|Year : 2014 | Volume
| Issue : 2 | Page : 102-105
Reversible MRI changes of prolonged hypoglycemia
Surinder Thakur1, NM Sharath Babu1, Jatinder K Mokta1, Sanjeev Sharma2
1 Department of Medicine, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
2 Department of Radiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
|Date of Web Publication||6-May-2014|
N M Sharath Babu
Department of Medicine, Indira Gandhi Medical College, Shimla, Himachal Pradesh
Source of Support: None, Conflict of Interest: None
Hypoglycemia is most commonly caused by drugs used to treat diabetes mellitus or by exposure to other drugs, including alcohol. Diverse neurologic manifestations of hypoglycemia have been reported frequently. These neurologic symptoms range from focal neurologic deficits to permanent dysfunction or death. Here, we report a case of prolonged hypoglycemia in an alcoholic who was unconscious and in whom there were reversible changes on magnetic resonance imaging.
Keywords: Hypoglycemia, magnetic resonance imaging, reversible changes
|How to cite this article:|
Thakur S, Sharath Babu N M, Mokta JK, Sharma S. Reversible MRI changes of prolonged hypoglycemia. J Med Nutr Nutraceut 2014;3:102-5
|How to cite this URL:|
Thakur S, Sharath Babu N M, Mokta JK, Sharma S. Reversible MRI changes of prolonged hypoglycemia. J Med Nutr Nutraceut [serial online] 2014 [cited 2021 Oct 23];3:102-5. Available from: https://www.jmnn.org/text.asp?2014/3/2/102/131963
| Introduction|| |
Hypoglycemia can cause serious morbidity; if severe and prolonged, it can be fatal. In healthy individuals, symptoms of hypoglycemia develop at a mean plasma glucose concentration of approximately 55 mg/dl (3.0 mmol/liter).  Radioimaging studies can show reversible changes on magnetic resonance imaging in specific locations which depend on severity and duration of hypoglycemia.
| Case Report|| |
A male patient aged 58 years was admitted with complaints of unconsciousness for 24 h. The patient was a chronic alcoholic. Also his intake was poor in the last 2 days. There was no history of similar complaints in the past. He was not a diabetic. On examination, patient was unconscious with Glasgow coma score of 5/15. Doll's eye reflex was present suggestive of intact brainstem. Pupils were equal with size of 2.5 mm, round and reactive to light. Fundus was normal. There were no meningeal signs. There was no history of fever. There were movements only to painful stimulus. Plantars were bilaterally extensor. Random blood sugar showed 35 mg/dl. So considering clinical findings and random blood sugar, patient was treated for hypoglycemia and further hypoglycemia was not recorded during routine monitoring at hospital stay.
On routine investigations, CBC, electrolytes, liver and kidney function tests, CSF analysis, skiagram chest, electrocardiogram were normal. On imaging studies of brain, magnetic resonance imaging showed hyperintensities in hippocampus, midbrain, middle cerebellar peduncle, insular cortex and parietal lobe on T2 and fluid attenuation and inversion recovery (FLAIR) sequences [Figure 1], restriction pattern in diffusion weighted imaging (DWI) and apparent diffusion coefficient (ADC) sequences [Figure 2]. Patient improved during hospital stay but memory disturbances persisted along with extrapyramidal signs.
On follow up, patient was reviewed after 8 weeks. Patient had improved without any hypoglycemic episodes, but had developed pseudobulbar effect with slowness in his activities. On repeat magnetic resonance imaging of brain, hyperintensities that were documented at first admission on T2 and FLAIR had disappeared except mild hyperintensity in hippocampus and midbrain [Figure 3] with no restriction on DWI and ADC sequences [Figure 4]. These were consistent with hypoglycemia findings which got improved. His present complaints were possibly due to sequelae of his hypoglycemia insult to brain.
|Figure 1: Hyperintensities on MR images (T2 and FLAIR) in middle cerebellar peduncle with restriction on DWI and ADC sequences|
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|Figure 2: Hyperintensities on MR images (T2 and FLAIR) in hippocampus, midbrain and parietal cortex with restriction on DWI and ADC sequences|
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|Figure 3: Middle cerebellar peduncle showing normal pattern without restriction|
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|Figure 4: Hyperintensities improved in all areas except hippocampus and midbrain(improving) without restriction|
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| Discussion|| |
Hypoglycemia is most documented by Whipple's triad: (1) Symptoms consistent with hypoglycemia, (2) low plasma glucose concentration measured with a precise method (not a glucose monitor), and (3) relief of those symptoms after the plasma glucose level is raised. In healthy individuals, symptoms of hypoglycemia develop at a mean plasma glucose concentration of approximately 55 mg/dl (3.0 mmol/liter).  Hypoglycemia can cause serious morbidity; if severe and prolonged, it can be fatal. It should be considered in any patient with episodes of confusion, an altered level of consciousness, or a seizure. In our patient Whipple's triad was demonstrated and suggestive of definite hypoglycemia.
Alcohol induced hypoglycemia is common in men and in malnourished patients on a low calorie diet. Fewer than 1% of alcoholic patients presenting to emergency room have hypoglycemia. However, because of high incidence of alcoholic intoxication relative to other causes of hypoglycemia, alcohol can be implicated in 18 to 52% of patients admitted in emergency department because of sustained hypoglycemia.  The mortality rate among hospitalized patients with alcohol induced hypoglycemia may be as high as 10%.  In healthy subjects, a minimum of 2 to 3 days of fasting is necessary to deplete hepatic glycogen storage. However, alcohol induced hypoglycemia could develop within 6 to 36 h of ingestion of a moderate to large amount of alcohol.  Our patient had similar presentation and it is a potential reversible cause of encephalopathy.
Hypoglycemia can cause various neurologic symptoms including profound memory loss, transient motor deficits, a persistent vegetative state, and death in 2-4% of cases. ,, Lesions are described that involve the temporal, occipital, and insular cortex; the hippocampus; and the basal ganglia,  with sparing of thalami. Additionally, the deep white matter may be involved, with hypoglycemic injury in the form of symmetric hyperintensity involving the internal capsule, corona radiata, and splenium on T2-weighted images. The lesions may show restricted diffusion.  In a recent article, Kang et al.  described typical areas of reversible restricted diffusions in hypoglycemic encephalopathy: Characteristically, the posterior limb of the internal capsule, cerebral cortex, corona radiata, centrum semiovale, hippocampus, and basal ganglia. Our patient had similar features on MRI in hippocampus, parietal cortex, insular cortex, and in middle cerebellar peduncle. Finelli has suggested that diffusion weighted magnetic resonance (MR) imaging in humans may better define the areas of involvement at an earlier time than conventional MR images and that the involvement of the basal ganglia may portend a poor outcome.  So, it is of relevance to get early imaging which can help in deciding outcomes depending on the areas involved even in a reversible cause.
The pathomechanism of hypoglycemic encephalopathy remains unclear. Some pathogenetic mechanisms for diffusion restriction in hypoglycemic encephalopathy thathave been proposed are: (1) Energy failure, (2) excitotoxic edema, and (3) asymmetric cerebral blood flow.  First, severe hypoglycemiacausing glucose deprivation leads to arrest of protein synthesis inmany 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. Second, excitotoxic edema is a cytotoxic form due to increased extracellular glutamate. The presence of glutamate leads to calcium and sodium entry into the cell and induces apoptosis. Last, when hypoperfusion complicates hypoglycemia, the brain is not exposed to an equal fall in perfusion. Due to thefocal loss of autoregulation, the frontal and parietal lobe areas have grossly decreased cerebral flow, whereas the cerebellum and brain stem show almost no fall in local cerebral blood flow.
Several different conditions like seizure, drug toxicity, viral encephalitis, and metabolic encephalopathy have reversible diffusion restrictions similar to those in hypoglycemia.  MR imaging findings in hypoglycemic encephalopathy include reversible diffusion restriction at characteristic locations. These findings can be helpful in the differential diagnosis. The prognosis or neurologic sequelae of hypoglycemic encephalopathy depends on the severity and duration of hypoglycemia.  Lo et al. described two cases of hypoglycemic coma in which transient white matter DW MR abnormalities were associated with complete recovery while widespread cortical lesions were associated with poor outcome and death.  In our case, all white matter abnormalities improved and among grey matter abnormalities, only hippocampus and midbrain hyperintensities did not improve completely. The striking difference in the neuroimaging patterns may be helpful in prognosis and differential diagnosis in hypoglycemic coma.
In patients with hypoglycemia, early diagnosis and treatment have a very important role in prognosis of the patient. The successful prevention of recurrent hypoglycemia is almost always associated with normal or near-normal neurologic outcome. The imaging studies help in differentiation from other metabolic causes depending on the specific sites involved in hypoglycemia. Also, as stated earlier, diffusion weighted MR has advantage over conventional MR in early diagnosis. The prognosis depends on severity and duration of hypoglycemia. 
| References|| |
Cryer P. The prevention and correction of hypoglycemia. In: Jefferson L, Cherrington A, Goodman H, editors. Handbook of physiology; Section 7, the endocrine system. Volume II. The endocrine pancreas and regulation of metabolism. New York: Oxford University Press; 2001.p. 1057-92.
Marks V, Teale JD. Drug-induced hypoglycemia. Endocrinol Metab Clin North Am 1999;28:555-77.
Marks V. Alcohol and carbohydrate metabolism. Clin Endocrinol Metab 1978;7:333-49.
Böttcher 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.
Finelli PF. Diffusion-weighted MR in hypoglycemia coma. Neurology 2001;57:933-5.
Shirayama H, Ohshiro Y, Kinjo Y, Taira S, Teruya I, Nakachi K, et al
. Acute brain injury in hypoglycaemia-induced hemiplegia. Diabet Med 2004;21:623-4.
Fujioka M, Okuchi K, Hiramatsu KI, Sakaki T, Sakaguchi S, Ishii Y. Specific changes in human brain after hypoglycemic injury. Stroke 1997;28:584-7.
Lo L, Tan AC, Umapathi T, Lim CC. Diffusion-weighted MR imaging in early diagnosis and prognosis of hypoglycemia. AJNR Am J Neuroradiol 2006;27:1222-4.
Kang EG, Jeon SJ, Choi SS, Song CJ, Yu IK. Diffusion MR imaging of hypoglycemic encephalopathy. AJNR Am J Neuroradiol2010;31:559-64.
Maekawa S, Aibiki M, Kikuchi K, Kikuchi S, Umakoshi K. Timerelated changes in reversible MRI findings after prolonged hypoglycemia. Clin Neurol Neurosurg 2006;108:511-3.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]