We review the key developments in our understanding of subcorneal pustular dermatosis (SCPD, also known as Sneddon-Wilkinson disease) over the past 50 years. SCPD is a rare, chronic, sterile pustular eruption that was first described by Sneddon and Wilkinson in 1956. The primary lesions are pea-sized pustules classically described as half-pustular, half-clear flaccid fluid blisters. Histologically the salient feature is a subcorneal accumulation of neutrophils, suggesting the presence of chemoattractants such as tumour necrosis factor (TNF)alpha in the uppermost epidermis. However, to date its exact pathophysiology is unknown. Cases in association with pyoderma gangrenosum, benign monoclonal IgA gammopathy and multiple myeloma are well documented. There are anecdotal reports of SCPD associated with other internal malignancies such as chronic lymphocytic leukaemia, thymoma, apudoma and epidermoid carcinoma of the lung. The treatment of choice is dapsone. Therapeutic alternatives include retinoids, phototreatment with psoralen ultraviolet (UV) A, broadband or narrow band UVB and corticosteroids. Anecdotal uses of tacalcitol, ketoconazole, azithromycin, tetracycline, minocycline, vitamin E, ciclosporin, colchicine, mizoribine, mebhydrolin, infliximab and adalimumab with mycophenolate mofetil have all been reported.

Background: Carotid stenosis is a common cause of ischaemic stroke and transient ischaemic attack (TIA). Despite rising recognition and centralization of stroke services there has been a decline in interventions for carotid stenosis in recent years. The aim of this study was to determine the current prevalence and management of carotid stenosis in the UK. Methods: This was a 1-year prospective observational study of consecutive patients presenting with ischaemic stroke, TIA or ischaemic retinal artery occlusion to a central London hyperacute stroke unit. Patients with significant carotid stenosis, defined as atherosclerotic narrowing of 50 per cent or greater, underwent multidisciplinary team (MDT) discussion to determine the cause of stroke/TIA and classify carotid stenosis as symptomatic or incidental. Results: In total, 2707 patients were seen; half had an ischaemic event and the majority had carotid imaging (1252 of 1444). Carotid stenosis of at least 50 per cent was seen in 238 (prevalence 19⋅0 (95 per cent c.i. 16⋅6 to 21⋅4) per cent). Patients with significant carotid stenosis were more likely to have hypertension, hypercholesterolaemia, diabetes and ischaemic heart disease. Carotid stenosis was deemed symptomatic in 99 patients (7⋅9 (6⋅3 to 9⋅5) per cent); of these, 17 had carotid occlusion, 17 were unfit for surgery and 58 patients were referred for carotid intervention. Among 139 patients with asymptomatic stenosis, 75 had carotid stenosis ipsilateral to the stroke but, after MDT discussion, the cause was deemed to be atrial fibrillation (32), small-vessel disease (15), another determined cause (5), or not determined owing to atypical imaging or clinical presentation. Conclusion: Carotid stenosis is common, affecting one in five patients presenting with stroke or TIA. Careful MDT discussion may avoid unnecessary intervention and should be the standard of care.

Introduction -Identification of patients who will benefit from carotid endarterectomy is not entirely

Artifact (ATA) was present in 16/16 participants with severe stenosis (>70%), p <.001), and were associated with absence of anterior communicating artery (11/16, p=.003). ATA was the best predictor of recent symptoms in internal carotid artery stenosis (13/16 participants with ATA had symptoms, p=004).