Due to a variety of clinical manifestations anti-N-methyl-d-aspartate (NMDA) receptor encephalitis may be difficult to diagnose. Magnetic resonance imaging (MRI) may be used as a component of the workup for encephalopathy. However, the use of MRI in anti-NMDA encephalitis is complicated by wide-ranging reports regarding the frequency of normal MRI findings in this disease. Positron emission tomography (PET) is a modality of imaging that may assess functional rather than structural disturbances. Therefore, this review was conducted to summarise published studies regarding the use of MRI and PET in the diagnosis of anti-NMDA receptor encephalitis. The terms (MR OR magnetic resonance OR PET OR positron emission tomography) AND (NMDA encephalitis OR N-methyl-d-aspartate encephalitis) were used to search the databases PubMed, EMBASE and Scopus on 10/5/2017. These searches returned 1534 results. Sixty studies met the inclusion criteria. The results indicated that fewer than half of MRIs in anti-NMDA receptor encephalitis show abnormal findings. When abnormal findings are present they most commonly include T2/FLAIR medial temporal and frontal hyperintensity, and leptomeningeal contrast enhancement. Cortical grey matter changes were reported in the same number of patients as subcortical white matter changes. The only MRI finding with prognostic significance at this stage is progressive cerebellar atrophy. FDG-PET has been assessed in a few small studies and can demonstrate abnormalities in cases where MRI does not. Further research should aim for larger sample sizes and to report (and attempt to control for) the time between symptom onset and the scan being conducted, and pre-imaging treatments.

For over 80 years, spontaneous coronary artery dissection (SCAD) has been recognised as a cause of myocardial infarction. SCAD is described as a non-iatrogenic, non-atherosclerotic coronary artery dissection, resulting in formation of a false lumen or intramural haematoma in the coronary artery wall that compresses the true lumen, often compromising myocardial blood flow. In early literature, the incidence of SCAD in acute coronary syndrome (ACS) was underestimated. Recent advances in awareness and widespread early angiographic investigation in ACS has led to important shifts in our understanding of the prevalence, predisposing causes, natural history, aetiology, clinical and angiographic features, management, and prognosis of SCAD. It is now well understood that SCAD predominantly affects women and is responsible for around 20% of ACS presentations in females below the age of 60. Despite this, SCAD is still often overlooked and misdiagnosed as atherosclerotic disease. Misdiagnosis is multifactorial; with contributing factors including a low clinical index of suspicion, particularly in young females, a lack of clinician familiarity with angiographic variants, and limitations of angiography. Although increasing evidence suggests that optimal management is distinct from atherosclerotic coronary artery disease, many questions remain unanswered regarding the pathogenesis and optimal treatment of SCAD, heralding prospective research to answer these questions. This review aims to give a current clinical perspective on SCAD and highlight the importance of familiarity and vigilance with this condition when diagnosing and treating ACS.

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Aims To systematic review and meta-analyse the association and mechanistic links between atrial fibrillation (AF) and cognitive impairment. Methods and results PubMed, EMBASE, and Cochrane Library were searched up to 27 March 2021 and yielded 4534 citations. After exclusions, 61 were analysed; 15 and 6 studies reported on the association of AF and cognitive impairment in the general population and post-stroke cohorts, respectively. Thirty-six studies reported on the neuro-pathological changes in patients with AF; of those, 13 reported on silent cerebral infarction (SCI) and 11 reported on cerebral microbleeds (CMB). Atrial fibrillation was associated with 39% increased risk of cognitive impairment in the general population [n = 15: 2 822 974 patients; hazard ratio = 1.39; 95% confidence interval (CI) 1.25–1.53, I2 = 90.3%; follow-up 3.8–25 years]. In the post-stroke cohort, AF was associated with a 2.70-fold increased risk of cognitive impairment [adjusted odds ratio (OR) 2.70; 95% CI 1.66–3.74, I2 = 0.0%; follow-up 0.25–3.78 years]. Atrial fibrillation was associated with cerebral small vessel disease, such as white matter hyperintensities and CMB (n = 8: 3698 patients; OR = 1.38; 95% CI 1.11–1.73, I2 = 0.0%), SCI (n = 13: 6188 patients; OR = 2.11; 95% CI 1.58–2.64, I2 = 0%), and decreased cerebral perfusion and cerebral volume even in the absence of clinical stroke. Conclusion Atrial fibrillation is associated with increased risk of cognitive impairment. The association with cerebral small vessel disease and cerebral atrophy secondary to cardioembolism and cerebral hypoperfusion may suggest a plausible link in the absence of clinical stroke. PROSPERO CRD42018109185.