J Neurointensive Care Search


J Neurointensive Care > Volume 2(1); 2019 > Article
You, Han, Kim, and Park: Central Pontine Myelinolysis After Non-Aneurysmal Perimesencephalic Subarachnoid Hemorrhage: Case Report and Review of the Literature


Central pontine myelinolysis (CPM) is one of the encephalopathy that results from extreme fluctuations in serum sodium concentration and plasma osmolality. CPM after non aneurysmal perimesencephalic subarachnoid hemorrhage (NPSAH) is very rare. A 53-year-old female patient aggravated her instabilty 3 weeks after treatment of after NPSAH. Brain CT showed a prominent low-density lesion in the central pons. Vasospasm, pontine infarct, multiple sclerosis must be excluded after subarachnoid hemorrhage. Her brain magnetic resonance imaging (MRI) of the brainstem revealed CPM. The peripheral fiber sparing, central trident appearance was observed. Peripheral fiber sparing is more prominent, but central trident is disappearing at long-term follow-up MRI. CPM can develop even after NPSAH as well as aneurysmal subarachnoid hemorrhage. Trident pattern in pons area and peripheral fiber sparing is differential diagnosis with vasospasm, cerebral infarct and multiple sclerosis after NPSAH.


Central pontine myelinolysis (CPM) was first described in 1959 by Adams and colleagues as a disease affecting alcoholics and malnourished people11). It is characterized by a loss of oligodendrocytes and myelin with relatively well preserved neuronal cell bodies and axons in the central pons9). CPM following after subarhanoid hemorrhage (SAH) caused by extreme fluctuations in serum sodium. However, CPM due to non-aneurysmal perimesencephalic SAH (NPSAH) is very rare. Here, we report and describe CPM after NPSAH.


A 53-year-old woman known to have asthma and hypertension was admitted to our emergency department with confused mentality. Initial brain computed tomography (CT) revealed SAH at the bilateral sylvian cisterns, basal cistern, and cortical sulci (Fig. 1A). Computed tomography angiography and transfemoral cerebral angiography were performed to rule out cerebral aneurysm. Neither aneurysmal dilatation nor vascular malformation was found even after repeated angiography (Fig. 1B).
The patient had severe hyponatremia (113 mmol/l) with low plasma osmolality (248 mOsm/kg). Urine sodium (25 mEq/l) and urine osmolality (201 mOsm/kg) were high. She was diagnosed with cerebral salt wasting (CSW) and was administered 3% hypertonic saline, which caused her serum sodium level to rise to 134 mmol/l within 48 hours.
When she was discharged from the hospital 3 weeks later, follow-up brain CT revealed that the SAH had resolved without CPM (Fig. 1C) and the patient was mentally alert without any neurologic symptoms. On clinical examination, her pulse rate was 72 beats/min, and her blood pressure was normal (110/70 mmHg). Her blood parameter including oxygenation, liver and renal tests were within normal limits. Her serum sodium was 136 mmol/L. She exhibited normal power in all four limbs, and her touch and pain sensation was normal.
Three weeks after discharge, however, the patient had a tendency to sway to one side when walking. She did not present dysphagia, but she had dysarthria. Brain CT showed a prominent low-density lesion in the central pons (Fig. 1D). Magnetic resonance imaging (MRI) of the brainstem revealed CPM, with a hyperintense lesion in the central pons on T2-weighted MRI and hypointensity on the T1-weighted image (Fig. 1E, 1F).
The patient was managed conservatively in outpatient care. Follow up one-year brain MRI showed some recovery brain stem lesion (Fig. 1G, 1H). Follow up one-year brain MRI showed some recovery brain stem lesion. Her clinical status was much improved; she can walk independently and returned to her daily job.


CPM after NPSAH is a very rare complication, with only a few reported cases to date. Hyponatremia is a common finding in acute brain disease, occurring in approximately 30% of neurosurgical patients with SAH, equal frequency after non-aneurysmal SAH and aneurismal SAH13). In our case, the hemorrhage was located at the bilateral sylvian cisterns, basal cistern, and cortical sulci. We have not found any aneurysmal dilatation. A falling sodium level can progressively lead to neurological problems such as confusion, lethargy, seizures, and coma2). CPM has traditionally been associated with rapid correction of hyponatremia, allcoholism, chronic malnutrition, and sodium imbalance are the primary conditions associated with CPM1). Although early case reports described CPM associated with alcoholism10), more recent studies have implicated rapid corrections of hyponatremia and hypernatremia as a cause of CPM or Osmotic demyelination syndrome (ODS)7). Reported cases in central pontine demylination after aneurysamal or non aneurysmal subarachnoid hemorrhage shown in Table 1.
Specifically, clinical studies suggest that rapid correction of hyponatremia, especially a large magnitude of correction (i.e., >25 meq/l in the first 24-48 hours) is associated with CPM18). As excessive natriuresis has been observed, the term CSW was coined for this syndrome. However, the proposed natriuretic factor was not identified, and after the discovery of antidiuretic hormone (ADH), the syndrome of inappropriate ADH secretion was favored as the causal mechanism2).
The preferential localization of myelinolysis to the central pons is thought to result from the grid arrangement of oligodendrocytes, which limits their mechanical flexibility and capacity to swell. Oligodendroglial cells are vulnerable to cellular dehydration, which may enhance apoptosis4). During hyponatremia, these cells can only adapt by losing more ions instead of swelling, making them prone to damage when sodium is replaced. Central trident sign and peripheral fiber sparing was observed at initial MRI, and peripheral sparing more prominent at long-term follow up MRI in this case.
ODS, which includes CPM and extrapontine myelinolysis, is evident on CT. However, MRI is the imaging technique of choice due to its greater sensitivity and superior capacity to detect the lesions. The typical radiologic feature of CPM is a trident-shaped, symmetric, hyperintense lesion in the central pons with sparing of the periphery on T2-weighted MRI and hypointensity on the T1-weighted image15). Diffusion-weighted imaging (DWI) with apparent diffusion coefficient mapping yields higher specificity for ODS lesions with early signal changes after the onset of neurologic symptoms14).
When osmotic demyelination occurs, it is usually irreversible and has no definitive management. Thus, prevention is more important. Indeed, the slow correction of hyponatremia does not appear to be associated with ODS either clinically or experimentally. Reports of individual cases or small case series suggest that treatments including steroids, intravenous immunoglobulin, and thyrotrophin-releasing hormone may have good outcomes, but these results have been difficult to interpret.


In conclusion, CPM can develop not only after aneurysmal SAH with thick subarachnoid hemorrhage but also after NPSAH. Brain MRI image showing brain stem lesion, and peripheral sparing can be detected after CPM at follow up MRI. Trident pattern in pons area and peripheral fiber sparing is differential diagnosis with vasospasm, cerebral infarct and multiple sclerosis after non-aneurysmal perimesencephalic subarachnoid hemorrhage.


No potential conflict of interest relevant to this article was reported.

Fig. 1.
A) Initial brain CT revealed SAH at the bilateral sylvian cisterns, basal cistern, and cortical sulci. B) No evidence of aneurysm, vascular malformation, or vasospasm was detected by CTA or transfemoral cerebral angiography. C) SAH at the bilateral sylvian cisterms, basal cistern, and cortical sulci resolved by the time of hospital discharge 3 weeks later. D) However, follow-up brain CT 3 weeks after discharge showed a prominent low-density lesion in the central pons. E) and F) Symmetric hyperintense lesion in the central pons with sparing of the periphery on T2-weighted MRI and hypointensity on the T1-weighted image, suggesting central pontine demyelination. G) and H) Follow-up MRI one year later showed improvement in central pontine demyelination. Peripheral fiber sparing is more prominent at long-term follow-up MRI.
Table 1.
Reported cases in central pontine demylination after subarachnoid hemorrhage
Study Cause Hyponatremia Metabolic cause
Maimaitili et al., 20138) Aneurysm Y SIADH
Saramma et al., 201316) Aneurysm Y CSW
Hannon et al., 20125) Aneurysm Y SIADH
Kubo et al., 20086) Aneurysm Y CSW
Sherlock et al., 200617) Aneurysm Y SIADH
Vrsajkov et al., 201219) Aneurysm Y CSW
Nakagawa et al., 201012) Aneurysm Y CSW
Wartenberg et al., 200620) Non- Aneurysm Y SIADH
Chandy et al., 20063) Aneurysm Y CSW

CSW: cerebral salt wasting; SIADH: Syndrome of inappropriate antidiuretic hormone secretion.


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;81:154–172.
crossref pmid
2. Betjes MG. Hyponatremia in acute brain disease: the cerebral salt wasting syndrome. Eur J Intern Med 2002;13:9–14.
crossref pmid
3. Chandy D, Sy R, Aronow WS, Lee WN, Maguire G, Murali R. Hyponatremia and cerebrovascular spasm in aneurysmal subarachnoid hemorrhage. Neurol India 2006;54:273–275.
crossref pmid
4. DeLuca GC, Nagy Z, Esiri MM, Davey P. Evidence for a role for apoptosis in central pontine myelinolysis. Acta Neuropathol 2002;103:590–598.
crossref pmid pdf
5. Hannon MJ, Behan LA, O'Brien MM, Tormey W, Ball SG, Javadpour M, et al. Hyponatremia following mild/moderate subarachnoid hemorrhage is due to SIAD and glucocorticoid deficiency and not cerebral salt wasting. J Clin Endocrinol Metab 2014;99:291–298.
crossref pmid
6. Kubo Y, Ogasawara K, Kakino S, Kashimura H, Yoshida K, Ogawa A. Cerebrospinal fluid adrenomedullin concentration correlates with hyponatremia and delayed ischemic neurological deficits after subarachnoid hemorrhage. Cerebrovasc Dis 2008;25:164–169.
crossref pmid
7. Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57–62.
crossref pmid
8. Maimaitili A, Maimaitili M, Rexidan A, Lu J, Ajimu K, Cheng X, et al. Pituitary hormone level changes and hypxonatremia in aneurysmal subarachnoid hemorrhage. Exp Ther Med 2013;5:1657–1662.
crossref pmid pmc
9. McCormick WF, Danneel CM. Central pontine myelinolysis. Arch Intern Med 1967;119:444–478.
crossref pmid
10. Messert B, Orrison WW, Hawkins MJ, Quaglieri CE. Central pontine myelinolysis. Considerations on etiology, diagnosis, and treatment. Neurology 1979;29:147–160.
crossref pmid
11. Musana AK, Yale SH. Central pontine myelinolysis: case series and review. WMJ 2005;104:56–60.

12. Nakagawa I, Kurokawa S, Nakase H. Hyponatremia is predictable in patients with aneurysmal subarachnoid hemorrhage--clinical significance of serum atrial natriuretic peptide. Acta Neurochir (Wien) 2010;152:2147–2152.
crossref pmid pdf
13. Rinkel GJ, Wijdicks EF, Vermeulen M, Hasan D, Brouwers PJ, van Gijn J. The clinical course of perimesencephalic nonaneurysmal subarachnoid hemorrhage. Ann Neurol 1991;29:463–468.
crossref pmid
14. Ruzek KA, Campeau NG, Miller GM. Early diagnosis of central pontine myelinolysis with diffusion-weighted imaging. AJNR Am J Neuroradiol 2004;25:210–213.
15. Sakamoto E, Hagiwara D, Morishita Y, Tsukiyama K, Kondo K, Yamamoto M. [Complete recovery of central pontine myelinolysis by high dose pulse therapy with methylprednisolone]. Nihon Naika Gakkai Zasshi 2007;96:2291–2293.
crossref pmid
16. Saramma P, Menon RG, Srivastava A, Sarma PS. Hyponatremia after aneurysmal subarachnoid hemorrhage: Implications and outcomes. J Neurosci Rural Pract 2013;4:24–28.
crossref pmid pmc
17. Sherlock M, O'Sullivan E, Agha A, Behan LA, Owens D, Finucane F, et al. Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J 2009;85:171–175.
crossref pmid
18. Sterns RH. Severe symptomatic hyponatremia: treatment and outcome. A study of 64 cases. Ann Intern Med 1987;107:656–664.
19. Vrsajkov V, Javanovic G, Stanisavljevic S, Uvelin A, Vrsajkov JP. Clinical and predictive significance of hyponatremia after aneurysmal subarachnoid hemorrhage. Balkan Med J 2012;29:243–246.
crossref pmid pmc pdf
20. Wartenberg KE, Schmidt JM, Claassen J, Temes RE, Frontera JA, Ostapkovich N, et al. Impact of medical complications on outcome after subarachnoid hemorrhage. Crit Care Med 2006;34:617–623; quiz 624.
crossref pmid
Share :
Facebook Twitter Linked In Google+ Line it
METRICS Graph View
  • 0 Crossref
  • 1,666 View
  • 24 Download
Related articles in JNIC


Browse all articles >

Editorial Office
Department of Neurosurgery, Korea University College of Medicine
73, Inchon-ro, Seongbuk-gu, Seoul 02841, Korea
Tel: +82-2-920-6833    Fax: +82-2-929-0629    E-mail: jnic.editor@gmail.com                

Copyright © 2019 by Korean Neurointensive Care Society. All rights reserved.

Developed in M2community

Close layer
prev next