A 37-year-old female patient was admitted to emergency room, because of unconsciousness. The patient's blood glucose was too low to measure. Computed tomography of the brain was performed. The next days, the patient was still in a coma. MR examination was performed for assessing the extent of brain damage.
Figure 1. An emergency non-contrast brain CT scan in the time of admission showed non-specific white matter hypodensities and diffuse supratentorial brain parenchyma (white cerebellum sign).
Figure 2. An emergency non-contrast brain CT scan in the time of admission showed non-specific white matter hypodensities and diffuse cerebral oedema.
MRI (magnetic resonance imaging) of brain (3T scanner) was performed using FLAIR, T2-weighted, T1-weighted, diffusion-weighted imaging, and contrast-enhanced T1-weighted sequences.
Figure 3. Transverse FLAIR magnetic resonance image showing bilateral cerebral cortical and subcortical patchy and confluent increased signal intensity. The caudate nuclei, the hippocampi as well as the insular cortices are seen involved.
Figure 4. Transverse FLAIR magnetic resonance image showing bilateral cerebral cortical and subcortical patchy and confluent increased signal intensity. The caudate nuclei, the hippocampi as well as the insular cortices are seen involved.
Figure 5. DWI magnetic resonance image revealed abnormal diffusion restriction involving the cerebral cortex in multiple locations.
Figure 6. T1-weighted gadolinium-enhanced image show no abnormal contrast enhancement inside the lesions.
Background: Hypoglycaemic encephalopathy is a neurologic manifestation of profound hypoglycaemia.
Clinical Perspective: The clinical course of this condition ranging from completely reversible neurologic deficits to irreversible coma.
Imaging Perspective: The lesion usually involves the frontal, parietal, temporal and occipital cortex and subcortex with relative sparing of the deep white matter. The basal ganglia are involved in severe cases. The thalami are always spared as well as the cerebellum. Serial CT scans and MR images showed diffuse brain oedema in the acute stage (within 1 week of onset) and showed diffuse brain atrophy in the chronic stage (from 2 weeks to 12 months after onset). [1,2]
Outcome: Poor prognostic factors include diffuse and extensive cortical involvement, prolonged and profound hypoglycemia, higher body temperature, and a low lactic acid level. 
Teaching Points: MRI reveals diffuse abnormal intensity in the cortex and basal ganglia region. DWI provides important information for diagnosis. [1,2,3]
Written informed patient consent for publication has been obtained.
 Shan Ren, Zhigang Chen, Ming Liu, Zhiqun Wang; The radiological findings of hypoglycemic encephalopathy. A case report with high b value DWI analysis. Medicine (Baltimore). 2017 Oct; 96(43): e8425.
 Witsch J, Neugebauer H, Flechsenhar J, Jüttler E; Hypoglycemic encephalopathy: a case series and literature review on outcome determination. J Neurol. 2012 Oct;259(10):2172-81.
 Sharma P, Eesa M, Scott JN; Toxic and acquired metabolic encephalopathies: MRI appearance. AJR Am J Roentgenol. 2009 Sep;193(3):879-86.