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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 3  |  Page : 307-308

Partial hypopituitarism: A sequel of extrapontine myelinosis

1 Department of Endocrinology, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India
2 Department of Medicine, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India

Date of Submission12-Mar-2013
Date of Decision29-Mar-2013
Date of Acceptance30-May-2013
Date of Web Publication16-Jul-2013

Correspondence Address:
Abhishek Singhai
Department of Medicine, Sri Aurobindo Medical College, Indore, Madhya Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.115075

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How to cite this article:
Banzal S, Singhai A. Partial hypopituitarism: A sequel of extrapontine myelinosis. Neurol India 2013;61:307-8

How to cite this URL:
Banzal S, Singhai A. Partial hypopituitarism: A sequel of extrapontine myelinosis. Neurol India [serial online] 2013 [cited 2021 Mar 1];61:307-8. Available from:


The concept of central pontine myelinolysis (CPM) first described by Adams et al. in 1959 [1] was extended from 1962 with the recognition that lesions can occur outside the pons, so-called extrapontine myelinolysis (EPM). The extrapontine sites include internal capsule, basal ganglion, cerebellum and cerebrum. [2] We here, probably describe the first case of partial hypopituitarism in a patient with extrapontine myelinolysis. [2]

A 22-year-old male presented with increased somnolence, dullness and anorexia of 4 days duration. He had abnormal behavior, change in voice and hiccoughs for 1 day. He was prescribed antihistaminic and steroid nasal spray for allergic rhinitis about 2 weeks ago. After taking these medications, he developed sleepiness and altered sensorium. On examination, patient was dull, drowsy, moving all limbs, had a puffy face. Vitals were normal and he looked mildly dehydrated. The relevant abnormal investigations: Hemoglobin 11.3 g/dl, serum creatinine 0.8 mg/dl, blood urea 21 mg/dl, serum sodium 92.1 mEq/L, serum potassium 3.9 mEq/L, chloride 101 mEq/L, total T4 3.6 mcg/dl (4.7-9.5), thyroid stimulating hormone (TSH) 11.9 mIU/ml (0.25-5.0), and urine for spot sodium 44 mEq/L (40-220). Ultrasound abdomen showed minimal ascites. Non-contrast computed tomography scan brain was normal. The diagnosis was primary hypothyroidism with severe hyponatremia. Patient was treated with hypertonic saline (1.6% NaCl) at the rate of 30 ml/h with other supportive treatment. After 24 h serum sodium improved to 111.6 mEq/L, it further improved to 122.1, 125.7, 137.6 mEq/L over next 3 days respectively. He was discharged in a stable condition on L-thyroxine 50 mcg/day after 5 days of hospital stay.

About a week of discharge patient again developed weakness of limbs, difficulty in walking, dribbling of saliva from mouth, staring look and slurring of speech. On examination, patient was drowsy with stiffness of limbs, facial tics, coarse tremors, dysarthria and ataxic gait. Investigations showed: serum sodium 135.4 mEq/L, serum potassium 3.89 mEq/L, serum cortisol level 1.0 mcg/dl (5-25), serum adrenocorticotropic hormone level 15.1 pg/ml (10-46). Repeat serum cortisol at 8 am confirmed lower value. Hormonal profile showed: serum follicle-stimulating hormone 3.94 mIU/ml (2.70-17.30), serum prolactin 3.89 ng/ml (0.0-15), and serum testosterone level was 3.17 (2.70-17.30). Magnetic resonance imaging (MRI) brain showed bilateral symmetrical hyperintensity in lentiform and caudate nucleus on fluid attenuated inversion recovery and T2-weighted images suggestive of osmotic myelinolysis [Figure 1]. MRI of the adrenal was normal. Patient was started on oral hydrocortisone along with thyroid replacement therapy. Gradually, he improved with treatment, but remained clumpsy. After 2 months of illness serum cortisol remained low, serum TSH became normal. He continued to improve neurologically. Oral hydrocortisone continued as his hypothalamic-pituitary axis had not improved. After 4 years of treatment, he is almost living normal life. Pituitary hormones were normal, but 8 am cortisol remained on the lower side (0.8 mcg/dl). Presently, he is on 10 mg hydrocortisone twice-a-day (8 am and 4 pm) and 75 mcg L-thyroxine.
Figure 1: Magnetic resonance imaging brain showing bilateral symmetrical hyperintensity in lentiform and caudate nucleus on fluid attenuated inversion recovery and T2 weighted images suggestive of osmotic myelinolysis

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In summary, CPM or EPM are devastating and often preventable conditions, with considerable morbidity and/or mortality. Prevention is certainly the key as current treatment only rarely leads to full recovery. Diligently avoid hypernatremia while correcting hyponatremia. [3] Patients who survive CPM/EPM likely require extensive and prolonged neurorehabilitation. Drugs known to give rise syndrome of inappropriate antidiuretic hormone should be prescribed cautiously in hypothyroidism, alcoholism, liver disease, immunosuppression after transplantation, malnourishment, renal disease, cancer, pregnancy, and in high-endurance exercise (in triathletes, marathon runners). [4] Pituitary functions should also be evaluated in osmotic demyelination whenever there is clinical suspicion of hormonal deficiency state.

  References Top

1.Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: A hitherto undescribed disease occurring in alcoholic and malnourished patients. AMA Arch Neurol Psychiatry 1959;81:154-72.  Back to cited text no. 1
2.Karp BI, Laureno R. Pontine and extrapontine myelinolysis: A neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 1993;72:359-73.  Back to cited text no. 2
3.Lien YH, Shapiro JI. Hyponatremia: Clinical diagnosis and management. Am J Med 2007;120:653-8.  Back to cited text no. 3
4.Goldman MB. The assessment and treatment of water imbalance in patients with psychosis. Clin Schizophr Relat Psychoses 2010;4:115-23.  Back to cited text no. 4


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