Nootropic effect of high-dose lurasidone in patient with cycloid psychosis and previous HSV-2 encephalitis: a case report

Leonhard described cycloid psychoses as acute and remitting disorders and states that “when the diagnosis of cycloid psychosis is made, then it necessarily follows that a complete remission will occur and even if the illness recurs no defect will be left behind.” Acute encephalitis (herpes simplex encephalitis, HSE) clinical manifestations are fever, confusion, psychiatric symptoms, personality change, memory loss, aphasia, seizures and focal symptoms; HSV is the most common cause of HSE. Diagnostic protocols for HSE contemplate cerebrospinal fluid, electroencephalography and magnetic resonance imaging. A 46-years old Venezuelan woman, with a previous diagnosis of HSE few months before, presented persecutory and poisoning delusions, refusal to eat resulting in a weight loss, perplexity, suspiciousness, bizarre behavior, insomnia and alterations in cognitive functions. Her symptoms overlapped with those experienced during the HSE. A differential diagnosis with brain imaging presented a case of cycloid psychosis. Psychotic and cognitive symptoms disappeared with the prescription of lurasidone 148 mg/day. Lurasidone promotes neuronal plasticity, modulates epigenetic mechanisms that control gene transcription and increases expression of brain derived neurotrophic factor (BDNF) in cortical and limbic regions. Chronic treatment with lurasidone increases BDNF levels in both hippocampus (ventral and dorsal) and the prefrontal cortex. Lurasidone enhances N-methyl-D-aspartate receptor function through an antagonistic action on 5HT7 receptors. Lurasidone has determined a gradual resolution of the psychotic symptoms associated with cycloid psychosis and cognitive alterations derived from cortical damage from both the cortical atrophy, with multiple gliotic areas, and previous HSE.