Journal of the History of the Neurosciences最新文献

After the end of the Spanish Civil War (1936-1939), an estimated 1,000 patients presented with lathyrism due to their excessive and prolonged consumption of grasspea (Lathyrus sativus L.) against the backdrop of poverty, drought, and famine. Based on 68 scientific communications between 1941 and 1962 by qualified medical professionals, the disease emerged in different geographical locations involving selective populations: (1) farmers from extensive areas of central Spain, traditionally producers and consumers of grasspea; (2) immigrants in the industrial belt of Catalonia and in the Basque Country, areas with little or no production of grasspea, which was imported from producing areas; (3) workers in Galicia, an area where the legume is neither produced nor consumed, who were seasonally displaced to high-production areas of grasspea in Castille; and (4) inmates of overcrowded postwar Spanish prisons. Original reports included failed attempts by Carlos Jiménez Díaz (1898-1967) to induce experimental lathyrism, the neuropathology of lathyrism in early stages of the disease in two patients, as reported by Carlos Oliveras de la Riva (1914-2007), and the special susceptibility of children to develop a severe form of lathyrism after relatively brief periods of consumption of the neurotoxic seed of L. sativus. In the Spanish Basque Country, L. cicera L. (aizkol) was cultivated exclusively as animal fodder. Patients who were forced to feed on this plant developed unusual manifestations of lathyrism, such as axial myoclonus and severe neuropsychiatric disorders, unknown in other regions of the country and previously unreported. The postwar epidemic of lathyrism in Spain represents the most extensively studied outbreak of this self-limiting but crippling upper motor neuron disease.

In 1949, William Stewart Alexander (1919-2013), a young pathologist from New Zealand working in London, reported the neuropathological findings in a 15-month-old boy who had developed normally until the age of seven months, but thereafter had progressive enlargement of his head and severe developmental delay. The most striking neuropathological abnormality was the presence of numerous Rosenthal fibers in the brain. The distribution of these fibers suggested to Alexander that the primary pathological change involved astrocytes. In the next 15 years, five similar patients were reported, and in 1964 Friede recognized these cases reflected a single disease process and coined the eponym "Alexander's disease" to describe the disorder. In the 1960s, electron microscopy confirmed that Rosenthal fibers were localized to astrocytes. In 2001, it was shown that Alexander disease is caused by mutations in the gene encoding glial fibrillary acidic protein, the major intermediate filament protein in astrocytes. Although the clinical, imaging, and pathological manifestations of Alexander disease are now well known, few people are familiar with Alexander's career. Although he did not make a further contribution to the literature on Alexander disease, his observations and accurate interpretation of the neuropathology have justified the continued use of the eponym "Alexander disease."

Efforts to treat epileptic seizures likely date back to primitive, manmade skull openings or trephinations at the site of previous scalp or skull injuries. The purpose may have been the release of "evil spirits," removal of "cerebral excitement," and "restoral of bodily and intellectual functions." With progressive discoveries in brain function over the past 100 to 300 years, the cerebral cortical locations enabling voluntary movements, sensation, and speech have been well delineated. The locations of these functions have become surgical targets for the amelioration of disease processes. Disease entities in particular cerebral-cortical areas may predispose to the onset of focal and or generalized seizures, which secondarily interfere with normal cortical functioning. Modern neuroimaging and electroencephalography usually delineate the location of seizures and often the type of structural pathology. If noneloquent brain regions are involved, open surgical biopsy or removal of only abnormal tissue may be undertaken successfully. A number of the early neurosurgical pioneers in the development of epilepsy surgery are credited and discussed in this article.

In contemporary neurosurgery little attention is currently paid to the pericranium. The purpose of this article is to present how past surgeons have viewed this membrane and how they have reacted to its appearances. In ancient times, the pericranium was considered formed by the dura through the sutures and it retained a relationship with the dura via vessels in the sutures. It was considered advisable to strip it totally from any area to be examined for fissure fractures and also for any area to be trepanned, as pericranial injury led to fever and inflammation. In the eighteenth century, a new idea arose that posttraumatic spontaneous separation of the pericranium from the bone was a reliable indicator of the development of intracranial suppuration. This idea was subsequently refuted. The development of the osteoplastic bone flap imposed on the surgeon the need to ensure postoperative craniotomy closure included accurate apposition of the margins of the pericranium. With modern free bone flaps, this is no longer required. For over two millenia, the pericranium was considered to be an important membrane requiring the close attention of the surgeon. It is no longer required to receive more than minimal attention.

On October 20, 1924, at the Waldorf-Astoria Hotel in New York City, two medical graduates of the University of Sydney delivered the John B. Murphy Oration to the American College of Surgeons on the topic of sympathetic ramisection for the treatment of spastic paralysis. The surgery was regarded as a triumph. The triumph, however, was short-lived, when one of the speakers, John Irvine Hunter, a promising anatomist, died prematurely. Norman Royle, an orthopedic surgeon, continued the research program and continued to perform these operations. Within a few short years, however, the theory of the dual nerve supply of skeletal muscle, which underpinned the procedure, and the results of surgery for spastic paralysis came under question. Nevertheless, Royle's sympathectomy found another indication and became the treatment of choice for peripheral vascular disease for several decades thereafter. Although Hunter and Royle's original work was discredited, their research turned their sorry saga into a scientific awakening of the sympathetic nervous system.

The cell doctrine-the theory of ventricular localization of the mental faculties-includes Galen's idea of a locking or valve mechanism between the middle and the rear ventricle. The anatomical substrate was the vermiform epiphysis, known today as the vermis cerebelli. This entity played a significant role in brain physiology even though its appearance, texture, and location changed over time. This article tells the story of the "worm's" transformation from Galen to Vesalius and beyond. Until the time of Albertus Magnus (c. 1200-1280 ce), the worm corresponded to the vermis cerebelli. From the beginning of the fourteenth century, under the influence of Mondino's Anothomia, the worm referred to the choroid plexus in the anterior ventricles; its Galenic heritage was abandoned. Contemporaneous illustrations confirm this anterograde movement. The contributions of post-Galenic natural philosophers and pre-Vesalian anatomists to this development are discussed. Today, the worm can serve as an example for different viewpoints and often deadlocked doctrines (religious, philosophic, scientific). In tracing beliefs about the worm from the Greeks to the Arabs and back to the Latin West, this article follows the history of neuroanatomy in the Middle Ages and the Renaissance.