Three cases of schizophrenia showing improvement after switching to blonanserin

Abstract

A 68-year-old man was admitted to the hospital because of auditory and visual hallucinations and persecutory delusions. Twenty years ago, he was diagnosed with chronic subdural hematoma after hitting his head, and he had been cured. Ten years earlier, he had visited a neurologist for gait instability and hearing impairment. Axial T2-weighted magnetic resonance imaging (MRI) scans revealed a rim of hypointensity around the cerebrum, brain stem and cerebellum. CSF analysis showed xanthochromia, an increased number of red blood cells and elevated iron and ferritin levels. The diagnosis of SSNS was made. His first experience of hallucination and delusion occurred at age 65 after moving to another city. After the move, he complained that neighbors were intentionally making loud noises, had bugged their home, changed their TV screen to red color and turned down his air conditioner. As the symptoms escalated in the following 3 years, he caused disturbances in the neighborhood and was taken to the hospital by his wife. On admission he showed auditory hallucinations and persecutory delusions. Physical examination showed tremor in upper limbs, dysarthria, complete hearing loss, and visual impairment. Laboratory tests and electroencephalography showed no significant abnormalities. MRI scans showed abnormal temporal cerebral and cerebellar atrophy in addition to the findings of 10 years ago. Single photon emission computed tomography showed mild low perfusion in the left frontal and the left temporal cerebral cortex and preserved perfusion in the other cerebral cortex, which indicated that the diagnosis of Alzheimer's disease was unlikely. Psychological tests showed mild cognitive impairment with the Mini Mental State Examination 20-23 points (indicating poor calculation and recall). The patient's Beck Depression Inventory II score was 14 and Hamilton Depression Scale score was 9, indicating an absence of severe depression. After admission, risperidone was started and increased to 5 mg/ day over 12 days. After 12 days he rarely hallucinated, and gradually stopped talking about delusions. On the 17th day he was discharged. At follow up, 23 days later, he showed neither hallucination nor delusion.In view of its pathology, SSNS can present with a variety of psychiatric symptoms, as occurred in this case. Iron is the cofactor for tyrosine hydroxylase, the late limiting enzyme in the synthesis of dopamine.3 The excessive iron may cause the overproduction of dopamine and lead to psychotic symptoms. A serotonin dopamine antagonist was effective in alleviating the psychotic symptoms. During differential diagnosis of psychotic patients, SSNS should be considered as a contributing factor, because the psychotic symptoms of SSNS can be sensitive to treatment with antipsychotic drugs, although the physical symptoms are progressive. 1 We report here three cases of schizophrenia improved by switching to blonanserin.Case 1 was a 30-year-old male college student with paranoid schizophrenia, strong delusions of being observed, and auditory ...

Simultaneous determination of blonanserin and its metabolite in human plasma and urine by liquid chromatography–tandem mass spectrometry: Application to a pharmacokinetic study

“…1 The results indicate that no significant matrix effect for blonanserin, blonanserin C, and the IS was implied in the method.…”

“…1(A)), first developed by Dainippon Sumitomo Pharma Company in Japan in 2008, is a novel atypical antipsychotic that is validated for the treatment of both positive and negative symptoms of schizophrenia, without extra-pyramidal symptoms [1][2][3][4][5][6]. It has a high affinity with dopamine D 2 and 5-HT 2A , while being much less potent in adrenergic-␣ 1 , histamine H 1 , and muscarinic M 1 antagonist activities [4].…”

Case report of bradycardia induced by blonanserin in schizophrenia

“…4 Furthermore, the case report published by Kurotaki mentioned that a 21-year-old male had improved tachycardia after switching to blonanserin, which corroborates the effect of blonanserin on HR. 5 We speculate that the bradycardia caused by blonanserin may be due to the influence of K + or Ca 2+ channels on the cell membrane, 6,7 but further studies are needed to elucidate the specific mechanisms. Considering that blonanserin has a low affinity for adrenergic receptors, the risk of bradycardia should be lower than other antipsychotics.…”