It was natural that most physicians appointed to the staff of the National Hospital for the Paralysed and Epileptic, Queen Square, after it opened in 1860, published versions of their lectures on the emerging discipline of clinical neurology; and many also wrote textbooks on the subject for students and practitioners. Some of this content was borrowed and much was based on astute observation of clinical cases, the experiments of nature; but of original research there was little, although several Victorian physicians did carry out laboratory studies in collaboration with Sir David Ferrier (1843–1928) and (Sir) Victor Horsley (1857–1916). Charles Edward Beevor (1854–1908) was appointed resident medical officer to the National Hospital in 1880; joined the staff as assistant physician in 1883; and, with responsibility for teaching, served soon after as first Dean of the Medical School. (Sir) Gordon Holmes (1876–1965) considered that, as a neurologist, Beevor was neither ‘distinguished nor an inspired teacher … courteous and considerate to his juniors, it cannot be claimed that his visits to the wards, which often lasted four hours or more, were popular’ (The National Hospital 1954; pp. 50–1). Methodologically industrious and scientifically cautious as a clinician, ‘ … no breath of slander ever passed his lips; his mind and thoughts were white and clear as those of a child. He never uttered an unkind word’ (Anon, Queen Square and the National Hospital 1860–1960; pp. 92–3). In 1886, Beevor was elected as a founder member of The Neurological Society of London; and he served as treasurer from 1894 to 1905, member of Council in 1893, vice-president in 1905–6, and as the Society’s last president in 1907-transferring in that capacity as foundation president of the section of neurology within the newly formed Royal Society of Medicine.

At their first meeting on 15 October 1907, held at 20 Hanover Square (London W1), Beevor was appointed by the Guarantors of Brain to the Committee of Management; and, with Horsley and (Sir) Henry Head (1861–1940), charged with negotiating terms with Macmillan and Co. But this was one of only four meetings of the committee that Beevor attended since he died suddenly aged 54, from ‘cardiac failure’, at his home (135 Harley Street London, W1) on 5 December 1908.

HK Lewis had published Beevor’s Diseases of the nervous system. A handbook for students and practitioners, a standard and highly successful work for its time, in the Lewis’s Practical Series (1898). Working with Horsley from 1883 to 1887 on the minute representation of movements in the cerebral cortex, Beevor had previously studied the impairment of action in muscles following cerebral palsy. This work formed the basis for his four Croonian Lectures delivered before the Royal College of Physicians in June 1903 and published as Muscular movements and their representation in the central nervous system (1904). Holmes acknowledges the importance of this contribution to neurology considering that ‘it did much to clarify fundamental questions on the cortical localisation of motor functions which had become confused in the spate of publications that followed the original investigations of (Eduard) Hitzig (1839–1907) and Ferrier’. Such was Holmes’s enthusiasm for the work that, on 7 March 1950, he advised the Guarantors to reprint Beevor’s 1904 Croonian Lectures; this was approved (500 copies at a cost of £192.10s.0d. plus 15% for charges from Macmillan, to be sold at 5s). As with most of the books and other occasional material published by the Guarantors, this did not sell especially well and the reprint failed to cover its costs.

Many of Beevor’s original articles, some co-authored with various colleagues, appeared in Brain: ‘On a case of tumour of the cerebellum with left hemiplegia’. Brain 1881; 4: 250–56; ‘On the condition of the knee-jerk, ankleclonus, and plantar reflex after epileptic fits in seventy cases; and on post-epileptic conjugate deviation of the eyes’. Brain 1882; 5: 56–61; ‘Case of glosso-labial paralysis, with progressive muscular atrophy and lateral sclerosis’. Brain 1882; 5: 403–11; ‘The cerebellar cortex’ Brain 1883; 6: 419–32; On the relation of the “aura” giddiness to epileptic seizures’. Brain 1884; 6: 487–96; ‘On staining “in toto” the central nervous system with Weigert's hæmatoxylin’. Brain 1885; 8: 239–42; ‘On Professor Hamilton’s theory concerning the corpus callosum’. Brain 1885; 8: 377–79; ‘A case of amyotrophic lateral sclerosis with clonus of the lower jaw’. Brain 1886; 8: 516–19 (see Brain 2012: 135; 2576–8); ‘On Professor Hamilton’s theory concerning the corpus callosum’. Brain 1886; 9: 63–73; ‘A case of almost complete anæsthesia with ataxia of the limbs’. Brain 1888; 11: 112–14; ‘Examination of the brain’. Brain 1889; 12: 349–57; ‘Case of tumour of the right temporosphenoidal lobe bearing on the localisation of the sense of smell and on the interpretation of a particular variety of epilepsy’. Brain 1889; 12: 346–9; ‘On some points in the action of muscles’. Brain 1891; 14: 51–62; ‘The accurate localisation of intra-cranial tumours, excluding tumours of the motor cortex, motor tract, pons and medulla’. Brain 1898; 21: 291–305; ‘A case of congenital spinal muscular atrophy (family type), and a case of hæmorrhage into the spinal cord at birth, giving similar symptoms’. Brain 1902; 25: 85–108; ‘On the pallio-tectal or cortico-mesencephalic system of fibres’. Brain 1902; 25: 436–43; ‘A contribution to the study of the cortical localisation of vision. A case of quadrantic hemianopia with pathological examination’. Brain 1904; 27: 153–62; ‘Removal of the gasserian ganglion’. Brain 1906; 29: 393–5; ‘On the movements of the tongue in hemiplegia, and from cortical stimulation—an apparent paradox; with a note on the movements of the tongue after paralysis of one hypoglossal nerve’. Brain 1907; 29: 487–93; and ‘The cerebral arterial supply’. Brain 1908; 30: 403–25.

Henry Head invited Dr Beevor to help in the selection of papers for publication in Brain from 1906. Now in our 136th year, the editorial team at Brain is, once again, very grateful to approximately 2500 reviewers who put aside time in 2012, many on several occasions, in order to help us select the 281 reviews, original articles and occasional papers published on 3844 printed pages as Volume 135. Apart from editorial material, we received 1997 original articles (an increase of 1.5% on 2011); 61 reviews (down by 7%); 37 occasional papers (up by 79%); 31 scientific commentaries (up by 61%), 13 book essays (steady); and 50 letters and responses (up by 30%) – a total of 2213 submissions. The Brain online system at Manuscript Central never closes (apart from occasional central down-time for maintenance); and, with 488 papers submitted in revision, we handled 2701 manuscripts, or 7.4 per day in 2012. The highest number of submissions, by country, came from the United States (21%) followed by the United Kingdom (15%); that order was reversed, exactly, for the percentage eventually accepted; other submissions came from Germany (10%), Italy (7%), France (6%), China (6%), The Netherlands (5%), Canada (5%), Australia (4%), Japan (3%), Spain (3%), Switzerland (2%), Belgium (2%) and 34 other countries making up the remaining 14%. We returned 49% of manuscripts without review, unreviewed beyond the editorial team, within 4.5 days of submission, for a variety of reasons, so that the authors could submit elsewhere without unnecessary delay; and a further 38% were rejected after review, the mean time to first decision slipping slightly to 37 days. Eventually, therefore, we rejected 87% of papers submitted as original articles; 87% of reviews; and 63% of occasional papers. We did not have a good year for producing issues online or in print on the designated date for each monthly issue. Most were late; and time from acceptance to publication online for each issue varied from 4.7 to 9.5 (range for individual papers, 2 to 12.8) weeks. The leading subject areas of papers published in 2012 were neurodegeneration and movements disorders (19%); neurogenetics (17%); Alzheimer’s disease and related disorders (16%); multiple sclerosis (6%); epilepsy (6%); stroke 6%); pain (5%); neuropsychiatry (5%); brain injury (4%); developmental disorders (3%) and with various other subject areas making up the remaining 13%. Authors opted for open access on 12% of manuscripts. Successful authors appeared well satisfied with the processing and appearance of their published article – those responding to a questionnaire giving an average score of 4.25/5 for speed, 4.25/5 for quality and 91% reporting that Oxford Journals provides a service equal to or better than other publishers. As usual, a proportion of those disappointed at not having their manuscripts reviewed or accepted appealed against those decisions; we aimed always to respond courteously to these cries of distress, variously expressed. Access to Brain increased in 2012. The combination of institutional, academic consortia and individual subscriptions was 6269; consortia deals and multi-site agreements increased slightly whereas, as in previous years, the number of personal and individual institutional subscriptions drifted down. Countless users have access to Brain's online content older than 12 months (back to 1996) as this content is free to all users. Electronic access increased by 3.73% in 2012 with more than 225 000 downloads per month either for HTML or PDF texts. Our impact factor increased marginally from 9.230 (2011) to 9.457 (2012) with a 5-year impact factor up from 10.143 (2011) to 10.545 (2012). Whilst the articles most often cited in Brain featured a variety of our sister journals, as well as ourselves, evidently that generosity of spirit was not so faithfully reciprocated by our competitors.

In the current issue, Mark Hallett reviews the newly published Marsden’s book of movement disorders, originally planned by David Marsden (1938–98) with Ivan Donaldson and now completed with the help of Susanne Schneider and Kailish Bhatia, setting out the lasting achievements of Professor Marsden, with whom Dr Hallett worked in London as a clinical fellow from 1975, and whose contributions to the science and clinical neurology of movement disorders are already legendary (page 682). Original papers on this topic include work by Sophie Winder-Rhodes and a team from Cambridge and London (UK) who show that 3.5% of patients with Parkinson’s disease derived from two population-based cohorts have pathological mutations of glucocerebrosidase (GBA), affected individuals progressing faster than others in terms of motor and cognitive decline (page 392). And Suzanne Lesage and colleagues from Paris, Lyon, Montpellier, Lille and Tours (France) and Montréal (Canada) extend the recently described association between mutations of C9orf72 and frontotemporal lobe degeneration and amyotrophic lateral sclerosis to include a small proportion of familial cases with the typical phenotype and drug responsiveness of Parkinson’s disease or related parkinsonian syndromes (page 385). Keith Josephs and investigators from Rochester and Jacksonsville (USA) assess the nature and degree of corticospinal tract degeneration in frontotemporal dementia with inclusions of TAR DNA-binding protein 43 (TDP-43) and highlight the association between severe and selective involvement of descending motor pathways without loss of lower motor neurons, and type-C pathology–long thick dystrophic neurites in the neocortex and Pick body-like inclusions in the dentate granular cells of the hippocampus–involving in particular the right temporal lobe and motor cortices (page 455).

Amongst five other papers on neurogenetics, Nancy Mokbel and colleagues from Sydney, Lucas Heights and Nedlands (Australia), London (UK), Helsinki (Finland), Rennes, Brest, Strasbourg and Grenoble (France), Bonn (Germany), São Paulo (Brazil) and Amsterdam (The Netherlands) add nemaline myopathy with arthrogryposis to the list of phenotypes associated with mutations in TPM2 and show that the disorder results from disrupted polymerization of beta-tropomyosin with consequential failure of incorporation into sarcomeres, and accumulation as nemaline rods leading to contractures through calcium-dependent hyper-contraction of muscle fibres (page 494). The mutation is an in-frame three base-pair deletion resulting in loss of a conserved lysine residue at the seventh amino acid position (p.K7del); and Ann Davidson and investigators from Ann Arbor, Springfield, Dallas, Marshfield and Iowa City (USA), Bristol, Birmingham and London (UK), and Dresden (Germany) add to this phenotype core-rod myopathy in familial autosomal distal myopathy and autosomal dominant trismus-pseudocamptodactyly syndrome, in which arthrogryposis is also a feature, modelling the molecular disruption to sarcomeres in zebrafish (page 508). Papers on tumours affecting the nervous system include work by Robin Doddrell and colleagues from Plymouth (UK), Buffalo (USA) and Erlangen (Germany) extending studies on loss of the Merlin tumour suppressor gene in schwannomas to show that alteration in specific transcription factors leads to loss of SOX10 protein with over-expression of platelet derived growth factor; correction of the SOX10 deficit in human Merlin null cells suppresses growth-factor dependent cell proliferation (page 549). Patrick Roth and a team from Zurich (Switzerland) and Tübingen (Germany) show that manipulation of αvβ3, αvβ5 and αvβ8 integrins, in vitro and in vivo, reduces the production of transforming growth factor on which many characteristics of malignant glioma–angiogenesis, invasiveness, stemness and local immunosuppression–may depend (page 564).

In one of two papers that deal directly with cerebrovascular disease, Yannick Béjot and colleagues from Dijon and Lille (France) ask whether the stable rates for intracerebral haemorrhage despite improved control of blood pressure reflect a rise in other causes; and they use incidence data gathered over 24 years to show a marked shift in the demography of brain haemorrhage with reduction in people aged ≤60 years and stable rates over the next decade but a sharp increase in those aged ≥75 years which they attribute to lobar haemorrhage resulting from use of anti-thrombotics in the elderly (page 658). They raise the issue of whether risk varies for different cerebral arteries. Many people consider that Charles Beevor’s most important research was his description of the arterial supply to the human brain. This was described, with much repetition, in two separate papers. The definitive version appeared in Philosophical Transactions of the Royal Society B (Charles E Beevor, ‘On the distribution of the different arteries supplying the human brain’ 1909; 200: 1–55), the paper having been read by David Ferrier on 5 December 1907 and submitted by him on 8 May 1908. Although Beevor did not live to see this in print, an abstract had appeared the previous year (Philosophical Transactions of the Royal Society B 1908; 80: 25–8). Beevor presented the specimens on which this work was based to a meeting of The Neurological Society of the United Kingdom on 14 July 1906; and he first published a detailed account of the studies in Brain (see above) as his presidential address to the Society given on 21 February 1907. Acknowledged as possessing rare artistic abilities, his work is based on fourteen horizontal (n = 2), sagittal (n = 6) and transverse (n = 6) brain sections, each of which was prepared as colour photographs and reproduced by the chromo-collotype process. ‘After many attempts he succeeded in injecting simultaneously the five arteries of the brain with different coloured substances held in solution in gelatine. By this means he determined exactly the blood supply to different parts of the brain and showed that the distribution of blood is purely anatomical and does not vary according to the physiological action of the parts’ [Leonard Guthrie, ‘Beevor, Charles Edward (1854–1908)’, revised, Caroline Overy, Oxford Dictionary of National Biography, Oxford University Press, 2004]. Of the fourteen original coloured images that were published, twelve survive. These came into the possession of Dr (Percy Whittington) Saunders (1877–1923), a Canadian physician appointed to the consultant staff of the National Hospital in 1916 who died from Hodgkin’s disease in 1923 [‘in a short, hard-working career, [Saunders] made his way, a stranger without social influence, entirely by his own merits and in spite of an ingrained reticence’ (Munk’s Roll 1955: IV; 555)]. The images passed to Dr James Purdon Martin (1893–1984) with a collection of Saunders’s books; from there, in 1967, to Dr Ralph Ross-Russell; thereafter to a drawer in the former Brain editorial office shared at that time with the Association of British Neurologists; and now destined, in due course, for the historical collection of the National Hospital for Neurology and Neurosurgery. The archive consists of a partial typescript summarizing the main findings, as reported in Philosophical Transactions of the Royal Society B, pp. 49–51); an explanation of lettering to the plates (pp. 53–5); a description of the colours depicting the distribution of the five main arteries [posterior communicating artery (brown); anterior choroidal artery (yellow); anterior cerebral artery (green); middle cerebral artery (carmine) and posterior cerebral artery (blue)]; and the twelve coloured images. The photographs are pasted to firm boards and with a transparent cover made of tracing paper on which is printed the outline contours of the main structures and the lettering that identifies each; on the back are figure legends but here there is a complication because, not only does the text not altogether match the legends that were eventually published, but the wrong texts are pasted to most of the photographic images, and numbering on the recto and verso of each is also incorrect. In From the Archives, we review ‘The cerebral arterial supply’ by Charles E Beevor, Brain 1908; 30: 403–25, reproducing the original coloured sections showing the distributions of the five arteries; and, for the benefit of those who may scrutinize this archival material in the future, we cross-reference the twelve surviving images (Figs 1 and 6 from the published paper are missing), text pasted on the verso of each, and corrections to the lettering made at proof stage with the relevant figures and their legends published in Philosophical Transactions of the Royal Society B and in Brain.