Osmotic demyelination

Classic MRI Patterns

The radiological presentation of osmotic demyelination syndrome consists of two main patterns of involvement, which can coexist:

1. Central pontine myelinolysis. Axial MR images demonstrate a typical isolated lesion in the central portion of the pons (pontine lesion). A key feature is that the corticospinal tracts remain intact (spared).
2. Extrapontine myelinolysis. In addition to brainstem changes, there is symmetric bilateral involvement of deep gray matter structures, primarily the basal ganglia.

MRI Signal Characteristics:

• DWI (DWI) and T2-FLAIR: On these sequences (including free-fluid signal suppression), demyelinating lesions appear hyperintense.
• T1-weighted images: The affected area shows a hypointense signal. Contrast enhancement is absent.
• ADC maps: The apparent diffusion coefficient (ADC) in the area of injury is paradoxically increased, which differentiates this process from classic cytotoxic edema with restricted diffusion.

Differential Diagnosis: Acute Hepatic Encephalopathy

Osmotic demyelination must be differentiated from other metabolic brain disorders. Acute Hepatic Encephalopathy (Acute Hepatic Encephalopathy, HE) develops against the background of acute hyperammonaemia (hyperammonaemia) and leads to cytotoxic edema, and in severe cases, intracranial hypertension.

MRI pattern in acute hepatic encephalopathy:

• DWI reveals increased diffusivity of the white matter, reflecting mild diffuse interstitial edema (changes are reversible upon restoration of liver function).
• T2 and FLAIR show bilateral symmetric signal changes.
• Cortical gray matter often demonstrates restricted diffusion. The insular cortex (insular cortex) and cingulate gyrus (cingulate gyrus) are predominantly affected. Meanwhile, the occipital and perirolandic cortices usually remain spared.
• The dorsal brainstem, thalami, posterior limb of the internal capsule, and periventricular white matter may also be involved.

Differential Diagnosis: Acute Glycemic Disorders

Acute carbohydrate metabolism disorders also present with a specific neuroimaging picture that must be distinguished from demyelination.

Severe Hypoglycaemia (Hypoglycaemia)

Occurs in cases of hypoglycemic drug overdose. Clinically manifests as coma, seizures, and neurological deficits.

• Early stage on MRI: Diffuse gyral swelling (diffuse gyral swelling), including the cerebellum.
• On T2: Diffuse hyperintense lesions appear. The basal ganglia, hippocampus, parietal, and occipital cortices are specifically involved. Unlike severe anoxia, the thalami usually remain spared.
• On DWI: Unlike osmotic demyelination, restricted diffusion is observed here with transiently decreased ADC values.

Hyperglycaemia Without Ketosis (Hyperglycaemia Without Ketosis)

Found in uncontrolled diabetes mellitus, accompanied by chorea, hemiballism, and seizures.

• Basal ganglia: CT shows spontaneous hyperattenuation, and T1 MRI shows unilateral or bilateral hyperintensity of the deep nuclei. On DWI, ADC is typically increased.
• Isolated cortical involvement: Manifests as subcortical hypointensity and cortical hyperintensity on T2. On DWI, the cortical lesion is hyperintense. A contrast pattern is possible (cortical or leptomeningeal enhancement). The mechanism of subcortical T2 hypointensity is not fully understood, but it is attributed to the accumulation of iron, free radicals, or intracellular dehydration of supporting tissue.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathophysiology of central pontine myelinolysis development during rapid correction of hyponatremia
• Comparison of MRI patterns in hypoglycemic encephalopathy and severe hypoxic-ischemic encephalopathy
• Mechanisms of cytotoxic edema formation in hyperammonemia
• Theories of subcortical T2 hypointensity in hyperglycemia without ketosis
• Clinical interpretation of ADC maps in metabolic brain disorders

Other topics in the Neuroimaging section

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