Manic symptoms associated with pregabalin in a patient with conversion disorder

Abstract

A previously well, 69-year-old woman was admitted to the psychiatric ward because of repeated sensory abnormality and retrograde and anterograde amnesia. On admission, her Mini-Mental State Examination (MMSE) score was 24/30. Physical and neuropsychological examination were normal apart from amnesia and brief sensory abnormality. Ictal electroencephalography (EEG) showed continuous highamplitude rhythmic lateralized sharp waves over the right temporal area. In spite of intensive screening for toxic, infectious, paraneoplastic and metabolic etiologies, no abnormality was detected. Thyroid function tests were within normal limits, but serum anti-thyroglobulin antibody titer was 2.3 U/mL (normal <0.3), and serum thyroid peroxidase antibody titer was 3.8 U/mL (normal <0.3). Autoantibodies against the amino (NH2)-terminal of a-enolase, a specific diagnostic marker of HE, were also positive.3 Brain MRI showed no apparent abnormality on fluid-attenuated inversion recovery (FLAIR), T1/T2-weighted imaging and diffusion-weighted imaging. Although focal abnormal lesions were not seen on brain single-photon emission computed tomography and 18 F-fluorodeoxyglucose positron emission tomography, hyperperfusion was clearly detected in the right hippocampus on CASLI. A diagnosis of HE presenting with LE was made. I.v. methylprednisolone 1000 mg for 3 days followed by oral prednisolone 30 mg/day was given. Dramatic improvement of amnesia was observed (MMSE score; 30/30) and sensory abnormality completely disappeared without using anticonvulsants, with normalization of EEG findings. CASLI 5 days after initial i.v. methylprednisolone treatment was normal for the right hippocampus.In the present case, hyperperfusion of the right hippocampus on CASLI was resolved rapidly after corticosteroid treatment, which suggests that hyperperfusion might reflect an inflammatory component such as vasculitis, which is suggested as the pathogenesis of HE.3 Reportedly, epileptic foci show hyperperfusion on CASLI during the interictal period.2 Thereby, epileptic foci in the right hippocampus might be another cause of hyperperfusion because the present sensory abnormality occurred frequently before corticosteroid treatment. The present case underscores the importance of including CASLI in the evaluation of LE to assess possible inflammatory changes and to provide another measure of response to treatment, especially in the absence of apparent positive findings on other neuroimaging modalities. A Japanese man aged 46 years and suffering from deviation of his head to the left and involuntary shaking of his head, was referred and admitted to the department of psychiatry in our hospital. His brain magnetic resonance imaging and electroencephalography were normal. Neurologists examined him, but no organic or symptomatic abnormalities were detected. A careful review of his psychiatric history did not reveal any history of manic/hypomanic or major depressive episodes. He was diagnosed with conversion disorder based on DSM-IV-TR diagnostic criteria. He was giv...