Neuroleptic malignant syndrome (NMS) is the most serious side effect produced by the administration of antipsychotic drugs. NMS shares many clinical similarities with malignant hyperthermia (MH), but the etiology of NMS and the relation between NMS and MH remain unknown. Anesthetic regimens for patients with NMS are not well established. We gave repeated anesthesia to a patient with a history of NMS undergoing electroconvulsive therapy for the treatment of depression. Propofol and vecuronium were used in twelve consecutive ECT sessions without complications. In this case report, we describe the safe and satisfactory repeated use of propofol in a patient with a history of NMS, and outline NMS and its questionable relation to MH.
高速らせん CT と 3 次元画像：新たな画像診断法の創成 林 宏光 隈崎達夫 日本医科大学放射線医学教室 図 1 左総腸骨動脈狭窄症 A：造影剤を静注し，約 50 秒間の高速らせん CT 検査から再構成した 3 次元 CT 血管造 影像．左総腸骨動脈に偏心性の 90％ 狭窄を認める (矢印) ．この狭窄部の血管壁には著明な石灰化を認める (矢 頭) ．B：動脈造影により左総腸骨動脈の狭窄が確認できる(矢印) ． 図 2 右大腿部動静脈奇形 A：背側上方より再構成した 3 次元 CT 血管造影像．右大腿部に無数の静脈の早期環流 を認める．矢印：治療後のプラチナコイル．B：閾値処理にて筋肉を抽出した 3 次元 CT．表在血管の奇形 (矢 印)が描出できるのみならず，二次的な筋肉の萎縮も評価し得る． 図 3 右頸部血管腫 2 カ月の男児．約 15 秒間の高速らせん CT 検査を施行し，閾値処理にて皮膚面から深部までの 腫瘍と周囲構造との関係を表示した 3
The effects of catecholamines (CAs) other than their transmitter action were investigated using clonal neuronal cells, ML-DmBG2-c2, derived from Drosophila in the larval central nervous system (CNS). All catecholamines tested, adrenaline (AD), dopamine (DA), noradrenaline (NA) and isoproterenol (ISO), prevented any increase in the number of cells during 2- to 7-day culture. alpha-, beta-adrenergic and dopaminergic antagonists did not block the effects of CAs on the number of cells. Adrenochrome, a product of the oxidative degradation of AD, also prevented any increase in the number of cells, as AD did. The effect of AD was partially blocked by an antioxidant, dithiothreitol (DTT). These results suggest that the inhibition of the increase in cell numbers by CA might be mediated by CAs themselves and/or oxidative products in the CA metabolic process. It is concluded that CAs inhibit cell proliferation but do not induce cell death in the Drosophila clonal cells.
We investigated the effectiveness of bright light therapy on cognitive disturbances and its effect on circadian (sleep-wake) rhythm in Alzheimer-type dementia (ATD). Twenty-seven patients with ATD were treated with bright light therapy in the morning for 4 consecutive weeks. We evaluated the cognitive functions and circadian rhythms of the patients as a whale, and as members of two groups (one: questionable and mild dementia: the other: moderate and severe dementia; both groups classified by the severity criteria of Clinical Dementia Rating). We assessed circadian rhythms by actigraphy and cognitive states by Mini-Mental-State Examination (MMSE) and Alzheimer's Disease Assessment Scale (ADAS) before and after light therapy. Bright light therapy improved circadian rhythm. Although bright light therapy had no Significant effect on the Severity of dementia, it improved the MMSE scores, cognitive functions of ADAS scores (memory > language) and non-cognitive functions of ADAS scores (behavior = mood), especially in the questionable and mild dementia group. These results suggest that bright light therapy improves cognitive functions with the modification of circadian rhythm, especially in the early stages of ATD.
