Editorial
Colin Blythe was put on to bowl his slow left-arm spinners on the last afternoon of the 1907 Headingley (cricket) test match against South Africa. He took eight wickets at little cost, winning a close match and securing the series for England. But the feat left him ‘completely knocked up’ and the selectors seldom picked him again since Blythe ‘suffered from strain on his nervous system caused by playing in a test match, and the effect lasts for some time’ (see Colin Blythe by Christopher Scoble, 2005: reviewed by Mick Imlah, Times Literary Supplement, July 1, 2005). A nervous disposition did not prevent Blythe being drafted to Flanders with the King's Own Yorkshire Light Infantry where, on November 8, 1917, a shell landed on his unit such that ‘One moment he was alive, the next he was dead.’ Many soldiers who survived the War also suffered strains on their nervous system. In ‘War and mental health: shell shock, battle exhaustion and PTSD’, Edgar Jones reviews Forgotten Lunatics of the Great War by Peter Barham; Hysterical Men, War, Psychiatry, and the Politics of Traumas in Germany, 1890–1930 by Paul Lerner; and Medicine and Victory, British Military Medicine in the Second World War by Mark Harrison. As professor of the history of medicine and psychiatry at Kings College, London, Professor Jones is well placed to explain how the experiences of those driven mad by war exposed deficiencies in the prevailing concepts of mental illness that led eventually to a radical change in attitudes, and revision of the asylum system. He discusses the emerging role of the scientific expert in society, and the tactics adopted by the French, German and British authorities for managing neuropsychiatric casualties, with the general aim of rapid return to the frontline, or—when, as was often the case, this failed—redeployment within the war economy. Edgar Jones identifies the best contemporary account of activities and outcomes of the four ‘Not yet diagnosed, nervous’ (NYDT) centres (War—neurasthenia, acute and chronic by D.W. Carmalt Jones. Brain 1919; 42: 171–213: ‘my plea is for men whose disabilities are as real and creditable as any wound...’). He considers whether the various functional somatic conditions defined after each major conflict—shell shock, exhaustion, low moral fibre and post-traumatic stress disorder—are identical or conditioned by the sociopolitical climates in which the various wars were waged. Professor Jones compares sympathetic treatment of the soldier who has fought hard and earned a ‘breakdown’ with the understandable wish of rational men and women to avoid injury and death by feigning symptoms: ‘war comes with a costly price tag in terms of mental health [for which] the only effective preventative measure is the maintenance of peace’.
The present issue contains four papers describing clinical and neuropathological features of the dementias. With Teodoro Del Ser and John Woulfe, David Munoz (page 1962) comments on the first large reported series of cases with semantic dementia, from Rhys Davies and others members of John Hodges' group in Cambridge (page 1984). His own paper with Andrew Kertesz and colleagues from London and Toronto, Ontario on the evolution and pathology of frontotemporal dementia (page 1996) correlates the various clinical syndromes making up this syndrome with their underlying pathological substrates. Each histological pattern favours a particular clinical phenotype, but the correlations are inexact. Thus, although the tau negative forms typically affect individuals with the behavioural variant of frontotemporal dementia, and the tauopathies are more usually seen in primary progressive aphasia, corticobasal degeneration and progressive supranuclear palsy, there is much overlap and a tendency for everything to merge with time. Debra Fleischman and authors from Chicago and Palo Alto report a prospective study showing that quantitative measures of Alzheimer pathology in the enterorhinal cortex correlate with impaired ante mortem performance on conceptual but not perceptual tests of implicit memory (page 2006); thus, particular memories are mediated by regions that are more or less affected by the neuropathology of Alzheimer's disease. This study assessed individuals in Religious Orders who also consented to autopsy, but Joseph Warren and investigators from the National Hospital for Neurology and Neurosurgery in London analyse the dividend for diagnosis of dementia from brain biopsy in life amongst a series of 90 cases sampled between 1989–2003 (page 2016); of these, 57% provided histology that was considered conclusive and, of the remainder, non-specific gliosis was the usual finding. Complications were appreciable (11%) but not long-lasting. The only biomarkers that might have avoided the need for obtaining brain tissue were cerebrospinal fluid pleocytosis indicating a potentially treatable inflammatory disorder. The diagnosis of Creutzfeld–Jacob disease (CJD) was made in 12%. Henriette Tschampa et al. from the Universities of Bonn, Göttingen and München evaluate the role of MRI in the diagnosis of CJD during life (page 2026). With some interobserver variations, the presence of hyperintensity in the caudate nucleus and putamen was agreed in 
50% of the 60 scans from individuals with CJD amongst 193 screened. MRI had high sensitivity (60–71%) and specificity (82–89%) for the diagnosis. Conversely, the detection of 14-3-3 protein in cerebrospinal fluid had a sensitivity of 91% and specificity of 44%; and the sensitivity of an abnormal EEG was 32% and its specificity 94%, respectively.
The medical applications of stem cell biology have yet to be realized, either as spare parts or as sophisticated delivery systems, but expectations are high. Ghazaleh Tabatabai and co-workers from departments of neuro-oncology, haematology and neurology in Tübingen, and neurosurgery and neuropathology in Erlangen, Germany report that adult human and murine haematopoetic progenitor cells show trophism towards glioma cells but not normal neurones (page 2200); the effect is mediated by a molecular pathway that involves the CXC chemokine and its ligand CXCL-12, matrix metalloproteinase-9, stem cell factor and transforming growth factor-ß. Here is a cell that is accessible and homes to glioma cells, where it could usefully deliver a lethal payload. On page 2189 Morten Moe and Mercy Varghase on behalf of co-authors from the Karolinska Institute in Stockholm and the Rikshospitalet in Oslo describe the developmental profile of multipotent progenitor cells harvested from the human temporal lobe; they differentiate into neurones expressing voltage-gated ion channels that propagate action potentials with mature waveforms and show neurotransmission across 
-amino butyric acid and glutamatergic synapses.
Apart from access to tissue, removal of the temporal lobe for the control of epilepsy provides other opportunities to study the human brain. Working in Uppsala, Sweden, Salomen Henschen first accurately charted projections of the retina through the visual pathways to the calcarine fissure (Kort öfversigt af lären om lokalisation I hejernbarken. Uppsala, LäkFören. Forh 1888; 27: 507–et seq., 601–et seq., and On the visual path and centre. Brain 1893; 16: 170–180). The details were finally elaborated by Harvey Cushing, Gilbert Horrax and Gordon Holmes. Much of their work derived from the neurosurgery of tumours and gunshot wounds, and included the clinicoanatomical correlation between superior quadrantinopia and damage to those lower fibres of the optic radiation that leave the upper tract and loop into the temporal lobe. On page 2123, Jason Barton and colleagues from Harvard Medical School and the University of British Columbia return to the anatomy of Meyer's loop. They report on correlations between the field defects in 24 patients undergoing temporal lobectomy for control of epilepsy, and an imaging based analysis of resection length along the anterior temporal–occipital pole line. Field defects were defined on the basis of area lost for three dioptres, with a novel scale for quantifying central vision. They conclude that the limit of Meyer's loop is 24–28 mm from the anterior temporal pole; resections in excess of 70 mm risk the lower quadrantic field; lack of congruity is confirmed with the nasal defect proving 15% larger than the temporal, whichever hemisphere is affected; the macula is not spared when the quadrantinopia exceeds 61%, and this corresponds to a resection length of 58 mm; the defects have a horizontal lower limit or slope down to the point of fixation. The authors propose a revised model for Meyer's loop in which the retinotopic organisation imposes a 90o rotation of the visual field—the most anterior fibres of Meyer's loop representing the superior field, not the vertical meridian as previously assumed. In From the Archives, we describe two papers from 1958 that also sought to define the significance of Meyer's loop for visual field defects following anterior temporal lobectomy for epilepsy.
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