MRI aspect of hypoglycaemic encephalopathy: An image to remember

A 44-year-old man with a history of type 1 Diabetes mellitus was discovered unconscious at home. On admission, he had a Glasgow Coma Scale score of 3 with an initial blood glucose level of 45 mg/dL. After normalization of blood glucose to 129 mg/dL, there was no clinical improvement.

Cranial computed tomography showed no abnormalities. A cerebral magnetic resonance imaging was performed 48 hours after the admission. It revealed on T2 weighted images, fluid-attenuated inversion recovery (FLAIR) (Figure 2), and diffusion-weighted imaging (DWI) (Figure 3) bilateral and symmetrical high signal intensity in both caudate and lentiform nuclei. The diagnosis of hypoglycaemic encephalopathy was made. Unfortunately, two weeks after admission, the initial neurological status of the patient did not improve, and he died later due to septicaemia.

Background

Hypoglycaemic encephalopathy (HE) is a critical condition characterised by low blood glucose levels leading to brain damage. It may cause reversible cytotoxic oedema, mostly in the cerebral cortices and deep-seated nuclei, particularly the globus pallidus. The exact pathophysiology is unknown. However, since glucose is the nervous system’s main energy source, severe hypoglycaemia can cause neurons to die. It is well-recognised that hypoglycaemia leads to cellular energy failure, as the brain is an obligate glucose metaboliser [1]. The consequences of this energy deficit are sodium/potassium pump failure, cellular swelling, and tissue alkalosis.

Clinical Perspective

Clinical signs of hypoglycaemia depend on the severity, duration, and responsiveness of serum glucose. When the hypoglycaemia persists, patients with HE may present with convulsions, hemiplegia, aphasia, and lethargy along with coma [2]. Hypoglycaemia is usually recognised clinically, and imaging is not routinely performed unless there is a complicated recovery.

Imaging Perspective

Cerebral neuroimaging is crucial in diagnosing HE. CT scans may be normal or show parietal and occipital hypodensities in the context of diffuse oedema. On MRI, there are characteristic changes typically affecting the posterior limb of the basal ganglia, internal capsule, cerebral cortex (particularly parieto-occipital and insula), and hippocampus. These are typically bilateral and symmetrical. The thalami, cerebellum, and brainstem are usually spared in adults [3]. The splenium of the corpus callosum can also be affected, producing the so-called boomerang sign. On T1-weighted images, there is usually a low signal of the affected areas. T2 and FLAIR show bilateral and symmetrical high intensities in those areas. While DWI/ADC can be an earlier and more sensitive tool, showing reversible diffusion restriction [4].

Outcome

Therapeutic options are usually intravenous glucose along with monitoring to keep blood glucose within the normal range. The outcome depends on the severity and duration of the hypoglycaemia, and the extent of brain damage, which is correlated with basal ganglia damage. If the latter is absent or minimal, residual deficits depend on cortical involvement. If basal ganglia damage is severe, the neurological outcome is usually poor [4].

Take Home Message / Teaching Points

• Key to diagnosis is a coma in a diabetic adult treated with insulin.
• MRI usually shows bilateral and symmetrical parietal/temporal/occipital and basal ganglia involvement.
• The thalami, cerebellum, and brainstem are usually spared in adults.

Written informed patient consent for publication has been obtained.