Lyme disease: diagnosis and management.

Lyme disease (borreliosis) is a tick-borne bacterial infection caused by the spirochaete Borrelia burgdoferi, transmitted by hard-backed Ixodes ticks. Actual numbers of cases are increasing and it appears that the distribution across the UK is widening; however, it occurs most frequently in area of woodland, with temperate climate. It typically presents in mid to late summer. Lyme disease is a multisystem disease. The nervous system is the second most commonly affected system after the skin. Other systemic manifestations, such as carditis, keratitis, uveitis and inflammatory arthritis, rarely occur in European Lyme disease. In 2018, the National Institute for Health and Care Excellence has updated its guidelines on the diagnosis and management of Lyme disease. Here, we highlight important aspects of this guidance and provide a more detailed review of the clinical spectrum of neuroborreliosis, illustrated by cases we have seen.

Critical cap thickness and rupture in symptomatic carotid plaques: the oxford plaque study.

BACKGROUND AND PURPOSE: Advances in carotid plaque imaging could allow quantification of fibrous cap thickness in vivo. While a cap thickness <65 microm is the accepted definition of rupture-prone plaque in the coronary circulation, the threshold value for carotid plaques is unknown. METHODS: We made detailed histological assessments of 526 carotid plaques from consecutive patients undergoing endarterectomy for symptomatic carotid stenosis. The thickness of the fibrous cap at the thinnest and most representative part was measured. RESULTS: Cap thickness could be measured reliably in 428 (81%) plaques. In the ruptured plaques (n=257), the median representative cap thickness was 300 microm (IQR 200 to 500 microm) and the median minimum cap thickness was 150 microm (80 to 210 microm; mean=181 microm), which is much greater than the mean cap thickness of 23 microm at the point of rupture that has been reported for coronary plaques. For nonruptured plaques, the median cap thickness values were 500 microm (300 to 700 microm) and 250 microm (180 to 400 microm), respectively. The optimum cut-offs for discriminating between ruptured and nonruptured plaques were a minimum cap thickness <200 microm (OR 5.00, 3.26 to 7.65, P<0.001), a representative cap thickness <500 microm (OR 3.38, 2.25 to 5.08, P<0.001), or a combination of both (OR 5.11, 3.19 to 8.19, P<0.001). Minimum and representative cap thickness were only modestly correlated (r(2)=0.30) and were both independently associated with cap rupture. CONCLUSIONS: Critical cap thickness is greater in carotid plaques than coronary plaques. Minimum and representative cap thicknesses were both independently associated with cap rupture. A combination of minimum cap thickness <200 microm and a representative cap thickness <500 microm identified ruptured plaques most reliably. Prospective imaging studies are required to establish whether these cut points predict clinical events in patients with asymptomatic carotid stenosis.

Pulse pressure is independently associated with carotid plaque ulceration.

BACKGROUND: Plaque rupture is the principal cause of acute coronary ischaemia, and unstable carotid plaques are associated with a high risk of ischaemic stroke. Carotid plaque ulceration also predicts acute coronary events, suggesting that systemic factors may determine plaque instability. One potentially important factor is pulse pressure. There is indirect evidence that cyclical haemodynamic forces affect plaque stability, and pulse pressure is a strong predictor of coronary events. OBJECTIVE: To study the association between pulse pressure and plaque ulceration. DESIGN AND METHODS: We studied angiograms from 3007 patients with recently symptomatic carotid stenosis in the European Carotid Surgery Trial. Presence of ulceration was related to the different components of blood pressure [pulse pressure, systolic blood pressure (SBP), mean arterial pressure (MAP), and diastolic blood pressure (DBP)], and adjustment was made for age, sex, diabetes, smoking, and the degree of vessel stenosis. RESULTS: Pulse pressure was the strongest independent predictor of ulceration of the symptomatic carotid plaque [adjusted odds ratio (OR) for the upper compared with the lower quintile 2.07, 95% confidence interval (CI) 1.25 to 3.44; P = 0.004]. This relationship was weaker for SBP (OR 1.66, 95% CI 1.05 to 2.62; P = 0.02), and non-significant for MAP (OR 1.58, 95% CI 1.01 to 2.48, P = 0.13) and DBP (OR 1.67, 95% CI 0.73 to 1.87, P = 0.50). CONCLUSIONS: Pulse pressure is independently associated with carotid plaque ulceration, supporting the hypothesis that pulsatile haemodynamic forces are an important cause of plaque rupture.

Cerebral venous sinus thrombosis.

Cerebral (or dural) venous sinus thrombosis (CVST) is a condition distinct from other cerebrovascular disease, which presents its own particular diagnostic difficulties and treatment controversies. The clinical presentation is variable and may mimic a wide range of other neurological disorders that include subarachnoid haemorrhage, encephalitis, eclampsia, idiopathic intracranial hypertension and arterial stroke.

Site of carotid plaque ulceration in relation to direction of blood flow: an angiographic and pathological study.

BACKGROUND: Rupture of atherosclerotic plaque is the main cause of acute coronary syndromes and carotid territory ischaemic stroke. Haemodynamic stress is important in early plaque formation and may affect the stability of mature plaques. There is some evidence that macrophage infiltration and plaque rupture tend to localise to the proximal (upstream) part of the plaque where shear stress is highest. However, previous studies have been too small to assess this reliably. We studied the site of ulceration in a large number of carotid plaques. METHODS: We studied angiograms of 3007 symptomatic carotid stenoses, and the pathological appearance of 119 carotid plaques (77 asymptomatic), to identify the presence and position of plaque ulceration. RESULTS: Angiographic ulceration, which was present in 421 patients (14%), was more likely to be PROXIMAL than DISTAL to the point of maximum stenosis (OR = 16.6, 95% CI = 11.6-26.9, p < 0.001). This trend increased with severity of stenosis (p = 0.002). Pathological examination of the 119 carotid plaques also showed that ulceration was more likely to occur proximal to the point of maximum stenosis (OR = 6.1, 95% CI = 2.8-13.6, p < 0.001). CONCLUSIONS: Ulceration of carotid plaques, visible on angiography or on pathological examination, is seen most often in the proximal (upstream) part where shear stress is highest.