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.

In sports medicine, chronic hip, groin and buttock pain is a common diagnostic problem. Because of the complex anatomy of this region and the many potential neurological causes for pain, few sports clinicians have a detailed understanding of this problem. This paper discusses the clinical aspects of nerve entrapment syndromes related to sport and takes a regional approach in order to provide a diagnostic framework for the general sports physician. The various neurological syndromes are discussed and the surgical management elaborated in detail. For some specific conditions, such as the so-called 'piriformis syndrome', the pathophysiological understanding has changed since the early descriptions and now this particular diagnosis is often ascribed to almost any cause of buttock and/or hamstring symptoms. We discuss the nature of the origin of local symptoms and note that the often described symptoms are more likely due to compression of structures other then the sciatic nerve. Furthermore, the role of piriformis hypertrophy or anatomical nerve variations in the genesis of this syndrome must be questioned. We suggest renaming this the 'deep gluteal syndrome' to account for all of the observed phenomena. As sports medicine continues to develop a scientific basis, the role of nerve entrapments as the basis for chronic symptomatology is undergoing a new understanding and clinicians need to be aware of the diagnostic possibilities and be able to advise patients accordingly on the basis of scientific fact not anecdotal fiction.

This surgical technique reduces pain and allows the majority of patients to return to sports; however, patients should be counseled that they may not be able to return to their preinjury level of exercise or remain pain-free.

Exercise-related leg pain is a common and yet difficult management problem in sports medicine. There are many common causes of such symptoms including stress fractures and muscle compartment syndromes. There are also a number of less common but important conditions including popliteal artery entrapment and nerve entrapment syndromes. Even for an astute clinician, distinction between the different medical causes may be difficult given that many of their presenting features overlap. This review highlights the common clinical presentations and raises a regional approach to the diagnosis of the neurogenic symptoms. In part, this overlapping presentation of different pathological conditions may be due to a common aetiological basis of many of these conditions namely, fascial dysfunction. The same fascial restriction that predisposes to muscle compartment syndromes may also envelop the neurovascular structures within the leg resulting in either ischaemic or neurogenic symptoms. For many athletes with chronic exercise-related leg pain, combinations of such problems often coexist suggesting a more widespread fascial pathology. In our clinical experience, we often label such patients as 'fasciopaths'; however, the precise pathophysiological basis of this fascial problem remains to be elucidated. This review discusses the various nerve entrapment syndromes in the lower limb that may result in exercise-related leg pain in the sporting context. The anatomy, clinical presentation, investigation, medical management and surgical treatment are discussed at length for each of the syndromes. It is clear from clinical experience that the outcome of surgical management of such syndromes fares much better where a clear dermatomal pain distribution is present or where focal weakness and/or sensory symptoms appropriate for the nerve are present. In many situations, however, nonspecific leg pain or vague nonlocalising sensory symptoms are present and in such situations, alternative diagnoses must be considered and investigated appropriately. As mentioned above, many different pathologies may coexist in the lower limb and may be a source of confusion for the clinician or alternatively may be the reason for poor treatment outcomes.

Analysis 1.4. Comparison 1 Open or arthroscopic subacromial decompression versus active non-operative treatment or placebo for impingem., Outcome 4 Success (reduction of 100% pain score from baseline). . . . . . . . Analysis 1.5. Comparison 1 Open or arthroscopic subacromial decompression versus active non-operative treatment or placebo for impingem., Outcome 5 Success and partial success (reduction 100% pain score or reduction 51-99% pain score from

GRADE Working Group grades of evidance High quality: Further research is very unlikely to change our confidence in the estimate of effect. Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate. Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate. Very low quality: We are very uncertain about the estimate.

Proximal hamstring syndrome occurs mainly in patients participating in competitive sports. Release of the proximal hamstring tendons in this active group resulted in decreased pain and increased strength, and the majority of patients were satisfied with the procedure.

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