Editorial
Vision is the favoured template in systems neuroscience for understanding how the brain works—from stimulus to perception, consciousness and behaviour. With its many special properties, some better developed in lower species but not evolutionarily conserved, seeing clearly is not the exclusive property of human primates. Yet the ability to relate the experiences of what it is to see and perceive, the relationship of vision to other sensibilities, the neuronal connectivity of the visual and other systems, the ability selectively to activate and study this feature or that, and the rich but tragic clinical repertoire of disordered vision have sustained the activities of many individuals working in clinical and basic neuroscience over several generations. Now, as Brain and Visual Perception, Oxford University Press have published the collaborative work of David Hubel and Torsten Wiesel, Nobel Laureates for Medicine or Physiology (1981, with Roger Sperry), with reprintings and commentaries on their joint work from 1958 to 1983. Aside from the content, this is a lovely book: sewn, the gathers bound in blind-stamped cloth with a headband and attractive dust wrapper; the free text in single column with a modern font and high-resolution illustrations; and the papers reset and presented in double-column format. In Measuring sight by sound, Semir Zeki tells the story of that collaboration and, with admiration and affection, adds another dimension to the historical record (page 1226). This is the story of V1, and the case for a hierarchical model of visual perception. It does not stray much outside area 17. Professor Zeki is at pains to establish that the scientific achievements of Hubel and Wiesel over this period were nothing if not systematic, one discovery building on another, despite the authors' claim to the repeated element of chance (in that, following another disarmingly modest giant of neuroscience, Sir Alan Hodgkin in Chance and Design, Cambridge University Press, 1992). In the best tradition of expert commentators, Zeki—himself no slouch when it comes to major insights into late 20th century vision neuroscience, and the discoverer of V5—leaves the stage entirely to his two players, making only one brief appearance to applaud, and in a joke at his own expense.
The present issue of Brain contains three papers on multiple sclerosis. Why the phenotype of demyelinating disease appears to be different in Asians and Japanese compared with Europeans is not well understood, and any hypothesis needs to take account of the apparent shift in frequency from the opticospinal to the so-called Western phenotype in individuals born during the last 40 years. A complex interplay of genetic, environmental and societal factors seems likely. Takaaki Ishizu and colleagues from Kyushu, Japan (page 988) back the possibility that these variations in clinical features reflect different immunological mechanisms: by studying a catalogue of cytokines and chemokines in samples of cerebrospinal fluid, they describe profiles of biomarkers for the two clinical phenotypes, and the mediators that are elevated in both, suggesting how these players might orchestrate distinct pathological processes. But the analysis leaves unanswered the issue of whether the complexity also denotes disease heterogeneity or merely divergent pathways downstream of the triggering events. Kakuri Omari, Gareth John, Stuart Sealfon and Cedric Raine from New York describe the upregulation of chemokine receptors on cells of the oligodendrocyte lineage in tissue from individuals with multiple sclerosis (page 1003): the corresponding ligands, expressed by astrocytes, are present in active lesions, and their production is stimulated in vitro by interleukin-1ß and interferon-
, suggesting to the authors a further role for the inflammatory process in promoting remyelination. Based on magnetic resonance spectroscopic studies at 3 Tesla, Radhika Srinivasan and colleagues from San Francisco suggest that oligodendrocyte depletion prevents glutamate removal in acute demyelinating lesions of multiple sclerosis and normal-appearing white matter but not chronic plaques, thus providing further indirect evidence for an excitotoxic contribution to acute axonal injury, in addition to the effects of nitric oxide already proposed (page 1016).
Ten years ago we published a study of superficial siderosis resulting from neuronal and glial loss due to deposition of ferritin following haemorrhage into the cerebrospinal fluid (Fearnley et al., Brain 118: 1051–66). Now, prompted by considerations of the cognitive role of the cerebellum, Natasja van Harskamp and members of the same team describe the neuropsychological and behavioural characteristics of this disorder (page 1082). All six patients showed impairments of speech, visual recall and executive function; theory of mind analyses revealed an impaired ability to represent other people's mental states, indicating a highly selective impairment of social interaction, attributable to dysfunction of the cerebellar vermis—selectively involved in superficial siderosis. This association resonates with the implication of cerebellar abnormalities in autism. Jeanne Bell and a team from Edinburgh representing the Scottish Paediatric Pathologists and Neuropathologists describe the findings in an epidemiologically defined resource of 70 children dying with neonatal asphyxia (page 1070). Using histological markers that separate antepartum from perinatal insults, they correlate neuronal karyorrhexes and increased ß-amyloid precursor protein deposition with birth asphyxia, especially when complicated by seizures; both are more sensitive and discriminating than ‘routine neuropathological examination’. Mechanistically, the findings suggest that neuronal damage is not just the result of discrete insults; rather the implication is for ongoing neuronal injury related to hypoxia and ischaemia. A population cohort studied prospectively for cognitive decline with assessments at five time points over a 9-year period yielded 215 cases of Alzheimer's disease amongst the 1265 participants from France (page 1093). Hélène Amieva and colleagues from INSERM units 593 and EO338 and the University of Bordeaux show that most were below baseline from the earliest assessments, with acceleration in the deterioration of cognitive performance in the 3-year run-up to presentation. The suggestion is made that this decline might be checked by strategies for cognitive education. At the practical level, when and what to biopsy in order to classify the individual with peripheral neuropathy is a common clinical conundrum: Jun Li and colleagues from Wayne State University, Detroit (USA), the University of Genova (Italy) and Limoges (France) show that skin biopsy provides a sufficient sample from which to make an accurate diagnosis of hereditary sensory motor neuropathy, achieving both a histological (with some novel features) and molecular genetic confirmation of PMP22 duplication or deletion (establishing the diagnoses of CMT1A and hereditary neuropathy with liability for pressure palsies, respectively; page 1168).
Warren Blume, Samuel Wiebe and Lisa Tapsell from London, Ontario (page 1209) define anterior, medial and lateral boundaries of the occipital lobe and use subdural recordings and/or the response to local resection to localize the epileptic focus in 41 patients with occipital epilepsy to mesial (20), lateral (11) or both (10) structures, respectively. Preoperative field defects, unformed visual auras and contralateral versive eye movements occurred more often in the mesial and mixed compared with the lateral cases. Conversely, abnormalities of the scalp electroencephalogram were observed in the lateral cases but in none of those with a mesial origin of seizures. Thus, seizure semiology may suggest a mesial origin and abnormalities of the scalp electroencephalograph a lateral source, but accurate localization within an occipital lobe requires subdural electrical recordings. Ten years ago, the surgical experience of Wilder Penfield (see From the Archives, April 2005), Theodore Rasmussen and Andre Oliver in patients with occipital epilepsy was reported from the Montreal Neurological Institute (Salonova et al., Brain 1992: 115; 1655–80). In turn, that report drew on the classical literature concerning the electrical properties and localization of function in the occipital lobe based on the writings, inter alia, of Sir David Ferrier and Sir Edward Sharpey Schäfer. Their exchanges were often acrimonious. We review Schäfer's two articles on the functional anatomy of the temporal and occipital lobes and the localization (or not) of vision, hearing, memory, taste and olfaction in From the Archives. Whereas the intimate visual experiences of monkeys studied by Schäfer and Ferrier were taken to their simian graves, Warren Blume and colleagues (drawing on the writings of Wilder Penfield, David Hubel, Torsten Wiesel and Semir Zeki, amongst others) are able to describe the unformed and formed experiences (coloured monsters, converging walls, complex colours, and enlargements) in their patients with occipital epilepsy.
Cambridge, UK
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