|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 3 | Page : 214-215
Central pontine myelinolysis following hypoglycemia
Rufus Demel1, Pratish George2, Uttam George3, Jeyaraj Pandian4
1 Department of Medicine, Christian Medical College, Ludhiana, Punjab, India
2 Department of Nephrology, Christian Medical College, Ludhiana, Punjab, India
3 Department of Radiology, Christian Medical College, Ludhiana, Punjab, India
4 Department of Neurology, Christian Medical College, Ludhiana, Punjab, India
|Date of Web Publication||17-Aug-2014|
Department of Nephrology, Christian Medical College, Ludhiana, Punjab
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Demel R, George P, George U, Pandian J. Central pontine myelinolysis following hypoglycemia. CHRISMED J Health Res 2014;1:214-5
|How to cite this URL:|
Demel R, George P, George U, Pandian J. Central pontine myelinolysis following hypoglycemia. CHRISMED J Health Res [serial online] 2014 [cited 2019 Oct 21];1:214-5. Available from: http://www.cjhr.org/text.asp?2014/1/3/214/138914
A 70-year-old lady was brought with unresponsiveness noticed in the morning after going to sleep with no apparent complaints at bed time. She was detected to have diabetes mellitus (DM) 8 years earlier and was on irregular control on 2 mg of glimipride, which was increased to 3 mg a week earlier. She had no addictions, indigenous or unprescribed medication intake, previous medical comorbidities, or surgeries. She was treated at a local hospital for hypoglycemia with Random Blood Sugar (RBS) of 40 mg/dL. Electrolytes were normal at referral and she did not receive sodium correction.
At referral, she was comatose with areflexic quadriplegia and bilateral extensor plantar reflex. She was normotensive with pallor and pitting pedal edema bilaterally. Investigations showed fractured neck of left femur with anemia (Hb 10.5 gm/dL), renal failure (blood urea 127 mg/dL, serum creatinine 5.1 mg/dL), metabolic acidosis (pH 7.3, pCO2 24.1 mmHg, HCO3 11.4 meq/dL, lactate 0.6 mmol/L), hypernatremia (147 meq/dL), hyperkalemia (potassium 6.1 meq/dL), and RBS 181 mg/dL. Differential diagnosis considered in the emergency room included brain stem stroke, nonconvulsive status epilepticus, osmotic demyelination, and uremic encephalopathy. Magnetic resonance imaging (MRI) of brain showed confluent hyperintensities in bilateral periventricular white matter, gangliocapsular region, and pons [Figure 1]a suggestive of osmotic myelinolysis. Electroencephalogram (EEG) showed generalized epileptiform abnormalities.
|Figure 1: (a and b) Axial T2 fl air images demonstrate hyperintensities involving (a) the pons and (b) periventricular white matter, intenal and external capsule|
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Her blood sugars were maintained between 150-250 mg/dl and underwent intermittent hemodialysis (10 sessions) till she recovered renal function 3 weeks later. She was managed as inpatient for another 5 weeks with no improvement in quadriplegia, sensorium, or MRI findings [Figure 1]b] and discharged for domicilary care.
Victor and Adams first described central pontine myelinolysis (CPM) in 1959. Osmotic demyelination syndrome develops because of rapid correction of a chronic osmolar abnormality when there is a deficit of organic osmolytes. As a result, brain cells, particularly oligodendrocytes, are at risk of cell shrinkage and hence demyelination.  Common causes of CPM are rapid correction of hyponatremia, alcoholism, liver transplantation, and malnutrition. Other causes include cirrhosis, severe burns, hypokalemia, hyperosmolar hyperglycemic state, acquired immunodeficiency syndrome (AIDS), post-pituitary surgery, post-urological surgery, psychogenic polydipsia, beer potomania, prolonged diuretic use, hypophosphatemia, folate deficiency, alcohol withdrawal, dialysis disequilibrium syndrome, correction of hyperammonemia, refeeding syndrome, lithium toxicity, hyperemesis gravidarum, and carbamate toxicity. CPM clinically presents with acute para- or quadraparesis, dysphagia, dysarthria, diplopia, loss of consciousness, and other neurological symptoms associated with brainstem damage. Characteristic MRI lesions show hypointense T1-weighted lesions and hyperintense lesions demonstrated on T2-weighted, proton density weighted and Fluid Attenuated Inversion Recovery (FLAIR) MRI. 
CPM is a rare complication of hypoglycemia. This lady had CPM secondary to hypoglycemia as evidenced by the clinical and MRI features and the absence of any of the other established etiology of CPM. Hypoglycemia causes CPM by failure of membrane ion channels,  oligodendrocyte apoptosis,  and oxidative stress of glucose reperfusion. 
There is no definite treatment for CPM and supportive management is recommended. The outcome may be death, disability, or recovery to a virtually normal level of function in rare cases. The delay in recognition and correction of hypoglycemia possibly induced CPM in this lady and early recognition and management of hypoglycemia is preventive.
| References|| |
|1.||Ghosh N, DeLuca GC, Esiri MM. Evidence of axonal damage in human acute demyelinating diseases. J Neurol Sci 2004;222:29-34. |
|2.||Brunner JE, Redmond JM, Haggar AM, Kruger DF, Elias SB. Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospect of magnetic resonance imaging study. Ann Neurol 1990;27:61-6. |
|3.||Hasegawa Y, Formato JE, Latour LL, Gutierrez JA, Liu KF, Garcia JH, et al. Severe transient hypoglycemia causes reversible change in the apparent diffusion coefficient of water. Stroke 1996;27:1648-55. |
|4.||Yan S, Rivkees SA. Hypoglycemia influences oligodendrocyte development and myelin formation. Neuroreport 2006;17:55-9. |
|5.||Suh SW, Gum ET, Hamby AM, Chan PH, Swanson RA. Hypoglycemic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase. J Clin Invest 2007;117:910-8. |