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BRIEF COMMUNICATIONS: T. Aoki, T. Sato, K. Hasegawa, R. Ishizaki, and M. Saiki Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma Neurology 2004; 63: 392-393 [Abstract] [Full text] [PDF]

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Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma

C.H.A. Tan, CC Tchoyoson Lim, T Umapathi   (27 September 2004)

Reply to Tan et al

Tomohiro Aoki   (27 September 2004)

Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma 27 September 2004
C.H.A. Tan, National Neuroscience Institute 11 Jalan Tan Tock Seng, Singapore 308433, CC Tchoyoson Lim, T Umapathi Send Correspondence to journal: Re: Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma tchoyoson_lim{at}nni.com.sg C.H.A. Tan, et al.	We thank Aoki et al for their case report. [1] Reversible hyperintensity on diffusion-weighted MRI affecting the white matter in a bilaterally symmetrical distribution has not yet been described. When we encountered a similar case, we almost made a misdiagnosis of cerebral infarction. Our patient was a 69-year-old diabetic man with episodes of difficulty talking and generalized weakness. While undergoing echocardiography, he suddenly became unresponsive, and we suspected embolic brainstem stroke from atrial fibrillation. An urgent MRI showed symmetrical diffusion-weighted MRI hyperintensities in the internal capsules and corona radiate bilaterally and the splenium of the corpus callosum. MR angiography and T2-weighted MR images were normal. These findings were interpreted as acute white matter embolic infarction. However, the patient had profound hypoglycemia, and recovered rapidly and completely after treatment. Repeat MRI including diffusion-weighted study 12 hours later was normal. The good prognosis and reversibility of MRI findings in our patient confirm the reported case, but return of diffusion MRI abnormalities was much more rapid. Previous animal and human studies have shown that severe prolonged hypoglycemic coma causes permanent neuronal damage in the cerebral gray matter. [2,3] However, the report by Aoki et al suggests that reversible decline in ADC values may be seen in the cerebral white matter, possibly reflecting water movement from the extracellular space into the intracellular compartment. [4] Perhaps the white matter tracts, which are highly oriented in direction (i.e., they exhibit anisotropic diffusion), may be more sensitive to this early and transient water diffusion phenomenon. We hope that our experience illustrates this phenomenon in “rule out stroke” patients with unsuspected hypoglycemic coma; such unusual findings may lead to misdiagnosis of cerebral infarction, especially since diffusion-weighted MRI is now common. References 1. Aoki T, Sato T, Hasegawa K, Ishizaki R, Saiki M. Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma. Neurology 2004;63:392-393. 2. Finelli PF. Diffusion-weighted MR in hypoglycemic coma. Neurology 2001;57:933. 3. Hasegawa Y, Formato JE, Latour LL, et at. Severe transient hypoglycemia causes reversible change in the apparent diffusion coefficient of water. Stroke 1996;27:27:1648-1655; discussion 1655-1656. 4. Pelligrino D, Almquist LO, Siesjo BK. Effects of insulin-induced hypoglycemic on intracellular pH and impedance in the cerebral cortex of the rat. Brain Res. 1981;221:129-147.
Reply to Tan et al 27 September 2004
Tomohiro Aoki Mizoshiri 150-11, Maiduru City, JAPAN Send Correspondence to journal: Re: Reply to Tan et al spetzler{at}hotmail.com Tomohiro Aoki	We thank Tan et al for their interest in our case report. The diffusion weighted MRI on hypoglycemic coma in both our and their cases showed bilateral symmetrical hyperintensity lesions. Sometimes these lesions will be misdiagnosed as cerebral infarction. One of the way to make a differential diagnosis is reversible change. However, diffusion weighted MRI on onset will not be able to distinguish hypoglycemic coma from cerebral infarction; it is important to consider the possibility of hypoglycemic coma. Sometimes the pattern of hyperintensity lesions, symmetrical white matter distribution and sparing of brain stem helps to determine differential diagnosis. The question is how long the hyperintensity lesions last after glucose infusion remains unclear.