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Clinically mild encephalopathy with a reversible splenial lesion and nonconvulsive status epilepticus in a schizophrenic patient with neuroleptic malignant syndrome
Author(s) -
Mogi Taichi,
Toda Hiroyuki,
Tatsuzawa Yasutaka,
Fukutomi Tsubasa,
Soga Shigeyoshi,
Shinmoto Hiroshi,
Yoshino Aihide
Publication year - 2017
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/pcn.12492
Subject(s) - neuroleptic malignant syndrome , medicine , status epilepticus , anesthesia , encephalopathy , splenium , stupor , catatonia , lesion , haloperidol , white matter , magnetic resonance imaging , pathology , epilepsy , schizophrenia (object oriented programming) , psychiatry , radiology , dopamine
M ILD ENCEPHALOPATHY WITH a reversible splenial lesion (MERS) is characterized by the magnetic resonance imaging (MRI) finding of a reversible lesion with homogeneously reduced diffusion in the splenium of the corpus callosum (SCC). Here, we report the case of a schizophrenic patient showing complications of MERS and nonconvulsive status epilepticus (NCSE) in the course of neuroleptic malignant syndrome (NMS). This study was performed in accordance with the provisions of the Declaration of Helsinki 2008 and was approved by the institutional review board of the National Defense Medical College. We obtained informed written consent and a signed release from the patient authorizing publication. His anonymity has been preserved. A 44-year-old man with schizophrenia was admitted to another psychiatric hospital for stuporous catatonia. After injection of 10 mg of haloperidol, he presented hyperthermia, tachycardia, muscular rigidity, diaphoresis, leukocytosis, hypernatremia (148 mEq/L), and an increase in serum creatine kinase, suggesting NMS. Administration of haloperidol was stopped and he was transferred to our hospital. The patient showed stupor, with no response to instructions and a motionless stare. Electroencephalogram (EEG) revealed continuous bilateral sharp and wave complex with frontal dominance, suggesting that NCSE was also present. Cerebrospinal fluid showed normal cell counts and increased protein, glucose, and sodium levels, but a normal immunoglobulin G level, and a myelin basic protein level <40 pg/mL. Diffusionweighted imaging of the brain revealed a hyperintense ovoid lesion in the SCC. On hospital day 2, he presented with generalized tonic–clonic seizures. As his respiratory condition rapidly deteriorated, ventilator management was started with continuous infusion of midazolam. On day 5, midazolam was tapered off, and ventilator management was subsequently ended. Level of consciousness recovered and muscle rigidity disappeared. On day 22, EEG showed no epileptiform discharges. By day 29, the hyperintense ovoid lesion in the SCC had disappeared from MRI. Takanashi noted that the most common neurological symptom of MERS is delirious behavior, followed by disturbance of consciousness and seizures, all of which completely recover within a month. The MRI findings and clinical course indicated that our patient suffered from MERS. Reversible splenial lesions develop from various etiologies, including hyperand hyponatremia. Interestingly, NMS may develop MERS as well as NCSE. To date, however, no cases of concomitant MERS and NCSE in a schizophrenic patient with NMS have been reported. Although the precise cause of the reversible splenial lesion with reduced diffusion could not be identified, our case suggests the importance of considering the possibility of MERS in the course of an NMS in catatonic schizophrenia.