SummaryBackgroundResults of small trials indicate that fluoxetine might improve functional outcomes after stroke. The FOCUS trial aimed to provide a precise estimate of these effects.MethodsFOCUS was a pragmatic, multicentre, parallel group, double-blind, randomised, placebo-controlled trial done at 103 hospitals in the UK. Patients were eligible if they were aged 18 years or older, had a clinical stroke diagnosis, were enrolled and randomly assigned between 2 days and 15 days after onset, and had focal neurological deficits. Patients were randomly allocated fluoxetine 20 mg or matching placebo orally once daily for 6 months via a web-based system by use of a minimisation algorithm. The primary outcome was functional status, measured with the modified Rankin Scale (mRS), at 6 months. Patients, carers, health-care staff, and the trial team were masked to treatment allocation. Functional status was assessed at 6 months and 12 months after randomisation. Patients were analysed according to their treatment allocation. This trial is registered with the ISRCTN registry, number ISRCTN83290762.FindingsBetween Sept 10, 2012, and March 31, 2017, 3127 patients were recruited. 1564 patients were allocated fluoxetine and 1563 allocated placebo. mRS data at 6 months were available for 1553 (99·3%) patients in each treatment group. The distribution across mRS categories at 6 months was similar in the fluoxetine and placebo groups (common odds ratio adjusted for minimisation variables 0·951 [95% CI 0·839–1·079]; p=0·439). Patients allocated fluoxetine were less likely than those allocated placebo to develop new depression by 6 months (210 [13·43%] patients vs 269 [17·21%]; difference 3·78% [95% CI 1·26–6·30]; p=0·0033), but they had more bone fractures (45 [2·88%] vs 23 [1·47%]; difference 1·41% [95% CI 0·38–2·43]; p=0·0070). There were no significant differences in any other event at 6 or 12 months.InterpretationFluoxetine 20 mg given daily for 6 months after acute stroke does not seem to improve functional outcomes. Although the treatment reduced the occurrence of depression, it increased the frequency of bone fractures. These results do not support the routine use of fluoxetine either for the prevention of post-stroke depression or to promote recovery of function.FundingUK Stroke Association and NIHR Health Technology Assessment Programme.

We present a practical overview of functional neurological disorder (FND), its epidemiology, assessment and diagnosis, diagnostic pitfalls, treatment, aetiology and mechanism. We present an update on functional limb weakness, tremor, dystonia and other abnormal movements, dissociative seizures, functional cognitive symptoms and urinary retention, and 'scan-negative' cauda equina syndrome. The diagnosis of FND should rest on clear positive evidence, typically from a combination of physical signs on examination or the nature of seizures. In treatment of FND, clear communication of the diagnosis and the involvement of the multidisciplinary team is beneficial. We recommend that patients with FND are referred to specialists with expertise in neurological diagnosis. FND is a common presentation in emergency and acute medical settings and there are many practical elements to making a positive diagnosis and communication which are useful for all physicians to be familiar with.

There have been many articles highlighting differences and similarities between complex regional pain syndrome (CRPS) and functional neurological disorders (FND) but until now the discussions have often been adversarial with an erroneous focus on malingering and a view of FND as ‘all in the mind’. However, understanding of the nature, frequency and treatment of FND has changed dramatically in the last 10–15 years. FND is no longer assumed to be only the result of ‘conversion’ of psychological conflict but is understood as a complex interplay between physiological stimulus, expectation, learning and attention mediated through a Bayesian framework, with biopsychosocial predisposing, triggering and perpetuating inputs. Building on this new ‘whole brain’ perspective of FND, we reframe the debate about the ‘psychological versus physical’ basis of CRPS. We recognise how CRPS research may inform mechanistic understanding of FND and conversely, how advances in FND, especially treatment, have implications for improving understanding and management of CRPS.

Functional neurological disorders are common problems in neurologic practice. In the past decade there has been an increasing interest in this group of disorders both from a clinical as well as research point of view. In this review, we highlight some of the most salient and exciting publications from recent years focusing especially on new findings illuminating mechanism and studies examining treatment.

BackgroundThe majority of patients presenting with suspected clinical cauda equina syndrome (CES) have no identifiable structural cause for their symptoms (‘scan-negative’ CES). Understanding these patients aids clinical differentiation and management in CES.MethodsA retrospective electronic note review was undertaken of patients presenting with suspected CES, defined as ≥ 1 of acute bladder, bowel, sexual dysfunction or saddle numbness, to a regional neurosciences centre. We investigated radiology, clinical features, psychiatric and functional disorder comorbidities and outcome of patients with ‘scan-negative’ CES and patients with MRI confirmed compression of the cauda equina (‘scan-positive’ CES).Results276 patients were seen over 16 months. There were three main radiologically defined patient groups: (1) ‘scan-positive’ CES (n = 78, mean age 48 years, 56% female), (2) ‘scan-negative’ CES without central canal stenosis but with lumbosacral nerve root compression not explaining the clinical presentation (n = 87, mean age 43 years, 68% female) and (3) ‘scan-negative’ CES without neural compromise (n = 104, mean age 42 years, 70% female). In the two ‘scan-negative’ groups (no neural compromise and nerve root compression), there were higher rates of functional disorders (37% and 29% vs. 9%), functional neurological disorders (12% and 11% vs 0%) and psychiatric comorbidity (53% and 40% vs 20%). On follow-up (mean 13–16 months), only 1 of the 191 patients with ‘scan-negative’ CES was diagnosed with an explanatory neurological disorder (transverse myelitis).ConclusionsThe data support a model in which scan-negative cauda equina syndrome arises as an end pathway of acute pain, sometimes with partly structural findings and vulnerability to functional disorders.Electronic supplementary materialThe online version of this article (10.1007/s00415-018-9078-2) contains supplementary material, which is available to authorized users.

IntroductionCauda equina syndrome (CES) is a potentially devastating condition caused by compression of the cauda equina nerve roots. This can result in bowel, bladder and sexual dysfunction plus lower limb weakness, numbness and pain. CES occurs infrequently, but has serious potential morbidity and medicolegal consequences. This study aims to identify and describe the presentation and management of patients with CES in the UK.Methods and analysisUnderstanding Cauda Equina Syndrome (UCES) is a prospective and collaborative multicentre cohort study of adult patients with confirmed CES managed at specialist spinal centres in the UK. Participants will be identified using neurosurgical and orthopaedic trainee networks to screen referrals to spinal centres. Details of presentation, investigations, management and service usage will be recorded. Both patient-reported and clinician-reported outcome measures will be assessed for 1 year after surgery. This will establish the incidence of CES, current investigation and management practices, and adherence to national standards of care. Outcomes will be stratified by clinical presentation and patient management. Accurate and up to date information about the presentation, management and outcome of patients with CES will inform standards of service design and delivery for this important but infrequent condition.Ethics and disseminationUCES received a favourable ethical opinion from the South East Scotland Research Ethics Committee 02 (Reference: 18/SS/0047; IRAS ID: 233515). All spinal centres managing patients with CES in the UK will be encouraged to participate in UCES. Study results will be published in medical journals and shared with local participating sites.Trial registration number ISRCTN16828522; Pre-results.

OBJECTIVECauda equina syndrome (CES) is a surgical emergency requiring timely operative intervention to prevent symptom progression. Accurately establishing the incidence of CES is required to inform healthcare service design and delivery, including out-of-hours imaging arrangements.METHODSA systematic literature search of MEDLINE, EMBASE, and Scopus was undertaken to identify original studies stating the incidence of CES, and the estimates were combined in a meta-analysis as described in the protocol registered with PROSPERO (registration no. CRD42017065865) and reported using the PRISMA guidelines.RESULTSA total of 1281 studies were identified, and 26 studies were included in the review. Data about CES incidence were available from 3 different populations: asymptomatic community populations, patients with nontraumatic low-back pain, and patients presenting as an emergency with suspected CES. The incidence of CES was 0.3–0.5 per 100,000 per year in 2 asymptomatic community populations, 0.6 per 100,000 per year in an asymptomatic adult population, and 7 per 100,000 per year in an asymptomatic working-age population. CES occurred in 0.08% of those with low-back pain presenting to primary care in 1 study, and a combined estimate of 0.27% was calculated for 4 studies of those with low-back pain presenting to secondary care. Across 18 studies of adults with suspected CES, 19% had radiological and clinical CES. Difficulties in comparison between studies resulted from the heterogeneous definitions of CES and lack of separation of more advanced CES with retention, which is unlikely to be reversible. In the studies of patients with suspected CES, the small sample size, the high number of single-center studies (18/18), the high number of studies from the United Kingdom (17/18), the retrospective nature of the studies, and the high number of abstracts rather than full texts (9/18) reduced the quality of the data.CONCLUSIONSFrom current studies, it appears that CES occurs infrequently in asymptomatic community populations and in only 19% of those presenting with symptoms. Determining accurate incidence figures and designing a bespoke service for investigation of patients with suspected CES would require a consensus clinical and radiological definition of CES and international multisite studies of patient pathways of investigation and management.

Aims: To study the frequency of pain, psychological, or functional disorders in patients with Fowler's syndrome. Methods: We carried out a retrospective chart review of patients with a diagnosis of Fowler's syndrome attending the Uro-Neurology centre at the National Hospital for Neurology and Neurosurgery between 2009 and 2013 looking at triggering events, physical and psychological comorbidities. Results: Of 62 patients with clinical and electromyographic diagnosis of Fowler's syndrome, 31 (50%) had unexplained chronic pain syndromes, 12 (19%) of these were taking opiates. Fifteen (24%) had ''functional'' neurological symptoms. Abdominopelvic surgery with general anesthesia was the leading trigger (n ¼ 21, 35%). Conclusions: We found high levels of co-morbidity with patients having some form of pain (50%), a probable functional disorder (24%), or psychological symptoms (31%). There are several potential explanations for this association including the effect of developing an apparently unexplained distressing condition, confounding effect of opiate use or referral bias. The findings suggest a need for prospective systematic study of comorbidity for this disabling condition. Neurourol. Urodynam. 35:601-603, 2016. # 2015 Wiley Periodicals, Inc.