Teaching Case

The patient presented with sudden unconsciousness and right-sided weakness in the morning. The patient was diabetic and had taken oral hypoglycaemic drugs in the night. In the emergency department, blood sugar was found very low. The patient became normal after glucose infusion.

MRI brain revealed diffusion restriction in posterior limb of bilateral internal capsule. Changes of cerebral atrophy were noted. Chronic ischaemic changes in bilateral periventricular white matter were seen.

Hypoglycaemia is a decrease in serum glucose level to less than 50 mg/dL, commonly induced by overuse of insulin or oral hypoglycaemic agents. [1]
Glucose is the main energy substrate and profound hypoglycaemia is known to cause neuronal death. In pathological studies, however, the vulnerability of different brain regions to neuronal damage in hypoglycaemia is different. [1]
Presentation of hypoglycaemic encephalopathy is variable and depends on the area affected in correlation to its vulnerability and the severity of hypoglycaemia. Neurological symptoms include giddiness, focal neurological deficits, coma and death and may present with hemiparesis and mimic acute stroke. [1, 2]
MRI diffusion demonstrates alteration of the diffusion of water within the extracellular space and between intracellular and extracellular spaces. It may also demonstrate changes suggestive of hypoglycemia by the restricted diffusion in the affected area. [1]
The basal ganglia, pons, the temporal and occipital cortices, hippocampus, splenium of corpus callosum and bilateral posterior limb of internal capsules are the commonly affected areas. [1, 2]
Pathogenic mechanisms for diffusion restriction in hypoglycaemic encephalopathy include energy failure, excitotoxic oedema and asymmetric cerebral blood flow. Glucose deprivation leads to arrest of protein synthesis, incomplete energy failure and loss of ion homeostasis, cellular calcium influx and intracellular alkalosis. Excitotoxic oedema in contrast to cytotoxic oedema does not imply neuronal damage, this is the reason why signal changes on MRI diffusion in hypoglycaemic encephalopathy are usually transitory and completely reversible after glucose infusion. [1, 2]
Diagnosing hypoglycaemic encephalopathy requires clinical suspicion and its confirmation with blood glucose is easily available, cost effective and should be the first step in diagnosis of hypoglycaemic encephalopathy instead of MRI. The role of MRI brain diffusion in hypoglycaemic encephalopathy is to evaluate the topographic distribution of signal abnormality of hypoglycaemia, which determines the severity and prognosis of hypoglycaemic encephalopathy. If signal abnormality is confined to white matter such as the corpus callosum, internal capsule or corona radiata and regresses on follow-up imaging, there are good chances for recovery without a neurological deficit. Lesions that are detected in the cerebral cortex, basal ganglia or hippocampus and do not regress on follow-up imaging are associated with a poor outcome. [1]