Editorial
The previous issue of Brain highlighted contemporary and historical work on the neurology of the symbols that individuals use to communicate (Brain 2005; 128: 1231–2, 1233–4, 1407–17). In ‘Talking up the use of language,’ Colin Renfrew reviews The first idea: how symbols, language and intelligence evolved from our primate ancestors to modern humans by Stanley Greenspan and Stuart Shanker. He brings an archaeological perspective to the interplay between language and the development of social behaviour (page 1763). Lord Renfrew is Professor Emeritus of Archaeology in the University of Cambridge, and in the McDonald Institute for Archaeological Research. His influential work on the origins of European culture and the Indo-European language has been recognized through the award of many international prizes. The idea that genetic mutations first enabled humans to speak seems undeniable, but when these events occurred, and how the processes evolved, are less clear. As Professor Renfrew outlines, the important concepts were first formulated in Charles Darwin's On the origin of species (1859), and in the meeting of minds involving Sir John Evans, Joseph Prestwich and Boucher de Perthes, in the same year, over the gravel pits of the Somme, where flint tools were found stratified with the bones of extinct mammals. Around 150 years later, the archaeogenetic evidence from mitochondrial DNA andY-chromosome dendrograms suggests rather little difference between the child born in 2005 and the offspring of Homo sapiens sapiens born 85000 years ago. Therefore, Professor Renfrew argues that changes in human behaviour have depended more on social and cultural development than on genetic mutations. In turn, the emergence of activities such as seafaring, agriculture and urbanism depended on language and the ability to store its messages in writing and symbolic artefacts. Homo erectus may even have possessed some of these cognitive abilities. Colin Renfrew explains how symbolic cognition is a product of social interaction and engagement with the material world, the skills being maintained in social groups through the learning that each new individual acquires during childhood. Thus, as Greenspan and Shanker set out with respect to the psychology of behaviour, and Professor Renfrew explores further in his analysis, ontogeny in the individual rehearses the story of phylogeny in the species, but on a timescale measured in years rather than the 40 millennia it took to establish these social and behavioural traits.Among the original publications in this issue, two papers address morbidity in children with epilepsy. Ron van Empelen and colleagues from Utrecht show that surgical procedures for epilepsy are not only effective for seizure control but may lead to improvements in motor performance in children with associated cerebral palsy (page 1536). Drawing on much the same clinical material, Kim Oostrom and others writing on behalf of the Dutch Study of Epilepsy in Childhood (page 1546) show that premorbid learning and behavioural characteristics, and parental attitudes, correlate better with cognitive outcome than the features of the seizures, their frequency or the requirement for drug treatment. Heidrun Golla, Peter Thier and Thomas Haarmeier from Tübingen address a controversial issue in systems neuroscience: is the concept of a cerebellar cognitive affective syndrome valid? They use saccadic eye movements in patients with cerebellar disorders to assess ‘attentional dysmetria’ under conditions that separate the accuracy of movements from responses requiring overt and covert shifts in attention. Their position is that ‘the contributions of the cerebellum to attention are confined to overt manifestations based on goal directed movements’. Mireia Coma and colleagues from Barcelona (page 1613) contrast the neuroprotective effect of oestrogen on amyloid ß-peptide induced toxicity of neurones with the stimulation of endothelial nitric oxide synthase and, hence, enhanced injury of endothelial cells—findings that have implications for oestrogen exposure in vascular disorders where oxidative stress contributes to the pathogenesis. In contrast, Jian Wang and Stella Tsirka from Stony Brook, New York, demonstrate the increased expression of matrix metalloproteinase-9 in neurones and endothelial cells in a mouse model of intracerebral haemorrhage. A broad spectrum metalloproteinase inhibitor provides neuroprotection with less inflammation, oxidative stress and brain oedema, and with functional improvement after the vascular insult. Also on the subject of stroke, Graham Teasdale and members of the Davie Cooper Scottish Aneurysm Study Group show a 2% recurrence risk for the relatives of probands with subarachnoid haemorrhage, the risk being highest in first-degree relatives (page 1677). An increased rate in families with more than one affected person, and reductions in risk with genetic distance from the proband, suggest genetic loading; however, overall, recurrence is low, and screening is indicated only in families with more than two affected members. Among other papers on neurogenetics, Adriano Jimenez-Escrig and colleagues from Madrid, Spain, describe four pedigrees from a genetic isolate with a new autosomal dominant late onset form of Alzheimer's disease. Onset is in the sixth decade, with dementia, seizures, myoclonus and Parkinsonism. The pathology shows neocortical neuritic plaques and neurofibrillary tangles, amyloid angiopathy and Lewy bodies. Linkage to existing loci is excluded, leaving the mutation handed down by the 18th-century founder yet to be determined. Also from Spain, Maria Sobrido and a team from several centres describe a single large multigenerational pedigree with dominantly inherited congenital fibre type disproportion myopathy affecting proximal limb and paraspinal muscles. Here, onset is in infancy but ambulation is preserved into adult life. Muscle histology is reasonably stereotyped among affecteds but not specific. Although the family is adequately powered for genetic analysis, once again the locus and gene mutation have yet to be mapped and identified.
Vestibular influences on the optokinetic response involved in gaze stabilization of rolling targets are described by Christine Lopez and colleagues from Marseille in 17 patients undergoing curative unilateral vestibular neurotomy for Ménière's disease (page 1511). As expected, torsional optokinetic responses are differentially influenced following stimulation of the damaged or intact side. Contralesional responses are decreased, whereas those from the denervated side are increased. The pattern changes but does not fully compensate over time. Thus, despite relief from vertigo, the persistent asymmetrical activity suggests a mechanism whereby impairment of normal torsional optokinetic nystagmus contributes to the long-term symptoms of unilateral vestibular loss. Quantitative measurement of vestibular function has a long history in clinical neurology. In ‘From the Archives’ we review three papers written by Gerald Fitzgerald, C. E. (Charles) Hallpike and (Sir) Terence Cawthorne in 1942 describing the human labyrinth in a variety of clinical situations, and supporting a novel synthesis of how the central nervous system integrates vestibular information.
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