Editorial
In retelling ‘The Discovery of Reflexes’ (1960), EGT Liddell reduces the story to four critical periods: the nerve cell and the microscope, animal electricity, experimental approaches, and ‘Sherrington and his times’. Manuscript lecture notes loosely inserted in Liddell's own copy of ‘Reflex Activity of the Spinal Cord’ (1932) written with RS Creed, D Denny-Brown, JC Eccles, and CS Sherrington trace how a millennium of post-Galenic darkness was systematically illuminated across the 15th–19th centuries by Leonardo da Vinci, Robert Whytt, Gilbert Blane, Georg Prochaska, Julien Le Gallois, Pierre Flourens, Marshall Hall, Johannes Müller, Richard Grainger, Eduard Pflüger, Friedrich Goltz and Alfred Vulpian before Sherrington provided his great synthesis of 1906 (The Integrative Action of the Nervous System). But, self-evidently, there was still unfinished business if the nature and role of reflex function, most easily characterized in the spinal cord, for the nervous system as a whole was to be understood. In ‘One small step for man’ Roger Lemon reviews ‘The Circuitry of the Human Spinal Cord: its Role in Motor Control and Movement Disorders’ by Emmanuel Pierrot-Deseilligny and David Burke. Making the point that, in work done by himself and later with Liddell, Sherrington warned against allowing ‘a tradition to grow up whereby it was scientifically and even clinically acceptable to think of the spinal cord as having an existence quite separate from that of the supraspinal centres’, and elevating the status of Hoffmann's description of the H-reflex in 1910, Professor Lemon brings his detailed knowledge of structure and function in the nervous system to bear on a critical analysis of this contemporary summary of how the human spinal cord participates in normal movement, and may go wrong in the context of neurological disease.This issue contains two scientific commentaries on the paper by Susan Ravizza and colleagues from the Universities of California, Davis and Berkeley, and Pittsburgh, USA, and Oxford, UK, describing deficits of verbal working memory in cerebellar disease (page 306). In 1998, we published a much cited review on the cerebellar cognitive syndrome (Schmahmann JD, Sherman JC. The cerebellar cognitive affective syndrome. Brain 1998: 121; 561–579), and Jeremy Schmahmann, now with David Caplan, considers the new evidence supporting that formulation (page 291). Conversely, the more classical doctrine of the cerebellum purely as the organ of motor coordination is preferred by Mitchell Glickstein (page 288).
In a previous issue, we explained the position of Brain with respect to open access (Brain 2005: 128; 2217–2218). As from January 6, 2006, authors may opt, at a charge, to make their paper freely available online to any reader immediately upon electronic publication as part of the Oxford Open initiative. Indeed, all authors are requested to indicate whether or not they wish to exercise this option. Details are available at http://www.oxfordjournals.org/oxfordopen.
In the year since the present editorial team took office, papers on many aspects of neurobiology and Parkinson's disease have been handled by Anders Bjorklund. Now, he wishes to step down, and we are pleased to welcome Dr Mark Hallett as Associate Editor of Brain. Mark is Chief of the Human Motor Control Section of the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health (NIH). His expertise in human motor control and its disorders is reflected in many scientific publications and recognized by a long list of distinguished awards. As a former member of the Editorial Board (now the Advisory Board) of Brain and, from 2000, Editor-in-Chief of Clinical Neurophysiology, Dr Hallett is ideally qualified to guide our editorial process on the many papers submitted that relate to movement and its disorders. Since more of the 1345 new manuscripts papers submitted to Brain in 2005 came from North America than any other country, we are additionally pleased to welcome a distinguished clinical neuroscientist from the USA to our board of Associate Editors.
That many sufferers from episodic migraine experience a crescendo frequency of headache in association with indiscriminate use of analgesics and other medication is not a new story; but Arnaud Fumal and a group from Liège, Belgium, and Aärhus, Denmark, report that, whereas metabolic dysfunctions in areas known to be associated with pain processing structures reverse with weaning from analgesics, there is persistent abnormality in the orbitofrontal cortex suggesting that these individuals are predisposed to drug dependence (page 543). Many studies seek to identify abnormal brain regions that anticipate the subsequent development of common neurodegenerative disorders. Based on a non-prejudicial screen using statistical parametric mapping, Christoph Scherfler and investigators from Innsbruck, Austria, now add to the list early diffusion-weighted and diffusion-tensor changes in the olfactory tract as a harbinger of Parkinson's disease—perhaps, not unexpectedly given the known frequency of anosmia in this condition (page 538). Global brain structure and function are studied by Sandra Witelson, Heather Beresh and Debra Kigar from Hamilton, Ontario, who (with some gender-related variations of theme) correlate prospective measures of verbal intelligence and visuospatial ability with brain size assessed at autopsy, raising issues with respect to ageing and imaging based surrogates of intelligence testing (page 386). These individuals were not known to have had neurological diseases in life, whereas Holger Schmidt and colleagues from Göttingen and Magdeburg, Germany, show that cognitive function is impaired long-term in patients recovering from meningitis, the impact on short-term and working memory, associative learning and executive functions being especially marked after bacterial infections (page 333); to some extent, these deficits could be predicted by severity of the acute neurological illness, and they correlate with subsequent brain atrophy. The consequences for global brain atrophy following a focal lesion are modelled in mice by Anna-Leena Sirén and investigators from Göttingen and Würzburg, Germany, and the Institute of Psychiatry in London who show that the secondary diffuse degeneration and its functional correlates are prevented by erythropoietin, adding to the status of that haematopoietic growth factor as a promising neuroprotectant (page 480). To date, the therapeutic role of individual growth factors has been disappointing, but Ann Logan and colleagues from Birmingham, UK, report that triple exposure to basic fibroblast growth factor, neurotrophin-3 and brain derived nerve growth factor acts synergistically to improve retinal ganglion cell survival and axonal outgrowth, through regulation of intramembraneous p75 neurotrophin receptor and shedding of the inhibitory molecule Nogo, thus reducing the inhibitory influence of Rho-A signalling (page 490). Protection from reperfusion ischaemic brain injury is described by Dong-Sheng Pei and a team from the Universities of Xuzhou, Hefei and Shanghai, China (page 465) who first show that this involves assembly of the GluR6/PSD-95/MLK3 molecular signalling complex, with activation of c-Jun N-terminal kinase (JNK) and phosphorylation of c-Jun and 14-3-3; this increases Fas ligand expression and bax translocation to the mitochondria with release of cytochrome c and caspase-3-activation—in short, energy failure and apoptotic cell death. Next, they show that this molecular cascade can be inhibited by the peptide construct Tat-GluR6-9c, thereby identifying another potential candidate for neuroprotection in the context of stroke. On the same general theme, Leonie Boven and investigators from Rotterdam and Amsterdam, Netherlands, suggest that the inflammatory response in evolving lesions of multiple sclerosis is curtailed at the point that macrophages ingest myelin and take on the appearance of foamy cells; now, they lack the ability to respond to inflammatory stimuli and no longer produce pro-inflammatory cytokines, only molecules that suppress inflammation (page 517).
Three papers focus on inherited disorders of the peripheral nervous system. Nens van Alfen and Baziel van Engelen from Nijmegen describe similarities and differences between 246 examples of idiopathic or hereditary neuralgic amyotrophy (page 438); against the typical background of pain lasting 
4 weeks, with motor and sensory involvement of discrete structures within the brachial plexus (most commonly the upper and middle trunks), and the majority of patients not making a satisfactory recovery even at prolonged follow-up, the hereditary forms present earlier, have more episodes, show involvement outside the brachial plexus, are weaker at peak severity, and do worse in the long term; differences in outcome and features observed during the acute phase are also dependent on gender. Elena Gallardo and colleagues from Santander, Spain, correlate detailed scores of motor function with MR appearances of limb muscles in 10 individuals with Charcot-Marie-Tooth disease type 1A; clinical severity correlates with the extent of fatty infiltration in muscles, spreading from the minimal appearance of abnormality in the pedal lumbricals (always resulting in pes cavus) to involvement of the lateral, anterior and superficial but not often the posterior compartments of the lower legs (page 426). Henry Houlden and investigators from University College London (including PK Thomas, former editor of Brain) and hospitals in East Anglia, UK, round up a large and deliberately heterogenous group of cases with sensory neuropathies—some known to be inherited and others not—and screen exons 5, 6 and 13 of SPTLC1, encoding serine palmitoyltransferase, finding mutations in one sporadic case and six of eight families with hereditary sensory and autonomic neuropathy type 1, all apparently originating from a common founder (page 411). There appears to be a marked variability in the clinical features and course amongst these cases sharing the same molecular lesion; thus, the phenotypic expression of this genotype is complex and presumably influenced by factors other than the point mutation in SPTLC1. Amongst the clinical features not well recognized is early and often severe motor involvement, especially in males. In ‘From the Archives’, we discuss an earlier publication in which the issue of motor involvement in hereditary sensory radicular neuropathy is debated, and the prescient conclusion reached that mixed motor and sensory phenotypes are indeed transitional examples of the same disorder (Campbell AMG, Hoffman HL. Sensory radicular neuropathy associated with muscle wasting in two cases. Brain 1964: 87; 67–74).
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Brain 1964 87: 67-74.[PDF]
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