Oketsu-night sweat was first mentioned in the “Yi lin gai cuo” by Wang Qing ren and the “Xue zheng lun” by? Tang Rong chuan, but there are few explanations of its disease condition. Thus we made pathological studies in Oriental medicine based on three cases (women), where Oketsu-sho was alleviated with Keppu-chikuo-to modification, and Teitou-gan and Tokaku-joki-to (Tao he cheng qi tang) modification. Common disease conditions were Netsu-sho or heat syndrome (summer incidences, redness, flushing during night sweat), and lower Oketsu symptoms (lower abdominal distention, distention and cramping of the lower abdomen, and increased urinary frequency). The theory of these disease conditions is as follows: During sleep, Wei-energy enters the blood. Because of this, Wei-energy of the body surface becomes asthenia making it easier to break out in sweat. The Wei-energy in the blood is depressed by Oketsu, and heat of Oketsu becomes stronger during the night. This fever heats and evaporates bodily fluids, and as a result fluids are pushed outward and cause night sweat. Therefore heat syndrome appears to be a pre-condition of Oketsu-night sweat. If the lower aspect of the body is taken to mean the liver, one would hypothesize that Oketsu-night sweat is more likely to emerge because blood accumulates in the lower area because it returns to the liver at night. Thus, it is thought to be necessary to consider Oketsu as one of the causes of night sweat.

Recently developed melatonin receptor agonists are expected to be effective for delayed sleep-wake phase disorder (DSWPD). To date, however, no study has described the effect of melatonin receptor agonists on DSWPD. We report the case of a 15-year-old girl with DSWPD who was successfully treated with ramelteon 4 mg at 7 PM. DSWPD symptoms were resolved; her sleep-wake and biological rhythms were normalized.

Maximal oxygen uptake (Vo₂max) and lactate threshold were measured during an incremental bicycle ergometer test in 40 healthy middle-aged and older runners between 43 and 79 years of age. Although the 10-km run time slowed with increasing age, there were no significant differences in recent training habits or relative amount of body fat between four age groups. However, our cross-sectional data revealed an annual decrement of -0.74 ml/kg/ min/yr, which was significantly greater than that reported in previous studies. Vo₂max values for the runners were greater than those for sedentary men of similar ages by about 50% in each age group. Significant correlations were found between the age at the onset of running training and Vo₂max (r=-0.600, p<0.05) . Vo₂@LT declined significantly but less rapidly with age (r=0.686, p<0.05) than Vo₂max. Both the mean maximal heart rate (HRmax) and HR@LT also declined with age. No significant differences in HRmax were observed between the runners and sedentary men of the respective age groups. Significant correlations were also found between the estimated HRmax and directly measured HRmax (r=0.600) . Neither systolic blood pressure nor diastolic blood pressure during submaximal-maximal exercise were found to increase with age. We suggest that maintenance of a higher lactate threshold in older runners when expressed as a percentage of Vo₂max is attributable to a greater age-dependent decline in Vo₂max with a smaller change in Vo₂@LT.

The management of clozapine (CLZ)-induced adverse events affects patient prognoses. Akathisia is a relatively rare adverse event related to CLZ administration and thus the management of this syndrome is not well established. Here, we report a case of treatment-resistant schizophrenia wherein CLZ-induced akathisia was successfully managed with gabapentin enacarbil (GE). The patient was a 39-year-old woman who had been treated with atypical antipsychotics other than CLZ for three years with poor tolerability. Initiation of CLZ (400 mg/day) attenuated her psychotic symptoms, but was followed by moderate akathisia. Neither benzodiazepines nor biperiden improved the akathisia; however, akathisia was finally diminished with co-administration of GE. GE facilitated a dosage increase in CLZ (450 mg/day) for the improved management of pyschotic symptoms, and thus indirectly contributed to treatment of the patient’s schizophrenia. We suggest that GE is a useful candidate for the management of CLZ-induced akathisia. The improved management of treatment-induced akathisia and other adverse events can extend the potential application of CLZ for treatment-resistant schizophrenia.
Adult ; Antipsychotic Agents ; Benzodiazepines ; Biperiden ; Clozapine ; Female ; Humans ; Prognosis ; Psychomotor Agitation* ; Restless Legs Syndrome ; Schizophrenia

Tardive dyskinesia and dystonia are intractable extrapyramidal symptoms caused by the blockade of dopamine receptors by antipsychotic drugs. In addition to the reduction or discontinuation of the causative drug, valbenazine for tardive dyskinesia and botulinum toxin for tardive dystonia have been reported to be effective. However, their efficacy has not been fully demonstrated. In this study, we report the case of a female patient with bipolar disorder, valbenazine-resistant tardive dystonia, and tardive dyskinesia who achieved improvement in extrapyramidal symptoms with electroconvulsive therapy. Additionally, we conducted a narrative literature review on the safety and efficacy of electroconvulsive therapy for tardive dyskinesia and dystonia.

Tardive dyskinesia and dystonia are intractable extrapyramidal symptoms caused by the blockade of dopamine receptors by antipsychotic drugs. In addition to the reduction or discontinuation of the causative drug, valbenazine for tardive dyskinesia and botulinum toxin for tardive dystonia have been reported to be effective. However, their efficacy has not been fully demonstrated. In this study, we report the case of a female patient with bipolar disorder, valbenazine-resistant tardive dystonia, and tardive dyskinesia who achieved improvement in extrapyramidal symptoms with electroconvulsive therapy. Additionally, we conducted a narrative literature review on the safety and efficacy of electroconvulsive therapy for tardive dyskinesia and dystonia.

Tardive dyskinesia and dystonia are intractable extrapyramidal symptoms caused by the blockade of dopamine receptors by antipsychotic drugs. In addition to the reduction or discontinuation of the causative drug, valbenazine for tardive dyskinesia and botulinum toxin for tardive dystonia have been reported to be effective. However, their efficacy has not been fully demonstrated. In this study, we report the case of a female patient with bipolar disorder, valbenazine-resistant tardive dystonia, and tardive dyskinesia who achieved improvement in extrapyramidal symptoms with electroconvulsive therapy. Additionally, we conducted a narrative literature review on the safety and efficacy of electroconvulsive therapy for tardive dyskinesia and dystonia.

Tardive dyskinesia and dystonia are intractable extrapyramidal symptoms caused by the blockade of dopamine receptors by antipsychotic drugs. In addition to the reduction or discontinuation of the causative drug, valbenazine for tardive dyskinesia and botulinum toxin for tardive dystonia have been reported to be effective. However, their efficacy has not been fully demonstrated. In this study, we report the case of a female patient with bipolar disorder, valbenazine-resistant tardive dystonia, and tardive dyskinesia who achieved improvement in extrapyramidal symptoms with electroconvulsive therapy. Additionally, we conducted a narrative literature review on the safety and efficacy of electroconvulsive therapy for tardive dyskinesia and dystonia.