Prolonged and repeated microemboli detection in acute ischemic stroke - The Norwegian Microemboli in Acute Stroke Study (NOR-MASS).

OBJECTIVES: Cerebral microemboli can be detected by transcranial Doppler monitoring (TCDM) and may elucidate stroke etiology, the effect of preventive therapy, and the risk of stroke recurrence. Microemboli detection is usually performed for up to 60 minutes, but due to temporal variability, microembolization may be missed if the monitoring time is too short. We aimed to assess the time course of microembolization in acute ischemic stroke and explore the utility of prolonged and repeated microemboli detection. MATERIALS AND METHODS: Patients with suspected ischemic stroke and symptom onset within 24 hours were examined with bilateral, stationary TCDM for one hour followed by unilateral, ambulatory TCDM for two hours. Unilateral TCDM was repeated for the following two days and after three months. RESULTS: We included 47 patients, of which 41 had ischemic stroke, five had transient ischemic attack, and one had amaurosis fugax. Microemboli were detected in 60 % of patients. The occurrence was highest within 24 hours after onset and significantly lower at three months. Prolonged and repeated microemboli detection yielded only one additional microemboli-positive patient. Hence, patients who initially were microemboli negative tended to remain negative. We could not demonstrate an association between microemboli occurrence and clinical outcome or stroke recurrence. CONCLUSIONS: Microembolic signals are frequent within 24 hours after ischemic stroke onset, but prolonged and repeated microemboli detection did not increase the yield of MES positive patients. CLINICAL TRIAL REGISTRATION-URL: http://www. CLINICALTRIALS: gov. Unique identifier: NCT03543319.

The Course of Carotid Plaque Vulnerability Assessed by Advanced Neurosonology.

Background: Carotid artery atherosclerosis is a major risk factor for ischemic stroke. This risk is related to plaque vulnerability and is characterized by plaque morphology, intraplaque neovascularization, and cerebral microembolization. Advanced neurosonology can identify vulnerable plaques and aid in preventing subsequent stroke. We aimed to assess the time course of cerebral microembolization and intraplaque neovascularization during 6 months of follow-up and to explore the utility of advanced neurosonology in patients with acute cerebral ischemia. Methods: Fifteen patients with acute cerebral ischemia and carotid artery plaques underwent comprehensive extra- and intracranial ultrasound examinations, including microemboli detection and contrast-enhanced ultrasound. The examinations were repeated after 3 and 6 months. Results: We examined 28 plaques in 15 patients. The ultrasonographic features of plaque vulnerability were frequent in symptomatic and asymptomatic plaques. There were no significant differences in stenosis degree, plaque composition, plaque surface, neovascularization, or cerebral microembolization between symptomatic and asymptomatic plaques, but symptomatic plaques had a higher number of vulnerable features. None of the patients had recurrent clinical stroke or transient ischemic attack during the follow-up period. We observed a decrease in cerebral microembolization at 6 months, but no significant change in intraplaque neovascularization. Conclusions: In patients with acute cerebral ischemia and carotid artery plaques, cerebral microembolization decreased during 6 months of follow-up, indicating plaque stabilization. Clinical Trial Registration:ClinicalTrial.gov, identifier NCT02759653.

Clinical manifestation of acute cerebral infarcts in multiple arterial territories.

OBJECTIVES: We aimed to assess frequencies and radiological aspects of single- and multiterritory clinical manifestation among patients with acute cerebral infarcts in multiple arterial territories (MACI). MATERIALS & METHODS: We retrospectively reviewed admission records and diffusion-weighted magnetic resonance imaging of patients with MACI admitted to our stroke unit between 2006 and 2017. MACI was defined as acute cerebral ischemic lesions in at least two out of three arterial cerebral territories, that is, the left anterior, right anterior and the bilateral posterior territory. Patients with single- and multiterritory clinical manifestation were then compared for topographical distribution of the ischemic lesions, the number of ischemic lesions, and The Oxfordshire Community Stroke Project classification. RESULTS: Out of 311 patients with MACI, 222 (71.4%) presented with single-territory clinical manifestation. Involvement of the left hemisphere (OR = 0.37, 95% CI 0.16-0.82), less than five ischemic lesions (OR = 0.58, 95% CI 0.35-0.97), and partial anterior circulation infarct clinical stroke syndrome (OR = 0.57, 95% CI 0.34-0.97) were associated with single-territory clinical manifestation. Involvement of all three territories (OR = 2.58, 95% = 1.48-4.50), more than 10 ischemic lesions (OR = 2.30, 95% CI 1.32-4.01) and total anterior circulation infarct clinical stroke syndrome (OR = 3.31, 95% CI 1.39-7.86) were associated with multiterritory clinical manifestation. CONCLUSION: Most patients with MACI present with single-territory clinical manifestation on admission. Diffusion-weighted magnetic resonance imaging is therefore necessary for a definite diagnosis.

Persistent Microembolic Signals in the Cerebral Circulation on Transcranial Doppler after Intravenous Sulfur Hexafluoride Microbubble Infusion.

BACKGROUND AND PURPOSE: Microembolic signals (MES) are detectable by transcranial Doppler monitoring and associated with increased risk of first or recurrent ischemic stroke. MES detection can also illuminate stroke etiology and the effect of prophylactic treatment. MES detection cannot accurately distinguish between stroke-related microemboli and ultrasound contrast agents. These agents contain microbubbles and are frequently used in neuro- and cardiovascular diagnostics. We aimed to assess how long after contrast infusion microbubbles are detectable by transcranial Doppler monitoring. METHODS: Ten healthy volunteers received an intravenous infusion of stabilized sulfur hexafluoride microbubbles (SonoVue®) for 30 minutes. The infusion was followed by continuous unilateral Doppler monitoring (TCD-X, Atys Medical, Soucieu-en-Jarrest, France) for 3.5 hours. RESULTS: MES persisted for 12 to 77 minutes (median 40.5 minutes), and the frequency tended to decrease gradually until cessation. CONCLUSIONS: None of the subjects had detectable MES for more than 77 minutes after ultrasound contrast infusion. MES detection with the intent to detect stroke-related microemboli should wait for at least this long after completed infusion.

Patent foramen ovale in an elderly male with multiple embolic infarcts.

Patent foramen ovale (PFO) is associated with embolic stroke, particularly in younger patients. In older patients, atrial fibrillation is a more common cause of embolic stroke. A PFO may be considered culpable at higher age when other potential embolic sources are absent or after recurrent stroke despite prophylactic treatment.

[A woman with pareses of the arms and legs]. / En kvinne med kraftsvikt i armer og bein.

BACKGROUND: Hypokalemic pareses are caused by low extracellular potassium levels which reduce the resting membrane potential of muscle cells and make them less excitable. It may be caused by an intracellular shift of potassium, renal potassium loss, reduced potassium intake or increased gastrointestinal loss. CASE PRESENTATION: A woman in her 60s presented with rapid-onset tetraparesis and hyporeflexia starting the day before admission. The patient history revealed several months of low food intake, increased alcohol consumption and diarrhoea. Laboratory tests showed severe hypokalemia (1.5 mmol/l) and hypomagnesemia (0.38 mmol/l), and ECG showed atrial fibrillation. She was admitted to the medical intensive care unit and treated with intravenous normal saline with added potassium and magnesium, with good effect on her symptoms. Urine tests showed high potassium-creatinine ratio (4.22 mmol/mmol creatinine) and increased fractional excretion of magnesium (18.6%). Abdominal CT scan revealed colonic wall thickening, and colonic biopsies showed mild inflammation. Faecal calprotectin was moderately elevated (294 mg/kg). INTERPRETATION: The patient had hypokalemic pareses for which there were several contributing factors. The renal causes were augmented excretion of magnesium and potassium, probably due to increased alcohol consumption. The extrarenal causes were increased gastrointestinal loss, with ulcerative colitis being the presumed explanation, and reduced food intake.