• Critically ill
• Hypernatremia
• Mortality
• Sodium
• Treatment

• Humans
• Hypernatremia/mortality
• Hypernatremia/therapy
• Length of Stay/statistics & numerical data
• Adult
• Hospitalization
• Hospital Mortality
• Fluid Therapy/methods

• case report
• central diabetes insipidus
• hypernatremia
• osmotic demyelination syndrome
• sodium correction

• normomatremia
• osmotic demyelination syndrome
• sodium
• traumatic brain injury

• desmopressin
• hypertonic saline
• hyponatremia
• osmotic demyelination syndrome
• syndrome of inappropriate antidiuresis

• Hyponatremia/therapy
• Hyponatremia/etiology
• Hyponatremia/diagnosis
• Hyponatremia/physiopathology
• Humans
• Intensive Care Units
• Sodium/blood
• Critical Illness/therapy
• Critical Care/methods
• Severity of Illness Index
• Arginine Vasopressin/blood

• complications
• hypernatremia
• hypokalemia
• hyponatremia
• malnutrition
• mortality risk
• osmolality
• outcomes
• risk factors
• water–electrolyte balance

• Hyponatremia/therapy
• Hyponatremia/blood
• Hyponatremia/diagnosis
• Humans
• Practice Guidelines as Topic
• Sodium/blood
• Severity of Illness Index

• Central Pontine
• Extrapontine
• Hyperammonemia
• Hyperbilirubinemia
• Myelinolysis

• Male
• Humans
• Aged
• Aged, 80 and over
• Female
• Hypernatremia
• Cohort Studies
• Retrospective Studies
• Correlation of Data
• Sodium

• Fructose
• SIADH
• hyponatremia
• osmotic demyelination syndrome
• polyol pathway

• Humans
• Hyponatremia/therapy
• Hyponatremia/complications
• Diuretics
• Inappropriate ADH Syndrome/complications
• Vasopressins
• Running

• P30 DK048520 NIDDK NIH HHS
• R01 DK121496 NIDDK NIH HHS

• hospital mortality
• prognostic factors
• restricted cubic splines
• sodium
• subarachnoid hemorrhage

Osmotic demyelination syndrome is a neurological disorder caused by damage to the myelin sheath of brain cells secondary to rapid correction of hyponatremia. Clinical features are variable depending on the location of demyelination, with diagnosis confirmed by MRI. Once diagnosed, treatment is supportive. We present a 49-year-old female recently discharged from an outside hospital who presented with symptoms of tremors, ataxia, slurred speech, and confusion. The patient was diagnosed with osmotic demyelination syndrome based on the classic trident sign on MRI imaging. A review of her records showed rapid correction of serum sodium during her initial hospital visit.

• Electrolytes
• Emergency
• Hyponatremia
• Sodium

A 76-year-old male presented with a recurrent depressive episode, an unsteady gait and cognitive impairment. Extensive blood tests, including hemogram, biochemical tests, folic acid, vitamin B12, and thyroid hormone, showed normal results. With the exception of the unsteady gait, neurological examination was negative. Brian magnetic resonance imaging (MRI) showed the typical feature of central pontine myelinolysis (CPM); however, there was no history of alcoholism, liver transplantation, malnutrition or rapid correction of hyponatremia. The patient had taken venlafaxine to treat major depressive disorder for more than 20 years. After discontinuation of venlafaxine, the unsteady gait gradually resolved, and subsequent MRI revealed reduction of the lesions over 6 months. We discuss herein the possible correlation between chronic use of venlafaxine and CPM.

• Myelinolysis
• Normonatremia
• Venlafaxine hydrochloride
• central pontine

Based on the symptoms, especially those affecting small vessels, it is difficult to distinguish multiple sclerosis (MS) from primary angiitis of the central nervous system (PACNS). Magnetic resonance imaging (MRI) helps understand the characteristics of deep gray matter lesions (DGML) in MS and PACNS. We aimed to compare the MRI characteristics of thalamus and basal ganglia lesions between relapsing-remitting MS and PACNS. In our study, 49 relapsing-remitting MS patients and 16 PACNS with MRI-confirmed thalamus or basal ganglia lesions were enrolled. Among the DGMLs in basal ganglia, putamen had significantly higher (P = 0.037) involvement in PACNS than in MS. More importantly, larger lesion sizes in thalamus helps to distinguish PACNS (12.4 ± 4.3 mm) from MS (7.9 ± 3.7 mm) (P = 0.006). But using lesions in basal ganglia, researchers were unable to differentiate the two disorders. Presently, our study shows that MRI performances of deep gray matter differ between MS and PACNS.

• MRI
• basal ganglia
• comparison
• multiple sclerosis
• primary angiitis of the central nervous system

Central pontine myelinolysis (CPM) usually occurs during rapid correction of serum osmolality, typically with brainstem lesions presenting uniform signals following enhancement on magnetic resonance imaging (MRI). We report a case of CPM caused by diabetes, which was characterized by glioma-like imaging features and the patient responded well to corticosteroids.

A 49-year-old man with type 2 diabetes was admitted due to numbness and weakness for 6 mo with progressive aggravation for 2 wk. His complete blood count, serum electrolytes, renal and liver function parameters were within the normal range. MRI showed mass lesions in the brainstem, with unusually inhomogeneous signal intensity after contrast-enhanced scans. His symptoms worsened after hypoglycemic therapy. Due to his clinical history and examination results, CPM was considered the most likely diagnosis. Treatment with corticosteroids was administered with a methylprednisolone pulse in the acute phase followed by dose tapering. During the 8-mo follow-up period, his clinical symptoms and imaging features significantly improved.

Diabetes could rarely be accompanied by CPM, and patients who experience this neurological complication could benefit from corticosteroid treatment. Clinicians should recognize the special relationship between diabetes and CPM, and improve awareness of early identification and appropriate treatment.

• Central pontine myelinolysis
• Diabetes
• Imaging
• Glioma
• Corticosteroids
• Case report

Central pontine myelinolysis (CPM) is a non-inflammatory demyelinating lesion of the pons. CPM and extrapontine demyelination (EPM) are together termed osmotic demyelination syndrome (ODS), a known and serious complication of acute correction of hyponatremia. Conversely, hyperglycemic hyperosmolarity syndrome (HHS) develops in patients with type 2 diabetes who still have some insulin secretory ability due to infection, non-compliance with treatment, drugs, and coexisting diseases, and is often accompanied by ketosis. HHS represents a life-threatening endocrine emergency (mortality rate, 10–50%) associated with marked hyperglycemia and severe dehydration. HHS may develop ODS, and some cases have been associated with hypernatremia.

The patient was an 87-year-old woman with hyperglycemia, dehydration, malnutrition, and potential thrombus formation during long-term bed rest. HHS was suspected to have developed due to progression of hyperglycemia and dehydration caused by pneumonia. Furthermore, ketoacidosis developed from ketosis and prerenal renal failure associated with circulating hypovolemia shock, which was also associated with disseminated intravascular coagulation. Treatment was started with continuous intravenous injection of fast-acting insulin and low-sodium replacement fluid. In addition, ceftriaxone sodium hydrate, heparin sodium, thrombomodulin α, human serum albumin, and dopamine hydrochloride were administered. Blood glucose, serum sodium, serum osmolality, and general condition (including vital, infection/inflammatory findings, and disseminated intravascular coagulation) improved promptly, but improvements in disturbance of consciousness were poor. Diffusion-weighted imaging of the brain 72 h after starting treatment showed no obvious abnormalities, but high-intensity signals in the midline of the pons became apparent 30 days later, leading to definitive diagnosis of CPM.

Fluctuation of osmotic pressure by treatment from hyperosmolarity due to hyperglycemia and hypernatremia in the presence of risk factors such as malnutrition, severe illness, and metabolic disorders may be a cause of CPM onset. When treating HHS with risk factors, the possibility of progression to ODS needs to be kept in mind.

• Central pontine myelinolysis
• Diffusion-weighted imaging
• Hyperglycemic hyperosmolarity syndrome
• Hypernatremia
• Osmotic demyelination syndrome

Acute demyelination of the pons or extrapontine areas results in an osmotic demyelination syndrome (ODS), previously referred to as central pontine myelinolysis (CPM) or extra pontine myelinolysis (EPM). It is caused by osmotic dysregulation in the brain. Multiple risk factors have been known to contribute to these osmotic disturbances. Among them, osmotic stress caused by rapid correction of hyponatremia is the most common cause. Other risk factors include liver failure, alcohol dependence, malnutrition, and malignancy. Symptoms can vary depending on the location of the demyelination. It has a high rate of morbidity and mortality. We present a case of ODS in a malnourished patient who was found to have alcoholic hepatitis and invasive colon cancer. The initial presentation was sepsis secondary to pneumonia. The patient was found to be severely hyponatremic at the time of admission, and the hyponatremia was corrected as per the recommendations. The initial non-contrast head computed tomography (CT) scan was unremarkable. However, the hospital course was complicated by a deteriorating neurological exam with encephalopathy despite not overcorrecting the sodium. A short-term follow-up brain magnetic resonance imaging (MRI) eventually revealed ODS. Initially, the findings of ODS were masked due to symptoms of alcohol withdrawal. However, the patient had a quick recovery with the improvement of all the neurological findings.

• alcohol withdrawal
• hyponatremia
• invasive colon cancer
• osmotic demyelination syndrome

• cell volume regulation
• clinical nephrology
• diabetes insipidus
• electrolytes
• hypernatremia
• hyponatremia
• osmolality
• outcomes
• pediatrics
• sodium
• water-electrolyte balance