Editorial
Ever since Ronald Reagan declared the 1990s to be the Decade of the Brain, society has had high expectations of neuroscience. Superficially, this is an agenda for solving big problems; inter alia, the nature of consciousness (Brain 2004; 127: 2558–63), cures for Parkinson's and Alzheimer's diseases, and brain repair. But the relationship between neuroscience and society goes deeper. If behaviour in the individual is just robotic brain function, are we simply the slaves of ion flux across cell membranes and chemical activity at synapses; or is there free-will? Is it appropriate for society to seek retribution and compensation when individual behaviour is aberrant, and the product of a deranged brain or mind? To what extent might society reasonably protect itself by engineering, through whatever means, the development of brain and behaviour? And how can behaviour best be studied: are performance of the individual and brain activations in single subjects informative with respect to how everything works when people interact to form social groups? For many, the problems are enshrined in the philosophy that it makes no sense philosophically for the brain to try and understand itself. These and many other issues relating to the discipline of social neuroscience are hammered out by Raj Persaud in ‘Why the Brain Shouldn't be Medicine's Second Favourite Organ’ (to misquote a Mr Woody Allen). Professor Persaud reviews five books (21st Century Brain: Explaining, Mending and Manipulating the Mind by Steven Rose; The New Brain Sciences: Perils and Prospects edited by Dai Rees and Steven Rose; Essays in Social Neuroscience edited by John Cacioppo and Gary Berntson; The Neuroscience of Social Interaction by Chris Frith and Daniel Wolpert; and Psychosomatic: Feminism and the Neurological Body by Elizabeth Wilson) that tackle matters ranging from how the decent folk of Louisville listened to claims that psychotropic medication had caused a mass murderer to act ‘innocently’ and uncontrollably in response to his altered brain chemicals ... and then used their common sense in considering Eli Lilly not to have been responsible for disrupting impulse control in the late Joe Wesbecker, to the conceptual and practical problem of performing functional MRI in individuals actually participating in social activities rather than merely imagining such behaviours. Professor Persaud has used television and radio to engage the public in a better understanding of psychiatry, psychology and brain sciences in the interests of encouraging more informed access by those who need these clinical services. Unlike many doctors who move into the media, he remains firmly committed to the practice of medicine as a consultant psychiatrist in London. Why the Brain Shouldn't be Medicine's Second Favourite Organ reveals a writer familiar with neuroscience but also in touch with the legitimate curiosities of society, and admirably able to communicate that knowledge.Whether Alzheimer's disease will eventually be solved by melting away protein aggregates remains to be seen, but on page 1778 Yang Liu and colleagues from Germany, the United Kingdom, Russia and Hungary show that the lipopolysaccharide receptor (CD14), implicated in innate immunity, promotes the phagocytosis of exogenous amyloid-ß peptide-42 by microglia in vitro and in tissue samples from affected individuals. Tackling another challenge in neuroscience still unsolved from the Decade of the Brain, Xiaodong Wang and a team from the People's Republic of China (page 1897) report that structure and function of the canine sciatic nerve can successfully be restored across a 30 mm (1.08 inch) gap using an artificial conduit made of chitosan and filaments of polyglycolic acid. Five papers in this issue deal with epilepsy—from susceptibility to surgical solution. Gianpiero Cavalleri and investigators from University College, London, round up all the usual genetic suspects for temporal lobe and other forms of epilepsy and retest these in a cohort of 1191 patients, the sample size necessarily reduced operationally by the need to stratify for defined phenotypes (page 1832): now, since nothing previously described is confirmed, the epilepsy community must confront the lesson, learned by others studying complex traits, that allelic associations are fickle. Despite the difficulty of capturing seizures during functional MRI, Paolo Federico and colleagues from Victoria, Australia, show a variety of blood oxygen level dependent (BOLD) features lasting several minutes before the onset of seizures, and not necessarily localised to the immediate vicinity of the seizure focus (page 1811). But what happens as the fit develops? Stéphan Chabardès and others from neurosciences departments in Milan, Italy, describe electrical activity originating in the hippocampus, before or simultaneously with the temporal pole; rapid onset and evolution of the episode distinguish these two groups, and involvement of the temporal pole cortex predicts a favourable outcome following surgery (page 1818). In patients with successful surgical results, Eun Teon Joo and colleagues from Seoul and Goyan City, Korea, reveal a distributed network of decreased and increased fluorodeoxyuglucose PET activity ipsilateral to the side showing hippocampal sclerosis (page 1802). They conclude that these signals reveal the propagation pathways of ictal and interictal discharges in mesial temporal lobe epilepsy, the post-operative activations reflecting loss of afferents normally innervating the sclerotic structures. Seizures arise from abnormal activities across ion channels, but the channelopathies have a broader significance for contemporary neurology. On page, Matthew Kiernan and investigators from New South Wales and Victoria, Australia, report a study of patients with epilepsy having mutations of the sodium channel ß1 subunit. They show alterations in peripheral nerve excitability attributable to transient and persistent abnormalities of sodium channel conductance arising from a reduced number rather than the gating of individual channels. Sulayman Dib-Hajj and colleagues from New Haven and Indiana, USA, report a mutation of the Nav1.7 sodium channel encoded by SCN9A in dominantly inherited erythromyalgia (page 1847); this alters activation and steady-state inactivation, leading to lower thresholds for firing in dorsal root ganglion neurones, thereby accounting for the burning pain in response to warmth or exercise.
Faced daily with patients whose presenting symptom is headache, and knowing that the vast majority are unpleasant but innocuous in terms of structural brain disease, every neurologist has nonetheless had the experience of discovering, sooner or later, the underlying brain tumour that initially seemed so unlikely. Even the indiscriminate use of brain imaging at presentation in every person with headache does not altogether eliminate these nasty frights; nor is such defensive practice necessarily desirable. On page 1921, Miles Levy and the Headache Group at the Institute of Neurology, London, describe the headaches at presentation in 84 patients with pituitary tumour. Of these, 76% were ‘chronic’ or ‘migrainous’. Hypophysectomy made many better (49%) but some got worse (15%). Somatostatin analogues helped most (64%) of those with acromegaly; and dopamine agonists improved some (25% of the whole series), whereas others deteriorated (21%). A minority had invasion of tissues outside the pituitary fossa (21%). So, what mechanisms are responsible for these disparate headaches? The authors attribute the presenting symptom to a combination of tumour activity, disturbance of the cavernous sinus and individual predisposition to headache. This is an old story newly told. In From the Archives, we review the thoughts of Sir David Ferrier writing on this topic in the first volume of Brain (1879).
Cambridge, UK
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