Editorial
Art and neurology have an obvious, but also a more subtle, relationship. Book illustration quickly followed the advent of printing with moveable type, and the brain was soon prominently displayed. Placed in a lush landscape, Jan von Calcar's plates for Vesalius's De fabrica (1543) are unambiguously artistic; and the colour lithography that decorated the neuropathological atlases of Robert Hooper (1826), Robert Carswell (1838) and Jean Cruveilhier (1829–1842), and the works of Charles Bell in the same era, are pictures—over and above their anatomical accuracies. Even when it was no longer necessary, many neuroscientists preferred to depict their work freehand rather than in photographs: thus, the works of Santiago Ramon y Cajal (1852–1934) and the surgical specimens of Harvey Cushing (1869–1939) sustained the role of the neuroscientist as artist. Turning the tables, painters have displayed neurological disorders in their works, as the anthologies of Paul Richer, and others, show. Thus, art and neuroscience are linked by the need to perceive artistic ephemera, and conversely to execute the works in various media. But treating the brain merely as the engine of artistic endeavour is too narrow an analysis. In his Clark Lectures (2005), Dr Rowan Williams, Archbishop of Canterbury, sets boundaries for the origins, purpose and legitimacy of art, rooted in the philosophy of Jacques Maritain (1882–1873) and explained through the works of Eric Gill (1882–1940), David Jones (1895–1974) and Flannery O'Connor (1925–1964). ‘Art is an action of the intelligence ... As such, it invites contemplation; that is, it sets out to create something that can be absorbed by intelligence, rather than a tool for use in a project larger than itself ... Art uncovers relations and resonances in the field of perception that ‘ordinary’ seeing and experiencing obscure or even deny ... It makes the world strange ... It opens up the dimension in which "things are more than they are", "give more than they have"’.In Secret harmonies: neurology and the arts, (page 948) Adam Zeman explores the relationship between (neuro)science and the arts through the act of imagination–the ability to ‘re-present’ or predict experience, unconstrained by time present. The difference is one of focus—art dealing with the experience and science the mechanism. Zeman claims no originality for his formulation but illustrates the analysis through scholarly reference to literature, music and the visual arts. In his review of Neurology and the Arts (edited by Frank Clifford Rose), Memory in Literature (Suzanne Nalbantian), The Psychology of Art and the Evolution of the Conscious Brain (Robert Solso) and The Cognitive Neuroscience of Music (edited by Isabelle Peretz and Robert Zatorre), Dr Zeman argues that, through memory and imagination, the cognitive brain liberates us from the constraints of immediate experience—to contemplate; and, in turn, art illuminates the workings of the human mind by leading the inner terrain of perception and experience in new directions, sometimes to extreme—a là Maritain and O'Connor.
Amongst five papers on neurogenetics, Amets Sáenz and colleagues from Spain, France, Italy and Germany review 238 examples of limb girdle muscular dystrophy type 2A, representing about half of those referred for molecular analysis of the calpain 3 gene (page 732). Despite a relatively stereotyped clinical phenotype characterized by onset in the teens, and a high expectation of wheelchair dependence by the fifth decade, 105 different CAPN3 mutations are identified, of which 50% are novel. Only the presence of two null mutations has a clinical correlate—disability at a relatively early age. Two papers inform the topic of degeneration and regeneration. Marc Ruitenberg and researchers from Australia and the Netherlands engineered olfactory ensheathing cells to express neurotrophin-3 (page 839); these increased the number of regenerating corticospinal tract fibres in a model of spinal cord injury, although not the behavioural recovery occurring in association with olfactory ensheathing cell implantation, and the consequent restriction of tissue damage seen without growth factor expression at the site of injury. Rates of axon degeneration differ in the central and peripheral nervous systems, perhaps explaining their different capacities for regeneration. Florence Perrin and colleagues explore the possibility that macrophage derived factors enhance regeneration by accelerating Wallerian degeneration (page 854). They show that the expression of monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1
(MIP-1) and interleukin-1ß is much increased in the regenerating mouse sciatic nerve by comparison with the spinal cord. Manipulating the availability of these cytokines, up and down, alters the dynamics of regeneration in both tissues, respectively.
The availability of imaging techniques that allow the distribution and activity of receptors to be mapped in the central nervous system, and the use of transcranial magnetic stimulation, increasingly are illuminating the pathophysiology of neurological disease. Martin Turner and colleagues from Kings and Imperial Colleges in London use the PET ligand [11C]-WAY100635 to map 5-HT1A receptors in the motor cortex of individuals with amyotrophic lateral sclerosis (page 896). Especially in patients with bulbar involvement, regional reductions in ligand binding principally affect the frontotemporal regions, and the cingulate and lateral pre-central gyri. Potential confounds, such as depression and drug treatment, are excluded, and the assumption is that these are the signatures of neuronal loss; but the authors cannot exclude reduced receptor expression or function on otherwise intact pyramidal neurones. Sarah von Spiczak and investigators from Imperial College, London and Göttingen, Germany (page 906) find no abnormality in distribution of the non-selective opioid receptor radioligand 11C-diprenorphine in patients with restless legs syndrome. However, pain severity correlates inversely with ligand binding in areas involved in the appreciation of pain – medial thalamus, amygdala, caudate, anterior cingulate, and insular and orbitofrontal cortex. Even if opioid release is merely a response to discomfort, the findings suggest interactions between sensory and motor systems in the mechanism of restless leg movements. The interplay of sensory input and motor response is also the focus of a study reported by Karin Rosenkranz and collaborators from the Institute of Neurology and the Royal College of Music, London (page 918). They use transcranial magnetic stimulation to tease apart abnormalities of motor control in musician's dystonia and writer's cramp – conditions that develop in the context of different requirements for repetitive hand movements – compared to healthy musicians and individuals lacking musical skill. Motor evoked potentials, reflecting the excitability of corticospinal outputs, to a muscle registering the sensory response to focal vibration are abnormal in both types of occupational cramp; but the neurophysiological properties observed in musician's dystonia lead the authors to suggest that the process of adaptation, normally associated with musical practice, spills out to disrupt rather than assist skilled movement in those who display musician's cramp.
This issue includes two papers describing case series. Nicole Grois, on behalf of the Langerhans Cell Histiocytosis Co-operative Group, describes 12 cases (page 829): eight presented with diabetes insipidus, as originally described by Alfred Hand (Proc Pathol Soc Philad 1893; 16: 282–84), Artur Schüller (Fortschr Geb Rontgenstr 1915–16; 23: 12–18) and Henry Christian (Contributions to medical and biological research dedicated to Sir William Osler. P. B. Hoeber, 1919: 1; 390–401), and nine eventually developed ataxia, dysarthria, cognitive deficits and headaches. The neuropathological findings are classified as circumscribed granulomas occupying the space between tissue planes; granulomas that also partially infiltrate the nearby brain parenchyma; or histiocytosis with degenerative cerebellar and brainstem lesions. Each is considered a proliferative disease of mesenchymal tissue. Given the immunological properties of dendritic cells, it is to be expected that intense T-cell inflammatory reactions should occur, but why these should accumulate is less clear. The features of peripheral neuropathy in patients with either Crohn's disease or ulcerative colitis are described by Francisco Gondim and investigators from Brazil and the USA (page 867). These neuropathies tend to affect males at an interval of around 11 and 26 years after the onset of inflammatory bowel disease in the Crohn's and ulcerative colitis cases, respectively. With axonal and demyelinating histology, sensory and sensorimotor clinical features, and many associated neurological disorders, the possibility of multiple causes and mechanisms arises. Not every confound was fully excluded, and particularly controversial is the possible effect of prior treatment with metrinadazole. But the authors conclude that the association is direct and the neuropathy immune-mediated.
Understandably, our editorial policy rarely to publish papers that explore physiological function in normal humans or animals frustrates many would-be authors. Several have pointed out that Brain has a rich past history of articles illuminating how the nervous system works in health. But with the advent of technical opportunities not foreseen by former authors and editors, the balance has shifted and our priority in recent years has been on the description of dis-order and the elucidation of disease mechanisms. The paper by Mario Campero and others from the USA is one of several exceptions to this editorial position (page 892). They use microneurography to map the cutaneous distribution of fascicles contained within the superficial radial nerve in the forearm, as it turns posteriorly beneath the tendon of the brachioradialis muscle and appears on the dorsum of the forearm, superficial to the abductor pollicis. From a study of 14 nerves, three patterns emerge: a fascicle supplying the radial aspect of the first dorsal interosseous space; one supplying the lateral aspect of the first metacarpal and the lateral aspect of the thumb; and another innervating the second interosseous space and the proximal phalanx of the index and middle fingers. These summate to produce the compound fascicular territory described classically for the superficial radial nerve. The functional status of these divisions is preserved during painful stimulation of each fascicle. The authors conclude that the experience of pain referred from one zone to another has nothing to do with cutaneous innervation but, rather, relates to nerve activity in afferent fibres from additional fascicles supplying deep tissue and muscles. Thus, classical dogma is challenged: ‘anatomical studies have shown that nerve fibres within a nerve trunk are subdivided into well defined fascicles, which by repeatedly uniting and dividing, engage in a plexus formation along the full length of a nerve. The expected result would be that the more distal the fascicle, the less often would topographic arrangement be found ... the fascicular arrangement of sensory fibres ... demonstrates that nerve fibres grouped in one single fascicle supply a continuous area of skin, and not separate cutaneous territories as might be expected by anatomical studies (Sunderland, 1945)’. But this may be a partial reading of Sir Sydney Sunderland's 1945 Brain paper, reviewed in From the Archives.
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