Editorial
Down the centuries, science and religion have often appeared to be in conflict, the requirement for evidence in scientific matters seeming to sit awkwardly with the basis in faith of theistic belief. For many, the apparent contest between creation and evolution through natural selection polarises the debate. This triggered the famous exchange between Charles Darwin's bulldog, TH Huxley, and William Wilberforce, Bishop of Oxford (who, for wit, in our opinion, has the better of the exchange) at the 1860 Oxford meeting of the British Association for the Advancement of Science: "would it be through his grandfather or his grandmother that [Huxley] claims descent from a monkey?" chided the Bishop; remarking to Sir Benjamin Brodie, seated by his side, ‘the Lord hath delivered him into mine hands’, Huxley replies that "he is not ashamed to have a monkey as an ancestor; but he would be ashamed to be connected with a man who used great gifts to obscure the truth"—remarks that evidently had an effect sufficient to cause ladies to faint, and journalists present to ‘jump out of their seats’ (see Leonard Huxley: Life and Letters of TH Huxley, 1900: Vol 1; pp 183–189). This exchange enlivened a session made rather dreary by Dr John William Draper of New York who had ‘droned out his paper’ on Intellectual development of Europe considered with reference to the views of Mr Darwin, a theme later developed in his monograph History of the conflict between religion and science (1873). WHR Rivers argued in his Fitzpatrick lectures to the Royal College of Physicians of London (1915–1916: published posthumously in 1924) that ‘Medicine, Magic and Religion’ are each abstract terms connoting social processes by means of which mankind seeks to safeguard life. Therefore, the differences are perceived not real, and the relationship is close. Religion involves the belief of some power greater than man himself, and magic co-opts man-made rites to explain morbidity, whereas medicine defines a set of social activities by which man seeks to control natural phenomena that disrupt physical and social functions. For Rivers, the common origin of these concepts is best revealed through studying the beliefs and practices of ‘rude cultures’—in his case, the peoples of Melanesia. In ‘Spirituality and wellbeing: some recent discussions’, Alister McGrath dispenses with the ‘warfare’ model of science and religion, separating spirituality from the ideas of traditional religions, and elevating worldviews of the individual person that aspire to ‘meaning in life’. Professor McGrath traces the need of individuals in a postmodernist world for freedom to contemplate more than just the favoured Rationalist model of human existence. And he hints at evidence, the stuff of science, that religious commitment does indeed affect wellbeing and longevity: in short, faith works. With a background in chemistry and molecular biophysics prior to studying theology, Alister McGrath, Professor of Historical Theology in the University of Oxford, is well placed to debate ‘an informed engagement between science and religion’. He reviews The spiral staircase: a memoir by Karen Armstrong; The sacred neuron: extraordinary discoveries linking science and religion by John Bowker; Spirituality and the healthy mind: science, therapy and the need for personal meaning by Mark Galanter; and Consciousness and the mind of God by Charles Taliaferro (page 278). His own most recent book is Dawkins's God: genes, memes and the meaning of life (2004). Avoiding any hint of evangelism, critical of anything that smacks of sophistry in hand-waving amateur neuroscience (Bowker), supportive of the position that attention to opinions on the meaning of life has to be part of understanding psychiatric morbidity (Galanter), unashamedly admiring of expressions of faith that articulate an integrative theism (Taliafero), and sensitive to events that challenge that faith (Armstrong), Professor McGrath has two messages: any who venture an opinion on human judgement should first acquire a passing acquaintance with contemporary neuroscience; and an evidence-base is beginning to emerge supporting the view that spirituality is conducive to wellbeing, and so of relevance to the study of health and disease.
In this issue, Johannes Sarnthein and colleagues from Zürich, Switzerland, use changes in the power spectra of surface electroencephalography following successful central lateral thalamotomy to show that chronic neurogenic pain is determined by tightly coupled thalomocortical loops (page 55). Amongst papers dealing with epilepsy, Robbert Notenboom and investigators from Utrecht, Netherlands and Toronto, Canada conclude that the specific increase in distribution of metabotropic glutamate receptors (mGluR5 but not mGluR1
) on the cell bodies and apical dendrites of hippocampal neurons in tissue removed from individuals with temporal lobe epilepsy, especially surviving neurons from individuals with hippocampal sclerosis, may explain the previous drug-resistance of these cases (page 96). Tiina Sairanen and colleagues from Helsinki provide support for a neuroprotective effect of the endogenous erythropoietin response in limiting penumbral tissue injury after stroke, by correlating markers of neuronal apoptosis with immunoreactivity for erythropoietin and its receptor in autopsy material, adding to the case for a neuroprotective role of erythropoein and the development of anti-apoptotic therapies in stroke (page 189). Mohammad Ikram and investigators from Rotterdam and Amsterdam, Netherlands, seek to reconcile whether the altered arterio-venular ratio of retinal vessels that correlates with cerebral small vessel disease is primarily arterial or venous in origin (page 182): large venular diameter emerges as the most reliable indicator of cerebral small vessel disease progression and incident lacunar infarctions, but the mechanism is unresolved. Rutger Goekoop and a team from Amsterdam, Netherlands, demonstrate altered fMRI activation in people with Alzheimer's disease recently exposed to galantamine (a cholinesterase inhibitor) during a face recognition task that probes memory retrieval and encoding, thereby supporting the cholinergic hypothesis for this disorder, and with qualitative differences shown between Alzheimer's disease and mild cognitive impairment (page 141). Tony Buchanan, Daniel Tranel and Ralph Adolphs from Iowa and California, USA, asked patients with surgical lesions of the anterior temporal lobe to recall their most poignant past emotional experiences: they show that those with right sided lesions enjoy a more pleasant ‘remembrance of things past’ selected from an intact catalogue reflecting the autobiographical memory bump of the second and third decades; thus, the right hemisphere is involved in the retrieval of negatively valenced, high intensity memories (page 115). Paul Dockree and colleagues from Dublin, Ireland, demonstrate that, as a result of damage to the prefrontal cortex, individuals with traumatic brain injury are vulnerable to misleading information, wrongly accepting this as true memory, and they lack the ability critically to evaluate uncertainty (page 128). Seeking to replace the Ashworth scale that has served the needs of clinical trials investigators for several decades, Jeremy Hobart and colleagues from Plymouth and London, UK, and Perth, Australia describe a new scale for the assessment of spasticity that incorporates patient-orientated aspects of participation, evaluated and refined in two cohorts of cases with multiple sclerosis (page 224).
Two papers in the current issue deal with Fragile X-associated tremor/ataxia syndrome. Claudia Greco and a group from California, USA, provide a quantitative and qualitative account of the neuropathology in 11 males dying at ages 67–87 years, emphasising the diffuse white matter disease with intranuclear neuronal inclusions in the brain and spinal cord and in astrocytes, each correlating with the number of CGG repeats (page 243). The same team of investigators, now under the authorship of Christine Iwahashi, has characterised candidate proteins accumulating within the ubiquitin-positive intranuclear inclusions associated with expansion of FMR1 that cause the presumed toxic gain-of-function: but no one of more than 20 identified by mass spectrometry and immunohistochemistry is dominant, and they conclude that the formation of inclusions is not likely to represent a breakdown in proteosomal degradation of nuclear proteins (page 256). Amongst other papers on neurogenetics, Claudia Cagnoli and colleagues from Turin, Milan and Bologna describe 11 members of a pedigree having a new variant of dominantly inherited juvenile onset, and slowly progressive spinocerebellar degeneration. Presenting with loss of balance, affected individuals later develop external ophthalmoplegia. Excluding repeat expansions of all known SCA genes, genome-wide screening revealed linkage to 18p11.22-q11.2 (maximum lod score 4.2) with the effect narrowed to a 7.9Mb interval encoding several positional candidates. In From the Archives, we review three papers that set standards for the description and classification of the spinocerebellar degenerations (Holmes G. A form of familial degeneration of the cerebellum. Brain 1907: 30; 466–489; Ferguson FR and Critchley M. A clinical study of an heredo-familial disease resembling disseminated sclerosis. Brain 1929: 52; 203–225; and Harding AE. The clinical features and classification of the late onset autosomal dominant cerebellar ataxias: a study of 11 families, including descendants of ‘the Drew family of Walworth’. Brain 1982: 105; 1–28).
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