Diffusion weighted imaging, apparent diffusion coefficient maps and stroke etiology

Objective : In acute ischemic stroke, the number and distribution of lesions on diffusion weighted imaging (DWI) have been shown to give clues to the underlying pathogenetic mechanisms. The objective of this study was to determine whether lesion features on DWI differ between stroke due to large artery atherosclerosis (LAA) and cardioembolism (CE), and to assess the role of apparent diffusion coefficient maps (ADC). Methods : We retrospectively studied 83 consecutive patients with stroke caused by either LAA (n = 40) or cardioembolism (n = 43). DWI lesions were characterized by number, size, distribution (i. e. lesion pattern) and signal intensity on ADC maps. In part A, all hyperintense DWI lesions regardless of their ADC were compared. In part B, only hyperintense DWI lesions with hypointense appearance on ADC maps (i. e. acute lesions) were assessed. Results : Part A: The frequency of multiple hyperintense DWI lesions (LAA: 28/40, CE: 21/43; p 1 circulation (i. e. anterior plus posterior or bilateral anterior circulations) was present in 5 LAA-patients (13 %) and 4 CE-patients (9 %). Lesion size did not differ between LAA-stroke (35.1 ± 33.7 mm) and CE-stroke (35.4 ± 27.8 mm). Part B: Multiple hyperintense DWI lesions with low ADC occurred in 23/40 LAA-patients and in 15/43 CE-patients (p 1 circulation occurred only in CE-stroke (n = 3; 7%) and never in LAA-stroke. Conclusions : (1) Multiple ischemic lesions occur significantly more often in LAA-stroke than in CE-stroke. (2) ADC maps are important in the comparison of DWI lesion patterns; DWI lesions in > 1 circulation can only be assigned to a cardioembolic etiology if they appear hypointense on ADC map

Recurrent post‐partum seizures after epidural blood patch

There are many causes for headaches after childbirth. Even though postdural puncture headache (PDPH) has to be considered in a woman with a history of difficult epidural anaesthesia, pre‐eclampsia should always be excluded as an important differential diagnosis. We report a case with signs of late‐onset pre‐eclampsia where administration of an epidural blood patch (EBP) was associated with eclampsia. A hypothetical causal relationship between the EBP and seizures was discarded on the basis of evidence presented in this report. Br J Anaesth 2003; 90: 247-5

Incidence of first-ever ischemic stroke in the Canton Basle-City, Switzerland: A population-based study 2002/2003

Our study sought to estimate the incidence rate of firstever ischemic stroke (FEIS) in the geographically well-defined population of the Canton Basle-City, Switzerland. An one-year prospective population-based study among the permanent residents of the Canton Basle-City (188015 inhabitants, census 2002) was carried out. Multiple overlapping sources of information were used. Stroke was defined according to the WHO criteria. The diagnosis of FEIS was based on clinical assessment and neuroimaging findings. 269 patients (114 males; mean age 72.8, standard deviation (SD) ± 12 and 155 females; mean age 78.4, SD ± 11) with FEIS were identified. The overall crude incidence of FEIS amounted to 143 per 100000 population (95% confidence interval (CI) 126 to 160) and it was higher among females (156; 95% CI 132 to 181) than in males (128; 95% CI 105 to 152). The age-specific incidence rates of FEIS approximately doubled with each decade of life, increasing from 17 (95 % CI 2 to 31) among 0-44 years old group to 1034 (95% CI 774 to 1293) for those aged 85 or more years. The overall incidence rate of FEIS adjusted for age to the European standard population was 76 per 100000 inhabitants (95% CI 66 to 86) and it was higher in males—89, 95% CI 72-106—than in females—66, 95 % CI 53-77. Moreover, in comparison with studies from other developed countries (e. g. Germany, Italy, Australia)—carried out in the middle of 1990s—the standardised incidence rates of FEIS were substantially lower in Switzerland. Our results indicate that the risk of ischemic stroke might be low in Switzerland. However, giving a major reduction in the age and gender specific stroke incidence over the past years our findings might—alternatively—mirror this favourable tren

Life-threatening orolingual angioedema during thrombolysis in acute ischemic stroke

Background: Orolingual angioedema can occur during thrombolysis with alteplase in stroke patients. However, data about its frequency, severity and the significance of concurrent use of angiotensin-converting-enzyme inhibitors (ACEi) are sparse. Objective: (1), to alert to the potentially life-threatening complication of orolingual angioedema. (2), to present CT-scans of the tongue which exclude lingual hematoma. (3), to estimate the frequency of orolingual angioedema. (4), to evaluate the risk associated with the concurrent use of ACEi. Methods: Single center, databank-based observational study on 120 consecutive patients with i. v. alteplase for acute stroke. Meta-analysis of all stroke studies on alteplase-associated angioedema, which provided detailed information about the use of ACEinhibitors. Across studies, the Peto odds ratio of orolingual angioedema for "concurrent use of ACEi" was calculated. Results: Orolingual angioedema occurred in 2 of 120 patients (1.7%, 95% CI 0.2-5.9 %).Angioedema was mild in one, but rapidly progressive in another patient. Impending asphyxia prompted immediate intubation. CT showed orolingual swelling but no bleeding. One of 19 (5%) patients taking ACEi had orolingual angioedema, compared to 1 of 101 (1%) patients without ACEi. Medline search identified one further study about the occurrence of alteplase-associated angioedema in stroke patients stratified to the use of ACEi. Peto odds ratio of 37 (95 % CI 8-171) indicated an increased risk of alteplasetriggered angioedema for patients with ACEi (p <0.001). Conclusion: Orolingual angioedema is a potentially life-threatening complication of alteplase treatment in stroke patients, especially in those with ACEi. Orolingual hematoma as differential diagnosis can be excluded by CT-sca

Hereditary Systemic Angiopathy (HSA) with cerebral calcifications, retinopathy, progressive nephropathy, and hepatopathy

Several hereditary conditions affecting cerebral, retinal and systemic microvessels have recently been described. They include CADASIL, CRV, and HERNS. We here report on a variant form of a hereditary systemic angiopathy (HSA) affecting two generations of a Caucasian family. Clinical symptoms of HSA appear in the mid-forties and are characterized by visual impairment, migrainelike headache, skin rash, epileptic seizures, progressive motor paresis and cognitive decline. Late symptoms include hepatic and renal failure. Retinal capillary microaneurysms and arteriolar tortuosity are associated with marked optic disc atrophy. Radiological hallmarks consist of multiple cerebral calcifications and tumor-like subcortical white matter lesions. Brain, peripheral nerve, muscle, kidney and colon biopsies have revealed a multi organ small vessel involvement with partly altered endothelium, perivascular inflammation and thrombotic microangiopathy. No curative therapeutic options are known for hereditary cerebral vasculopathies. The use of cyclophosphamide, azathioprine and methotrexate was of no benefit in our cases of HSA. Early diagnosis of hereditary systemic angiopathies is important in order to prevent patients from repetitive invasive diagnostic measures and to avoid the use of inappropriate and potentially harmful drug