Asian Journal of Psychiatry 14 (2015) 73–74
Contents lists available at ScienceDirect
Asian Journal of Psychiatry journal homepage: www.elsevier.com/locate/ajp
Letter to Editor Central pontine myelinolysis-induced mania: A case study Dear Editor, Central pontine myelinolysis (CPM) is a disease of the pons with unclear aetiology and pathogenesis (Mochizuki et al., 2003). It is strongly correlated with alcoholism and uncorrected hyponatremia (Mochizuki et al., 2003). Clinical presentation can include psychiatric changes, neurological dysfunction (Lampl and Yazdi, 2002) and acute confusion (Mochizuki et al., 2003). CPM is formally diagnosed via magnetic resonance imaging (MRI) showing symmetrical lesions in the central portion of the pontine base (Graff-Radford et al., 2011; Martin and Young, 1995). 25% of
patients present with psychiatric features alone, with neurological deficits notable in their absence (Lampl and Yazdi, 2002). This case report describes just such an atypical presentation, and the resulting need for greater clinical awareness of the possibility of CPM in alcoholics presenting with mania alone. Ms. MA is a 41 year old woman with a history of depression and alcohol dependence with resulting intermittent hepatitis. She presented with a recent onset delirium. Extensive organic investigations did not identify a clear aetiology; in particular her sodium was noted to be normal and her chronically deranged liver function tests had not significantly changed. Neurological examination was normal. An MRI was positive for CPM (Fig. 1), however this diagnosis was initially dismissed as there were no neurological deficits.
Fig. 1. MRI brain: signal change in the central pons demonstrating CPM. http://dx.doi.org/10.1016/j.ajp.2015.01.007 1876-2018/ß 2015 Elsevier B.V. All rights reserved.
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Letter to Editor / Asian Journal of Psychiatry 14 (2015) 73–74
Ms. MA’s delirium persisted for two weeks before her clinical picture evolved to mania. On transfer to the psychiatric ward Ms. MA was elevated, distractible and intrusive with bizarre behaviour and marked insomnia. Her speech was pressured and circumstantial. Neuropsychological assessment was undertaken on two separate occasions, and both were consistent with deficits associated with CPM. Three weeks of quetiapine and lorazepam settled her mood symptoms, but deficits in executive function and language persisted beyond discharge despite ongoing quetiapine therapy. Ms. MA initially presented with delirium, then shifting into a mania in keeping with an organic mood disorder. Most CPM cases display neurological deficits accompanying psychiatric manifestations; commonly behavioural, psychotic or mood disturbance (Lampl and Yazdi, 2002). Mania as a result of CPM has been reported (Yu et al., 2004), but not specifically in the absence of neurological deficit. Given the reliance on the presence of motor symptoms in the diagnosis of CPM, it is possible that patients presenting with behavioural disturbance in the absence of neurological features may go undiagnosed and untreated. Alcohol dependence is a highly prevalent condition (Hasin et al., 2007) associated with CPM, and as such CPM in the context of alcoholism might be an under-recognised entity that warrants greater attention and research. This is especially true given the poor prognosis of CPM; mortality rates are between 5 and 10% (Martin, 2004). As such, CPM should be part of the differential diagnosis when presented with a chronic alcoholic patient with acute confusion and/or mania. Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. Conflict of interest The authors disclose no conflicts of interest. References Graff-Radford, J., Fugate, J.E., Kaufmann, T.J., et al., 2011. Clinical and radiologic correlations of central pontine myelinolysis syndrome. Mayo Clin. Proc. 86 (11), 1063–1067. Hasin, D., Stinson, F.S., Ogburn, E., Grant, B.F., 2007. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States. Arch. Gen. Psychiatry 64 (7), 830.
Lampl, C., Yazdi, K., 2002. Central pontine myelinolysis. Eur. Neurol. 47 (1), 3–10. Martin, P.J., Young, C.A., 1995. Central pontine myelinolysis: clinical and MRI correlates. Postgrad. Med. J. 71, 430–432. Martin, R.J., 2004. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry 75 (Suppl. 3), 22–28. Mochizuki, H., Masaki, T., Miyakawa, T., et al., 2003. Benign type of central pontine myelinolysis in alcoholism – clinical, neuroradiological and electrophysiological findings. J. Neurol. 250 (9), 1077–1083. Yu, J., Zheng, S.S., Liang, T.B., Shen, Y., Wang, W.L., Ke, Q.H., 2004. Possible causes of central pontine myelinolysis after liver transplantation. World J. Gastroenterol. 10 (17), 2540–2543.
Rachel Goggin* Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia Nicholas Nguyena,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Prashant Tibrewala,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Rohan Dhillona,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Ben Finlay Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia Daphne Law Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia *Corresponding author at: The Queen Elizabeth Hospital, 28 Woodville Rd, Woodville South, SA 5011, Australia. Tel.: +61 8 8222 6000 E-mail address: [email protected] (R. Goggin). Received 10 January 2015
Contents lists available at ScienceDirect
Asian Journal of Psychiatry journal homepage: www.elsevier.com/locate/ajp
Letter to Editor Central pontine myelinolysis-induced mania: A case study Dear Editor, Central pontine myelinolysis (CPM) is a disease of the pons with unclear aetiology and pathogenesis (Mochizuki et al., 2003). It is strongly correlated with alcoholism and uncorrected hyponatremia (Mochizuki et al., 2003). Clinical presentation can include psychiatric changes, neurological dysfunction (Lampl and Yazdi, 2002) and acute confusion (Mochizuki et al., 2003). CPM is formally diagnosed via magnetic resonance imaging (MRI) showing symmetrical lesions in the central portion of the pontine base (Graff-Radford et al., 2011; Martin and Young, 1995). 25% of
patients present with psychiatric features alone, with neurological deficits notable in their absence (Lampl and Yazdi, 2002). This case report describes just such an atypical presentation, and the resulting need for greater clinical awareness of the possibility of CPM in alcoholics presenting with mania alone. Ms. MA is a 41 year old woman with a history of depression and alcohol dependence with resulting intermittent hepatitis. She presented with a recent onset delirium. Extensive organic investigations did not identify a clear aetiology; in particular her sodium was noted to be normal and her chronically deranged liver function tests had not significantly changed. Neurological examination was normal. An MRI was positive for CPM (Fig. 1), however this diagnosis was initially dismissed as there were no neurological deficits.
Fig. 1. MRI brain: signal change in the central pons demonstrating CPM. http://dx.doi.org/10.1016/j.ajp.2015.01.007 1876-2018/ß 2015 Elsevier B.V. All rights reserved.
74
Letter to Editor / Asian Journal of Psychiatry 14 (2015) 73–74
Ms. MA’s delirium persisted for two weeks before her clinical picture evolved to mania. On transfer to the psychiatric ward Ms. MA was elevated, distractible and intrusive with bizarre behaviour and marked insomnia. Her speech was pressured and circumstantial. Neuropsychological assessment was undertaken on two separate occasions, and both were consistent with deficits associated with CPM. Three weeks of quetiapine and lorazepam settled her mood symptoms, but deficits in executive function and language persisted beyond discharge despite ongoing quetiapine therapy. Ms. MA initially presented with delirium, then shifting into a mania in keeping with an organic mood disorder. Most CPM cases display neurological deficits accompanying psychiatric manifestations; commonly behavioural, psychotic or mood disturbance (Lampl and Yazdi, 2002). Mania as a result of CPM has been reported (Yu et al., 2004), but not specifically in the absence of neurological deficit. Given the reliance on the presence of motor symptoms in the diagnosis of CPM, it is possible that patients presenting with behavioural disturbance in the absence of neurological features may go undiagnosed and untreated. Alcohol dependence is a highly prevalent condition (Hasin et al., 2007) associated with CPM, and as such CPM in the context of alcoholism might be an under-recognised entity that warrants greater attention and research. This is especially true given the poor prognosis of CPM; mortality rates are between 5 and 10% (Martin, 2004). As such, CPM should be part of the differential diagnosis when presented with a chronic alcoholic patient with acute confusion and/or mania. Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors. Conflict of interest The authors disclose no conflicts of interest. References Graff-Radford, J., Fugate, J.E., Kaufmann, T.J., et al., 2011. Clinical and radiologic correlations of central pontine myelinolysis syndrome. Mayo Clin. Proc. 86 (11), 1063–1067. Hasin, D., Stinson, F.S., Ogburn, E., Grant, B.F., 2007. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States. Arch. Gen. Psychiatry 64 (7), 830.
Lampl, C., Yazdi, K., 2002. Central pontine myelinolysis. Eur. Neurol. 47 (1), 3–10. Martin, P.J., Young, C.A., 1995. Central pontine myelinolysis: clinical and MRI correlates. Postgrad. Med. J. 71, 430–432. Martin, R.J., 2004. Central pontine and extrapontine myelinolysis: the osmotic demyelination syndromes. J. Neurol. Neurosurg. Psychiatry 75 (Suppl. 3), 22–28. Mochizuki, H., Masaki, T., Miyakawa, T., et al., 2003. Benign type of central pontine myelinolysis in alcoholism – clinical, neuroradiological and electrophysiological findings. J. Neurol. 250 (9), 1077–1083. Yu, J., Zheng, S.S., Liang, T.B., Shen, Y., Wang, W.L., Ke, Q.H., 2004. Possible causes of central pontine myelinolysis after liver transplantation. World J. Gastroenterol. 10 (17), 2540–2543.
Rachel Goggin* Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia Nicholas Nguyena,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Prashant Tibrewala,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Rohan Dhillona,b University of Adelaide, Adelaide, Australia b Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia a
Ben Finlay Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia Daphne Law Department of Psychiatry, Queen Elizabeth Hospital, Adelaide, Australia *Corresponding author at: The Queen Elizabeth Hospital, 28 Woodville Rd, Woodville South, SA 5011, Australia. Tel.: +61 8 8222 6000 E-mail address: [email protected] (R. Goggin). Received 10 January 2015
