Keywords

Diabetes, post-hypoglycemic brain injury, MRI brain scan

Diverse neurologic manifestations of hypoglycemia have been reported. These neurologic symptoms range from focal neurologic deficits to permanent dysfunction or death.1-3 The accumulation of excitatory amino acids and not simply glucose starvation of the neuron, seems to play an important pathogenetic role.4 Brain magnetic resonance imaging (MRI) is a useful technique to evaluate hypoglycemic brain damage. We describe herein characteristic brain MR diffusion imaging features in a diabetic patient who had severe hypoglycemia.

Case Report

A 45-year-old diabetic female was brought comatose in the casualty outdoor. On physical examination, her pulse rate was 108/min, blood pressure 100/70 mmHg and respiratory rate 26/min. Her extremities were cold clammy with profuse sweating. Jugular venous pressure (JVP) was normal. There was no pedal edema, cyanosis, icterus or lymphadenopathy. Lungs were clear. Neurological examination revealed power >3/5 in both upper and lower limbs with normal tone. Bilateral plantar reflex was extensor. Pupils were normal in size and reactive to light. Patient was then shifted for MRI brain scan, which showed hyperintense areas of restricted diffusion involving the bilateral basal ganglia (Fig. 1) characteristic of posthypoglycemic brain injury. Immediately blood glucose levels was then done, which confirmed hypoglycemia (blood sugar - 40 mg%). Patient was given 100 mL intravenous infusion of 25% dextrose stat. She regained consciousness. During her further hospital stay her insulin dose was resetted to optimal dose with proper instructions for dietary pattern and she was discharged on 10th day.

Discussion

Hypoglycemia can cause various neurologic symptoms including profound memory loss, transient motor deficits, a persistent vegetative state and death in 2-4% of cases.5 Some pathogenetic mechanisms for diffusion restriction picture in MRI brain have been proposed as follows:

1. Energy failure
2. Excitotoxic edema
3. Asymmetric cerebral blood flow.

Glucose deprivation leads to arrest of protein synthesis in many regions, incomplete energy failure and loss of ion homeostasis, cellular calcium influx and intracellular alkalosis. Consequently, neuroactive amino acid (aspartate) release into the extracellular space occurs and results in selective neuronal necrosis, predominantly in the cerebral cortex, caudoputamen and hippocampus.6 However, protein synthesis in the cerebellum, brainstem and hypothalamus remains unaffected because of the greater activity of the glucose transport mechanisms.7

Further in contrast to ischemic brain damage, inability to produce lactic acid during hypoglycemia is thought to account for the fact that infarction is not seen in controlled experimental conditions producing a pure hypoglycemic insult to the brain. Thalamic lesions exist in ischemic encephalopathy, but not in hypoglycemic coma. In hypoglycemia, due to focal loss of autoregulation, the frontal and parietal lobe areas have grossly decreased cerebral flow, whereas the cerebellum and brainstem show almost no fall in local cerebral blood flow as seen in our patient also. There was a characterisitic band like area localized to right parietal lobe (Fig. 1). The predominant release of aspartate into the extracellular fluid in hypoglycemia differs from the rise in extracellular glutamate in ischemia.8 Second, unlike ischemia, energy failure is only moderate during hypoglycemia because of the remaining glucose supply and oxidation of endogenous nonglucose fuels by the brain.8 In contrast to cytotoxic edema, excitotoxic edema does not imply neuronal damage, because glutamate induces edema of glial cells and myelinic sheaths might protect axons from intracellular edema and irreversible damage. In addition, glutamate reuptake systems are not impaired in hypoglycemia. According to these mechanisms, hypoglycemic brain injury is usually transitory and MRI abnormalities normalize with time.9

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