Journal of the History of the Neurosciences最新文献

The amygdaloid complex is a crucial component of the basal forebrain that participates in the modulation of many homeostatic functions, emotional behaviors, and learning. These features require a widespread pattern of connections with several brain structures. In the past, the amygdaloid complex was divided into corticomedial and basolateral groups. The existence of a neuronal continuum linking the central amygdaloid nucleus to the lateral bed nucleus of stria terminalis through the subpallidal area was first revealed by José de Olmos (1932-2008) with the aid of his cupric-silver technique. This observation gave birth to the concept of the extended amygdala, a conceptual framework that is useful for understanding the anatomofunctional organization of the amygdaloid complex, with relevance for basic neuroscience and clinical interventions. Traditional tract-tracing staining methods were complicated and tedious to reproduce. Axonal terminal endings were lost among a myriad of normal fibers. The need to visualize these terminals drove de Olmos to develop cupric-silver methods that revealed disintegrating synaptic terminals, without staining normal fibers. In this article, we describe the historical events leading to the development of the cupric-silver technique that evolved into the amino-cupric-silver technique, which developed hand-in-hand over the years.

Most historical articles have named Johann Jacob Wepfer as the first author to describe a case of chronic subdural hematoma (CSDH). However, the question arises whether these cases truly describe CSDH. Two other names that appear in literature as the first authors to describe a case of CSDH are Thomas Willis and Giovanni Battista Morgagni. In our attempt to find the first description of a CSDH, we studied the original cases described by Willis, Wepfer, and Morgagni. The cases described by Willis and Wepfer cannot be interpreted as cases of CSDH. Willis's university scholar is more likely to have experienced venous infarction with an underlying septic thrombosis than a CSDH. Wepfer's cases seem to represent an intraparenchymal hemorrhage from the rupture of a branch or branches of the internal carotid artery, a subarachnoid hemorrhage complicated with hydrocephalus, and a hydrocephalus in tuberculous meningitis. Morgagni's case described in Letter III, Article 20 in the Sedibus in 1761 seems to be the first accurate historical description of a CSDH, and we believe it should be cited as such. With these early cases of alleged CSDH, we emphasize the importance of misquotation and blind copying of references, which are important citation errors.

The origins of Edward Flatau's "The Law of Eccentric Location of Long Pathways in Spinal Cord" are discussed, considering newly examined archival documents from Central State Archive of Moscow and Museum of the I. M. Sechenov University (former medical faculty of Imperial Moscow University [IMU]). These documents, together with German and Polish records, illustrate the international character of Flatau's education and shed light on the bigger question of interactions between Moscow and Berlin fin de siècle neurologists. Flatau's peregrinations between these two cities are documented, together with difficulties encountered due to his nationality and the changing political environment.

The collective efforts of Australasian neuroscientists over the past 50 years to forge a binational presence are reviewed in this article. The events in the 1970s leading to the formation of an informal Australian Neurosciences Society are discussed in the context of the international emergence of neuroscience as an interdisciplinary science. Thereafter, the establishment in 1980 of the Australian Neuroscience Society, subsequently renamed as the Australasian Neuroscience Society (ANS), is described. The achievements of ANS-including its active role in developing national, regional, and global cooperation to promote neuroscience-are chronicled over successive decades, followed by a discussion of the future challenges facing the society and its associated neuroscience institutions.

Medical interest in the knee-jerk reflex began in about 1875 with simultaneous and independent publications by Wilhelm Heinrich Erb (1840-1921) and Carl Friedrich Otto Westphal (1833-1890) contending that the knee jerk was absent (and the ankle clonus was present) in all clear cases of locomotor ataxia (tabes dorsalis). Physicians in the medical communities of Europe, Great Britain, and North America responded with case and large group studies that tested this contention. These studies revealed the usefulness of the knee jerk and other myotatic reflexes, but also unexpected characteristics. The knee jerk, apparently so simple, proved to be a complex phenomenon depending the strength of the strike on the patella, induced muscle tension, and inhibition from the brain. Was it a reflex with afferent and efferent nerves and an intervening process in the spinal cord, or was it a local phenomenon confined to the muscle itself? Experimental studies directed at the reflex issue investigated latencies from patella strike to leg extension or muscle contraction and compared them with latencies from direct muscle strikes and theoretical calculations based on reflex components. Such studies were unable to resolve the reflex issue during the nineteenth century. The physicians were shown to be limited, like all scientific explorers of the unknown, by their knowledge, methodology, and technology.

Among William Gowers's many contributions to neurology, the concept of abiotrophy ("an essential failure of vitality") has been relatively overlooked. In this article, we review the echoes of Gowers's concept in neurology, ophthalmology, and aging research. We also argue that abiotrophy is broader than both heredodegeneration and neurodegeneration. Unlike the common view that it simply means premature aging, abiotrophy currently can be understood as a progressive degenerative process of a mature specialized tissue, which is nonsynchronous with normal aging and may affect organs or systems early in life, resulting from the age-dependent effects of genetic mutations or variants, even if environmental factors may also causally contribute to the process. Although the term has largely fallen out of use, there are likely to be everlasting echoes of Gowers's concept, through which he is to be considered a source of the modern thinking about the etiology and nosology of neurological diseases.