Seitelberger F
Aktuelle Gerontol. 1982 Nov;12(6):200-5.
Pick's disease (circumscribed lobar atrophy of the brain) in its typical form, is a so-called presenile type of dementia, i.e. a cerebral disease which begins in the sixth decade of life, and leads to a progressive loss of intellectual capacity traits. Neuropathologically, Pick's disease is characterised by severe focal atrophy of the cerebral cortex, mainly of basal parts of the temporal and frontal lobe. In the long run, all the nerve cells of the affected areas and their processes are destroyed. This also involves the subcortical white matter (loss of nerve fibres and cicatrisation). Concomitant atrophies of other parts of the brain are frequent. The article reports on the results of the clinico-neuropathological examination of 30 cases of Pick's disease basing on the author's own observations. Special emphasis is placed on "neuronal atrophising dystrophy" of cortical systems as a characteristic change caused by Pick's disease; this phenomenon is interpreted as an endogenous disturbance of the neuronal structural metabolism. This process is, as a matter of principle, identical with the physiological "atrophising dystrophy" which represents part of cerebral aging. There are also pathogenetical parallels to orthological neuronal reactions to damaging of the axis cylinder processes. Pick's disease is characterised by the pathological extent and type of manifestation of "neuronal atrophising dystrophy". This pathological distortion of physiological processes is probably due to a specifically genetic and sometimes hereditary constellation. Finally, the article discusses the functional neuropathology or neuropsychology of Pick's disease. The importance of the basal temporofrontal cortex for the quality and preservation of human personality is emphasised; the changes of the high-class performances of the human brain, as caused by Pick's disease, are interpreted. Referring to the peculiarities of Pick's disease compared with normal cerebral aging, particular attention is drawn to the concept of "disease" and the definition of senile cerebral aging.
匹克氏病（大脑局限性叶萎缩）的典型形式是一种所谓的早老性痴呆，即一种始于生命第六个十年的脑部疾病，并导致智力能力特征的逐渐丧失。从神经病理学角度来看，匹克氏病的特征是大脑皮质严重局灶性萎缩，主要累及颞叶和额叶的基底部分。从长远来看，受影响区域的所有神经细胞及其突起都会被破坏。这也涉及皮质下白质（神经纤维丧失和瘢痕形成）。大脑其他部位的伴随性萎缩很常见。本文基于作者自己的观察报告了30例匹克氏病临床神经病理学检查的结果。特别强调皮质系统的“神经元萎缩性营养不良”是匹克氏病引起的特征性变化；这种现象被解释为神经元结构代谢的内源性紊乱。这个过程原则上与生理性的“萎缩性营养不良”相同，生理性“萎缩性营养不良”是大脑衰老的一部分。在轴突损伤时神经元的反应方面也存在发病机制上的相似之处。匹克氏病的特征在于“神经元萎缩性营养不良”的病理程度和表现类型。这种生理过程的病理扭曲可能是由于特定的遗传因素，有时是遗传性因素组合所致。最后，本文讨论了匹克氏病的功能性神经病理学或神经心理学。强调了颞叶额叶底部皮质对人类个性品质和维持的重要性；解释了匹克氏病导致的人类大脑高级功能的变化。与正常大脑衰老相比，针对匹克氏病的特殊性，特别关注了“疾病”的概念和老年大脑衰老的定义。
