American Journal of Physical Medicine & Rehabilitation:
From the Department of Neurology, Korea University Medical Center, Korea University College of Medicine, Seoul, Korea.
All correspondence and requests for reprints should be addressed to Byung-Jo Kim, MD, Department of Neurology, Korea University Medical Center, Korea University College of Medicine, Anam-Dong 5 Ga 126-1, Seongbuk-Gu, Seoul (136-705), Korea.
A 41-yr-old woman was admitted to our hospital after an episode of drowsiness attributable to hypoglycemia (25 mg/dl), which improved immediately after she received an infusion of 50% dextrose solution at another hospital. She had no history of diabetes, trauma, recent infection, or drug overuse.
She was hemodynamically stable on admission, and her blood tests were normal except for profound hypoglycemia (23 mg/dl). Her serum glucose level was immediately restored to within the normal range, but there was no improvement in her state of consciousness. She opened her eyes, withdrew both arms, and made meaningless sounds in response to noxious stimuli. Her brainstem reflexes were normal, and no pathologic reflexes were elicited. Her neck was supple, and there were no skin lesions or evidence of any trauma. The results of all other laboratory tests, including an examination of the cerebrospinal fluid, were normal. Electroencephalography showed generalized delta waves but no epileptic form discharge.
T2-weighted images showed high signal intensities in the bilateral caudate nucleus and putamen without cortical involvement. Gadolinium-enhanced T1-weighted images showed strong enhancement in these areas (Fig. 1A and B). The lesions showed high signal intensities on diffusion-weighted magnetic resonance images (b-value, 1000 sec/mm2) and low signal intensities on apparent diffusion coefficient maps (Fig. 1C and D). She is currently in a persistent vegetative state.
Brain lesions caused by hypoglycemia are known to involve the posterior limb of the internal capsule, splenium of the corpus callosum, corona radiata, cerebral cortex, basal ganglia, and hippocampus.1 Glucose deprivation is known to lead to brain energy failure, dysfunction of the cell membrane ionic pump, and consequent cytotoxic edema.2 The vegetative state can result from both traumatic and nontraumatic injuries, such as stroke, metabolic disorders, and congenital malformations of the central nervous system.3 Neuroimaging studies are not only useful for the differential diagnosis and identification of the underlying pathophysiological mechanisms in patients in a persistent vegetative state, but they may also be used for prognostic assessment and treatment planning.4 Diffusion-weighted magnetic resonance imaging is rarely performed in patients with hypoglycemia. The images presented in this study demonstrate the signal changes typically seen on diffusion-weighted images of patients with hypoglycemia-induced encephalopathy, and they suggest that cytotoxic edema caused the hypoglycemic coma and persistent vegetative state to occur.
1. Albayram S, Ozer H, Gokdemir S, et al: Reversible reduction of apparent diffusion coefficient values in bilateral internal capsules in transient hypoglycemia-induced hemiparesis. AJNR Am J Neuroradiol
2. Hasegawa Y, Formato JE, Latour LL, et al: Severe transient hypoglycemia causes reversible change in the apparent diffusion coefficient of water. Stroke
3. The Multi-Society Task Force on PVS: Medical aspects of the persistent vegetative state— first of two parts. N Engl J Med 1994;330:1499–508
4. Joseph TG, Joy H, Nicholas S, et al: Funtional neuroimaging applications for assessment and rehabilitation planning in patients with disorders of consciousness. Arch Phys Med Rehabil