Editorial
Electoral franchise and the right to emphatic political opinion expressed without the need for explanation or fear of retribution are enshrined in the democratic process enjoyed widely but by no means universally throughout the world. What constitutes the mental process that integrates the analysis of fact and rhetoric, and from which emerges the decision on how to vote, is less clear. In ‘Swaying the swingers: how neuroscience influences voting behaviour’ David Owen reviews The political brain: the role of emotion in deciding the fate of the Nation by Drew Westen, The myth of the rational voter: why democracies choose bad policies by Bryan Caplan, and Microtrends: the small forces behind today's big changes by Mark Penn (page 591). The debate is whether or not individual voting behaviour is rational, based on honest appraisal of the relevant issues, and reliable in terms of an outcome that history might judge to have been right for the times. Trained in clinical neurology at St Thomas's Hospital until the mid-1960s, elected to Parliament in 1966 and representing constituencies in Plymouth until 1992, holding Ministerial Offices including the portfolios for Health and for Foreign Affairs in the 1970s, founder of the Social Democratic Party in 1981 and its leader from 1983 to 1992 (with a brief interruption over the issue of merger with the Liberal Party), European Union peace negotiator in the former Yogoslavia, and now actively involved with the issues of global business in America, Europe and Russia, Lord Owen is well qualified to comment.Based on evidence from functional brain imaging in committed Democrats and Republicans, Drew Westen concludes that voters are able to detect contradictions made by a rival party candidate but not those perpetrated by their own candidate even when deliberately lying or misrepresenting the facts. He endorses the view proposed by David Hume that ‘reason is the slave of emotion’ and concludes that ‘the political brain is an emotional brain’. Lord Owen acknowledges that political opinion is modulated by personality and cognitive style. He refers to the alarming study of swing voters whose brain scans were activated variously and changeably in regions associated with reward, anxiety and disgust in response to videos of contemporary candidates for the US Presidential election, and how the tactics of these politicians may have altered as a consequence; but he joins Nature (November 22, 2007) in blowing the whistle on the flimsy provenance of this popular ‘research’ and the undeclared conflicts of interest underlying these images. Although Lord Owen notes the differential preparedness and ability of the US parties to exploit emotionality in voting, the use of dirty advertising tricks, the distinctions between those who parade emotion (Tony Blair and Bill Clinton) and the politically more stuffed shirts (Al Gore, John Kerry and Gordon Brown), he takes the view that a much greater proportion of the electorate is floating emotionally and therefore amenable to manipulation in tweaking its vote than Westen suggests; and he considers that voters are well able to judge the important issues and ‘ensure the alternation of power’—as Lord Owen found to his own cost when removed from Ministerial Office following the General Elections of 1970 and 1979.
David Owen has written revealingly on disease, dementia and depression in Heads of State (Quarterly Journal of Medicine 2003; 96: 325–336) and the effect of illness on Anthony Eden's decision making during the Suez crisis (Quarterly Journal of Medicine 2005; 98: 387–402): ‘In sickness and in power’ will be published in 2008, a chapter from which has already appeared as ‘The hubris syndrome: Bush, Blair and the intoxication of power’ in which, whilst not dealing with conventional illness as in other leaders, he suggests that power can go to the heads of politicians, intoxicating their actions and helping to explain the sense of massive incompetence felt by many over the planning and aftermath of the Iraq war. In his Brain review, Lord Owen argues the need for devolution, decentralization and disaggregation of power with greater involvement of unelected but expert decision makers—seeking thereby to remedy the mistakes he perceives to exist at Westminster with respect to influence on the European Union, and the devolved political machinery of Scotland, Northern Ireland and Wales.
On the theme of emotion, Sophie Schwartz and colleagues from Geneva and Zurich (Switzerland) show funny pictures to individuals with the cataplexy–narcolepsy syndrome, mapping the supra-pontine brain regions implicated in cataplexy to a circuit in which orexin neurones in the hypothalamus influence the processing of emotional inputs within the amygdala (page 514, and see cover). Amongst six papers on movements disorders, Caroline Williams-Gray, Adam Hampshire, Roger Barker and Adrian Owen from Cambridge (UK) pursue their evaluation of the early cognitive decline to show that medicated individuals with Parkinson's disease possessing the catechol O-methyltransferase (COMT) genotype (val/val) that confers high fronto-striatal dopaminergic activity are capable of preferential shifts in attention within dimensions, whereas those with the low activity COMT genotype (met/met) fail to establish this attentional ‘set’; thus they propose a neurobiological basis for these novel genotype–phenotype correlations (page 397). Mikhail Bogdanov and investigators from New York and Bedford, MA (USA) use metabolomics to propose products of oxidative damage (8-hydroxy-2-deoxyguanosine, uric acid and glutathione) as biomarkers for the diagnosis and disease progression in Parkinson's disease (page 389). Clinical, imaging and (in a single case) pathological correlations in the context of spasmodic dysphonia are described by Kristina Simonyan and members of seven branches at the National Institutes of Health and the Armed Forces Institute of Pathology (USA): diffusion-weighted imaging steered the pathological inquiry to reveal axonal loss in the genu of the internal capsule with abnormalities of calcium, phosphorus and iron deposition there and in the striatum and cerebellum—locating the defect to descending motor pathways and their connections needed for voice control (page 447). Zeshan Ahmed and colleagues from the Mayo Clinics (Florida and Minnesota, USA) select from a large series of individuals with progressive supranuclear palsy examined pathologically, eight with distinguishing features more suggestive of pallido-nigro-luysian atrophy; and they chart differences in the clinical presentation and evolution to a phenotype that eventually is indistinguishable from other examples of supranuclear palsy (page 460). Following our cluster of articles on brain injury in October 2007, the present issue contains two further papers on this topic. Vanessa Raymont and investigators from Bethesda, MA (USA) report on veterans suffering penetrating head injuries during the Vietnam War to show accelerated rates of cognitive decline at >30 years follow-up, especially affecting those with lower pre-morbid intelligence scores and individuals with genotypes placing them at-risk for neurodegeneration following brain trauma (page 543).
Brain does not often publish on therapeutic interventions in man but the present issue contains three such papers. Paul Bentley, Jon Driver and Ray Dolan from London (UK) show that sophisticated stimulus and task-dependent components of defects in visual attention in Alzheimer's disease improve with physostigmine, and with increased activation in various extrastriate and frontoparietal brain regions that showed altered activations pre-treatment, whereas pro-cholinergic exposure may perturb different cognitive functions and brain activations in normal individuals (page 409). Craig Takahashi and colleagues from California (USA) show that subject-initiated robotic support of the force and dynamics of motor control improves hand movement during recovery from stroke and with task-specific reorganization of sensorimotor cortical motor maps (page 425). Roy Raymann and investigators from Amsterdam (The Netherlands) exploit the observation that a rise in temperature increases activity in neurones implicated in sleep regulation to show—what cats who choose the warmest spot in which to snooze know well— that even a 0.4°C increase in skin temperature improves normal sleep and that of insomniacs, doubling the amount of slow wave sleep and reducing the frequency of early morning waking (page 500). Without wishing to engage the can of worms recently opened by James Watson on ethnicity and intelligence, our series of occasional papers includes an updated account by Alla Vein and Marion Maat-Schieman from Leiden (The Netherlands) on brain structures in two intellectually elite Russians—Alexis Yakovlievich Kozhevnikov and Sergei Korsakov—neither included in the analyses reported from 1928 by the Moscow Brain Research Institute but earlier studied briefly by AA Kaputsin (1925) who claimed a larger left hemisphere and more complex convolutions of the frontal and parietal lobes for both of these cherished Russian neuroscientists (page 583). Finally, we publish papers illuminating aspects of a disorder of mitochondrial function in which mutation of an autosomal gene hitherto associated only with dominant optic atrophy is newly implicated as the cause of familial progressive external ophthalmoplegia (pages 329, 338; and 352 and see Commentary by Massimo Zeviani, page 314). A mosaic histochemical defect was first described in chronic progressive external ophthalmoplegia by John Morgan Hughes (for example, Petty et al. Brain 1986; 109: 915–938): later, with Ian Holt and Anita Harding, John Morgan Hughes added single mtDNA deletions to this description; Massimo Zeviani provided a definitive report showing single mitochondrial DNA deletions in the Kearns Sayre syndrome (Zeviani et al. Neurology 1988; 38: 1339–1346) and shortly after alerted the research community to disorders of mitochondrial disease in which the propensity to form multiple mtDNA deletions is inherited as an autosomal trait (Zeviani et al. Nature 1989; 339: 309–311). As always, these accounts traded on earlier clinical descriptions of phenotypes that only gradually came to be associated with the defined molecular defects, to which is now added a fifth culprit, and pathological mechanisms underlying the mitochondrial cytopathies. In From the Archives, we review ‘Progressive dystrophy of the external ocular muscles (ocular myopathy)’ by LG Kiloh and S Nevin (Brain 1951; 74: 115–143).
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