of osmotic demyelination syndrome during the last months of pregnancy and immediately postpartum. All the possible predisposing risk factors for central pontine myelinolysis were ruled out through history, physical examination, and relevant investigations. The case study of the patient hypothesized that: (1) pregnancy should be considered as a risk factor for central pontine myelinolysis in pregnant and postpartum patients presenting with clinical features of the disease, (2) clinical features of central pontine myelinolysis in pregnancy can have a more gradual onset of symptoms compared to other causes of central pontine myelinolysis. Although, this case report signifies a relationship between pregnancy and osmotic demyelination syndrome. However, further studies should be done to develop a causal relationship and preventive measures for the condition.

A 73-year-old African American male presented with altered mental status, severe hyperglycemia, and acute kidney injury. His metabolic derangements including hyperglycemia and hyponatremia were initially thought to be the cause of his encephalopathy. While managing his hyperglycemic hyperosmolar non-ketotic state, he received intravenous rehydration with almost three times his physiologic requirement for normalization of his electrolyte abnormalities. After the correction of the metabolic derangements, he remained confused with dysarthria and labile mood. Magnetic resonance imaging of the brain revealed osmotic demyelination syndrome.

BACKGROUND: Osmotic demyelination syndrome (ODS), which embraces central pontine and extrapontine myelinolysis, is an uncommon neurological disorder that occurs due to plasma osmotic changes.
METHODS: We present the case of a 55-year-old man, who presented with severe hyponatremia due to repeated vomiting, antidepressant treatment and consumption of large amounts of water. Fifteen days after sodium correction, the patient showed fluctuation of vigilance, dysarthria and dysphagia, tremor, cogwheel rigidity, bilateral facial palsy, ophthalmoplegia and tetraparesis. A brain MRI scan revealed extrapontine and later on pontine myelinolysis. He received intravenous steroids and subsequently immunoglobulin. His status began to improve gradually after completion of immunoglobulin and at three month-follow-up had no neurological deficit.
METHODS: A comprehensive literature search of all reported ODS cases that received immunoglobulin, steroids or plasmapheresis was conducted in the electronic databases PubMed and Web of science.
CONCLUSIONS: Improvement was seen in most cases that received immunoglobulin either during treatment or in the first days after treatment. With regard to steroids, although most cases reported improvement in the following months their effect on the outcome is unclear. Most cases treated with plasmapheresis reported favorable outcome at variable follow-up time. Immunoglobulin and steroids have immunomodulatory effects, which could contribute to promotion of myelin repair in ODS. Plasmapheresis has effects on the immune system beyond removing myelinotoxins from the circulation. More evidence is required to support their use in ODS. However, in view of the disease severity, these therapeutic choices should be considered in the clinical management of ODS.

Osmotic demyelination syndrome (ODS) is a clinical syndrome seen following aggressive correction of severe hyponatremia. Chronic alcohol use, malnutrition, and electrolyte derangement are additional risk factors promoting the demyelination in ODS. A 49-year-old female with a history of untreated mood disorder, hypertension, alcohol, and tobacco abuse presented to the emergency department (ED) with a three-month history of generalized body weakness. She also had a history of recurrent falls, difficulty walking, inadequate food and water intake, progressively worsening jaundice, and confusion which started about the same time. Her vital signs were normal; some of the significant physical examination findings were: sclera icterus, abdominal distension, bilateral pedal edema, hand tremors, rotary nystagmus, paraparesis, 1+ bilateral knee jerk, and absent bilateral ankle jerk. She had moderate hyponatremia, mild hypokalemia, deranged liver function test with a cholestatic pattern and transaminitis, hypoalbuminemia, elevated ammonia, lipase, in keeping with alcoholic liver disease and acute pancreatitis. In the ED, she received a normal saline infusion, and her serum sodium rose by just 6 mmol/L within the first 24 hours. She had drainage of her ascitic fluid and treatment with thiamine, folic acid, prednisone, lactulose, rifaximin, furosemide, spironolactone, and Ceftriaxone with improvement in clinical and laboratory abnormalities. Her lower extremity weakness persisted despite physical therapy, prompting neurologic evaluation. MRI of the lumbar spine showed an old compression fracture and lumbar spinal stenosis, while MRI brain findings were consistent with Osmotic demyelination. At the time of discharge to a rehabilitation facility, her serum sodium was 132 mmol/L, but her leg weakness persisted. Although rare, ODS can occur in the setting of moderate hyponatremia if there are additional risk factors that lower the threshold for demyelination.