Hypoglycaemic encephalopathy is a brain injury that results from prolonged or severe hypoglycaemia.
On imaging, it can manifest on MRI as bilateral areas of increased signal on both T2 and FLAIR affecting the posterior limb of the internal capsule, cerebral cortex (in particular parieto-occipital and insula), hippocampus and basal ganglia. Restricted diffusion can be an earlier and sensitive tool, and is commonly reversible.
Severe symptoms of hypoglycaemia are present, such as altered conscious state, loss of consciousness, seizures, etc.
The pathophysiology is uncertain, but altered cellular physiology results in neuronal death 4-5,7. It is known that hypoglycaemia leads to a cellular energy failure, as the brain is an obligate glucose metabolizer. The resulting energy shortage results in sodium/potassium pump failure and cellular swelling and tissue alkalosis 8. Some theories are based on cell damage due to increased extracellular aspartate and glutamate 7.
Any cause of profound hypoglycaemia 4:
- overdose of hypoglycaemic medication (usually in diabetics)
- pancreatic insulinoma
As hypoglycaemia is usually recognised and managed promptly, MRI scans are not routinely performed unless there is a complicated recovery.
There are characteristic changes affecting the posterior limb of the internal capsule, cerebral cortex (in particular parieto-occipital and insula), hippocampus and basal ganglia 1,3. These are typically bilateral. The cerebellum, brainstem and thalami are usually spared in adults but they are also involved in neonates 3,4,8. The splenium of the corpus callosum can also be affected, producing the so-called boomerang sign.
- T1: low signal
- T2: high signal
- DWI: can be an earlier and sensitive tool showing reversible diffusion restriction 6
Treatment and prognosis
The clinical outcome has a direct relation with the severity and duration of the hypoglycaemic insult.
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