Editorial
In 1965, we published a paper by Norman Geschwind (1926–1984) on ‘Disconnection syndromes in animals and man’ (Brain 1965; 88: 237–294 and 585–644). Merely to describe this as a landmark paper is not to do the scholarship justice. ‘Disconnection syndromes in animals and man’ illuminated otherwise incomprehensible neurological syndromes, but the exposition also allowed the reader to consider rival concepts on how the cerebrum is organized and to ponder the strictly disconnectionist formulation that Geschwind proposed to explain bizarre clinical phenomenology. It seemed so simple to understand that occlusion of the left posterior cerebral artery causes a right homonymous hemianopia and, at the same time, lesions the posterior part (splenium) of the corpus callosum thus isolating an intact right visual cortex from the left angular gyrus needed to decode visual engrams, but leaving unaffected the ability to generate graphemes already learned, thus resulting in alexia without agraphia. Geschwind presented the primary 19th century literature from which, in the context of his own subspecialty of speech and language, emerged the concept that syndromes are localized without this necessarily indicating that those same brain regions subserve the normal functions so disrupted. It was the chance reading of Jules Dejerine's paper on alexia without agraphia and his own recognition of a similar case in 1961 that led Geschwind to discuss his ideas on callosal disconnections with Oliver Zangwill, then an associate editor of this journal, who persuaded him to expand these ideas into the article that appeared in 1965. Now, Marco Catani and Dominic ffytche (page 2224; and see cover) celebrate the 40th anniversary of this paper by reviewing Norman Geschwind's ‘Manifesto for behavioural neurology’, debating the rises and falls of disconnection syndromes in the light of tractography and functional imaging techniques not available to those who used clinical and neuroanatomical analyses, and experimental lesions in animals, to formulate ideas on order and disorder of higher cortical functions in man.Geshwind's paper fired the imagination. That is also the role of literature. The need for stories, and the reassurance they offer by elevating romantic characters and exorcising demons through caricature needs no explanation. Literary critics explain that reading is goal-orientated, allowing us to understand other minds. They argue that literary competence requires some appreciation of social cognition. In turn, cognitive scientists see a connection between the real mind and that portrayed in fiction. In ‘The story on neurology’ (page 2470), Alastair Wilkins and Simon Shorvon review three books: Epileptic by David B, A curious incident of the dog in the night-time by Mark Haddon, and Saturday by Ian McEwan. Each orientates its story around neurological illness. Dr Wilkins and Professor Shorvon rehearse examples and argue the purpose of describing neurological disease in works of fiction. They discuss how such representations can inform lay readers about the realities of illness, and explore what—if anything—the neurologist may gain from a fictional account of disorders encountered on a daily basis. The comic-strip approach to portraying everyday life for the chronic Epileptic clearly does succeed in revealing nuances of that disorder, informative even to a distinguished epileptologist. But, for the rest, our reviewers are left concluding that we all need stories and ‘a novel is just a novel’.
For 127 years, Brain has charged its readers. At first, each quarterly issue cost 3 shillings and 6 pence: now, the annual personal subscription is £215 ($366) and the institutional rate £410 ($697) for 12 printed issues. Electronic access is available for £389 ($661), and both print and electronic versions can be obtained by institutions for £432 ($734). Recent declarations of intent from major funding agencies on the requirement to make the research they support publicly available challenge this conventional business model. Is it reasonable to re-charge these organisations and their beneficiaries for the privilege of reading the products of those investments? Placing everything in the public domain suits funding agencies, individual authors and host institutions, each of whom obtains maximum exposure of the work. But if a journal makes its copy freely available, who—other than archivists that distrust electronic storage and the odd paper-bound Luddite—will pay to subscribe? At one extreme, the solution is to switch from ‘reader pays’ to ‘author pays’. But, even if the cost per paper could be agreed, have those who advocate this revolution thought through the issue of how to budget in advance for the number and location of articles that may, or may not, eventually emerge from a given grant; or ensured that the ability to pay, and access to funding from commercial sources, do not enable the publication of certain articles and suppress the appearance of others? More fundamentally, it should matter to the champions of immediate access that the editorial and peer review processes remain reliable if the currency of work appearing in highly rated journals is not to be devalued (see Brain 2004; 127: 1689–90 for a discussion of the merits and demerits of publishing in Brain and Cosmopolitan). At a rough guess, our journal requires 
50 h work distributed amongst the editorial team per week: we contact 20 referees every day and the c.1400 manuscripts processed annually are eventually commented upon by 3000 experts. Some of our sister journals are busier. The quality of reviews we obtain is outstanding. The attention to detail is meticulous, many reports offering presentational suggestions and correcting errors in addition to providing expert opinion and editorial advice. Most referees are happy to repeat the process when revisions are submitted, and many help us on multiple occasions throughout the year. This work depends on unsung professionalism of the anonymous reviewer. Although we do not publish lists, the debt owed to these individuals is enormous, and hereby acknowledged. Since all of this work is entirely honorary, its motivation must somehow be maintained so that papers in Brain can be trusted as accurate, novel and worthwhile accounts of their subject. Therefore, the value of peer review and the editorial process also need to be reckoned before the present model of academic publication is changed, however laudable the aims of public access. Whilst these complex matters are still being considered, Brain has (along with some other journals in our field) agreed, as a first step, to make all content freely available online 12 months after online publication and to allow authors also to deposit post-prints (traditionally, manuscripts that have been peer reviewed but not copy edited or typeset) of their articles 12 months after online publication (generally 2 months before the print version appears) into subject repositories, such as PubMedCentral and institutional systems. Authors may also deposit their URL providing a link to the final electronic online publication and its supplementary appendices. We are considering the step, already taken by other journals published at Oxford University Press, of allowing authors the option of paying to have their article immediately available.
Amongst a series of papers in the present issue on Parkinson's disease, Tao Wu and Mark Hallett (page 2250) exploit the difficulty these patients have in performing complex automatic learned movements to show that performance requires increased regional brain activation to compensate for the basal ganglia dysfunction. In asymptomatic carriers of the Parkin gene, Carsten Buhmann and colleagues from Italy and Germany (page 2281) reveal differences in the brain activation patterns and reaction times for motor tasks requiring internal motivation, again indicating reorganization of striatocortical motor loops as compensation for the impending loss of nigrostriatal function. Four other papers describe novel aspects of neurogenetic disorders. Amongst these, Bryan Neville from London, and collaborators from Malta, add Sepiaterin reductase deficiency to the list of levodopa responsive disorders of childhood that may mimic cerebral palsy (page 2291). Kumaraswamy Sivakumar and a group from the United States, Cyprus, France and Australia describe clinical and laboratory features of 60 patients from 5 families with mutations of the glycyl-tRNA synthetase (GARS) gene at 7p15 manifesting initially as focal upper limb wasting and weakness but progressing to mimic a generalized spinal muscular atrophy, with laboratory evidence for sensory involvement (page 2304). The identification of Rapsyn as the molecular target in some cases of acetylcholine receptor negative myasthenia gravis was an important discovery: now Mario Losen working with colleagues from Maastrict and Utrecht, and with Angela Vincent in Oxford (page 2327), show that increased expression of Rapsyn rescues animals from the loss of acetylcholine receptors in experimental autoimmune myasthenia gravis, and that the levels of Rapsyn may determine severity. Spinal cord injury continues to offer tantalizing prospects for treatment using a variety of neurobiological strategies. In the present issue, Grégoire Courtine and a team from institutions in California (page 2338) analyse in detail the motor consequences, and patterns of recovery over time, for the ipsi- and contra-lateral limb in monkeys undergoing unilateral lesions of the lateral corticospinal tract, as the basis for informing rehabilitation and repair strategies in man: and Bryan Hains, Carl Saab and Stephen Waxman from Yale and Brown University in the United States, show that plasticity manifesting as altered sodium channel expression extends to the thalamus after injury of sensory pathways in the spinal cord (page 2359).
Marieke Wermer and colleagues from Utrecht (page 2421) report on the dividend from screening patients who have successfully undergone clipping of an intracranial aneurysm for additional lesions that might cause intracranial bleeding: at around nine years follow-up, 96 of 610 (16%) patients had a total of 129 aneurysms representing recurrence at the same site (24: 19%), previously detected but remote lesions (40: 31%) and de novo swellings (19: 15%). The risk of developing a new neurological problem due to aneurysm correlated with having had multiple lesions at initial presentation, smoking and hypertension. Thus, aneurysms represent a chronic neurological disorder in which recurrence and new events are to be expected. This study emphasizes that developmental defects in the arterial wall may be important underlying causes, but secondary events such as hypertension seem to influence the onset and type of clinical presentation. In From the Archives, we review an earlier post mortem analysis of smaller intracerebral miliary aneurysms showing that these are also strongly associated with chronically raised blood pressure during life (R Ross Russell. Observations on intracerebral aneurysms. Brain 1963; 86: 425–442).
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