Association of auditory Charles Bonnet syndrome with increased blood flow in the nondominant Brodmann area 22.

Aim: Auditory Charles Bonnet syndrome (aCBS) is characterized by musical hallucinations (MHs) that accompany acquired hearing impairments. This hallucination is the acoustic perception of music, sounds, or songs in the absence of an outside stimulus, and it may be associated with hyperactivity of the superior temporal lobes. Some studies have reported the possibility of improving MH with antiepileptics. To elucidate in detail the brain regions responsible for aCBS, we analyzed the regions that changed functionally after treatment. Methods: Before and after treatment with carbamazepine (four cases), clonazepam (one case), and a hearing aid (one case), cerebral perfusion single-photon emission computed tomography (SPECT) and the Auditory Hallucination Rating Scale (AHRS) were applied to six patients with hearing-loss-associated MHs. Results: Cerebral blood flow analysis using SPECT revealed hyperperfusion in Brodmann area (BA) 22-the posterior region of the superior temporal gyrus-in the nondominant hemisphere in all six patients in the pretreatment phase. After treatment, the hyperperfusion region improved in all patients. The area percentages with hyperperfusion in the nondominant BA22 were strongly positively correlated with the AHRS score. Conclusion: The results suggest that aCBS, which was treatable with antiepileptics or hearing aids, was involved in hyperexcitement in BA22, and that MH strength was correlated with degree of excitement.

Predicting postpartum depression by evaluating temperament during pregnancy.

AIM: The purpose of this study was to investigate premorbid temperaments to predict postpartum depression in pregnant women with no previous psychiatric history and to clarify the correlation between postpartum depression and the factors included in the Postpartum Depression Predictors Inventory-Revised (PDPI-R) and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Auto questionnaire (TEMPS-A)/Munich Personality Test (MPT). METHODS: A total of 170 eligible pregnant women filled out both questionnaires, the first between the 8th and 23rd week of gestation, and the latter between the 34th and 38th week of gestation. Participants filled out The Edinburgh Postnatal Depression Scale (EPDS) one month postpartum to measure for postpartum depression symptoms. All participants delivered full-term healthy babies. RESULTS: Seventeen (10%) women met the criteria for postpartum depression with a score of 9 or higher on the EDPS. The factors significantly related to developing postpartum depression were schizoid and melancholic temperament on the TEMPS-A/MPT and marital dissatisfaction on the PDPI-R. The total score on the PDPI-R was significantly correlated with depressive, cyclothymic, irritable, and anxious temperaments on the TEMPS-A/MPT. A lack of social support on the PDPI-R was significantly correlated with depressive, irritable, and anxious temperaments on the TEMPS-A/MPT. CONCLUSION: The findings suggest that postpartum depression may be related to schizoid and melancholic temperaments and marital dissatisfaction. The hyperthymic temperament was identified as a significant predictor in preventing PPD. Careful observation during puerperium is recommended if a pregnant woman is likely to have these temperaments or psychological conditions. Temperament evaluation should be done during pregnancy as a form of postpartum depression screening.

Sleep Disorders in Four Patients With Myotonic Dystrophy Type 1.

Sleep disturbances such as excessive daytime sleepiness, central and obstructive sleep apneas, restless legs syndrome, and rapid eye movement sleep dysregulation are prominent in patients with myotonic dystrophy type 1 (DM1). Mild intellectual deficits presented in many patients with DM1. In addition, psychosocial issues caused by neuropsychiatric symptoms are a clinical problem. We herein present the cases of four DM1 patients with sleep disturbances and neuropsychiatric symptoms in the preceding stage of clinically significant muscle symptoms. One of the cases exhibited a sleep disorder and neuropsychiatric symptoms before electromyography showed myotonic discharge, suggesting that careful follow-up is also important. Patients 1 and 2 were first referred to our department due to daytime sleepiness. Patients 3 and 4 were objectively suffering from daytime sleepiness of which they were not subjectively aware of. Patients 1, 3, and 4 obtained high apnea-hypopnea index (AHI) scores, which reflected central and/or obstructive apnea, whereas patient 2 had an AHI score of zero. The daytime cerebrospinal fluid (CSF) orexin levels of all patients ranged from the normal lower limit to low, although they were not as low as those observed in narcolepsy with typical cataplexy. Neuropsychological tests of patients 1 and 2 showed frontal lobe dysfunction. Patients 3 and 4 were diagnosed with mild intellectual disability and autism spectrum disorder, respectively. All patients exhibited indifference toward their own symptoms, which may have resulted from the cognitive decline caused by DM1. Based on family history and/or neurological findings such as myotonia, we suspected DM1 as the cause of their sleep disturbances. Molecular analysis using the triplet repeat-primed polymerase chain reaction (TP PCR) method and Southern blotting, which provided a genetic confirmation of the diagnosis of DM1, were performed. These clinical features of sleep disturbances were unrelated to the length of CTG repeats and are caused by unknown molecular mechanisms. Clinicians should take into account that multisystem involvement in DM1 is hugely variable, and thus, a disabling sleep disorder could overshadow muscle impairment in DM1 patients.

Differences in two mice strains on kainic acid-induced amygdalar seizures.

Seizure susceptibility and neurodegeneration induced by microinjection of kainic acid (KA) into the left amygdala (LA) in C57BL/6 and FVB/N mouse strains were compared. Mice were administered 0.5 microg of KA into the LA. Electroencephalograms (EEGs) and behavior were monitored for 48 h after KA microinjection. Neuronal cell damages in the CA1 and CA3 regions of hippocampus were assessed at 2 and 48 h after KA microinjection. We demonstrated that the FVB/N mice showed longer duration of seizure activity than the C57BL/6 mice in EEGs and behavioral observation. The C57BL/6 mice were resistant to neurodegeneration while the FVB/N mice were vulnerable as measured 2 and 48 h after KA microinjection. These differences might be associated with genetic background.