Osmotic demyelination syndrome is a rare condition reported mainly in the case of rapid correction of hyponatremia, but it can occur even in the case of complicated diabetes mellitus either during rapid correction of hyperglycemia or anytime during the complicated diabetes mellitus. We report a case of complicated diabetes mellitus developing osmotic demyelination syndrome. The patient had presented with altered sensorium and seizure, which was initially diagnosed as hyperglycemia, but during his treatment, the magnetic resonance imaging of brain revealed central pontine myelinolysis. Our search on the causes of osmotic demyelination syndrome other than rapid correction of hyponatremia has revealed several other causes like autoimmune liver disease, Sjogren’s syndrome and non-Hodgkin’s lymphoma in addition to diabetes mellitus.

Central pontine myelinolysis (CPM) is a neurological disorder typically caused by rapid correction of severe chronic hyponatremia. Conditions causing a hyperosmolar state can also cause CPM, but it is rarely seen in diabetes.

Here we describe a case of a 34-year-old female with longstanding uncontrolled diabetes mellitus who presented with bilateral upper and lower limb weakness and dysphagia. Examination showed decreased muscle strength, and laboratory investigations showed high HbA1c, high blood glucose, increased serum osmolality, and normal sodium. A diagnosis of CPM was made after MRI showed restricted diffusion in the bilateral pons and CT showed pontine hypodensities. The patient was started on insulin therapy, and she showed clinical improvement with improving blood glucose levels. After five days of hospital stay, she was discharged home with appointments to neurology and endocrinology clinics.

This case shows that CPM is a potential complication of uncontrolled diabetes mellitus in the presence of normal serum sodium. Timely treatment of hyperglycemia can lead to improvement of symptoms, but it is a potentially fatal condition. Thus, a diagnosis of CPM should be considered in diabetic patients who present with neurological symptoms and hyperglycemia.

• blood glucose
• central pontine myelinolysis
• diabetes mellitus
• hyperglycemia
• osmotic demyelination syndrome

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

Patients with diabetes mellitus are at increased risk for bone fragility fracture secondary to multiple mechanisms. Hyperglycemia can induce true dilutional hyponatremia. Hyponatremia is associated with gait instability, osteoporosis, and increased falls and bone fractures, and studies suggest that compromised bone quality with hyponatremia may be independent of plasma osmolality. We performed a case-control study of patients with diabetes mellitus matched by median glycated hemoglobin (HbA1c) to assess whether hyponatremia was associated with increased risk of osteoporosis and/or fragility fracture.

Osteoporosis (n = 823) and fragility fracture (n = 840) cases from the MedStar Health database were matched on age of first HbA1c ≥6.5%, sex, race, median HbA1c over an interval from first HbA1c ≥6.5% to the end of the encounter window, diabetic encounter window length, and type 1 vs type 2 diabetes mellitus with controls without osteoporosis (n = 823) and without fragility fractures (n = 840), respectively. Clinical variables, including coefficient of glucose variation and hyponatremia (defined as serum [Na⁺] <135 mmol/dL within 30 days of the end of the diabetic window), were included in a multivariate analysis.

Multivariate conditional logistic regression models demonstrated that hyponatremia within 30 days of the outcome measure was independently associated with osteoporosis and fragility fractures (osteoporosis OR 3.09; 95% CI, 1.37 to 6.98; fracture OR, 6.41; 95% CI, 2.44 to 16.82).

Our analyses support the hypothesis that hyponatremia is an additional risk factor for osteoporosis and fragility fracture among patients with diabetes mellitus.

• diabetes mellitus
• fractures
• hyponatremia
• osteoporosis
• sodium