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Osmotic Demylination Syndrome (ODS)

Formerly known as Central Pontine Myelinolysis, ODS is a devastating condition which can occur after rapid overcorrection of hyponatremia. It is a clinical diagnosis with a delayed presentation up to 7 days after the rapid correction. The symptoms can vary and are dependent on which anatomical structure in the brain demyelinates. ODS most commonly affects the pons, however other structures can be affected including the cerebellum or basal ganglia. Commonly described symptoms include ataxia, quadriplegia, cranial nerve palsies, and the ‘locked-in’ syndrome. Risk factors for ODS: 1. elderly, 2. malnourished state, 3. chronic severe hyponatremia, 4. hypokalemia.

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 Central Pontine Myelinolysis - What it is and How to Prevent it

Central Pontine Myelinolysis (CPM) is a largely irreversible, dreaded neurologic complication caused by osmotic demyelination, as a result of increasing sodium levels too rapidly. It is definitively diagnosed via Brain MRI. Symptoms may include dysphagia, dysarthria, paraparesis, quadriparesis, lethargy, seizure, or even coma, and usually begin within 2 to 6 days following sodium elevation (i.e. may not be apparent in the emergency department). If the hyponatremic patient is symptom-free, treat conservatively by restricting oral fluid intake to less than 1500 mL per day. Isotonic fluids (i.e. 0.9% normal saline) may be used, particularly if the patient is dehydrated. If the hyponatremic patient is symptomatic, hypertonic saline (i.e. 3%, start with 100 mL bolus) may be used. Increase sodium level by no more than 1.5 to 2 meq/L per hour for the first 3 to 4 hours until symptoms resolve. Increase by no more than 10 meq/L in the first 24 hours. Take Home Point: Prevent devastation of CPM by treating asymptomatic hyponatremia conservatively and by closely monitoring rate of sodium increase.

Articles of Interest

Acute Demyelinating Disorders

The greatest risk occurs if patients transition from chronic hyponatremia to hypernatremia. Hypernatremia should be aggressively avoided in patients who are recovering from hyponatremia.

Annals of B-Pod: Osmotic Demyelination Syndrome

ODS includes the more common central pontine myelinolysis (CPM), as well as extrapontine myelinolysis (EPM), which occurs in addition to CPM in approximately 10% of cases. Osmotic demyelination syndrome typically presents two to six days following overcorrection or rapid correction of hyponatremia.

Central Pontine Myelinolysis

CAUSES... Most important: Rapid correction of hyponatremia (typically chronic).

Central pontine myelinolysis

Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. There are no inflammatory changes, and blood vessels are normal. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis, and the locked-in syndrome. Magnetic resonance imaging of the brain, the imaging procedure of choice, shows an area of prolonged T1 and T2 relaxation in the central pons, which may have a characteristic shape. Recovery varies...

Central Pontine Myelinolysis as a Result of Ideally Corrected Hyponatremia in a Post-Covid Patient

Central pontine myelinolysis (CPM) is a non-inflammatory neurological condition with various clinical features and onset patterns and also with a very wide prognostic spectrum ranging from asymptomatic cases to encephalopathy and mortality. In this case report we, aim to present the first case of central pontine myelinolysis as a result of an optimally corrected hyponatremia in a post-COVID-19 patient our knowledge while assessing the clinical and radiological findings.

Central Pontine Myelinolysis, Osmotic Demyelination Syndrome...

Simplified but still detailed explanation about an important clinical topic in Neurology, Central Pontine Myelinolysis. How to avoid the disease and how bad the prognosis could be if we didn't pay attention to the optimum patients' clinical approach.

Central Pontine Myelinolysis: A Metabolic Disorder of Myelin

CPM was first documented in 1959, in patients with alcoholism.7,8 The association with hyponatremia and rapid correction of the low sodium did not occur until many years later.1–4 The defining neuropathological characteristics of CPM are symmetric, sharply demarcated lesions of the central pons, with selective destruction of myelin sheaths and loss of oligodendrocytes, presence of fat-laden macrophages, and absence of inflammatory infiltrate.

Central pontine myelinolysis: electrolytes and beyond

Central pontine myelinolysis (CPM), which is a component of the osmotic demyelination syndrome (ODS), is a frequent neurological complication that follows rapid correction of hyponatraemia. However, there are other predisposing risk factors (chronic alcoholism, hypokalaemia) that perpetuate the development of ODS.

Extra-pontine Myelinolysis After Rapid Correction of Hyponatremia Responding to Levodopa

Osmotic demyelinating disease of the central nervous system has two variants: central pontine myelinolysis and extra-pontine myelinolysis (EPM). Up to 10% of cases of osmotic demyelination syndrome are associated with EPM, which mostly affects the thalamus and basal ganglia. It is commonly associated with the rapid correction of hyponatremia.

The piglet andthe trident sign inosmotic demyelination syndrome

These findings are typical of osmotic demyelination syndrome (ODS) and have been compared with a pig’s snout or a trident sword (piglet sign or trident sign). One month later, he was alert with spastic teraparesis, still under mechanical ventilation.

The Role of Nurses in Managing Severe Hyponatremia and Preventing Central Pontine Myelinolysis

Extreme caution must be taken in correct serum sodium levels in hyponatremic patients, particularly when there should be a higher index of suspicion for a more chronic nature. Though commonly thought of as a neurologic disorder limited to this scenario, it has also been described in patients with acute hypernatremia and overly rapid lowering of the serum sodium level.

Resources

CPM Surviors or Family Members Central Pontine Mylinolisis

For anyone who has suffered CPM and survived or their family members.

CMAJ

Central pontine myelinolysis was first described by Adams and colleagues in 1959 in a clinicopathologic study with alcoholic or malnourished patients. Chronic alcoholism, electrolyte disturbances and liver transplant are associated with an increased risk of central pontine myelinolysis, and it may occur after rapid correction of hyponatremia. Decreasing levels of consciousness is the most common manifestation of central pontine myelinolysis. Other symptoms include horizontal gaze paralysis, pseudobulbar palsy and quadriplegia.

Physiopedia

Central pontine myelinolysis (CPM) [now termed osmotic demyelination syndrome (ODS)], characterized by damage to regions of the brain (most commonly pontine white matter tracts) after rapid correction of metabolic disturbances such as hyponatremia.

StatPearls

Central pontine myelinolysis (CPM) is a component of osmotic demyelination syndrome (ODS). It is characterized by damage to regions of the brain, most commonly pontine white matter tracts, after rapid correction of metabolic disturbances such as hyponatremia. Central pontine myelinolysis (CPM) was first described in 1959 by Adams and his colleagues in a report of four patients with pseudobulbar palsy and quadriplegia.