Psychotic disorder in a patient with central and extrapontine myelinolysis

Lim, Linda; Krystal, Andrew D.

doi:10.1111/j.1440-1819.2007.01648.x

Cited by 14 publications

(15 citation statements)

References 16 publications

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“…With increasing MRI availability, asymptomatic or mildly symptomatic cases have been described [12,18]. Neuropsychiatric manifestations are beginning to be recognized, although there are no large series [8,9,20].…”

Section: Introductionmentioning

confidence: 99%

Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis

2010

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The objective of this study is to review the presentation, outcome and aetiology of central pontine and extrapontine myelinolysis (CPEPM) in a tertiary hospital center. The study method is a case series and included identification of patients from University of Montreal Health Centre archives database (1995-2007). All diagnoses were confirmed by neuroimaging or brain autopsy. Twelve individuals (25-66 years old) presented heterogeneous manifestations. Co-morbidities included diabetes insipidus (n = 2), haemodialysis (n = 1), cirrhosis (n = 3), gastroenteritis (n = 2) and potomania (n = 1). Aetiologies included rapid correction of severe hyponatremia (n = 6)/acute hypernatremia (n = 1); immediate (n = 2) or remote (n = 1 with recurrent cirrhosis) orthotopic liver transplantation (OLT) with tacrolimus-induced immunosuppression (n = 3); and chronic alcoholism (n = 4, two with hyponatremia). Four individuals died acutely. Two were lost to follow-up. Six had good motor or cerebellar recovery. Neuropsychological evaluations (n = 5/6) revealed a subcortical/frontal dysfunction. Cognitive impairment represented the major remaining lasting sequel (n = 4). Three salient clinical syndromes were observed: (1) predominant cerebellar presentation in individuals with alcoholism (n = 4); (2) significant alteration of consciousness at presentation (n = 4), all resulting in death (OLT, n = 3); (3) seizures persisting after natremia correction (n = 2). Clinical presentation of CPEPM is heterogeneous and can even include seizures. Cognitive impairment should be screened as it is a significant factor limiting return to normal life.

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Section: Introductionmentioning

confidence: 99%

Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis

2010

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“…In EPM, demyelinating lesions occur in brain structures other than the pons, including the basal ganglia (e.g., caudate nucleus), cerebellum, internal capsule, and thalamus. Recent literature has suggested that extrapontine lesions are associated with reversible movement disorders, such as parkinsonism, dystonia, catatonia, mutism, myoclonic jerks, and/or choreoathetosis [2, 9, 11–13]. Both CPM and EPM make up the spectrum of osmotic demyelination syndrome, which affects oligodendrocytes with relative preservation of neuronal axons [9].…”

Section: Discussionmentioning

confidence: 99%

“…The timeline for the onset of psychiatric manifestations in CMP/EPM is a conflict between many authors. Some state that psychiatric disturbances occur within two weeks after the onset of motor symptoms, while others report that motor symptoms can present in the two weeks after initial psychiatric disturbance is observed [3, 4, 11, 25]. To date, the exact pathophysiology of the psychiatric and behavioral manifestations in CPM remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…Rapid correction of hyponatremia has been proven as one of the most common and important etiologic factors [9, 10]. Although central pontine and extrapontine myelinolysis can present with behavioral and neuropsychiatric manifestations, there is limited literature available describing behavioral manifestations (personality changes, labile affect, disinhibition, poor judgment, paranoid delusions, emotional lability, delirium, hallucinations, and catatonia) in patients with CPM without any focal neurological deficits [3–6, 11–13]. Diffusion-weighted MRI (DWI) characteristically shows restricted diffusion in the central pons, and Positron Emission Tomography (PET) scan has been demonstrated to detect central pons hypermetabolism in patients with CPM [14–18].…”

Section: Introductionmentioning

confidence: 99%

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Acute Psychosis as Main Manifestation of Central Pontine Myelinolysis

Gopal

Parasram

Patel

et al. 2017

Case Reports in Neurological Medicine

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Central pontine myelinolysis (CPM) is an acute demyelinating neurological disorder affecting primarily the central pons and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy, and encephalopathy of various degrees; however, coma, “locked-in” syndrome, or death can occur in most severe cases. Rarely, CPM presents with neuropsychiatric manifestations, such as personality changes, acute psychosis, paranoia, hallucinations, or catatonia, typically associated with additional injury to the brain, described as extrapontine myelinolysis (EPM). We present a patient with primarily neuropsychiatric manifestations of CPM, in the absence of focal neurologic deficits or radiographic extrapontine involvement. A 51-year-old female without significant medical history presented with dizziness, frequent falls, diarrhea, generalized weakness, and weight loss. Physical examination showed no focal neurological deficits. Laboratory data showed severe hyponatremia, which was corrected rather rapidly. Subsequently, the patient developed symptoms of an acute psychotic illness. Initial brain magnetic resonance imaging (MRI) was unremarkable, although a repeat MRI two weeks later revealed changes compatible with CPM. This case demonstrates that acute psychosis might represent the main manifestation of CPM, especially in early stages of the disease, which should be taken into consideration when assessing patients with acute abnormalities of sodium metabolism.

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“…The clinical presentation varies among patients, with some showing no obvious neurological symptoms and only abnormal MRI findings, and others showing a combination of neuropsychiatric (such as emotional lability, disinhibition, and other bizarre behaviors) and neurologic (such as confusion, impaired cognition, dysarthria, dysphasia, gait instability, weakness or paralysis, and generalized seizures) symptoms [1, 8, 9]. The extent of radiologic signal abnormality or the severity of hyponatremia may not be associated with clinical outcomes.…”

Section: Discussionmentioning

confidence: 99%

Diffuse large B-cell lymphoma presenting with central pontine myelinolysis: a case report

et al. 2015

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IntroductionThe most common cause of central pontine myelinolysis is an overly rapid correction of hyponatremia, although it can also occur in patients with any condition leading to nutritional or electrolyte stress. We report a case of diffuse large B-cell lymphoma with central pontine myelinolysis developing at the onset of disease. To the best of our knowledge, hematological malignancies presenting with central pontine myelinolysis have been rarely reported, especially in previously untreated patients, as in our case report.Case presentationA 78-year-old Japanese woman presented to a neighborhood clinic with persistent high fever, edema, and general weakness. Despite the absence of specific neurological findings, brain magnetic resonance imaging showed an abnormal lesion in the central pons area of her brain (hyperintense on T2-weighted and hypointense on T1-weighted sequences), compatible with central pontine myelinolysis. She was admitted to our emergency department in a state of shock one month later. The results of her blood tests showed greatly elevated C-reactive protein and lactate dehydrogenase levels. She had severe hypoalbuminemia and mild hyponatremia, and showed signs of disseminated intravascular coagulation. Mild bilateral pleural effusion, prominent subcutaneous edema, and splenomegaly were detected on her systemic computed tomography scan. Her body fluid cultures did not show signs of infection and her spinal aspiration did not show pleocytosis or abnormal cells. A diagnosis of diffuse large B-cell lymphoma was made based on the results of her bone marrow examination. As she was critically ill before the diagnosis was made, she was treated with methylprednisolone pulse therapy, followed by systemic chemotherapy (rituximab with modified THP-COP regimen, including cyclophosphamide, pirarubicin, vindesine, and prednisolone), which resulted in complete remission and recovery without any neurological defects, and resolution of her abnormal findings on magnetic resonance imaging.ConclusionsCentral pontine myelinolysis is a serious condition that may result in neuropathological sequelae and mortality, and clinicians should be aware of its potential presence in patients with malignancies.

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Psychotic disorder in a patient with central and extrapontine myelinolysis

Cited by 14 publications

References 16 publications

Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis

Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis

Acute Psychosis as Main Manifestation of Central Pontine Myelinolysis

Diffuse large B-cell lymphoma presenting with central pontine myelinolysis: a case report

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