Editorial
Mid-summer can be an anxious time for editors since this brings the new list of Impact Factors that increasingly serve as markers of worthiness in academic publishing. Ours is stable—rising from 7.535 (2005) to 7.617 (2006 - current), having reached a peak (to date) of 8.201 in 2004 following a steady rise from 7.122 in 2002. Even when topping the list of journals specializing in clinical neuroscience, we were careful not to be self-congratulatory, sensing that pride has a nasty habit of coming before a fall. Our sister journals are evidently not so reticent: Lancet Neurology acquired an enviable Impact Factor of 12.167 based on exclusive publication of review articles but has seen a fall to 9.479 as the effect of also including original papers starts to make itself felt; at 8.051, Annals of Neurology has now substantially reduced the number of papers published. Should Brain play games in chasing the fickle Impact Factor statistic by cutting back on the number of papers we publish, and so risking fewer passengers that attract low citations, or filling our pages with reviews? The answer is ‘no’. We will continue to publish 20–21 original articles and one review each month (together with occasional papers, editorial contributions and a book essay) irrespective of whether some papers that we publish offer a low prospect of high citation by nature of the topic they address. Nor will we chase papers just because we judge these as likely to boost our numerator in determining future Impact Factors. Rather, we will maintain our role, dating from 1878, as the repository of discovery and knowledge across the spectrum of clinical neuroscience. Nevertheless, we hope that our selections are well cited.After many years of glacial progress, the search for genes that increase susceptibility to complex genetic traits is at last proving productive. The factors that impeded success, and which are now partially corrected, include the focus on linkage rather than case-control studies; insufficient reagents with which to explore the genome at high density; grossly under-powered sample sizes; and failure to appreciate that statistical analysis needs thresholds for significance several orders of magnitude more stringent than those often adopted. The rate of attrition for provisional results has been high. As a result, association studies claiming to have identified markers of disease susceptibility, and those suggesting exclusion, have become untrustworthy and difficult to evaluate. The spate of whole genome association screens that has started to illuminate complex traits and phenotypes that might not previously have been considered even to constitute discrete diseases—now bearing the ‘low-hanging’ fruit on the back of the human genome project and haplotype map, the merging of resources and samples through formation of cooperative consortia, and the adoption of appropriate analytical methods—already includes several previously somewhat recalcitrant neurological diseases. Of course, these limitations did not inhibit the mapping and identification of genes for very many Mendelian disorders; and the revolution of molecular genetics has in turn, defined new phenotypes and disease mechanisms that suggest effective remedies for previously untreatable conditions. At Brain, we consider ourselves to have been reasonably indulgent in publishing studies that merely map novel loci for neurological disorders. But as the new era of neurogenetics dawns, that threshold is bound to rise and our readers are likely only to be served studies that combine topography with functional data, mechanistic insights and phenotypic clarifications. Meanwhile we publish three papers that map susceptibility loci for existing or newly defined neurological phenotypes based on whole genome and candidate gene approaches. Veerle Bogaerts and colleagues from Antwerp (Belgium), Tübingen (Germany) and Jacksonville (Florida, USA) use whole genome family linkage to map a locus for dementia with Lewy bodies and parkinsonism to 2q35-q36 that is close to but separate from Park11; sequence analysis has not revealed the gene (page 2277). Masatoyo Nishizawa and investigators from Niigata, Sado and Kuroishi (Japan) exclude recognized genetic disorders and map autosomal dominant adult onset benign chorea without dementia to 8q21.3-q23.3; they dub the condition benign hereditary chorea type 2 (BHC2: page 2302). Dalia Kasperaviciute and a team from London, Birmingham and Sheffield (UK), Durham (North Carolina, USA) and Würzburg (Germany) report a candidate gene study in which pathways involved in axonal transport, xenobiotic metabolism and neurodegeneration form the basis for selecting 134 candidate genes, and a reasonably high density of markers covers the regions of interest tested in a primary population and validated in replication cohorts; in the event, this is a negative study that effectively excludes these pathways from further genetic exploration (page 2292).
Five papers in the present issue address various aspects of brain structures that allow us to sense and interact with the visual world. Cristina Becchio and colleagues from Torino and Padua (Italy), Melbourne (Australia) and London (UK) show that autistic children fail to appreciate the cue provided by observing the direction of gaze in others carrying out a reaching task that they themselves then have to mimic, when the model is or is not distracted (page 2401): therefore the eye gaze that normally plays an important role in eliciting the motor contagion constituting a first step in mentalizing is defective in the context of autism. Ergun Uc and a team from Iowa City (Iowa, USA) test individuals with Parkinson's disease for their ability to simulate navigation in a motor car (page 2433): patients make more incorrect turns, get lost more often and commit more errors than controls on the route finding task; and these navigational weaknesses result from poor performance on tests of memory, attention, executive function and visual perception rather any associated motor difficulties. Roger Kalla and investigators from Munich (Germany) and London (UK) hypothesize that increasing the excitability of cerebellar Purkyne cells with the potassium channel blocker 4-aminopyridine might improve the oscillations of downbeat nystagmus (page 2441): with some variations dependent on aetiology, 4-AP does restore gaze-holding ability due to an effect on vertical and horizontal neural integrator function. Ayse Saygin from London (UK) and San Diego (USA) shows that patients with unilateral strokes predominantly affecting the superior temporal or premotor areas have impaired biological motion perception, irrespective of lateralization, implicating damage to a network normally activated in motion perception that results in failure to engage the action observation system (page 2452).
Finally, Robert Ward and Isabel Arend from the University of Wales (Bangor) describe deficits in two individuals with discrete lesions to show that spatial coding in the pulvinar respects both retinotopic and object-based (those that relate spatial position to a reference object) frames amongst the many that convert visual stimuli into coherent percepts (page 2462). This study pre-empts the position taken by Jon Kaas in ‘The thalamus revisited: where do we go from here?’, where he reviews The thalamus by Edward Jones and Exploring the thalamus and its role in cortical function by Murray Sherman and Ray Guillery—each published in a second edition, 21 and 5 years after their original appearances, respectively (page 2470). Professor Kaas sympathizes with the mystique expressed by Jerzy Rose in 1940, and re-quoted by Edward Jones: ‘the thalamus is like the flying Dutchman: many have heard of it, some believe in it, but few have actually seen it’. He much admires Professor Jones's comprehensive comparative anatomy depicted in photomicrographs of thalamic sections from many species—including but not confined to the human brain and including tree shrews, galagos and egg-laying monotremes; and he applauds Jones's history of thalamic discovery brought up to date from 1985—detailed, personalized and rich in opinion. The concept that one scheme of thalamic organization does not fit all emerges from Professor Jones's magisterial work despite the emphasis on thalamic structures that appear conserved across species. Jon Kaas offers an equally admiring critique of Exploring the thalamus, linking Sherman and Guillery's 2001 formulation that the thalamus contains neurones acting as drivers, not only of connections involved in relaying information from lower centres to the cortex but more especially those that form cortico-thalamo-cortical connections involving the neocortex, and modulators of these pathways that impose the conditioning influences of attention and awareness on these drivers. And they advocate a detailed cataloguing of response patterns in each thalamic nucleus and each cortical area—correcting the designations of Brodmann's ‘organs of the brain’ and their projections onto thalamic architectures with definitions conditioned by function and not the, often incorrect, anatomical boundaries. Because the cortico-thalamo-cortical system of drivers and modulators is intimately correlated, Professor Kaas warns us to expect no less complexity in thalamic organization to that clearly apparent in cortical arrangements. As Centennial Professor of Psychology at Vanderbilt, and a devoted student of brain structure and function, Jon Kaas’ own studies have traced the evolution of the neocortex and dorsal thalamus in mammals. Complexities of the pulvinar are particularly instructive: here, the extrageniculate visual thalamus has evolved in markedly different ways across mammalian species depending on their visual competencies, indicating that studies in rats and mice cannot necessarily inform the arrangements that pertain to primates and to man.
We have previously considered structure and function of the thalamus and the issue of its connections with the cortex and other brain structures. In 1932, Sir Wilfred Le Gros Clark published his Arris and Gale Lectures given at the Royal College of Surgeons on February 17th and 19th 1932 as ‘The structure and connections of the thalamus’ (Brain 1932: 55; 406–470); and in From the Archives, we review ‘On the structure and functional relations of the optic thalamus’ by Ernest Sachs (Brain 1909: 32; 95–186).
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