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The first chapter of Part I begins by taking stock of European theories of fever, and of the importance of the work of the Hippocratic revival, particularly as reflected in the work of Sydenham, Boerhaave, and Hoffman. The discussion then turns to medical work in the tropical colonies during the sixteenth and seventeenth centuries, placing British medicine in the context of earlier work by the Portuguese and Dutch. The chapter examines both the East and the West Indies. It shows the growing importance of climate and morbid anatomy in theories of disease and how ideas about disease had a bearing on concepts of race. The strongly natural‐historical orientation of colonial practice is emphasized, along with its connections to the politics of medical reform in Britain.

Chapter 2 shows how British practitioners, many from Dissenting backgrounds or trained at the University of Edinburgh, sought to apply the insights of Sydenham and Boerhaave to their work on disease in the tropical colonies. Again, it stresses the centrality of place and climate to their understanding of disease and the vital part played by morbid anatomy. The chapter traces a number of important intellectual networks, spanning both the East and West Indies, and Britain and the American colonies. Some of these were Dissenting networks which linked surgeons in the Army, Navy, and East India Company to figures such as John Fothergill and Benjamin Rush in Britain and America; others were more formal, such as the Royal Society of London and ties to universities such as Edinburgh.

This chapter focuses on William Farr. In the latter half of the 19th century, both the concept of environment and the numerical approach to the understanding of related public health problems were firmly entrenched. Yet for much of the century, most British epidemiologists and many elsewhere were guided largely by Sydenham's theory of the interaction of miasmata with the ‘epidemic constitution’ of seasons. Accordingly, they had followed a general line of research into environmental effects. Among them was William Farr. Farr can be properly assigned a major role as a founder of epidemiology in its modern analytic form. Perhaps his greatest accomplishment was to institute and write the Annual Reports of the Registrar General, the first appearing in 1839. These described and analyzed the health status of the country in terms of the database he had himself devised to enumerate births, marriages, and deaths.

This chapter focuses on the historical development of the notion of transmissible infection. In the late 18th century, developments in the field of infection began to tail off. The great and influential physician Thomas Sydenham gave a new lease of life to miasma with a theory that gave currency to a refinement: the ‘epidemic constitution’ he posited arose from the emanations of miasma. The theory invoked vernal and autumnal entities of disease attributed to changes in season and atmosphere in the spring and fall respectively. The theory was plausible to the degree that epidemic infections do in reality vary by season. In consequence, the concept of contagion lost ground both in theory and practice. Only in the mid-1800s, did intimations of contagion sustain a strong challenge to miasma theory. Within the following decade, other seminal works indirectly fortified the likelihood that infection was transmissible from person to person whether by direct contact, inhalation, or ingestion. The contributions of Peter Ludwig Panum, Alexander Gordon, Ignác Semmelweis, Joseph Lister, John Snow, and William Budd are discussed.

This chapter argues that, given our lack of epistemic access to the inner natures of substances, Locke believed that the correct method of natural philosophy is the construction of Baconian natural histories. The evidence adduced for this claim includes Locke's involvement with Robert Boyle's natural histories; his interest in travel literature; his lists of queries; his emphasis on natural histories of disease; and his various divisions of the sciences.

This chapter explores the origin and infectivity of the measles virus in the course of human history. How measles first came to infect humans is not clear. Definitive proof is hard to come by since measles virus infection was once nearly impossible to distinguish from smallpox virus infection. Consequently, both had been lumped together as a single entity. As early as the tenth century, the Arab physician Abu Becr first attempted to distinguish between the two. However, it was not until the seventeenth century that English physician Thomas Sydenham actually documented the clinical entity of measles infection. Once it was understood that infection with measles virus confers lifelong protection from the disease and that humans are the natural host, interest turned toward developing a preventive vaccine. The chapter then considers the purported evidence that measles virus vaccines may be harmful. Such misinformation is often propagated for personal reasons yet greatly affects public health and individual lives.

This chapter continue the focus on the law of correlation’s imbrication with mid-Victorian modernity, exploring its close relation to the central symbol of this new age of entrepreneurship, industry and consumerism: the Crystal Palace. It considers both the Great Exhibition and then the commercial reconstruction of the Crystal Palace at Sydenham, examining how, with the expensive life-sized models of prehistoric creatures built at the latter, the demands of mid-nineteenth-century commerce gave a new impetus to the endorsement of the law of correlation, ensuring that it remained central to the new forms of print culture, and modes of visual education and entertainment that were emerging in the 1850s.

This introductory chapter explores and establishes the Sydenham Crystal Palace in relation to existing scholarship on the Great Exhibition of 1851. The Sydenham Palace combined education, entertainment and commerce, and spans both nineteenth and twentieth centuries. We resituate it as an important location within the London art world and establish the broader connections it had with rival ventures such as the South Kensington Museum and the numerous international exhibitions in the period. We set out the new possibilities for the analysis of both nineteenth- and twentieth-century visual and material cultures opened up by this unique venue, problematising the periodisation of art works and attitudes into discretely ‘Victorian’ and ‘Edwardian’ categories.

The Exhibition was an immediate commercial success, but it also had a legacy that went way beyond the event itself. The final chapter of this book shows both the short and long-term manifestations of the Exhibition’s impact. It includes material taken from the debates about the appropriate use of the Exhibition’s surplus funds and the future of the Crystal Palace along with an account of the closing ceremony. It provides reports about the rebuilding of the Palace at Sydenham and its destruction by fire in 1936. The long-term material benefits of the Exhibition are represented through the work of the Royal Commission and its scholarships and its lasting impact on the architecture of South Kensington in London. The chapter evaluates the role that the Exhibition has played, and continues to play, in debates about nationalism, imperialism, and the significance of British culture.

We can uncover the causes and reasons for Locke’s acceptance of corpuscularianism by considering his life and projects before he writes the first draft of the Essay, and looking at the illustrations and arguments in the Essay itself. At Oxford, Locke is exposed to corpuscularianism but also engages in physiological inquiries in the chemical traditions of Jan van Helmont and Thomas Willis. After moving to London, collaborating with Thomas Sydenham, and practicing medicine, Locke begins to doubt our ability to explain empirical phenomena, but he still thinks of corpuscularian explanations as being justified by way of analogy. In particular, he thinks there are interesting analogies between deductive inferences and inferences concerning seventeenth-century machines. In contrast, Aristotelian inferences concerning living things fall short of this mathematical ideal since they are only reliable for the most part, but they fail in cases of malformation.

■ Receives inputs from the frontal eye field (FEF), supplementary eye field (SEF), dorsolateral prefrontal cortex (DLPC), internal medullary lamina of the thalamus, and substantia nigra pars compacta (SNpc, the dopaminergic portion) ■ Projects to substantia nigra pars reticulata (SNpr) and the globus pallidus ■ Receives inhibitory inputs from the caudate nucleus ■ Sends inhibitory signals to intermediate layers of the superior colliculus Parkinson’s disease is a progressive neurodegenerative disorder that affects about 1% of adults over 60 years of age. 1. Loss of pigmented dopaminergic neurons in the SNpc 2. Presence of Lewy bodies (not specific for Parkinson’s disease) 3. Decreased dopamine reaching the striatum causes increased inhibitory output from the globus pallidus internal segment and SNpr, thereby inhibiting movement 1. Standard therapy: levadopa and carbidopa (a peripheral decarboxylase inhibitor to reduce motor fluctuations and dyskinesia) e.g., such as Sinemet or Sinemet CR 2. Monoamine oxidase-β inhibitor (e.g., Selegiline); may have neuroprotective effect 3. Dopamine agonist (e.g., bromocriptine, a D2 agonist, and apomorphine, a D1 and D2 agonist) 4. Anticholinergics (e.g., Benzhexol) 5. Amantadine (seldom used) 6. Surgery ■ Thalamotomy or thalamic deep brain stimulation of the ventral lateral nucleus to reduce medically refractory tremor. The mechanism of action is unknown; these procedures may destroy autonomous neural activity (synchronous bursts) that has the same frequency as the limb tremor. ■ Pallidotomy or pallidal stimulation to reduce contralateral dyskinesia (e.g., bradykinesia, rigidity, and tremor).