Editorial

Amongst the many questions for which society looks to neuroscience for an answer is whether differences exist between man and animals other than the obvious alterations in structure dependent on evolution. Faced with much diversity of opinion and ambiguity on this and related topics, the thinking person can often turn with confidence to the analyses and formulations of Ray Tallis—philosopher, literary critic, poet, novelist and former professor of gerontology in the University of Manchester. Professor Tallis is never afraid to say what he thinks. He has particularly trenchant views on flaky philosophy; and, at a time when its general interest and influence on society have made neuroscience something of an intellectual fashion accessory, Ray Tallis is an ardent neuro-protectionist. Most recently he has tackled the literary critic masquerading as neuroscience groupie—proving not very flattering to AS Byatt in commenting on her neuronal formulation of why reading John Donne is thrilling, dimming the seductive bright fMRI lights of the ‘John Donne centre’ (anterior cingulate and striatum) and the search for ‘love amongst the neurones’ (see the Times Literary Supplement for 11 April 2008). Rather, Professor Tallis argues that cramming mind back into the cranium is mere neuro-mythology, brain being necessary but not sufficient for mental experience; and that cognition and consciousness belong to a community of minds, not the individual. Professor Tallis argues that not only in the realm of creativity are we distanced from animals, rejecting the unhelpful simplifications and de-mystifying stance of materialism that sees aesthetic appreciation as nothing more than brain activity, gently evolved over many millions of years but common to animals and man.

In reviewing The human animal in Western art and science by Martin Kemp (page 3103), Professor Tallis brings wit and wisdom to his analysis of why, especially in Greek medicine and Renaissance art, animals were used to represent and explain human natures—the majestic lion, he with piggy eyes, the foxy gentleman—and how this animalization extends into the fable and metaphor of La Fontaine and Narnia, and the less palatable freak and circus shows exhibiting the Elephant-Man and the Man-Monkey (William Henry Johnson). But in rehearsing contemporary value judgements of individuals, society and literary commentators, Professor Tallis declares co-registration of animals and man on the same metric as mistaken, and closure of the gap between slime-mould and homo sapiens as plain wrong. He applauds Martin Kemp in considering that, although the origin of the species is animal, our evolved state is not retrospectively and reciprocally embedded within those ancestors: ‘thus we are human animals but animals are not human’. And in concluding with an optimistic and lofty view of humankind that recommends leaving behind the foothills of nihilism that perpetuate a naturalistic account of humanity, Ray Tallis deplores the man–machine metaphor and the forcing of aesthetics, consciousness and personal identity back into the skull.

Amongst six papers on movement and balance in the current issue, Andreas Zwergal and colleagues from Munich (Germany) describe 14 patients with discrete lesions of the anteromedial pontomesencephalic hindbrain in whom the vertical is subjectively displaced in the roll plane in the absence of any other ocular symptoms or signs, observations that stimulate lesion tracking in primates leading to the identification of a graviceptive pathway running close to the medial lemniscus and connecting the vestibular nuclei to the ipsilateral posterolateral thalamus (page 2928). Sigurros Davidsdottir and investigators from Boston (USA) correlate veering in Parkinson's disease with laterality of motor symptoms to show that patients with left dominant symptoms are less able to use visual feedback in preventing the tendency to sway to the right through failure to perceive an egocentric midline rather than mistaking optic flow speed asymmetries (page 2882). And on navigation, Madeleine Fortin and a team from institutions in Montréal (Canada) compare the effect of early-onset and more recent blindness to show that those who cannot see have superior navigational skills and a bigger hippocampus than blindfolded individuals with normal vision, irrespective of when sight was lost (page 2995, and see cover).

In anticipation of clinical trials that evaluate new treatments for dementia, David Knopman and investigators from the Mayo Clinics (Rochester, Jacksonville and Scottsdale), San Francisco, Los Angeles and Seattle (USA) show measurable deterioration as part of the natural history in a cohort of patients with fronto-temporal dementia syndromes, recruited in sufficient numbers over a relatively short period, studied at baseline and 12 months for alteration in cognitive composites that assess language and executive function and two global measures, whereas behavioural scales are insensitive (page 2957). And in the context of sporadic Alzheimer's disease and fronto-temporal dementia, Stefan Klöppel and colleagues from Freiburg (Germany), London and Haywards Heath (UK), Scottsdale and Rochester (USA), Melbourne and Heidelberg (Australia), Paris (France) and Rome (Italy) assess whether neuroradiologists working independently and without consulting each other are better at classifying MR scans than support vector machines that can be exchanged between centres: the machines win both on sensitivity and specificity (page 2969).

Whether substance abuse alters brain structure is much debated. Maartje de Win and investigators from Amsterdam and Utrecht (The Netherlands) prospectively study markers of neuronal injury, connectivity and axonal integrity in drug-naïve individuals to show that those who subsequently use ecstasy acquire regional alterations in brain microvasculature, abnormalities of white matter maturation and non-specific axonal damage suggesting (but not yet confirming) that ecstasy is rapidly neurotoxic even after recent and modest exposure (page 2936). María-Salud García-Ayllón and a team from Alicante and Valencia (Spain) implicate the cholinergic system in the pathogenesis of hepatic encephalopathy showing that post-mortem levels of acetylcholinesterase but not choline acetyltransferase are increased in fatal hepatic coma and in a rodent model of liver failure in which the consequent reduction of acetylcholine is corrected by the acetylcholinesterase inhibitor, rivastigmine, whereas manipulating ammonia has no effect (page 2946). Teresa Sevilla and colleagues, also from Valencia (Spain), evaluate vocal cord and diaphragmatic function to show a high frequency of involvement in ganglioside-induced differentiation-associated protein 1 gene (GDAP1) mutations that develops late in the disease and—given the preferential involvement of the left recurrent laryngeal nerve—in a length-dependent pattern, culminating in life-threatening respiratory failure (page 3051). The four papers on aspects of demyelinating disease include work from Laura Piccio and investigators at St Louis (USA) and Milan (Italy) showing that soluble levels of the anti-inflammatory and pro-phagocytic ‘triggering receptor expressed on myeloid cells 2’ (sTREM-2) are increased in cerebrospinal fluid but not serum from individuals with relapsing–remitting and progressive multiple sclerosis, and the receptor is detected on monocytes and infiltrating macrophages from the lesions of affected individuals, suggesting that there may be mileage in therapeutic targeting of the TREM-2 pathway (page 3081).

On neurogenetics—Huntington's disease and various muscle disorders—Marie Louise Sveen and investigators from Copenhagen (Denmark) and Julie Murphy and her colleagues from Newcastle-upon-Tyne (UK), Dallas (USA) and Montréal (Canada) describe the effects of resistance training in Becker muscular dystrophy and mitochondrial cytopathy (pages 2824 and 2832; and see commentary, page 2809). For neurologists trained after the 1970s, the concept of mitochondrial disease as the basis for several myopathies and encephalopathies must seem commonplace. But these disorders, and elucidation of the biochemical pathways on which they depend, emerged at that time from the mists of nosological and mechanistic uncertainty and ambiguity. It is therefore appropriate that the Association of British Neurologists (ABN) should recently have recognized John Morgan-Hughes, one of the pioneers in this field, as the ABN Medallist for 2008 in recognition of his many contributions to the science and practice of neurology. In From the Archives, we review ‘A mitochondrial myopathy characterised by a deficiency in reducible cytochrome b by JA Morgan-Hughes, P Darveniza, SN Kahn, DN Langdon, RM Sherratt, JM Land and JB Clark (Brain 1974: 100; 617–640)’.