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A syndrome of vaccine-induced immune thrombotic thrombocytopenia (VITT) has recently been reported following the ChAdOx1 nCoV-19 (Oxford–AstraZeneca) recombinant adenoviral vector vaccine encoding the spike glycoprotein of SARS-CoV-2.1–4 Previously described patients developed thrombosis, mainly affecting cerebral venous sinuses, with thrombocytopenia and antibodies to platelet factor 4 (PF4), but the characteristics of VITT with arterial thrombosis have not previously been described. Here, we report three patients with VITT who presented with ischaemic stroke. Patient 1, a 35-year-old Asian woman, developed episodic right temporal and periorbital headache 6 days after receiving the ChAdOx1 nCoV-19 vaccine. Five days later, she awoke with left face, arm and leg weakness, right gaze preference and drowsiness. Non-contrast CT and CT angiography (CTA) revealed occlusion of the right middle cerebral artery (MCA) distal M1 segment with extensive ischaemia and haemorrhagic transformation (figure 1A-C)). Subsequent imaging revealed right portal vein thrombosis. The platelet count was 64 x 109/L (reference range 150 –400 x 109/L); D-dimer was raised at 11 220 µg/L (reference range 0–550); and the Asserachrom HPIA IgG assay for anti-PF4 antibodies was positive (76.1%). The patient underwent urgent decompressive hemicraniectomy …

Neurological complications due to the HIV itself became apparent early on in the course of the AIDS epidemic. The most feared were the cognitive and motor complications termed AIDS dementia complex or HIV-associated dementia. With the introduction of combination antiretroviral therapy, the incidence of HIV-associated dementia has been dramatically reduced. However, the prevalence of less severe forms of the disorder remains around 20%. There is controversy about whether some patients may continue with progressive cognitive decline despite adequate suppression of the HIV. The salient issues are those of cerebrospinal fluid (CSF) drug penetration, drug neurotoxicity and persistent immune activation and inflammation. This review will also discuss other newly encountered complications, including the compartmentalisation (or CSF escape) and immune reconstitution inflammatory syndromes.

Background Intracerebral haemorrhage (ICH) is an uncommon but devastating complication of regular antiplatelet use: identifying high-risk patients before treatment could potentially reduce this hazard. Brain microbleeds on gradient-recalled echo (GRE) T2*-weighted MRI are considered a biomarker for bleeding-prone small-vessel diseases. The authors hypothesised that microbleeds are a risk factor for antiplatelet-related ICH, and investigated this in a hospital-based matched case–control study. Methods Cases of spontaneous ICH were ascertained, using overlapping methods, from a prospective database of 1017 consecutive unselected patients referred to our stroke unit and associated clinics. For each case of antiplatelet-related ICH, two controls matched for age, sex and hypertension without history of ICH on antiplatelet therapy were selected. Microbleeds were identified by a trained observer blinded to clinical details. Results Microbleeds were more frequent in antiplatelet users with ICH than in matched antiplatelet users without ICH (13/16 (81%) vs 6/32 (19%), p=0.004) and patients with non-antiplatelet-related ICH (13/16 (81%) vs 15/33 (45%), p=0.03). The frequency of lobar microbleeds was 11/16 (69%) in antiplatelet-related ICH versus 11/33 (33%) in non antiplatelet-related ICH (p=0.032). Microbleeds were more numerous in antiplatelet users with ICH compared with controls (p=0.016). The number of microbleeds was associated with the risk of antiplatelet-related ICH (adjusted OR 1.33 per additional microbleed, 95% CI 1.06 to 1.66, p=0.013). Conclusions Brain microbleeds are associated with antiplatelet-related ICH. In patients with a large number of lobar microbleeds, the risk of ICH could outweigh the benefits of antiplatelet therapy. Larger prospective studies to investigate the prognostic significance of microbleeds in regular antiplatelet users are warranted.

Imaging occupies an important role in the investigation of dementia and neurodegenerative disease. The role of imaging in prion disease used to be one of exclusion of other conditions. Over the past decade, the non‐invasive nature of MRI, the improved range of magnetic resonance sequences and the availability of clinical and neuropathological correlation have led to a more prominent position of MRI and its inclusion in the diagnostic criteria for variant Creutzfeldt–Jakob disease. As experience of imaging in human prion disease increases, patterns of change related to strain and genotype may improve the diagnostic potential of imaging in the future, may reduce the need for more invasive testing and prove useful in future therapeutic trials. This paper reviews the current knowledge of imaging appearances in human prion disease.

A 31 year old HIV infected woman developed neuropsychiatric problems soon after starting highly active antiretroviral therapy (HAART). Despite modifying and subsequently stopping HAART her condition progressively worsened. Cranial magnetic resonance imaging revealed multiple areas of abnormal signal suggestive of either a vasculitis or demyelination.

Magnetic resonance imaging (MRI) is often divided into structural MRI and functional MRI (fMRI). The former is a widely used imaging technique in research as well as in clinical practice. This review describes the more important developments in structural MRI in recent years, including high resolution imaging, T2 relaxation measurement, T2*-weighted imaging, T1 relaxation measurement, magnetisation transfer imaging, and diffusion imaging. The principles underlying these techniques, as well as their use in research and in clinical practice, will be discussed.

Background Subclinical acute ischaemic lesions have recently been described in spontaneous intracerebral haemorrhage (sICH). We hypothesised that they are related to MRI markers of small vessel disease [SVD] (hypertensive arteriopathy or cerebral amyloid angiopathy [CAA]) in a multicentre, cross-sectional study. Methods We studied consecutive patients with sICH from four stroke centres, and age-matched stroke referrals without sICH. Acute ischaemic lesions were assessed on MRI ( Results We included 114 sICH patients (39 with probable CAA); and 47 controls. The prevalence of DWI lesions was 9/39 (23%) in probable CAA-related ICH vs 6/75 (8%) in the remaining patients with sICH (p=0.024); no DWI lesions were found in controls. DWI lesions were associated with WMC score (OR 1.14 per unit increase, p=0.024) and strictly lobar CMBs (OR 3.85, p=0.029). Conclusion Acute, subclinical ischaemic brain lesions are frequent after sICH, and three times more common in CAA-related ICH than in other ICH types. They are associated with WMC and CMBs, suggesting that they result from an occlusive small vessel arteriopathy. They contribute to the overall burden of vascular-related damage in ICH, and may be a useful surrogate marker of ongoing ischaemic injury from SVD.

Objectives Vascular cognitive impairment and Alzheimer9s disease (AD) may interact and co-exist. We investigated the prevalence and impact of mesial temporal lobe atrophy (MTA), a radiological marker for AD, in a population of stroke patients. Methods Patients referred to a stroke service underwent detailed neuropsychological testing and standardised imaging, including GRE T2* MRI and FLAIR. We assessed MTA on FLAIR images using a newly developed and validated visual rating scale based on the Scheltens scale (scores 0 to 4; mild MTA Findings 396 patients with full neuropsychological testing and complete MRI sequences were included (358 mild and 38 severe MTA). 171 patients (43%) showed some degree (score ≥1) of MTA. Patients with severe MTA were older (76 vs 64, p=0.000), more hypertensive (97% vs 66%, p=0.000), and had more severe WMC (median 9 vs 5.5, p=0.000) than patients with mild or no MTA. In adjusted multivariate analyses, MTA was a predictor of verbal memory impairment (OR 1.81, p=0.004) and frontal executive dysfunction (OR 1.48, p=0.023). Conclusions MTA is common in stroke patients and is independently associated with verbal memory and frontal executive deficits. Alzheimer pathology may play an important role in cognitive impairment in patients with cerebrovascular disease.

Background Although conventional MRI (cMRI) has been reported to show specific abnormalities in parkinsonism, the diagnosis of the underlying pathology can be challenging. We report the radiological diagnostic accuracy, and the sensitivity, specificity, positive (PPV) and negative predictive values (NPV) of cMRI abnormalities in a pathologically confirmed cohort of Parkinson9s disease (PD), progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and corticobasal degeneration (CBD). Method cMRI of donors to a neurological brain bank was reviewed by two experienced neuroradiologists blinded to clinical details. Images were systematically reviewed for the presence of specific reported abnormalities. Results 48 pathologically confirmed cases (23 PSP, 6 PD, 13 MSA and 6 CBD) and nine controls were studied. The final clinical diagnosis was supported in 68% and the radiological diagnosis in 60%. Using cMRI 55% of PSP, 67% of PD, and 77% of MSA were correctly identified. In this study the Hummingbird sign has 68% sensitivity, 100% specificity and PPV for PSP and the Hot Cross Bun has 62% sensitivity, 100% specificity and PPV for MSA. Conclusion The confirmation that using cMRI key diagnostic features with very high specificity and PPV have low sensitivity endorses the development of newer MR techniques (e.g., high field diffusion tensor imaging) as useful biomarkers early in disease.

Background Adult low-grade gliomas (LGG) are usually WHO grade II and have a propensity to transform into malignant gliomas at some point in their natural history. Prognostic factors for patients treated with radiotherapy include increasing age and tumour diameter, but may not be applicable to patients who have not received any oncological treatment. We have carried out a prospective multimodality imaging study of 47 untreated adult patients with supratentorial LGG to determine which factors are independently associated with a poor prognosis, using time to progression as the primary endpoint. Methods Patients were recruited from the neuro-oncology clinic and followed up from January 1999 to December 2006. Baseline clinical and radiological data were collected and Kaplan–Meier, univariate and multivariate analysis using Cox proportional hazards regression model, were carried out. Results 28 patients (60%) had progressed by the end of the study. Median progression-free survival was 35.4 (9.9–93.3) months. In univariate analysis, 6 out of 12 prognostic variables reached significance at the 10% level. Multivariate analysis showed that only baseline tumour volume as well as lead time between first seizure and first MRI study were significant at the 5% level. Conclusions Tumour volume, measured with an easily reproducible method on standard MR sequences, is of prognostic value in predicting tumour progression in patients with untreated LGG.