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LETTER TO EDITOR
Year : 2021  |  Volume : 69  |  Issue : 1  |  Page : 209-210

Pituitrin-induced Extrapontine Myelinolysis without Rapid Osmolar Shifts


1 Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China
2 Department of Neurology, Tongling People's Hospital, Tongling, Anhui, China

Date of Submission21-Jul-2019
Date of Decision04-Nov-2019
Date of Acceptance22-Jan-2020
Date of Web Publication24-Feb-2021

Correspondence Address:
Jie-Ping Lu
Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, NO.17, Lujiang Road, Luyang District, Hefei, Anhui 230001
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.310101

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How to cite this article:
Lu JP, Wang CY, Tang QQ. Pituitrin-induced Extrapontine Myelinolysis without Rapid Osmolar Shifts. Neurol India 2021;69:209-10

How to cite this URL:
Lu JP, Wang CY, Tang QQ. Pituitrin-induced Extrapontine Myelinolysis without Rapid Osmolar Shifts. Neurol India [serial online] 2021 [cited 2021 Apr 23];69:209-10. Available from: https://www.neurologyindia.com/text.asp?2021/69/1/209/310101




Sir,

The osmotic demyelination syndrome (ODS), an uncommon disorder comprising of central pontine myelinolysis and extrapontine myelinolysis (EPM), is primarily related to the aggressive osmolar correction.[1],[2] In addition to the rapid osmolarshifts, ODS has an increasing risk in patients with alcoholism, malnutrition, liver transplantation, hemodialysis, severe burns, etc.[3] There have been a few reports of ODS caused by the rapid correction of hyponatremia associated with pituitrin/deamino arginine vasopressin.[4],[5],[6],[7] Herein, we describe a patient presenting with encephalopathy and delayed-onset dystonia, but without any preceding rapid osmolar shifts or other common risk factors of ODS following the intravenous administration of pituitrin.

A 37-year-old woman was admitted to neurology department with three days of insomnia, psychiatric symptoms, and gait disorder. Eleven days earlier, the patient had begun to receive continuously the intravenous injection of pituitrin at a rate of 1.5 U/h via a pump for eight consecutive days because of hemoptysis. During that period, she did not suffer from hyponatremia or rapid osmolar shifts. The patient had no history of poisoning, alcoholism, or malnutrition. Physical examination revealed restlessness, normal orientation, and festinating gait. There was no muscle weakness, abnormal muscle tension, or sensory disturbance. Blood tests showed serum sodium 135 mmol/L. Other serum electrolyte concentrations and ceruloplasmin levels were also within a normal range. Liver and renal function tests showed no abnormality. The slit-lamp examination found no Kayser–Fleischer ring of the cornea. Brain magnetic resonance imaging revealed bilateral caudate nuclei and putamina of low T1 and high T2 signaling, which were consistent with EPM [Figure 1]. The patient received corticosteroid therapy and her clinical conditions improved gradually. She developed delayed-onset dystonia consisting of oromandibular dystonia and spasmodic torticollis 3.5 months later. We treated her with trihexyphenidyl, baclofen, and clonazepam, and she partially responded to this drug treatment.
Figure 1: Brain magnetic resonance imaging showed symmetrical lesions in the basal ganglia. (a) Axial T1-weighted image showed bilaterally symmetrical hypointense areas in the caudate nuclei and putamina (red arrow). (b) Axial T2-weighted image showed bilaterally symmetrical hyperintense areas in the caudate nuclei and putamina (red arrow)

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Pituitrin, extracted from the posterior pituitary, consists of oxytocin and vasopressin. It is often used in the treatment of gastrointestinal and pulmonary hemorrhage due to its vasoconstrictive properties. Hyponatremia is a rare adverse event of vasopressin administration, and attention should be drawn especially when high-dose therapy is used.[8] Patients may develop ODS in case of the rapid correction of hyponatremia induced by vasopressin.[4] Our patient did not experience any rapid osmolar shifts. She also had no other common risk factors for EPM, whereas she received intravenous pituitrin before the onset of neurological symptoms. Therefore, the use of pituitrin was considered as the most probable cause of EPM.

The basal ganglia lack collateral circulation and are susceptible to ischemia. Müller et al. found that therapeutic level arginine vasopressin might significantly reduce the cardiac output and carotid blood flow by increased vascular resistance.[9] Another experimental observation showed arginine vasopressin reduced cerebral blood flow and increased cerebrovascular resistance due to vasoconstriction via activation of vasopressin V1 receptors.[10] Therefore, the pathogenesis of EPM in our case was postulated to be owing to basal ganglion ischemia resulted from the cerebral hypoperfusion associated with pituitrin administration, but the exact mechanism needs to be further studied. In summary, clinicians should be aware that EPM may still occur in patients who receive pituitrin even without rapid osmolar shifts.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Harsha KJ, Parameswaran K. Newly described additional sites of extrapontine myelinolysis along with typical pontine and extrapontine myelinolysis. Neurol India 2017;65:181-2.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Srivastava T, Singh P, Sharma B. Pontine and extrapontine myelinolysis following rapid correction of hyponatremia. Neurol India 2000;48:97.  Back to cited text no. 2
    
3.
Singh TD, Fugate JE, Rabinstein AA. Central pontine and extrapontine myelinolysis: A systematic review. Eur J Neurol 2014;21:1443-50.  Back to cited text no. 3
    
4.
Zhuang L, Xu Z, Li Y, Luo B. Extrapontine myelinolysis associated with pituitrin: Case report and literature review. BMC Neurol 2014;14:189.  Back to cited text no. 4
    
5.
Achinger SG, Arieff AI, Kalantar-Zadeh K, Ayus JC. Desmopressin acetate (DDAVP)- associated hyponatremia and brain damage: A case series. Nephrol Dial Transplant 2014;29:2310-5.  Back to cited text no. 5
    
6.
Ranger A, Szymczak A, Levin S, Salvadori M, Fraser DD. Osmotic myelinolysis with malignant cerebellar edema occurring after DDAVP-induced hyponatremia in a child. Pediatr Neurosurg 2010;46:318-23.  Back to cited text no. 6
    
7.
Xu DH, Yuan M, Wang JW, Hu YZ. Osmotic demyelination syndrome after correction of severe hyponatremia associated with pituitrin. Int J Clin Pharmacol Ther 2015;53:408-11.  Back to cited text no. 7
    
8.
Obritsch MD, Jung R, Fish DN, MacLaren R. Effects of continuous vasopressin infusion in patients with septic shock. Ann Pharmacother 2004;38:1117-22.  Back to cited text no. 8
    
9.
Müller S, How OJ, Hermansen SE, Stenberg TA, Sager G, Myrmel T. Vasopressin impairs brain, heart and kidney perfusion: An experimental study in pigs after transient myocardial ischemia. Crit Care 2008;12:R20.  Back to cited text no. 9
    
10.
Fernández N, Martínez MA, García-Villalón AL, Monge L, Diéguez G. Cerebral vasoconstriction produced by vasopressin in conscious goats: Role of vasopressin V (1) and V (2) receptors and nitric oxide. Br J Pharmacol 2001;132:1837-44.  Back to cited text no. 10
    


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