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BackgroundThe association between fire-setting behavior and psychiatric or medical disorders remains poorly understood. Although a link between fire-setting behavior and various organic brain disorders has been established, associations between fire setting and focal brain lesions have not yet been reported. Here, we describe the case of a 24-year-old first time arsonist who suffered Todd’s paralysis prior to the onset of a bizarre and random fire-setting behavior.Case presentationA case of a 24-year-old man with a sudden onset of a bizarre and random fire-setting behavior is reported. The man, who had been arrested on felony arson charges, complained of difficulties concentrating and of recent memory disturbances with leg weakness. A video-EEG recording demonstrated a close relationship between the focal motor impairment and a clear-cut epileptic ictal discharge involving the bilateral motor cortical areas. The SPECT result was statistically analyzed by comparing with standard SPECT images obtained from our institute (easy Z-score imaging system; eZIS). eZIS revealed hypoperfusion in cingulate cortex, basal ganglia and hyperperfusion in frontal cortex,. A neuropsychological test battery revealed lower than normal scores for executive function, attention, and memory, consistent with frontal lobe dysfunction.ConclusionThe fire-setting behavior and Todd’s paralysis, together with an unremarkable performance on tests measuring executive function fifteen months prior, suggested a causal relationship between this organic brain lesion and the fire-setting behavior. The case describes a rare and as yet unreported association between random, impulse-driven fire-setting behavior and damage to the brain and suggests a disconnection of frontal lobe structures as a possible pathogenic mechanism.

Purpose: Clozapine has been reported to be effective for refractory schizophrenic patients. However, there have been few reports investigating whether clozapine responders are likely to suffer from more or fewer extrapyramidal symptoms. The aim of the present study is to investigate the association between clinical effects of clozapine and extrapyramidal symptoms in clozapine-treated patients. Methods: Ten patients were divided into Improvement Group with CGI-I scores ranging from 1 to 3 and Non-improvement Group with CGI-I scores ranging from 4 to 7. The Drug-Induced Extrapyramidal Symptoms Scale (DIEPSS) scores were compared between these two groups just before starting clozapine treatment and after 12 weeks of clozapine treatment. Results: Although there was no significant difference in any DIEPSS scores between Improvement Group and Non-improvement Group just before clozapine treatment, Improvement Group had significantly fewer extrapyramidal symptoms in DIEPSS scores than Non-improvement Group after 12 weeks of clozapine treatment. Moreover, there was a significant interaction between overall severity of extrapyramidal symptoms assessed by DIEPSS and improvement measured by CGI-I across the 12 weeks of clozapine treatment. Discussion: These findings suggest that clozapine responders are less likely to suffer from extrapyramidal symptoms.