Objective
To identity clinical features that distinguish between cerebral amyloid angiopathy (CAA)-associated convexity subarachnoid haemorrhage (cSAH) and suspected TIA.
Methods
We undertook a ...single-centre, retrospective case–control study. We identified cases patients with cSAH presenting with transient focal neurological episodes (TFNE) from radiological and clinical databases of patients assessed at the National Hospital for Neurology and Neurosurgery and UCLH Comprehensive Stroke Service. We identified age- and gender-matched controls at a 1:4 ratio from a database of consecutive suspected TIA clinic attendances at UCLH. We compared presenting symptoms and vascular risk factors between cases and controls.
Results
We included 19 patients with cSAH-associated TFNE and 76 matched controls with suspected TIA. Migratory (spreading) symptoms (32% vs. 3%, OR 17.3;
p
= 0.001), sensory disturbance (47% vs. 14%, OR 5.3;
p
= 0.003,) and recurrent stereotyped events (47% vs. 19%, OR 3.7;
p
= 0.02,) occurred more frequently in patients with cSAH compared to controls. Hypercholesterolaemia was less common in patients with cSAH (16% vs 53%, OR 0.17;
p
= 0.008).
Conclusion
Simple clinical features could help distinguish cSAH-associated TFNE from suspected TIA, with relevance for investigation and management, including the use of antithrombotic drugs.
Summary Background The risk of recurrent stroke is up to 10% in the week after a transient ischaemic attack (TIA) or minor stroke. Modelling studies suggest that urgent use of existing preventive ...treatments could reduce the risk by 80–90%, but in the absence of evidence many health-care systems make little provision. Our aim was to determine the effect of more rapid treatment after TIA and minor stroke in patients who are not admitted direct to hospital. Methods We did a prospective before (phase 1: April 1, 2002, to Sept 30, 2004) versus after (phase 2: Oct 1, 2004, to March 31, 2007) study of the effect on process of care and outcome of more urgent assessment and immediate treatment in clinic, rather than subsequent initiation in primary care, in all patients with TIA or minor stroke not admitted direct to hospital. The study was nested within a rigorous population-based incidence study of all TIA and stroke (Oxford Vascular Study; OXVASC), such that case ascertainment, investigation, and follow-up were complete and identical in both periods. The primary outcome was the risk of stroke within 90 days of first seeking medical attention, with independent blinded (to study period) audit of all events. Findings Of the 1278 patients in OXVASC who presented with TIA or stroke (634 in phase 1 and 644 in phase 2), 607 were referred or presented direct to hospital, 620 were referred for outpatient assessment, and 51 were not referred to secondary care. 95% (n=591) of all outpatient referrals were to the study clinic. Baseline characteristics and delays in seeking medical attention were similar in both periods, but median delay to assessment in the study clinic fell from 3 (IQR 2–5) days in phase 1 to less than 1 (0–3) day in phase 2 (p<0·0001), and median delay to first prescription of treatment fell from 20 (8–53) days to 1 (0–3) day (p<0·0001). The 90-day risk of recurrent stroke in the patients referred to the study clinic was 10·3% (32/310 patients) in phase 1 and 2·1% (6/281 patients) in phase 2 (adjusted hazard ratio 0·20, 95% CI 0·08–0·49; p=0·0001); there was no significant change in risk in patients treated elsewhere. The reduction in risk was independent of age and sex, and early treatment did not increase the risk of intracerebral haemorrhage or other bleeding. Interpretation Early initiation of existing treatments after TIA or minor stroke was associated with an 80% reduction in the risk of early recurrent stroke. Further follow-up is required to determine long-term outcome, but these results have immediate implications for service provision and public education about TIA and minor stroke.
OBJECTIVE:Many guidelines recommend emergency assessment for patients with ≥2 TIAs within 7 days, perhaps in recognition of the capsular warning syndrome. However, it is unclear whether all patients ...with multiple TIAs are at high early risk of stroke and whether treatable underlying pathologies are more prevalent in this group.
METHODS:We studied clinical characteristics, Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, and risk of stroke in 1,000 consecutive patients with incident and recurrent TIAs in a prospective, population-based study (Oxford Vascular Study).
RESULTS:Of 1,000 patients with TIAs, 170 had a further TIA within 7 days (105 within 24 hours). Multiple TIAs were not associated with carotid stenosis or atrial fibrillation, and much of the 10.6 (95% confidence interval CI 6.5−15.9) risk of stroke during the 7 days after the first TIA was due to patients with small-vessel disease (SVD) etiology (10 of 24 vs 8 of 146, odds ratio OR = 12.3, 95% CI 3.7–41.9, p < 0.0001), particularly those with motor weakness (i.e., capsular warning syndrome) compared with hemisensory events (9 of 15 60%, 95% CI 35.3–84.7 vs 1 of 9 11.1%, 95% CI 0–31.7, p = 0.03). The 7-day risk of stroke after a recurrent TIA was similar to the risk after a single TIA in patients with non-SVD TIA (8 of 146 5.5% vs 76 of 830 9.2%, OR = 0.58, 95% CI 0.25–1.3, p = 0.20). Of the 9 patients with stroke after a capsular warning syndrome, all had the recurrent TIA within 24 hours after the first TIA, and the subsequent stroke occurred within 72 hours of the second TIA in 8. The ABCD2 scores of all preceding TIAs were ≥4 in all 9 patients with capsular warning syndrome before stroke.
CONCLUSIONS:Capsular warning syndrome is rare (1.5% of TIA presentations) but has a poor prognosis (7-day stroke risk of 60%). Otherwise, recurrent TIA within 7 days is not associated with a greater stroke risk than that after a single TIA.
GLOSSARYCI confidence intervalGP general practitionerOR odds ratioOXVASC Oxford Vascular StudySVD small-vessel diseaseTOAST Trial of Org 10172 in Acute Stroke Treatment
The ABCD(2) score predicts the early risk of stroke after transient ischemic attack. The early risk of recurrence after minor stroke is as high but the only validated prognostic scores for use in ...minor stroke predict long-term risk of recurrence: the Essen Stroke Risk Score and the Stroke Prognosis Instrument II.
We determined the prognostic value of the ABCD(2) score, Essen Stroke Risk Score, and Stroke Prognosis Instrument II in a prospective population-based study in Oxfordshire, UK, of all incident and recurrent stroke (Oxford Vascular Study). Minor stroke was defined as an National Institutes of Health Stroke Scale score ≤5 at the time of first assessment. The 90-day risks of recurrent stroke were determined in relation to each score. Areas under the receiver operator curves indicated predictive value.
Of 1247 first events in the study period, 488 were transient ischemic attacks, 520 were minor strokes, and 239 were major strokes. The ABCD(2) score was modestly predictive (area under the receiver operator curve, 0.64; 0.53 to 0.74; P=0.03) of recurrence at 7 days after minor stroke and at 90 days (0.62; 0.54 to 0.70; P=0.004). Neither Essen Stroke Risk Score (0.50; 0.42 to 0.59; P=0.95) nor Stroke Prognosis Instrument II (0.48; 0.39 to 0.60; P=0.92) were predictive of 7-day or 90-day risk of recurrent stroke. Of the traditional vascular risk factors, etiologic classification (Trial of ORG 10172 in Acute Stroke Treatment) and variables in the ABCD(2) score, only blood pressure >140/90 mm Hg (hazard ratio, 2.75; 1.18 to 6.38; P=0.02) and large artery disease (hazard ratio, 2.21; 1.00 to 4.88; P=0.05) were predictive of 90-day risk.
The predictive power of the ABCD(2) score is modest in patients with minor stroke, and neither the Essen Stroke Risk Score nor the Stroke Prognosis Instrument II predicts early recurrence. More reliable early risk prediction after minor stroke is required.
A high prevalence of antiphospholipid antibodies has been reported in case series of patients with neurological manifestations and COVID-19; however, the pathogenicity of antiphospholipid antibodies ...in COVID-19 neurology remains unclear.
This single-centre cross-sectional study included 106 adult patients: 30 hospitalised COVID-neurological cases, 47 non-neurological COVID-hospitalised controls, and 29 COVID-non-hospitalised controls, recruited between March and July 2020. We evaluated nine antiphospholipid antibodies: anticardiolipin antibodies aCL IgA, IgM, IgG; anti-beta-2 glycoprotein-1 aβ2GPI IgA, IgM, IgG; anti-phosphatidylserine/prothrombin aPS/PT IgM, IgG; and anti-domain I β2GPI (aD1β2GPI) IgG.
There was a high prevalence of antiphospholipid antibodies in the COVID-neurological (73.3%) and non-neurological COVID-hospitalised controls (76.6%) in contrast to the COVID-non-hospitalised controls (48.2%). aPS/PT IgG titres were significantly higher in the COVID-neurological group compared to both control groups (p < 0.001). Moderate-high titre of aPS/PT IgG was found in 2 out of 3 (67%) patients with acute disseminated encephalomyelitis ADEM. aPS/PT IgG titres negatively correlated with oxygen requirement (FiO2R=-0.15 p = 0.040) and was associated with venous thromboembolism (p = 0.043). In contrast, aCL IgA (p < 0.001) and IgG (p < 0.001) was associated with non-neurological COVID-hospitalised controls compared to the other groups and correlated positively with d-dimer and creatinine but negatively with FiO2.
Our findings show that aPS/PT IgG is associated with COVID-19-associated ADEM. In contrast, aCL IgA and IgG are seen much more frequently in non-neurological hospitalised patients with COVID-19. Characterisation of antiphospholipid antibody persistence and potential longitudinal clinical impact are required to guide appropriate management.
This work is supported by UCL Queen Square Biomedical Research Centre (BRC) and Moorfields BRC grants (#560441 and #557595). LB is supported by a Wellcome Trust Fellowship (222102/Z/20/Z). RWP is supported by an Alzheimer's Association Clinician Scientist Fellowship (AACSF-20-685780) and the UK Dementia Research Institute. KB is supported by the Swedish Research Council (#2017-00915) and the Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement (#ALFGBG-715986). HZ is a Wallenberg Scholar supported by grants from the Swedish Research Council (#2018-02532), the European Research Council (#681712), Swedish State Support for Clinical Research (#ALFGBG-720931), the Alzheimer Drug Discovery Foundation (ADDF), USA (#201809-2016862), and theUK Dementia Research Institute at UCL. BDM is supported by grants from the MRC/UKRI (MR/V007181/1), MRC (MR/T028750/1) and Wellcome (ISSF201902/3). MSZ, MH and RS are supported by the UCL/UCLH NIHR Biomedical Research Centre and MSZ is supported by Queen Square National Brain Appeal.
We present a case of a 49M with a large left MCA territory ischaemic stroke and combined venous arterial thrombosis. His past medical history was significant for Crohn’s disease and anabolic steroid ...use for body building. Young stroke screen was negative except for a severely elevated homocysteine, and folate deficiency. He was also found to be a homozygous carrier of the methylenetetrahydrofolate reductase enzyme mutation (MTHFR 667 C->T). The aetiology of this stroke was a hypercoagulable state induced by raised serum homocysteine. Anabolic steroids have been shown to increase serum homocysteine levels. The MTFHR enzyme mutation is known to increase stroke risk. Patients who have this mutation and abuse anabolic steroids or have poor folate levels may be higher risk for stroke.In summary ischaemic stroke can occur in the setting of severe elevations of homocysteine. Anabolic steroid use is an important risk factor to consider in cases of young stroke with elevated serum homocyst- eine. Testing for MFTHR mutations in stroke patients with raised homocysteine and low folic acid levels may be useful to guide secondary stroke prevention through adequate vitamin supplementation. Further studies looking into primary and secondary stroke prevention in the high risk MTHFR mutation cohort are necessary.
Stroke lesion size and location are understood to be more accurate predictors of recovery from aphasia than demographic variables such as age, education, or socioeconomic status.
We hypothesise that ...markedly high premorbid language function can influence functional recovery from aphasia.
This case study reports the recovery of a 64-year-old right-handed male, with large left posterior cerebral artery territory infarct involving the thalamus, occipital lobe and posteromedial temporal lobe. The report is informed by retrospective review of clinical notes, language assessment, and interviews with the participant and his family. Premorbidly, he had acquired fluency in five additional languages in early adulthood, followed by a career in senior roles within corporate communications.
Following severe expressive aphasia in the acute period, the subacute and chronic phases were characterised by residual mild anomia and cognitive communication difficulties apparent on formal assessment, yet masked in functional contexts through compensatory strategies and preservation of an authoritative premorbid communication style.
The current report provides single-case evidence that individuals with markedly high premorbid metalinguistic skills may, in functional contexts, be able to compensate for expressive aphasic deficits and preserve their communicative competence. The discrepancy between the participant's performance on formal versus informal language assessment underscores the necessity for both perspectives for accurate diagnosis of aphasia. Consideration of premorbid language function can usefully guide clinical decision-making about intervention for individuals with aphasia.
Migrainous headaches and transient ischaemic attacks are amongst the commonest acute neurological presentations seen in the UK. Our case highlights a rare complication of a rare disorder presenting ...as a mimic for these common neurological conditions.A 68 year-old woman presented with gradual onset severe frontotemporal headache with vomiting, mild photophobia and transient aphasia. Previously, she had experienced episodes of sudden onset left arm weakness and numbness spreading to the face, associated with complete aphasia, lasting for ten minutes. Examination was unrevealing.Contrast head MRI showed enhancing leptomeningeal disease. An IgM kappa paraprotein was detected in serum, with a lymphoplasmacytic lymphoma diagnosed on bone marrow aspirate/trephine. CSF was highly cellular containing a population of predominantly CD20+ lymphocytes, in keeping with a B-cell lymphoplasmacytic lymphoma infiltrating the leptomeninges. A diagnosis of Waldenstrom’s macroglobulinaemia (WM) presenting with Bing-Neel syndrome was made. She was started on chemoimmunotherapy with MATRix regimen.Bing-Neel syndrome is a rare complication of WM that results from infiltration of the central nervous system, and rarely peripheral nervous system, by malignant lymphoplasmacytic cells. Neurological manifestations are diverse and protean. The diagnosis should be considered with unexplained neurological symptoms in the presence of macroglobulinaemia.
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