Neurol India Home 
 

LETTER TO EDITOR
Year : 2011  |  Volume : 59  |  Issue : 3  |  Page : 475--476

Reversible splenial abnormality in hypoglycemia

Dhananjay Duberkar, Vivek Lal 
 Department of Neurology, Postgraduate Institute of Medical Education & Research, Chandigarh, India

Correspondence Address:
Vivek Lal
Department of Neurology, Postgraduate Institute of Medical Education & Research, Chandigarh
India




How to cite this article:
Duberkar D, Lal V. Reversible splenial abnormality in hypoglycemia.Neurol India 2011;59:475-476


How to cite this URL:
Duberkar D, Lal V. Reversible splenial abnormality in hypoglycemia. Neurol India [serial online] 2011 [cited 2021 Dec 4 ];59:475-476
Available from: https://www.neurologyindia.com/text.asp?2011/59/3/475/82752


Full Text

Sir,

Magnetic resonance imaging (MRI) techniques, particularly diffusion-weighted imaging (DWI), have facilitated detection of early neuronal injury in hypoglycemia. [1],[2] MR signal changes have been described in the basal ganglia, pons, temporal, occipital cortex, and hippocampus. [1],[2],[3],[4] The splenium of corpus callosum may be another area of selective vulnerability to hypoglycemia. [5],[6] We report a patient with hypoglycemia with reversible focal neurological deficits and reversible DWI changes restricted to splenium of corpus callosum and internal capsule.

A 32-year-old lady presented with a history of three episodes of altered sensorium in a period of 7 days. The first two episodes were characterized by encephalopathy and right hemiparesis, which subsided within 3-4 hours of administration of intravenous glucose. She was admitted to our hospital during the third episode of altered sensorium. She was not a known case of diabetes mellitus or hypertension. On neurological examination, she was drowsy, not obeying commands and with no focal signs. Her pulse and blood pressure were within normal limits. Admission blood glucose was 19 mg/dl and other blood biochemistry was normal. Brain MRI revealed bilaterally symmetrical areas of hyperintensity on DWI sequence, with decreased apparent diffusion coefficient (ADC), in both the posterior limb of the internal capsule and splenium of the corpus callosum [Figure 1]a and b. The T2-weighted sequences and MR angiography were normal. The patient regained consciousness soon after treatment with intravenous 25% dextrose. Follow-up imaging revealed complete resolution of the hyperintense lesions on DWI, with normalization of the ADC values [Figure 1]c and d. Review of her history revealed ingestion of tablet glibenclamide 2.5 mg on all the three occasions. The patient was evaluated for insulinoma. Computer tomography of abdomen and 72 hour fasting for ruling out insulinoma were normal. She is asymptomatic on follow-up 1 year later.{Figure 1}

Neurochemical changes in hypoglycemia include an arrest of protein synthesis in many regions, incomplete energy failure, and loss of ion homeostasis, cellular calcium influx, intracellular alkalosis, and a release of neuroactive amino acids, especially aspartate, into the extracellular space of the brain. [7] Excessive release of excitatory amino acids, particularly aspartate, results in selective neuronal necrosis, predominantly in the cerebral cortex, caudoputamen, and hippocampus. The splenium of corpus callosum represents an area of selective vulnerability. [5] In our patient, the transient hypoglycemic episodes were related to glibenclamide intake, and the clinical symptoms included focal deficits and encephalopathy. MRI brain disclosed different region of involvement than what is seen commonly in hypoglycemic coma. Profound MR signal changes in the splenium of corpus callosum have been reported in a variety of different pathological conditions such as infectious diseases and treatment with or withdrawal from antiepileptic drugs, partially based on histopathological studies, without unravelling the reason for this localized vulnerability. [8] Identification of this mechanism may help understand hypoglycemia-induced brain injury. We emphasize that while assessing changes on DWI, clinicians should include hypoglycemia in the differential diagnosis.

References

1Shirayama H, Ohshiro Y, Kinjo Y, Taira S, Teruya I, Nakachi K, et al. Acute brain injury in hypoglycemia-induced hemiplegia. Diabet Med 2004;21:623-4.
2Finelli PF. Diffusion-weighted MR in hypoglycemia coma. Neurology 2001;57:933.
3Chan R, Erbay S, Oljeski S, Thaler D, Bhadelia R. Case report: Hypoglycemia and diffusion-weighted imaging. J Comput Assist Tomogr 2003;27:420-3.
4Fujioka M, Okuchi K, Hiramatsu KI, Sakaki T, Sakaguchi S, Ishii Y. Specific changes in human brain after hypoglycemic injury. Stroke 1997;28:584-7.
5Kim JH, Choi JY, Koh SB, Lee Y. Reversible splenial abnormality in hypoglycemic encephalopathy. Neuroradiology 2007;49:217-22.
6Terakawa Y, Tsuyuguchi N, Nunomura K, Murayama N, Fujishige M, Yamamura A, et al. Reversible diffusion weighted imaging changes in the splenium of corpus callosum and internal capsule associated with hypoglycemia - case report. Neorol Med Chir (Tokyo) 2007;47:486-8.
7Auer RN, Siesjo BK. Hypoglycaemia: Brain neurochemistry and neuropathology. Baillieres Clin Endocrinol Metab 1993;7:611-25.
8Böttcher J, Kunze A, Kurrat C, Schmidt P, Hagemann G, Witte OW, et al. Localized reversible reduction of apparent diffusion coefficient in transient hypoglycemia-induced hemiparesis. Stroke 2005;36:e20-2.