Editorial
Unravelling the complexities of neuroscience is now a multi-disciplinary enterprise. This general interest transcends biology and, apart from interactions with the physical sciences, increasingly involves such novel intellectual alliances as social-neuroscience, neuro-economics, neurophilosophy and neuro-ethics. The complex relationship between medicine, the style of its practitioners, behaviour—alone or in groups—and the reciprocal attitudes of society are all represented in these emerging disciplines. But is neuroethics merely an awareness of doctrines enshrined in the Declaration of Helsinki, first formulated by the World Medical Association General Assembly in June 1964 and since serially amended down to 2004, whereby clinical research is only conducted with informed personal or surrogate consent, and never in violation of the basic principles of human experimentation, ensuring that the practice of neurological medicine is ethical; or does neuro-ethics have a status that might justify the distinction from, say, cardioethics, nephro-ethics or colono-ethics? In ‘Rights, wrongs and neurons’, Neil Manson from the Institute for Philosophy and Public Policy, Lancaster University (UK) rapidly disposes of this dichotomy and focuses on the neuroscience of ethics, rather than the ethics of neuroscience. Dr Manson reviews Neuroethics: Defining the Issues in Theory, Practice and Policy, edited by Judy Iles, and The Ethical Brain by Michael S. Gazzaniga. He parks the rhetorical position that knowing how the brain works does not of itself help us to consider what ought and what ought not to be done, arguing that—although the disciplines of ethics, law and philosophy can proceed nicely without needing to touch base in the brain—behaviour, the stuff of ethical expression, is brain-derived, albeit attenuated by folk psychology and social practices that influence intention, deliberation and reason. Comfortable, therefore, with the notion that neuroscience can inform the study of morality and responsibility, Neil Manson draws back from total neuroscience reductionsism in considering rationality, justice and morality; and he does not like the suggestion that the neuroscience formulation might replace those folk psychological concepts from which emerged successful social practices such as the criminal justice system.In the present issue, we publish—on the topic of vision—accounts of things present that are not seen; things not present that are seen; and things seen after they have disappeared. R. Jarrett Rushmore and investigators from Boston (USA, including the late Dr Bertram Payne), London (Canada), and Bremen (Germany) manipulate the feline brain with cold probes and study regional 2-deoxyglucose uptake to show that, in the context of visual neglect, the superior colliculus influences the balance of inhibition and hyper-excitability in the posterior and inferior parietal cortices (page 1803). Sandra Leh, Heidi Johansen-Berg and Alain Ptito from the University of Oxford (UK) and the Montreal Neurological Institute (Canada) use diffusion tensor-weighted imaging tractography to demonstrate that hemispherectomized individuals with field defects who show the phenomenon of attention-blindsight open up connections to the contralateral primary and association visual areas, and regions of the parietal, prefrontal and frontal lobes, in addition to the ispilateral pathways present in normal individuals that are unaltered in subjects without blindsight (page 1822). Alex Shepherd from the University of London (UK) studies pattern adaptation in migraineurs to disaggregate the separate contributions of changes in local networks and individual cellular responses responsible for visual motion after-effects (page 1833), showing that cellular recovery is slowed differentially across areas of the visual cortex, and people with migraine have widespread suppression of regional networks that results from increased intracortical excitability not directly due to loss of cortical inhibition.
Three papers describe different aspects of motorneuron diseases. Based on proteomics screening and protein expression, Clare Wood-Allum and colleagues from Sheffield (UK) and the Karolinska Institute, Huddinge (Sweden), identify reduction in the mitochondrial anti-oxidant peroxiredoxin-3 as a promising molecular candidate in a cell-culture-based model of superoxide dismutase-1 familial amyotrophic lateral sclerosis—the defect being corrected by the anti-oxidant peroxiredoxin-3 agonist, ebselen (page 1693). Chris Panzeri and a team from centres in Monza, Milan, Rende, Conegliano and Padova (Italy) and the Institute of Psychiatry, London (UK), report a first homozygous missense mutation in ALS2, that normally encodes alsin—already implicated in several spinal cord neurodegenerative disorders including juvenile onset primary lateral sclerosis—and go on to show disruption of endosomal protein localization, rendering neurons more susceptible to spontaneous and induced apoptotic cell death through the Bcl-xL/Bax system (page 1710). Olga Ciccarelli and investigators from University College London and the University of Oxford (UK) analyse data captured by diffusion tractography of the corticospinal tracts to compare the sensitivity of summary connectivity measures of fibre organization, and reduced fractional anisotropy—a measure of directional coherence in fibre tracts—as markers of disease progression in amyotrophic lateral sclerosis (page 1859).
Three other papers focus on the subthalamic nucleus. James Bernard Luys (1828–1897) described his ‘corpus’ in 1865 as a ‘substance grise accessoire des olives supérieures’—by ‘olives supérieures’, he meant the red nucleus—speaking of a ‘noyau de substance grise accessoire du locus niger’ identical in location and shape to the corpus Luysii or, as it is now less personally known, the subthalamic nucleus. Luys noted connections of his corpus with the globus pallidus or ‘corps jaune’ (Luys J. B. Recherches sur le système nerveux cérébrospinal, Paris, 1865). On page 1748, Fernando Alonso-Frech and colleagues from the University of Pamplona (Spain) directly record field potentials in the presence of dopamine agonists and in the ‘off’ medication state, correlating the development of dyskinesias with onset of 4–10 Hz activity in the opposite subthalamic nucleus. João Costa and colleagues from Barcelona (Spain), Lisbon (Portugal) and Innsbruck (Austria) explore the physiological basis of the glabella tap sign in Parkinson's disease showing that, in the context of reduced auditory and somatosensory inhibition of the blink reflex, subthalamic nucleus deep brain stimulation reduces the R2 component of the orbicularis oculi response to supra-orbital stimulation by increasing prepulse inhibition in the circuit that connects the basal ganglia to the pontine tegmental nuclei (page 1758). Lastly, Puneet Plaha and a team from Bristol (UK) challenge the dogma that the preferred site for deep brain stimulation is the body of the subthalamic nucleus itself, by comparing relocation of electrodes to the zona incerta and the pallido-fugal fibres that reciprocally connect this structure to the globus pallidus (page 1732; and see cover): their comparisons, based on components of the Unified Parkinson's Disease Rating Scale observed in 35 patients with Parkinson's disease, suggest that improvement is better with deep brain stimulation applied directly to the zona incerta than in the subthalamic nucleus, or structures dorsomedial to the corpus Luysii. Clearly, readers will want to consider these clinical outcomes and evaluate the confidence with which placements in these small and juxtaposed structures were reliably achieved before asking neurosurgical colleagues to swing their electrodes more medially. In ‘From the Archives’, we review contributions made over a period of 30 years to the clinical neurology of lesions affecting the subthalamic nucleus and the zona incerta by Dr James Purdon Martin (Hemichorea resulting from a local lesion of the brain. The syndrome of the body of Luys). Brain 1927; 50: 637–651; Hemichorea associated with a lesion of the corpus Luysii. Brain 1934; 57: 504–516; and Hemichorea [hemiballismus] without lesions in the corpus Luysii. Brain 1957; 80: 1–10).
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