Department of Psychiatry, Tokyo Metropolitan Matsuzawa Hospital, Tokyo, Japan.
Department of Psychiatry, Nagoya University, Nagoya, Japan.
Neuropathology. 2021 Apr;41(2):127-132. doi: 10.1111/neup.12711. Epub 2021 Jan 20.
Anorexia nervosa (AN) is a serious eating disorder characterized by self-starvation and extreme weight loss. It has the highest mortality rate among all psychiatric disorders. Recent research indicates that malnutrition in AN patients induces various kinds of functional brain damage, but the pathophysiology of AN remains unclear. We report here the neuropathological findings of a 31-year-old Japanese woman. At age 24, she had a fear of gaining weight and reduced her dietary intake; she had extremely low body weight associated with overeating then self-induced vomiting. She was clinically diagnosed as having AN and was admitted to a psychiatric hospital with severe depression and suicidal thoughts. At age 31, she died despite intensive physical care and psychotherapy. Neuropathological examination revealed increased capillary blood vessels and slight fibrillary gliosis in the mammillary bodies, with similarities to Wernicke encephalopathy. The brainstem exhibited the characteristic features of central pontine myelinolysis, characterized by a sharply demarcated region of myelin pallor and relative sparing of axons. Senile changes, including neurofibrillary tangles/senile plaques, were not significant. Severe fibrillary gliosis was prominent around periventricular regions, including the caudate nucleus and nucleus accumbens, which are associated with cognition, emotion, and emotional behaviors via the dopaminergic pathways. These findings indicate that prolonged malnutrition in AN patients may induce brain damage, leading to dysfunction of the reward-related dopaminergic pathways. Furthermore, they represent the first pathological evidence that dysfunction of the cortico-limbic-striatal circuitry is involved in the pathophysiology of psychiatric symptoms in AN patients.
神经性厌食症（AN）是一种以自我饥饿和极度体重减轻为特征的严重进食障碍。它在所有精神障碍中的死亡率最高。最近的研究表明，AN 患者的营养不良会导致各种功能性脑损伤，但 AN 的病理生理学仍然不清楚。我们在这里报告了一位 31 岁日本女性的神经病理学发现。她在 24 岁时害怕体重增加并减少了饮食摄入量；她的体重极低，伴有暴食后自我诱导呕吐。她被临床诊断为患有 AN，并因严重抑郁和自杀念头被送进精神病院。在 31 岁时，尽管进行了密集的身体护理和心理治疗，她还是去世了。神经病理学检查显示在乳头体中毛细血管增多和轻微的纤维状神经胶质增生，与威尼克脑病相似。脑干表现出中央桥脑髓鞘溶解症的特征性特征，其特征是髓磷脂苍白区域明显分界，轴突相对保留。神经原纤维缠结/老年斑等老年性改变不明显。严重的纤维状神经胶质增生在脑室周围区域明显，包括尾状核和伏隔核，这些区域通过多巴胺能途径与认知、情绪和情感行为有关。这些发现表明，AN 患者长期营养不良可能导致脑损伤，导致与奖励相关的多巴胺能途径功能障碍。此外，它们代表了第一个病理学证据，表明皮质边缘纹状体电路功能障碍与 AN 患者精神症状的病理生理学有关。
