Editorial
The history of medicine tells how, within the contexts of existing beliefs and techniques, various societies shaped their knowledge concerning the prevention of disease and the preservation of human health. Not all these systems survive but the origins of modern scientific (one might say, Western) medicine lie in the practices and cultures of these many civilizations. For a long time, many such societies remained isolated from the benefits (and also the dangers) of Western science; and the local traditions of folk medicine persisted. Tropical medicine developed through an awareness of the special medical conditions prevailing in certain geographical locations, and the work of medical scientists, trained in Western medicine, in those places. Garcia d'Orta (1501–1568) wrote the first book on tropical medicine in India (Coloquios dos simles, e drogas he cousas mediçinais da India, 1563) but not until 1764 did this discipline formally come into existence through activities of the Indian Medical Service of the British Army. (Sir) Ronald Ross (1857–1932) studied malaria, as a young officer in the Indian Medical Service, from 1889, discovering the oocyst and working out the life cycle of the mosquito through his observations in Calcutta. In 1880, Griffith Evans (1835–1935), an army veterinary surgeon in India, described a form of trypanosomiasis (in Africa, ‘sleeping sickness’). Charles Donovan (1863–1951) identified Leishmania donovani in Madras; and in the same year, James Homer Wright (1870–1928) named the organism responsible for Delhi boil as Leishmania tropica. Neurology, as a subspecialty of tropical medicine, has an even more recent history but the pattern is similar: medical travellers seeing at first hand the spectrum of neurological disease; pioneering citizens training in neurology in the West; and these founders of the discipline creating schools of neurological excellence in their own countries. In ‘Neurology in the developing world’, Charles Poser and Joan Crawford Poser review ‘Neurological practice: an Indian perspective’, edited and much of the text written by Dr Noshir Wadia but co-authored with 32 colleagues (page 1624). Dr and Mrs Poser trace the emergence of tropical neurology following World War II, identifying the leaders from Asia, India, Africa, and Central and South America who founded neurology in their countries, and those from the West who were influential and supportive of their efforts. They consider the emergence of writings on tropical neurology, concluding that Dr Wadia's book is now the standard text on the subject. Charles and Joan Poser are well qualified to comment: for more than 50 years, they have travelled the world—as expert in clinical neurology and companion sensitive to the local culture and language, respectively—motivated by scholarship and an interest in neurological illness as it affects all societies, and securing many lasting friendships in the process.The present issue includes five papers on neurogenetics, including identification of the gene responsible for congenital neuronal ceroid-lipofuscinosis (page 1438; and see Scientific Commentary, page 1351). Naoki Atsuta and colleagues from Nagoya University, Nagoya, Japan, present a retrospective analysis of the natural history over 20 years in 223 cases of spinal and bulbar muscular atrophy resulting from CAG repeat expansion of the androgen receptor: the pattern is for symptoms to progress from hand tremor (in the 30s) to immobility (by the early 60s); life expectancy is reduced with death from respiratory complications; and the number of expansions determines age at onset of the individual features but not their prognosis. Stephan Klebe and a group of investigators from the Salpêtrière and institutions in Paris, Evry, Gerardmer and Strasbourg, France, and from Rabat, Morocco report a new (the 30th) locus for autosomal recessive spastic paraplegia, with peripheral neuropathy and mild cerebellar atrophy, mapping to 2q37.3 (SPG30) that does not explain 10 other newly studied families, thus providing yet more evidence for genetic heterogeneity. Three papers discuss muscle disease, amongst which Maria Elena Farrugia and a team from Oxford (including our associate editor, Angela Vincent, and former editor, John Newsom-Davis) describe atrophy and fatty infiltration of facial, tongue and bulbar muscles in cases of myasthenia gravis having antibodies directed at muscle specific kinase (MuSK), but not the acetylcholine receptor (page 1481): the independent contribution of MuSK antibodies, or other primary components of the disease process, from the effect of prolonged treatment with corticosteroids remains to be established. It could be argued that not much progress has been made in elucidating the nature of the environmental factor in multiple sclerosis since Pierre Marie declared, in 1884: ‘the fact, thank God, has been well established, viz. that the cause of insular sclerosis (multiple sclerosis) is intimately connected with infectious disease’. On page 1493, Jan Lünemann and investigators from the National Institutes of Health, Bethesda, and Rockefeller University, New York, USA, and the Charité University, Berlin, Germany, add to the evidence implicating Epstein Barr virus (EBV), showing an increased range and repertoire of EBVA1-specific T cells in people with multiple sclerosis compared to HLA-DR matched controls: the authors suggest that the build-up of these cells sustains autoimmunity by molecular mimicry with autoantigen, or through bystander mechanisms.
Two papers deal with aspects of regeneration in the central nervous system. Zubair Ahmed and colleagues from the University of Birmingham, UK, explore the pathway involving the NoGo, p75 neurotrophin, and epidermal growth factor receptors, eventually leading to actin depolymerization and growth cone collapse (page 1517): they show that the ability of Schwann cell grafts to promote axon growth relates to their release of factors that cleave Nogo-A and its receptor, thus preventing epidermal growth factor receptor activation and many aspects of the down-stream signalling cascade that normally collapses the growth cone. Romana Vavrek and a group from Edmonton and Vancouver, Canada, report that—compared to local delivery of neurotrophin-3 (NT-3)—brain derived nerve growth factor (BDNF) applied to the cell body (i.e. motor cortex) of corticospinal neurones that are experimentally damaged in the dorsal spine increases collateral sprouting and connectivity through propriospinal interneurons at the site of the lesion, but not in normal animals, indicating cell body based plasticity of the injured central nervous system (page 1534). Emmanuel Mignot and investigators from Stanford and Madison, USA, document the prevalence of narcolepsy (
2 sleep onset rapid eye movement periods during the multiple sleep latency test) in the Wisconsin Sleep Cohort Study (page 1609): 6% of all men and 1% of women have narcolepsy, as defined; risk factors include HLA type, shift work patterns and sleep restriction, and the use of anti-depressants but not age, body mass or markers of sleep apnoea. Amongst four papers relating to various aspects of stroke medicine, Asaf Gilboa and colleagues from Toronto, Canada, and Haifa, Israel, aim to reconcile the nature of confabulation in survivors from ruptured anterior communicating artery aneurysms (page 1399): performance on continuous recognition and free recall of semantic narratives suggests the model of general retrieval failure with temporal confusion due to early, rapid and pre-conscious errors, rather than one based on true memories that have become displaced in time.
On page 1385, Keith Josephs and colleagues from the Mayo Clinic, Rochester, USA, correlate the presence of speech apraxia and aphasia with pathological anatomy and the biochemical basis for structural abnormalities: they allow five categories of speech disorder and show a strict correlation between tau pathology and the presence of apraxia, which usually reflects involvement of the premotor and supplemental motor cortices, whereas non-fluent aphasia results from damage to the anterior peri-Sylvian region. Dorothee Saur and investigators from Freiburg, Hamburg and Aachen, Germany, report on the dynamics of language reorganization after stroke (page 1371; see Scientific Commentary, page 1351, and the cover). In From the Archives, we review an earlier classification of disorders resulting in apraxia and aphasia, together with abnormalities of reading and writing, based on disconnectionist theory, cerebral localization and the analysis of individual cases that also predicted recovery of language due to plasticity within the cerebral circuits for language (On aphasia. By L. Lichtheim, Brain 1885: 7; 433–84).
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