- Email: [email protected]
An Overlooked Cause of Acute Symptomatic Seizures: Psychogenic Polydipsia
CLINICAL COMMUNICATION TO THE EDITOR
An Overlooked Cause of Acute Symptomatic Seizures: Psychogenic Polydipsia To the Editor: Metabolic encephalopathy and seizures are well-known serious manifestations of severe hyponatremia, because water equilibrates with cells leading to brain edema.1 Psychogenic polydipsia is a rare and often overlooked cause of hyponatremia, mostly described in the past in institutionalized patients with long-standing schizophrenia. However, psychogenic polydipsia has been observed recently in the community setting and outside an obvious psychiatric context; thus, little is actually known about the clinical relevance and neurologic complications of this disorder in this large and various population.2 We report the case of a dysthymic patient from the community who developed acute seizures related to severe hyponatremia. Acute water intoxication, induced by unrecognized potomania, was finally revealed as the provoking cause. A 51-year-old woman was referred to the emergency department in postictal coma, after 2 tonic-clonic seizures without clear focal symptoms. Severe hypo-osmolar hyponatremia (admission serum Na⫹ 112 mmol/L, normal value: 135-146 mmol/L; plasma osmolarity 246 mOsm/L, normal value: 275-295 mOsm/L) was found on laboratory examinations, along with low urine osmolarity (232 mOsm/L, normal value: 400-1500 mOsm/L) and sodium (23 mmol/24 h, normal value: 40-220 mmol/24 h). Serum total protein, triglycerides, creatinine, plasma adrenocorticotropin, serum cortisol, and thyroid hormones were in the normal range. Blood glucose values were satisfactory. She appeared euvolemic, and the whole clinical examination did not show abnormalities. Computed tomography scan and magnetic resonance imaging of the brain were normal, as well as routine and sleep electroencephalograms.
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Camilla Cicognani, MD, Medicine Unit, Ospedale Bellaria, Azienda USL Bologna, via Altura n.5, 40139, Bologna, Italy. E-mail address: [email protected]
0002-9343/$ -see front matter © 2013 Elsevier Inc. All rights reserved.
Water restriction (⬍1.5 L/d) was prescribed, and normal plasma sodium was obtained 1 week after admission. No clinical symptoms occurred after seizures resolved. The history of the patient was unremarkable for neurologic pathology. She was affected by insulin-dependent type 1 diabetes without recent decompensations and stable dysthymia with anxious traits treated with low-dose citalopram. Her grandmother was epileptic, and her brother’s son has had epilepsy since the age of 3 years. However, details on the epilepsy type were unavailable. A subsequent clinical interview revealed a history of psychogenic polydipsia and chronic hyponatremia (123-132 mmol/L), with the recent superimposition of water intoxication due to anxiety decompensation. Water restriction was recommended on discharge, and the patient’s blood electrolytes were normal 6 months later. The patient’s overall clinical picture is suggestive for seizures provoked by severe hyponatremia as a consequence of self-induced water intoxication. The patient did not have a history of seizures and had normal electroencephalograms and negative brain magnetic resonance imaging. Therefore, apart from a possible generic “predisposition” to epilepsy as suggested by a positive family history, the patient did not show any other potential cause of seizures except for severe hyponatremia, which, in turn, was likely to be induced by compulsive water drinking. Other causes of hyponatremia were excluded by extensive diagnostic workup. Typically, psychogenic polydipsia has been described in chronic schizophrenic inpatients, most commonly presenting with seizures. However, recently it has been shown in middle-aged women with anxiety disorder and in chronic alcoholics, but reports on the neurologic complications of psychogenic polydipsia in these cases are rare. Cronin3 described a group of 11 patients with potomania-induced hyponatremia, mostly with a history of alcoholism, and in this group grand mal seizures were the most common complication. We emphasize that acute symptomatic seizures can be the only manifestation of potomania, even as an isolated behavioral disorder in the context of compensated dysthymia. Psychogenic polydipsia is not always obvious, and often only a detailed clinical interview finally reveals a potomanic attitude. This highlights the difficulties in detecting psychogenic polydipsia and related neurologic complications in the community and suggests the risk of overlooking this disorder as a cause of acute symptomatic seizures.
e2
The American Journal of Medicine, Vol 126, No 5, May 2013 Camilla Cicognani, MDa Chiara Vezzadini, MDb Roberto Zoni, MDa Roberto Michelucci, MDc
Ospedale Bellaria Bologna, Italy
http://dx.doi.org/10.1016/j.amjmed.2013.01.003
a
Medicine Unit Ospedale Bellaria Bologna, Italy b Endocrinology Unit Ospedale Maggiore Bologna, Italy c Neurology Unit IRCCS Neurological Sciences
References 1. Fraser CL, Arieff AI. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy. Am J Med. 1997;102:67-77. 2. Dundas B, Harris M, Narasimhan M. Psychogenic polydipsia review: etiology, differential, and treatment. Curr Psychiatry Rep. 2007;9:236-241. 3. Cronin RE. Psychogenic polydipsia with hyponatremia: report of eleven cases. Am J Kidney Dis. 1987;IX:410-416.
An Overlooked Cause of Acute Symptomatic Seizures: Psychogenic Polydipsia To the Editor: Metabolic encephalopathy and seizures are well-known serious manifestations of severe hyponatremia, because water equilibrates with cells leading to brain edema.1 Psychogenic polydipsia is a rare and often overlooked cause of hyponatremia, mostly described in the past in institutionalized patients with long-standing schizophrenia. However, psychogenic polydipsia has been observed recently in the community setting and outside an obvious psychiatric context; thus, little is actually known about the clinical relevance and neurologic complications of this disorder in this large and various population.2 We report the case of a dysthymic patient from the community who developed acute seizures related to severe hyponatremia. Acute water intoxication, induced by unrecognized potomania, was finally revealed as the provoking cause. A 51-year-old woman was referred to the emergency department in postictal coma, after 2 tonic-clonic seizures without clear focal symptoms. Severe hypo-osmolar hyponatremia (admission serum Na⫹ 112 mmol/L, normal value: 135-146 mmol/L; plasma osmolarity 246 mOsm/L, normal value: 275-295 mOsm/L) was found on laboratory examinations, along with low urine osmolarity (232 mOsm/L, normal value: 400-1500 mOsm/L) and sodium (23 mmol/24 h, normal value: 40-220 mmol/24 h). Serum total protein, triglycerides, creatinine, plasma adrenocorticotropin, serum cortisol, and thyroid hormones were in the normal range. Blood glucose values were satisfactory. She appeared euvolemic, and the whole clinical examination did not show abnormalities. Computed tomography scan and magnetic resonance imaging of the brain were normal, as well as routine and sleep electroencephalograms.
Funding: None. Conflict of Interest: None. Authorship: All authors had access to the data and played a role in writing this manuscript. Requests for reprints should be addressed to Camilla Cicognani, MD, Medicine Unit, Ospedale Bellaria, Azienda USL Bologna, via Altura n.5, 40139, Bologna, Italy. E-mail address: [email protected]
0002-9343/$ -see front matter © 2013 Elsevier Inc. All rights reserved.
Water restriction (⬍1.5 L/d) was prescribed, and normal plasma sodium was obtained 1 week after admission. No clinical symptoms occurred after seizures resolved. The history of the patient was unremarkable for neurologic pathology. She was affected by insulin-dependent type 1 diabetes without recent decompensations and stable dysthymia with anxious traits treated with low-dose citalopram. Her grandmother was epileptic, and her brother’s son has had epilepsy since the age of 3 years. However, details on the epilepsy type were unavailable. A subsequent clinical interview revealed a history of psychogenic polydipsia and chronic hyponatremia (123-132 mmol/L), with the recent superimposition of water intoxication due to anxiety decompensation. Water restriction was recommended on discharge, and the patient’s blood electrolytes were normal 6 months later. The patient’s overall clinical picture is suggestive for seizures provoked by severe hyponatremia as a consequence of self-induced water intoxication. The patient did not have a history of seizures and had normal electroencephalograms and negative brain magnetic resonance imaging. Therefore, apart from a possible generic “predisposition” to epilepsy as suggested by a positive family history, the patient did not show any other potential cause of seizures except for severe hyponatremia, which, in turn, was likely to be induced by compulsive water drinking. Other causes of hyponatremia were excluded by extensive diagnostic workup. Typically, psychogenic polydipsia has been described in chronic schizophrenic inpatients, most commonly presenting with seizures. However, recently it has been shown in middle-aged women with anxiety disorder and in chronic alcoholics, but reports on the neurologic complications of psychogenic polydipsia in these cases are rare. Cronin3 described a group of 11 patients with potomania-induced hyponatremia, mostly with a history of alcoholism, and in this group grand mal seizures were the most common complication. We emphasize that acute symptomatic seizures can be the only manifestation of potomania, even as an isolated behavioral disorder in the context of compensated dysthymia. Psychogenic polydipsia is not always obvious, and often only a detailed clinical interview finally reveals a potomanic attitude. This highlights the difficulties in detecting psychogenic polydipsia and related neurologic complications in the community and suggests the risk of overlooking this disorder as a cause of acute symptomatic seizures.
e2
The American Journal of Medicine, Vol 126, No 5, May 2013 Camilla Cicognani, MDa Chiara Vezzadini, MDb Roberto Zoni, MDa Roberto Michelucci, MDc
Ospedale Bellaria Bologna, Italy
http://dx.doi.org/10.1016/j.amjmed.2013.01.003
a
Medicine Unit Ospedale Bellaria Bologna, Italy b Endocrinology Unit Ospedale Maggiore Bologna, Italy c Neurology Unit IRCCS Neurological Sciences
References 1. Fraser CL, Arieff AI. Epidemiology, pathophysiology, and management of hyponatremic encephalopathy. Am J Med. 1997;102:67-77. 2. Dundas B, Harris M, Narasimhan M. Psychogenic polydipsia review: etiology, differential, and treatment. Curr Psychiatry Rep. 2007;9:236-241. 3. Cronin RE. Psychogenic polydipsia with hyponatremia: report of eleven cases. Am J Kidney Dis. 1987;IX:410-416.