うつ病の治療中にアカシジアとジスキネジアを呈した一例

症例は60歳代男性，15年前より当科にてうつ病，アルコール依存症として治療していた．２年前より町内会の仕事で多大なストレスを感じ，１年前より身体不調から仕事を退職した．その後，過剰な飲酒が始まり，精神科病院に入院しアルコール依存症の治療が行われ，その際にオランザピンが投与された．その後は断酒ができていたが，町内会での大きな役割が回ってくる不安感からイライラ感が強くなり，オランザピンの増量，クロルプロマジンへの変更などを行ったが精神症状は改善せず，薬剤変更１ヶ月後より終日じっとしていられないアカシジア様症状と，舌が勝手に動く口舌ジスキネジア様症状，首下がり症状が出現した．抗精神病薬を中止したが症状改善せず，次第に食事摂取困難となり体重が減少，状態悪化のため当科入院となった．入院後，薬剤調整による抗うつ治療を行ったが改善なく，希死念慮の増悪を認めたため修正型電気けいれん療法（modified-electroconvulsive therapy: m-ECT）の適応と考えられ，全13回のm-ECT を施行した．m-ECT 施行により精神症状，アカシジア，ジスキネジア，首下がりが徐々に改善し，最終的には病状が著明に改善した．本症例のジスキネジアは薬剤性としては発現が急であり，また首下がりの症状を伴っていたため，パーキンソン病の存在が疑われた．頭部MRI，ドパミントランスポーターシンチグラフィでは異常はなかったが，MIBG 心筋シンチグラフィではFDG 集積の低下を認めた．入院時軽度の左右差のあるパーキンソニズムがあり，筋電図にて頸部伸展筋ミオパチーと診断された．以上から身体症状の原因は，臨床症状発現前のパーキンソン病を背景とする抗精神病薬の副作用であると考えられた．アカシジア，ジスキネジアは薬剤性に起因するものが多数であるが，その他の疾病の有無を注意深く観察することが必要であると考えられた．Here, we present a case study of a man in his sixties, under treatment for depression and alcoholism at our department for the past 15 years. 2 years ago, he began to experience high stress levels that he attributed to his work at the neighborhood association. One year after that, he retired from his job because of poor health. After his retirement, he began to consume alcohol excessively. Subsequently, he was admitted to our hospital and was treated for alcoholism with the antipsychotic drug olanzapine. Although he achieved abstinence, his frustration gradually increased because of the stress associated with his prominent role in his neighborhood association several months ahead. Therefore, he was administered a higher dose of olanzapine, which was then changed to chlorpromazine. However, his psychological symptoms did not improve. After about one month, he began to display symptoms of akathisia, characterized by an inability to stay still throughout the day. Additionally, his tongue began to move involuntarily, which is a common symptoms of dyskinesia. He also presented with the dropped head syndrome. His symptoms did not improve upon termination of antipsychotic drugs. He was subsequently hospitalized because of gradually decreasing appetite and weight. Because the antidepressant treatment had no effect and his suicidal feelings had exacerbated, he was subjected to 13 rounds of modified-electroconvulsive therapy (m-ECT). His mental condition improved and the akathisia, dyskinesia, and dropped head symptom decreased gradually. Parkinson’s disease would not have likely caused dyskinesia without long term medication with dopaminergic drugs. Additionally, because dyskinesia generally appears several years after initiation of antipsychotics therapy, dyskinesia in our case could not have occurred due to antipsychotic drugs in acute course of the symptoms. Head MRI and dopamine transporter scintigraphy did not show any abnormalities. In contrast, metaiodobenzylguanidine (MIBG) scintigraphy showed a decrease heart/mediastinum ratio (H/M ratio). He had been recognized as showing symptoms of parkinsonism with a slight laterality when he was initially hospitalized, and his EMG showed neck extensor myopathy, which is a characteristic of Parkinson’s disease. Thus, his physical symptoms were likely a side effect of short-term use of antipsychotic drugs for preclinical Parkinson’s disease. The most common cause of akathisia and dyskinesia is antipsychotics drug use, however it is necessary to check carefully for other diseases as well

Temporal dispersion in vasculitic neuropathy: its microscopic ultrastructural findings

　症例は35歳男性．32歳のときに右腓腹神経・足底神経支配領域の異常感覚で発症し，その後，左腓腹神経・足底神経領域，両側尺骨神経領域に感覚障害が拡大した．神経伝導検査では，左脛骨神経複合筋活電位において，時間的分散の所見が認められた．腓腹神経生検では，神経上膜にフィブリノイド壊死を伴う壊死性血管炎を認めた．エポン包埋トルイジン青染色では、有髄神経線維の脱落が著明であり，髄鞘の薄い再生軸索が認められた．電子顕微鏡による観察では，脱髄は認められず，軸索の再生が認められたが，髄鞘再生に乏しい thin myelin が特徴的であった．神経伝導検査で，伝導ブロックや時間的分散といった脱髄を疑う所見を呈する血管炎性ニューロパチーについて24例の報告があるが，これまで電子顕微鏡による観察はされていない．血管炎性ニューロパチーによって惹起される時間的分散の出現機序について，微細構造所見を基に考察する．　A previously healthy 35-year-old man developed abnormal sensation in the right sural and medial plantar nerve territory 2 years ago. The sensory impairment gradually spread to the left sural and medial plantar nerve regions, then bilateral ulnar nerve regions. Nerve conduction study showed temporal dispersion in the left tibial nerve. Sural nerve biopsy revealed necrotizing vasculitis with fibrinoid necrosis in the epineurium. Toluidine blue staining of Epon-embedded tissue showed significant loss of myelinated nerve fibers without demyelination, even in the teased nerve fiber preparations. Electron microscopy showed immature regenerated nerve fibers with thin myelin sheaths. Even including 24 reported cases of vasculitic neuropathy with either conduction block, pseudo-conduction block, or temporal dispersion, this is the first case examined by electron microscopy. Herein, we discuss the ultrastructural background of“temporal dispersion”in vasculitic neuropathy

A case of variant angina treated with a pacemaker for cardiopulmonary arrest due to complete atrioventricular block and pulseless electrical activity

A 55-year-old woman with variant angina was hospitalized for cardiopulmonary arrest because of pulseless electrical activity (PEA). Despite intensive postresuscitation drug therapy, another episode of angina occurred, with complete atrioventricular block and PEA. There was no confirmed ventricular fibrillation or ventricular tachycardia. Coronary arteriography did not show significant stenosis, and acetylcholine-loading test was positive. The patient was diagnosed with coronary spastic angina, and a pacemaker was implanted to stabilize hemodynamics during attacks. The pacemaker settings required some ingenuity: a high output was selected to avert pacing failure, and a rate drop response setting was selected to ensure efficient pacing