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Background Awareness of stroke risk factors is important for stroke prevention. Knowledge of stroke symptoms and awareness regarding the necessity of seeking urgent stroke treatment are vital to provide rapid admission to a stroke unit. Data on this specific knowledge in Luxemburg are lacking. METHODS We investigated 420 patients from the Department of Neurology and their relatives using a questionnaire. There were 44% men and 56% women; 25% were immigrants and 75% Luxemburgish nationals; 13% already had had a stroke or transient ischemic attack (TIA); and the mean age was 55 years ranging from 18 to 87 years. Results A total of 88% of participants knew that a stroke occurs in the head/brain. In all, 10% of participants did not know any symptom of a stroke. The most frequently quoted symptoms (>15%) were paralysis/weakness (36%), speech disorders (32%), cranial nerve deficit (16%), vertigo (15%), and visual disorders (15%). Sensory deficits were mentioned by only 4% of patients. Known risk factors (>15%) were smoking (40%), hypertension (32%), alcohol (32%), poor nutrition (28%), high cholesterol (26%), stress (23%), and lack of exercise (19%). Age (4%), diabetes (6%), carotid stenosis (2%), and heart disease (1%) were less frequently known. In all, 11% of participants did not know any risk factor of a stroke. A total of 89% of participants would correctly call the 112 (emergency phone number). The following groups were better informed: Luxemburgish nationals, younger people, and participants with higher education level. Stroke/TIA patients were better informed concerning stroke symptoms, but unfortunately not concerning how to react in the case of a stroke. There was no relevant gender difference. Discussion Although most of the participants knew what to do in the case of a stroke, they did not know the relevant stroke symptoms and risk factors. Future campaigns should therefore focus on risk factors and symptoms, and should address immigrants, elderly persons, less-educated persons, and patients who had already suffered a stroke/TIA.

Background: A Mediterranean diet, with and without small daily amounts of red wine, and physical activity reduce the risk of cerebrovascular disease and improve cognition. An increase in cerebral blood flow may be the underlying mechanism. Under normal conditions, cerebral blood flow velocity changes in the internal carotid arteries and in large basal cerebral arteries correlate closely with cerebral blood flow changes, as the diameter of these vessels hardly changes and only the smaller vessels downstream change their diameter. Methods: A prospective randomized controlled trial was performed in 108 patients with carotid atherosclerosis (mean age 64 years, 67% men, 66% on statin therapy). Half of them were advised to follow a polyphenol-rich modified Mediterranean diet including 1-2 tomatoes, 3-5 walnuts and a bar of dark chocolate (25 g) a day and to perform moderate physical exercise for 30 min/day (lifestyle changes). Within these two groups, half of the patients were randomized either to avoid any alcohol or to drink 100 ml of red wine (women) or 200 ml of red wine (men) daily. Bilateral middle cerebral and internal carotid blood flow velocity (peak systolic, peak end-diastolic and mean) was measured at baseline and after 4 and 20 weeks using colour-coded duplex ultrasound. Insonation depth and insonation angle were used to identically place the sample volume during follow-up investigations. A general linear model with Tukey-Kramer adjustment for multiple comparisons was used to assess the primary end points. For the analysis we used the mean values of the right and left artery. Results: Neither lifestyle changes nor red wine had an effect on peak systolic, peak end-diastolic or mean cerebral blood flow velocity. Conclusions: Advice on lifestyle changes, including a modified polyphenol-rich Mediterranean diet, a glass of red wine daily and physical exercise, did not affect middle cerebral and internal carotid blood flow velocity in our patient group with carotid atherosclerosis. An increase in cerebral blood flow is thus unlikely to be the cause of the reduced risk of cerebrovascular disease and improved cognitive functioning described in the literature. One possible explanation for the fact that blood flow velocity was not affected by red wine, diet and physical activity advice is that two thirds of our patients were already on statin therapy. Statins increase cerebral blood flow and vasomotor reactivity via nitric oxide.

Background: Regular consumption of small amounts of red wine improves blood lipids. However, there is concern whether this beneficial effect might be counterbalanced by an increase in blood pressure (BP) and heart rate (HR), which are risk factors for cerebro-cardiovascular disease. In particular, we studied whether regular consumption of red wine with and without lifestyle changes (LC; healthy diet and physical activity advice) results in an increase in BP and HR. Methods: A prospective, unblinded randomized trial was performed in 108 patients (67% men) with carotid atherosclerosis documented by ultrasound, a mean BP of 122/79 mm Hg and a mean HR of 71 bpm at inclusion in the study. Sixty-eight percent were known and treated hypertensives. The mean 24-hour BP at baseline was 122/79 mm Hg. Half of the study participants, the control group, was seen by a nurse at baseline, after 4 and after 20 weeks, and was instructed not to change their eating and physical activity habits. In the other half, a dietician performed five sessions of 30 min each (at baseline, after 1 week and after 2, 3 and 4 weeks) giving advice on healthy eating based on a Mediterranean diet and physical exercise. The recommendations given were the following: 5 portions of fruit/vegetables per day, a diet low in absolute fat, a preference of vegetable oil (olive or rapeseed oil), whole-grain products, poultry, low-fat dairy products, 1 fat and 1 lean fish meal per week, reduced consumption of red meat, and avoidance of pork, ready-made meals, sugar and excessive salt intake. In addition, regular consumption of 1 bar of dark chocolate (25 g, >70% of cacao), 1-2 tomatoes, and 3-5 walnuts as well as at least 30 min of moderate daily physical activity were recommended. Within these two groups, half of the patients were randomized either to avoid alcohol completely or to drink 100 ml (women) or 200 ml of red wine (men) daily. Results: Neither LC nor red wine had an effect on the mean systolic and diastolic 24-hour BP and HR after 4 and 20 weeks, as analyzed by general linear modeling. No difference was found for diurnal and nocturnal values. Conclusions: The possible beneficial effect of regular consumption of small amounts of red wine is not counterbalanced in the long term by an increase in the mean BP or HR in mainly normotensive and well-treated hypertensive patients with carotid atherosclerosis, neither in the patients given healthy lifestyle advice nor in those with a standard lifestyle. Yet, we remain cautious about actively advice patients to drink alcohol regularly given the well-known risks.

There is conflicting evidence in the literature as to the potential effect of continuous positive airway pressure (CPAP) on cerebral perfusion. Compromising cerebral perfusion could possibly outweigh the benefit of improved oxygenation. Patients with the obstructive sleep apnea syndrome (OSAS) have been claimed to have a higher cerebrovascular reactivity to changes in end-tidal pC02. In this study, we investigated 23 patients with OSAS and 7 6 healthy young adults in the waking state. Both groups performed a series of lOmin of normal breathing, 20min with 9 cmH20 nasal CPAP, and then TOmin of normal breathing while wearing a nasal CPAP mask. The following parameters were assessed: bilateral transcranial Doppler signal of the middle cerebral artery, systolic and diastolic blood pressure assessed manually, and cerebrovascular reactivity to changes in pC02 during hyperventilation and rebreathing into an airbag. Continuous end-tidal pC02 measurements were performed in 74 subjects. As compared with normal breathing middle cerebral artery blood flow velocity and pC02 remained unchanged during CPAP. Systolic and diastolic blood pressure increased slightly by 1.2mmHg (p = 0.015) and 1.1 mmHg (p = 0.007), respectively. Cerebrovascular reactivity did not differ in the two groups. Nasal CPAP of 9 cmH20 is a safe treatment with respect to the maintenance of cerebral blood flow. Our study gives further evidence for the autoregulation's capacity to maintain cerebral blood flow velocity constant during different levels of intrathoracic pressure and different cerebral perfusion pressures. We could not demonstrate any difference in cerebrovascular reactivity between patients with OSAS and healthy persons. [Neurol Res 1999; 21: 737-741].

Extracranial and transcranial colour-coded duplex sonography (TCCD) are used routinely in clinical practice to assess physiologic and pathologic arterial blood flow to the brain. Such investigations are straightforward, safe, and cost effective, and can be repeated frequently for patient follow-up. In addition, the portability of extracranial colour-coded duplex sonography and TCCD provides the option of bedside investigations, particularly useful for evaluation of the critically ill patient. However, duplex ultrasound can be hampered by insufficient acoustic penetration, an unfavourable insonation angle, or by conditions of low or no flow. Echocontrast agents capable of surviving pulmonary and capillary transit have been developed, and such agents increase the Doppler signal and, therefore, the success rate of neurosonographic investigations. Approximately 20% of TCCD studies involve poor insonation conditions and, therefore, the use of echocontrast agents is of particular interest for this application. Levovist® and SonoVue® are the two agents currently approved for use in neurosonography. Such agents have a relatively long-lasting effect (up to 7 min), and can be administered as a single injection or, alternatively, a fractionated injection protocol can be used, depending on the quality of the window.

This study compares the additional benefit of diffusion-weighted MRI (DWI) and microembolus detection by transcranial Doppler ultrasonography (TCD) in the assessment of stroke etiology.Fifty-five acute anterior circulation stroke or TIA patients were investigated by both cranial DWI and bilateral TCD of the middle cerebral arteries (1 hour).In one of the 13 patients without acute ischemic lesions visualized on DWI, microembolic signal (MES) detection was positive. However, in 33 out of 44 patients without MES, DWI revealed at least one lesion. In two patients with unilateral territorial infarction and otherwise normal cardiovascular work-up, bilateral MES were found thus localizing the embolic source into the aortic arch or the heart. In a further patient with a dissection, the occurrence of contralateral MES raised doubts on a dissection to be the cause of the infarct.There is a contribution of both techniques to the understanding of stroke etiology. The impact of DWI is, however, superior to that of MES detection. Longer TCD recording times may diminish this discrepancy.

Clinically silent microembolic signals (MES) can be detected by transcranial Doppler sonography (TCD). There is theoretical evidence that lower ultrasound emission frequencies may lead to a higher signal intensity and thus sensitivity to detect MES. We compared a 1-MHz probe with a 2-MHz probe regarding sensitivity in the detection of MES. Moreover, embolus detection by transcranial Doppler ultrasound is very time consuming and semi-automated detection is mandatory. Therefore, we studied an on-line algorithm using the bi-gate technique and the two transmission frequencies.After defining detection thresholds ofor = 12 dB (1 MHz) andor = 10 dB (2 MHz) with eight normal subjects as MES-negative controls, taking into account natural fluctuations of the Doppler spectrum, we studied 36 patients with ischaemic events and five asymptomatic patients with incidental embolic sources. All patients subsequently underwent a 1-hour unilateral embolus detection from the middle cerebral artery (MCA) or the posterior cerebral artery (PCA), respectively, using 1 and 2 MHz for 30 minutes each in a randomized order. The software algorithm was compared with a blinded off-line analysis by an experienced observer as a gold standard.The investigator detected 198 MES (range 0-41 MES) in the recordings of 29 patients out of the 41 patients using the 1-MHz probe and 101 MES (range 0-32 MES) in the recordings of 14 patients using the 2-MHz probe (p = 0.0007). Sensitivity of the software to detect MES confirmed by the investigator was 31% using 1 MHz and 41% using 2 MHz. The positive predictive value was 6 and 30%, respectively.The sensitivity and positive predictive values of the automated algorithm to detect MES were unacceptably low for clinical practice with both frequencies. The use of 1 MHz instead of 2 MHz may, however, be useful when evaluating the recordings off-line by an experienced blinded observer.

Objectives: Proper assessment of the intracranial arteries by transcranial color-coded duplex sonography (TCCD) is occasionally made difficult by an insufficient temporal bone window, an unfavorable insonation angle, or low flow velocity or volume. In these cases, echocontrast could be helpful to increase the diagnostic confidence or to make the diagnosis at all. Material and Methods:We investigated 67 temporal windows of 47 patients with insufficient native transtemporal insonation conditions before and after the application of the second-generation (gas-filled) microbubble contrast agent Sonovue® (in 20 patients out of these 47, both temporal windows were insufficient, in the remaining 27 only one side). Results: As compared to the precontrast scans, echocontrast allowed for more segments to be evaluated by pulsed Doppler sonography (p < 0.0001) and for longer lumen segments to be displayed on color mode (p < 0.0001). With the help of contrast medium, flow velocity in the middle cerebral artery could be measured through 65 windows as compared to only 26 windows before contrast was applied (p < 0.0001). Conclusions: In patients with poor precontrast visualization of intracranial arteries, echocontrast-enhanced TCCD is very helpful.

Neurosonological investigations of the extracranial and intracranial brain supplying arteries are helpful in the assessment of stroke and stroke-prone patients.In this paper we review the indications, application and advantages of second-generation (gas-filled) microbubble contrast agents such as SonoVue.Gas-filled microbubbles have a strong echo enhancing effect and produce enhancement for several minutes, enabling the sonographer to perform the investigation with a single injection or two or three repeated injections without the need for continuous administration. Echocontrast agents provide better delineation of normal blood flow, occlusions, pseudo-occlusions, stenoses, and collaterals in the extracranial and intracranial vascular beds. They are of particular value during transcranial color-coded transcranial duplex investigations via the temporal and occipital window.Echocontrast agents give additional information on the patient's vascular situation that is often crucial to planning further diagnostic and therapeutic steps. The use of second-generation gas-filled microbubbles, such as SonoVue in transcranial neurosonology, may help to avoid unnecessary, expensive and potentially harmful additional investigations such as intra-arterial DSA. Future applications include the visualization of brain tissue perfusion.

Background and Purpose: The major limitation of native transcranial colour-coded duplex sonography (TCCS) in older stroke patients is the relatively frequent occurrence of an insufficient temporal window. Our goal was to investigate the relationship between the in vivo Doppler ultrasound image quality of the temporal bone, and computed tomography (CT)-determined thickness, density, and homogeneity of cadaver temporal bone. Methods: Thirty-three moribund neurological patients who eventually died were examined by TCCS using the transtemporal approach. The sonographer categorized the quality of the TCCS image (excellent, intermediate, and poor). During autopsy, a rectangular sample of the temporal squama was removed, which corresponded to the area of the in vivo acoustic window. The thickness of the whole temporal bone, cortical, and cancellous (= diploe) bone as well as the density and homogeneity were determined by high-resolution CT. Results: Thirty-seven temporal bones were obtained. The quality of the acoustic window was classified as excellent in 13, intermediate in 6 and poor in 18 cases. A significant correlation between the complete bone thickness, as well as between the absolute thickness of the diploe and the quality of the acoustic window was found: the thinner the bone/diploe, the better the colour Doppler signal. The thickness of the cortical plates and the homogeneity of the bones were identical in the three image quality categories. Conclusion: The transtemporal TCCS image quality depends mainly on the thickness of the cancellous component of the temporal bone.

Clinically silent circulating microembolic signals (MES) can be identified by transcranial Doppler ultrasound (TCD). It is not yet clear whether their occurrence is always linked to the presence of embolic sources. 24 terminally ill patients (7 women, 17 men; mean age 68 years) were investigated by TCD of the middle cerebral arteries. These findings were correlated with a complete post-mortem examination of potential embolic pathways. Four patients out of the 24 under investigation showed MES, 2 of them bilaterally. All these 4 MES-positive patients had a definite embolic source, i. e. bilateral carotid artery occlusive disease, endocarditis with thrombotic valvular adhesions and severe plaques in the aortic arch, dilated left atrium and a patent foramen ovale, or severe plaques in the aortic arch and a dilated left atrium, respectively. In the investigated patient group, we could demonstrate that MES can only be found when an embolic source is present. The finding of MES justifies an extensive clinical and laboratory search for potential embolic sources including extracranial and intracranial colour-coded duplex ultrasound, ECG, Holter-ECG, and TEE.

Objectives – Arterial hypertension is, besides age, the number one risk factor for ischaemic stroke. Patients with arterial hypertension frequently present with additional coexisting vascular risk factors interacting in a complex way. Material and methods – This paper reviews the benefit of antihypertensive treatment, as well as different treatment options of arterial hypertension and their side-effects. Results – Patients with definite arterial hypertension, but also patients with so-called normal or high-normal blood pressure are at increased risk to develop stroke and other cardiovascular complications. Vascular remodelling of small and large vessels provoked by arterial hypertension is the initial step in the development of atherosclerosis and lipohyalinosis. Vascular remodelling can be improved or even normalized by antihypertensive treatment with angiotensin-converting-enzyme inhibitors and angiotensin-I-receptor antagonists showing the most convincing effects. Angiotensin-converting-enzyme inhibitors and angiotensin-I-receptor antagonists have the lowest rate of side-effects, however, economic restraints hinder their general application. Statins are needed to treat dyslipidaemia. They also lower blood pressure and have a synergistic effect with the above two antihypertensive components in lowering blood pressure. In hypertensive patients, risk of stroke and other cardiovascular complications is determined by the blood pressure level and the presence or absence of target organ damage and the interaction with other risk factors, such as cigarette smoking, dyslipidaemia, and diabetes. These high-risk patients should be treated even more aggressively than usual. Conclusions – In the vast majority of patients and healthy individuals, target blood pressure should be as high as or below 120/80 mmHg to minimize the occurrence of stroke and other cardiovascular complications.

Carotid bruits are supposed to indicate the presence of high-grade common carotid or extracranial internal carotid artery stenosis in a large proportion of patients. Using a stethoscope, we prospectively auscultated 273 carotid arteries of 145 patients blinded to the results of a complete extracranial and intracranial Doppler investigation including extracranial color-coded duplex ultrasound. Fifty-four arteries showed stenosis of > or = 50%-99%, or occlusion of the extracranial internal or the common carotid artery. In 25 of these arteries, a bruit was present. In 9 out of 16 patients with extracranial stenosis from 70%-99%, a bruit was detected. In one additional patient with a middle-grade external carotid artery stenosis, a bruit was also present. In seven additional patients, a bruit was present in the absence of any carotid artery stenosis, cardiac vitium or goiter. The sensitivity of carotid auscultation for the detection of a 70%-99% stenosis of the common or extracranial internal carotid artery was 56% and specificity was 91%. The positive predictive value of a bruit found during carotid auscultation was 27%, and the negative predictive value of a normal auscultation was 97%. Carotid auscultation is a useful screening procedure in the detection of carotid stenosis or occlusion, but requires confirmation by carotid ultrasound.

Although most therapeutic efforts and experimental stroke models focus on the concept of complete occlusion of the middle cerebral artery as a result of embolism from the carotid artery or cardiac chamber, relatively little is known about the stroke mechanism of intrinsic middle cerebral artery stenosis. Differences in stroke pathophysiology may require different strategies for prevention and treatment. We prospectively studied 30 consecutive acute ischemic stroke patients with middle cerebral artery stenosis detected by transcranial Doppler and magnetic resonance angiography. Patients underwent microembolic signal monitoring by transcranial Doppler and diffusion-weighted magnetic resonance imaging. Characteristics of acute infarct on diffusion-weighted magnetic resonance imaging were categorized according to the number (single or multiple infarcts) and the pattern of cerebral infarcts (cortical, border zone, or perforating artery territory infarcts). The data of microembolic signals and diffusion-weighted magnetic resonance imaging were assessed blindly and independently by separate observers. Diffusion-weighted magnetic resonance imaging showed that 15 patients (50%) had single acute cerebral infarcts and 15 patients had multiple acute cerebral infarcts. Among patients with multiple acute infarcts, unilateral, deep, chainlike border zone infarcts were the most common pattern (11 patients, 73%), and for single infarcts, penetrating artery infarcts were the most common (10 patients, 67%). Microembolic signals were detected in 10 patients (33%). The median number of microembolic signals per 30 minutes was 15 (range, 3-102). Microembolic signals were found in 9 patients with multiple infarcts and in 1 patient with a single infarct (p = 0.002, chi(2)). The number of microembolic signals predicted the number of acute infarcts on diffusion-weighted magnetic resonance imaging (linear regression, adjusted R(2) =0.475, p < 0.001). Common stroke mechanisms in patients with middle cerebral artery stenosis are the occlusion of a single penetrating artery to produce a small subcortical lacuna-like infarct and an artery-to-artery embolism with impaired clearance of emboli that produces multiple small cerebral infarcts, especially along the border zone region.

Background: Intracranial arterial stenosis is a rare cause of stroke in Caucasians. Detection of clinically silent circulating microemboli by transcranial Doppler sonography is now widely investigated in patients with carotid artery disease in the hope to identify patients at increased risk for stroke. Methods: In 33 patients with intracranial internal carotid (n = 12), middle cerebral (n = 18), posterior cerebral (n = 2), or basilar artery stenosis (n = 1), we performed a 1-hour microembolus detection downstream to the stenosis in the middle or in the posterior cerebral artery, respectively. The stenosis was assessed by transcranial Doppler and duplex ultrasound. 18 patients had been symptomatic in the dependent territory. Results: Five patients with ischaemic symptoms within the last 8 days and with a peak systolic flow velocity of ≧210 cm/s in the stenosis showed microembolic signals at a rate of 3–25 events/h, despite effective anticoagulation. All these 5 patients had a lesion pattern on cranial CT or MRI scan suggesting embolic origin. All the asymptomatic patients (n = 15) and all the patients with a peak systolic intrastenostic velocity of 160 to Conclusion: Microembolic signals occur in recently symptomatic patients with high-grade intracranial arterial stenosis indicated by a sonographically measured stenotic peak flow velocity of ≧210 cm/s. Therapeutic anticoagulation was not sufficient to suppress microemboli formation.

We report the case of a young woman with progressive cognitive decline and epilepsy. She showed ischemic cerebrovascular disease and proximal livedo racemosa. Antiphospholipid antibody (aPL) could not be detected and there were no microemboli on continuous transcranial Doppler ultrasonography monitoring. Histology of cerebral vessels showed intimal hyperplasia in small leptomeningeal venous vessels and micronecrosis of grey and white matter. We subsequently made the diagnosis of aPL-negative Sneddon Syndrome (SNS). Anticoagulation with warfarin could not be initiated because of a drug-resistant epilepsy with the risk of falls and subsequent bleeding; immunosuppression with steroids and azathioprine was ineffective, as was initial antiplatelet therapy with clopidogrel alone. However, when we intensified antiplatelet therapy by combining clopidogrel and ASS, a slowing of disease progression, as assessed by neuropsychological testing and magnetic resonance imaging, was noted on a follow-up after 6 months. Therapeutic options in SNS in both aPL-positive and aPL-negative patients with SNS are discussed.

Background and Purpose: Cardiac right-to-left shunts (RLS) can be identified by transesophageal echocardiography (TEE) as well as by transcranial Doppler ultrasound (TCD) using contrast agents, such as Echovist®-200 or Echovist®-300 in conjunction with a Valsalva maneuver (VM) as provocation procedure. Both Echovist preparations are in use. Currently, the appropriate timing of the VM is still under debate. Methods: Sixty-four patients were investigated by both TEE and bilateral TCD of the middle cerebral arteries. The following protocol was applied in a randomized way: (1) no VM, (2) VM for 5 s starting with the beginning of Echovist-300 injection, (3) VM for 5 s starting 5 s after the beginning of Echovist-300 injection, (4) VM for 5 s starting 10 s after the beginning of Echovist-300 injection, and (5) VM for 5 s starting 5 s after the beginning of Echovist-200 injection. Results: In 27 patients, an RLS was demonstrated by both TEE and contrast TCD (shunt-positive). Twenty-two patients were negative in both investigations, no patient was positive on TEE but negative on TCD, 15 patients were only positive on at least one TCD investigation but negative on TEE. Tests 3 and 5 were the most appropriate ones; test 3 was slightly superior to test 5. Conclusions: TCD using Echovist-300 or Echovist-200 is a sensitive method to identify TEE-proven cardiac RLS. To achieve the best diagnostic accuracy, the VM should be performed for a duration of 5 s starting at 5 s following the beginning of contrast injection.

Background and Purpose: Visualization of normal or pathological flow in the intracranial arteries using transcranial colour-coded duplex sonography (TCCS) is occasionally obstructed by insufficient temporal bone windows, unfavourable insonation angles, or low flow velocities or volumes. SonoVue® (BR1) is a new, long-acting echocontrast agent, which could be helpful in these instances. Methods: SonoVue was studied in two separate multicentre investigations of patients with insufficient bone windows (BR1-014 with 73 patients and BR1-017 with 40 patients) using an identical protocol. The agent was given intravenously as a bolus in four different doses (0.3, 0.6, 1.2 and 2.4 ml). Evaluation was performed on-site and off-site with video clips. Results: The contrast agent was well tolerated. As compared to the precontrast scans, SonoVue facilitated the visualization of vessel patency, stenosis, occlusion, and collateral flow, decreased the need for additional tests, and had an impact on the patient’s treatment. In 66–74%, a non-diagnostic investigation was converted into a diagnostic investigation. The highest dose (2.4 ml) allowed for a clinically useful signal enhancement of a median 1.9–6.3 min. Conclusions: SonoVue at a single dose of 1.2 or 2.4 ml is effective in increasing the detection of normal or pathological flow in the intracerebral arteries in patients who do not have a fully diagnostic unenhanced TCCS examination.

Proper assessment of intracranial arteries by transcranial Doppler sonography (TCD) in patients with intracranial stenoses is occasionally made difficult by an insufficient temporal bone window, an unfavourable insonation angle, or low flow velocity or volume. This condition is frequently found in Chinese. In these cases, echocontrast could be helpful. We investigated 48 temporal windows of 24 acute Chinese stroke patients with insufficient native transtemporal insonation conditions before and after the application of the echo enhancer Levovist® (galactose/palmitic acid) by an injection pump. We classified the signal quality from four segments of the main intracranial arteries: anterior cerebral artery (A1), main stem of the middle cerebral artery (MCA, M1), intracranial segment of the carotid artery (C1), and posterior cerebral artery (P1). The signal quality was classified as follows: 0 = no signal, 1 = poor, envelope curve does not follow spectrum, 2 = adequate, envelope curve follows spectrum. As compared to the pre-contrast scans, echocontrast allowed for more segments to be evaluated by pulsed Doppler sonography. Before Levovist, only 12% of the segments could be detected, after Levovist 63%. For all arteries, signal quality was better after Levovist, p between 0.0180 and 0.0003. In 3 patients, MCA stenoses with peak systolic Doppler flow velocities above 160 cm/s were found only after Levovist. In patients with poor pre-contrast detection, echocontrast-enhanced TCD allows for more arterial segments to be insonated and for the detection of stenoses unnoted during the non-enhanced investigation.

Electrical cardioversion (CV) of atrial fibrillation (AF) is associated with an increased risk of stroke, and its appropriate prevention is still a matter of debate. It is known that, besides dislodgement of pre-existing intra-atrial thrombi, the ‘stunned’ atrium after CV is an important cause of thrombus formation and subsequent embolism. We investigated whether CV of AF is associated with occurrence of circulating microemboli (ME) representing a sensitive marker of the actual thromboembolic activity. Twenty-nine patients (22 men) aged 54 ± 13 years suffering from valvular (n = 5) or nonvalvular (n = 24) AF were studied. All but 1 patient (with recent-onset AF) had been put on oral anticoagulation (INR >2.0) for at least 3 weeks before and 4 weeks after successful CV. In all patients, exclusion of internal carotid artery stenosis and atrial thrombus was performed prior to CV. Five unilateral 1-hour transcranial Doppler ME monitorings over the middle cerebral artery were performed (1) before CV, and (2) immediately, (3) 4–6 h, (4) 24 h, and (5) 2–4 weeks after CV. Total absence of circulating ME was found before CV as well as during a cumulative monitoring time of 115 h after successful CV. Electrical CV of AF after at least 3 weeks of effective anticoagulation is not associated with occurrence of cerebral circulating ME. This finding requires further investigation including high-risk patients with AF undergoing CV based on different treatment protocols.

In carotid artery stenosis both the degree of the lesion and its plaque morphology are thought to be associated with the carrier's thromboembolic risk. In this study we evaluated the diagnostic preciseness of non-invasively B-mode ultrasound in predicting the histopathological plaque structure. We examined 44 patients with > 50% ICA stenosis by B-mode within 6 weeks prior to carotid endarterectomy. At the affected bifurcations, up to 10 different regions of interest (ROI) per artery were investigated. Plaque appearance was classified according to 6 subtypes considering different ultrasonic plaque features. Postoperatively, plaque specimens were examined histopathologically for their relative content of calcification, fibrous tissue and different soft tissue. B-mode ultrasound was compared with histopathological features in ROI. A total of 265 regions of interest were evaluated. In mainly echolucent types of plaques, atheromatous debris was most frequently seen, whereas fibrosis was rare. Homogeneous echolucent plaques showed a high proportion of cholesterol and/or recent haemorrhage. Thrombosis at the plaque surface was often seen in "completely echolucent" plaque type (each P

The present study was designed to perform follow-up transcranial Doppler investigations for microembolic signals (MES) in acute stroke patients by means of a strict protocol. The number of MES was correlated with stroke etiology and the strength of antithrombotic treatment. Concurrently, we wanted to demonstrate that MES in acute stroke patients are solid in nature and not gaseous. Nineteen patients with middle cerebral artery ischemic events, 16 with completed stroke and 3 with transient ischemic attack (TIA) were investigated within 24 h following the onset of symptoms. Six 1-hour recordings on days 1, 2, 3, 4, 7 and 14 were performed from the affected middle cerebral artery. The four-gate technique and recently established criteria for the identification of MES were used. Eight of 19 patients showed MES in at least one recording. Variability was high and showed no uniform tendency with respect to time since onset of symptoms or treatment. All 3 patients with internal carotid artery dissection showed MES. In 3 patients with lacunar stroke, no MES were detected. Two patients with MES suffered recurrent TIAs during the observation period, whereas none of the patients without MES suffered a recurrent ischemic event. In the acute phase following stroke, ongoing, emerging and vanishing embolization in some patients may reflect individual active processes of remodelling, healing and disruption or disappearance of the embolic source.

Background: The anterior communicating artery is a key collateral pathway in patients with internal carotid artery (ICA) occlusions. Diagnostic balloon or manual occlusion of the ICA is a qualified test for the collateral function of the circle of Willis. The aim of our study was to test whether transcranial Doppler sonography (TCD) with manual carotid compression is able to predict the degree of cross-over flow and tolerance of ICA occlusion. Methods: A prospective study was performed on 88 patients suffering from neck tumors or inoperable ICA aneurysms with planned ligation or permanent balloon occlusion of the ICA. Preceding a balloon occlusion lasting 20 min we performed TCD with manual carotid compression test. Insufficient cross-over flow during transient carotid occlusion was defined angiographically as missing opacification of the middle cerebral artery (MCA) after selective injection of contrast media in the contralateral ICA, and sonographically as a decrease greater than 60% in flow velocity of the MCA ipsilateral to the carotid occlusion. Results: TCD and angiography could be compared in 70 of 88 patients. Angiography showed no or insufficient collateral flow in 26%. All patients (n = 10) with a decrease in MCA velocity greater than 60% on angiography showed missing or poor cross-over flow. A greater than 50% increase in the anterior cerebral artery (ACA) predicted moderate or good cross-over flow in 98%. Clinical observation revealed 11 transient neurological deficits. Eight of them showed insufficient cross-over flow angiographically and sonographically. In 2 of 11 only TCD revealed such low collateral supply. Neither technique predicted hemodynamic ischemia in only 1 of the 11. Conclusion: TCD with carotid compression test is a valid method for predicting interhemispheric flow and clinically relevant hemodynamic compromise in cases of occlusion of the ICA.

B-waves are rhythmic oscillations of intracranial pressure (ICP) with a wavelength of 0.5-2 min. These oscillations are accompanied by corresponding fluctuations of arterial blood pressure (BP). There is controversy in the literature whether the ICP oscillations precede or follow the BP oscillations. This relationship, however, is important for the understanding of the origin and the interactions of ICP B-waves with other parameters. ICP and BP were monitored continuously for one night in nine patients with suspected symptomatic normal pressure hydrocephalus (NPH). Forty-five B-waves were identified and the time delays between the peaks and the onsets of B-waves and their BP-equivalents were measured. The mean (+/- standard deviation) of the time delays between the peaks of ICP B-waves and corresponding BP-oscillations was 4.2 +/- 2.4 sec and between the onsets of the oscillations 10.3 +/- 6.6 sec. In all but two B-waves, the ICP peak preceded the BP peak, in all the 45 B-waves the onset of the ICP increase preceded the BP increase (p0.004). Our study demonstrates that ICP B-waves precede concomitant changes in BP by several seconds.

Transcranial Doppler sonography has become a widely used method for detecting cerebral circulating microemboli (ME) arising from the carotid arteries or the heart. Yet, studies on subgroups of patients with distinct cardiac sources of embolism are still limited. The same holds true for investigations on the relationship between microembolization and hemorheological parameters. A total of 142 patients suffering from left ventricular aneurysm (LVA, n = 52), severe left ventricular dysfunction (LVD, n = 43), or chronic atrial fibrillation (AF, n = 47) were enrolled in this study. All patients had been neurologically asymptomatic for at least 1 month. Further relevant embolic disorders of the carotid arteries and the heart had been excluded. Unilateral monitoring for ME over the middle cerebral artery was performed for 30 min. Blood was drawn after each monitoring for determination of plasmatic coagulation parameters, as well as plasma viscosity, and platelet reactivity. The overall prevalence of ME was 31%, with a slightly higher prevalence in patients with LVA (37%) compared to patients suffering from AF (30%) or LVD (26%). With single-factor analysis, a trend towards higher ME prevalences was found with (a) a history of remote embolic events, (b) ineffective anticoagulation, (c) increased platelet aggregation, or (d) increased plasma viscosity (all p > 0.1). The combination of ineffective anticoagulation in conjunction with increased platelet aggregation, however, was significantly associated with higher ME rates even after adjustment for other factors by logistic regression analysis. Our results demonstrate a low ongoing microembolic activity in asymptomatic patients suffering from LVA, LVD and AF. An activated plasmatic coagulation system together with increased platelet aggregation contributes to ME generation.

Besides the degree of carotid artery stenosis, the composition of the plaque may help to predict the thromboembolic risk. Low echogenicity on ultrasound and hemorrhage into the atheroma demonstrated histopathologically have been shown to be associated with a higher risk of embolism. Twenty-nine consecutive patients with carotid artery stenosis and scheduled for carotid endarterectomy were investigated preoperatively by B-mode ultrasound. Post-operatively the endarterectomy specimens were examined histopathologically. Neither atheroma with hemorrhage nor atheroma without hemorrhage were significantly associated with echolucent ultrasound presentation. Out of the 10 lesions echolucent and homogeneous on ultrasound, six corresponded to atheroma with hemorrhage, two corresponded to atheroma with hemorrhage plus thrombus, two corresponded to fibrous plaque plus thrombus, and one corresponded to pure thrombus. Out of the 4 lesions heterogeneous and predominantly echolucent, one corresponded to atheroma without hemorrhage plus thrombus, one corresponded to atheroma with hemorrhage, one corresponded to atheroma with hemorrhage plus thrombus, one corresponded to atheroma with hemorrhage plus fibrous plaque. Seven out of the 18 atheromas with hemorrhage did not present as purely or predominantly echolucent lesions, six of them were even homogeneously echogenic. Plaque surface could not reliably be predicted by ultrasound. In our study, there was no significant correlation between ultrasound and histology of the lesion.

Periodic leg movements (PLM) in sleep are supposed to constitute a frequent cause of insomnia. There is some controversy whether PLM are the cause of insomnia by provoking microarousals or whether they are simply and epiphenomenon not casually related to the insomnia. We examined four patients with PLM by overnight polysomnography and concomitant transcranial Doppler sonography (TCD) monitoring, 13 patients with suspected normal pressure hydrocephalus by concomitant overnight polysomnography and intracranial pressure recording, and 10 healthy volunteers by concomitant overnight polysomnography and TCD monitoring. EEG arousals occurred more frequently before than after the PLM. PLM were associated with increase in heart rate, breathing amplitude, and cerebral blood flow velocity assessed by TCD. PLM occurred with a mean wavelength of 40.5 s. This mean wavelength corresponded to similar values calculated for intracranial pressure B-waves (43.3 s) in 13 patients with suspected normal-pressure hydrocephalus, TCD B-wave equivalents (42.2 s) in 10 healthy young adults and the frequency of the cyclic alternating pattern in EEg recordings (40 s). Our date suggest that these cyclic variations with a wavelength of about 40 s are part of a common endogenous rhythm. PLM seem to be an epiphenomenon of this rhythm and not the cause of insomnia.

Circulating cerebral emboli can be detected by transcranial Doppler (TCD) sonography. However, there has been little systematic study of parameters necessary for optimal embolus detection. Both the in

The in vivo correlates of microembolic signals (MES) are still unknown. Platelet-associates (PA) with monocytes or granulocytes or platelet aggregates only may represent these correlates.Thirty patients with asymptomatic carotid stenosis50% and 16 patients with acute (4 days) atherothrombotic stroke were investigated. PA, P-selectin and thrombospondin expressions on platelets were assessed by flow cytometry. Soluble P-selectin (sPS) levels were assessed. MES detections were performed by transcranial Doppler sonography for 1 hour. PA, P-selectin and thrombospondin expressions on platelets and sPS levels were compared between MES-positive (MES+) and MES-negative (MES-) patients.Eight patients (27%) with asymptomatic carotid stenosis had 1-26 MES/h. Degree of stenosis was 78 +/- 10% in MES- and 88 +/- 8% in the MES+ (p=0.01). There were no differences in percentages of PA. P-selectin and thrombospondin surface expression was lower in MES+, but this was not significant. sPS levels were higher in MES+ (122 +/- 27 ng/ml versus 80 +/- 25 ng/ml in MES-, p=0.01). Seven (44%) patients with stroke had 1-39 MES/h. There were no differences in percentages of PA. MES+ had higher sPS levels (178 +/- 43 versus 121 +/- 44 ng/ml, p=0.02) and less P-selectin surface expression than MES- (9.0 +/- 3.4 versus 4.5 +/- 1.6%, p=0.004).High levels of sPS in MES+ and lower expression of platelet activation markers on platelets' surface suggest shedding of activation markers from the platelets' surface and thus enhanced activation of platelets of MES+ compared with MES-. PA are probably not the clinical correlates of MES, but platelets seem to be the main cellular element of solid cerebral microemboli.

Five different calliper methods for assessing the degree of carotid artery stenosis and visual estimation ("eyeballing") of postmortem carotid arteriograms were compared with the planimetric gold standard of the area reduction at the site of the stenosis.During autopsy 53 carotid specimens were removed in toto from 31 neurological patients. Carotid arteries were ligated and redistended to a physiological degree for standardised three-plane arteriography. Afterwards, the entire specimen was filled with an embedding medium under the same conditions and sectioned. Slices at the site of stenoses were histologically processed. Computerised planimetric analysis of the lumen area reduction was performed and compared with the arteriographic findings. Arteriograms were evaluated by two independent observers by means of linear Common Carotid Artery (CC), the European Carotid Surgery Trial (ECST) and the North American Symptomatic Carotid Endarterectomy Trial (NASCET), and squared measurements (NASCET2, ECST2) after applying the pi r2 function. Further, three independent observers performed eyeballing of the degree of stenosis from the postmortem arteriographies.Planimetry was carried out in 29 internal carotid artery (ICA) and 17 common carotid artery (CCA) stenoses ranging from 8.5 to 100%. The smallest mean differences of the degree of stenosis in % between planimetry and arteriography were -0.5 and 0.6%. The narrowest 95 %-limits of agreement covered a range of +/-24.1 and 26.3% of stenoses, and the highest correlation coefficients were both 0.9 for the CC and ECST2 techniques, respectively. By eyeballing, the degree of stenosis was underestimated by 13.5 to 15.8% on average. The narrowest limits of agreement between two observers for eyeballing covered a range of 35%.Three-plane arteriography has only a moderate accuracy and reproducibility in detecting and measuring carotid artery stenosis independent of the technique of measurement used.

High-intensity transient signals (HITS) detected by transcranial Doppler (TCD) ultrasound may correspond to artifacts or to microembolic signals, the latter being either solid or gaseous emboli. The goal of this study was to assess what can be achieved with an automatic signal processing system for artifact/microembolic signals and solid/gas differentiation in different clinical situations. The authors studied 3,428 HITS in vivo in a multicenter study, i.e., 1,608 artifacts in healthy subjects, 649 solid emboli in stroke patients with a carotid stenosis, and 1,171 gaseous emboli in stroke patients with patent foramen ovale. They worked with the dual-gate TCD combined to three types of statistical classifiers: binary decision trees (BDT), artificial neural networks (ANN), and support vector machines (SVM). The sensitivity and specificity to separate artifacts from microembolic signals by BDT reached was 94% and 97%, respectively. For the discrimination between solid and gaseous emboli, the classifier achieved a sensitivity and specificity of 81% and 81% for BDT, 84% and 84% for ANN, and 86% and 86% for SVM, respectively. The current results for artifact elimination and solid/gas differentiation are already useful to extract data for future prospective clinical studies.

Background: Transesophageal echocardiography (TEE) and transcranial Doppler sonography (TCD) can identify right-to-left-shunts that predispose to paradoxical embolism. In a large cohort we compared the results of both techniques. Methods: 222 patients were investigated by both techniques using the contrast agent Echovist®-300 and performing each test once without and once with the Valsalva maneuver (VM). Results: TEE-proven right-to-left-shunts were detected by TCD with a high sensitivity of 94%. In addition, TCD revealed shunts not noted during TEE in about 20% of all patients studied. These shunts are in general smaller than those concordantly identified; however, 9% of the patients without a TEE-proven shunt presented with a shunt that allows a considerable amount of contrast medium to pass. There were 12% more microbubbles detected in the right middle cerebral artery than in the left middle cerebral artery during the TCD test performed with VM, but not during the TCD test performed without VM. Conclusions: Contrast-enhanced TEE and TCD are complementary methods in the assessment of stroke and stroke-prone patients. The side difference of microbubbles may indicate a selective streaming of cardiac emboli during VM.

Fabry’s disease is a sex-linked recessive storage disorder leading to cerebrovascular symptoms in many cases. Whether the primary origin of cerebrovascular symptoms in these patients is due to autochthonous thrombosis of small vessels or embolic infarction from large vessels is under debate. Microembolic signals (MES) indicative of an active embolic source can be recorded by transcranial Doppler sonography. We report four patients (34, 44, 62 and 66 years old) with Fabry’s disease from one kindred in whom we carried out microembolus detection recordings to disclose active embolic sources. Three of the patients had had transient focal neurological deficits. Two patients had angina pectoris and one had exercise dyspnea, but no patient had clear evidence of disease of the large coronary vessels or brain-supplying arteries. No MES were found in 1-hour recordings in any patients, supporting the hypothesis that early cerebrovascular symptoms arise from small vessel occlusion and not from embolic sources as an indicator of disease of large brain-supplying arteries or cardiac embolism.

Symptomatic atherothrombosis in one vascular bed is usually indicative of disseminated disease. Indeed, involvement of multiple beds is common in everyday clinical practice, and these patients are at much higher risk of ischaemic events. The prevention of manifestations following atherothrombosis is therefore an important therapeutic goal in these patients. Some causative risk factors demonstrate affinities to particular arterial domains. Cigarette smoking, for example, is particularly associated with atherothrombotic involvement of the pelvic and lower limb arteries, whereas arterial hypertension is associated with the intracranial cerebral arteries. The degree, spread and progression of atherosclerosis can be assessed using various non-invasive and invasive modalities: high-resolution Doppler ultrasound, ankle-brachial index (ABI) measurement, magnetic resonance (MR), computed tomography (CT) and intra-arterial angiography. Indicators of atherothrombotic risk include increased carotid artery intima-media thickness, microembolic signals on transcranial Doppler ultrasonography and low ABI. There is a strong rationale for the inclusion of the ABI measurement as part of the routine clinical examination to assess the cardiovascular risk in patients with identified risk factors. Furthermore, detection of a low ABI should serve as a trigger for patient management with aggressive antiplatelet therapy. The generalized nature of atherothrombosis and the methods for evaluating the spread of disease are illustrated through the case history of a patient with disseminated atherothrombotic disease.

Background and Purpose: Carotid and vertebral artery dissections are frequently complicated by cerebral embolism. Detection of clinically silent circulating microemboli by transcranial Doppler sonography (TCD) is now widely investigated in patients with carotid artery disease in the hope to identify patients at increased risk for stroke. Methods: In 20 patients with carotid (n = 17) or vertebral (n = 2) artery dissection, or both (n = 1), we performed a 1-hour microembolus detection downstream to the dissection in the middle or in the posterior cerebral artery, respectively. Results: Five patients with a carotid artery stenosis of ≧90% or with carotid artery occlusion showed microembolic signals at a rate of up to 15 events/h. In all these patients, the onset of the dissection was within the last 58 days. Patients with lower degrees of stenosis or onset of symptoms beyond 58 days did not show microembolic signals at all. Three patients who had presented with recurrent ischaemic events prior to TCD monitoring unexceptionally had microembolic signals. Conclusion: Microembolic signals occur in patients with high-grade stenosis or occlusion due to acute cervical artery dissection. Patients with microemboli seem to be at increased macroembolic risk, i.e. stroke recurrence, and may require close-meshed clinical follow-up and possibly stronger antithrombotic treatment.

Background: Clinically silent circulating microemboli can be detected by transcranial Doppler sonography. Case Description: We report the case of a 45-year-old man with congenital cyanotic heart disease, elevated haematocrit, low platelet count and decreased protein C and protein S activity. Before and following several haemodilutions, we performed 5 1-hour transcranial Doppler recordings from one or both middle cerebral arteries (MCAs) on different days. The number of microembolic signals per hour varied from 54 to 134. During the bilateral recording, the microemboli occurred on both sides (55 in the right and 45 in the left MCA, respectively). There was no relation to red blood cell count, platelet count, the spontaneously lowered prothrombin time or the spontaneously prolonged activated partial thromboplastin time. Conclusions: The origin of the large number of microembolic signals found in this patient remains unclear, but may be presumed in the intra-abdominal or crural venous system.

Atrial fibrillation (AF) is a well-recognized independent risk factor of ischemic stroke. The aim of this study was to investigate the amount of microembolic signals (MES) in 15 patients with ‘lone’ AF representing the subgroup of AF patients with the lowest lifelong risk of stroke. All patients had been put on effective anticoagulation due to a scheduled electric cardioversion. Additional cardiac and arterial sources of embolism were excluded by echocardiography and extracranial color-coded duplex sonography of the carotid arteries. Unilateral one-hour transcranial Doppler monitorings revealed complete absence of MES in this series. This observation fits the concept that the amount of microembolisation is related to the risk of manifest thromboembolism. Further studies on this patient group treated with less intensive antihemostatic therapy should be undertaken to define more clearly the disease-specific microembolic activity. [Neurol Res 1999; 21: 566–568]

Objectives - By means of transcranial colour-coded duplex sonography (TCCD) through the foramen magnum, the intracranial vertebral artcries (VAs) and the basilar artery (BA) can be investigated. In this study we evaluated the additional diagnostic value of echocontrast administration in patients with an insufficient pre-contrast TCCD investigation of the vertebrobasilar system. Material and methods - In 22 patients the intracranial VAs and the proximal, middle and distal BA were evaluated before and after the application of 4 g of the echocontrast agent Levovist®. The length of the different vessel segments visualized on colour modc before and after echocontrast, and the diagnostic benefit and the diagnostic confidence were assessed. Results - Echocontrast enlarged in cach vessel segment the length that could be visualized. Using echocontrast, in 5/22 patients (23%) definite and probable pathological findings unnoted in the native scans were detected. In 12 additional paticnts (55%) the investigator and the clinician became confident with thc vascular diagnosis by echocontrast to a degree that angiography could be avoided. In only 3/22 patients (14%) no gain and in 2/22 paticnts (9%) an insufficient diagnostic gain was noted. Conclusions - Our study demonstrates that echocontrast provides effective Doppler signal enhancement and considerably increases the diagnostic gain of TCCD in the intracranial vertebral and basilar vasculature.

Cerebral ischaemia in young adults is a well-recognised disease, and approximately half of the cases remain aetiologically unclear despite extensive investigations. Thrombophilias are known to cause a subset of ischaemic strokes in this population. The factor V Leiden (FVL) mutation, causing resistance to activated protein C, has recently been recognised as the most important genetic thrombophilia in the Western population. Carriers of this gene mutation have a sevenfold increased risk of phlebothrombosis. We undertook this study to evaluate whether the FVL mutation constitutes a risk factor for juvenile cerebral ischaemias. A total of 225 patients agedor = 45 years at onset of cerebral ischaemia and 200 age-matched healthy controls were investigated. The overall frequency of heterozygosity for the FVL mutation did not differ significantly between patients (8.4%) and controls [6.0%; odds ratio (OR) 1.4, 95% confidence interval (CI) 0.7-3.1]. In the subgroup of patients with cryptogenic cerebral ischaemia (n = 94), however, a significantly higher frequency of this gene defect (15.9%) was found compared with the controls (OR 3.0, CI 1.3-6.6). Further trends towards higher frequencies of the FVL mutation were found in patients with patent foramen ovale (OR 1.9), individual (OR 2.1) or family history of previous thrombembolisms (OR 2.0), and in those aged 25 years at onset of disease (OR 1.9, all not significant). In conclusion, the FVL mutation is not a risk factor for cerebral ischaemia of the young. However, our results suggest that this gene mutation plays an aetiological role in the subgroup of patients suffering from 'cryptogenic' ischaemic events.

Patent foramen ovale (PFO), but not uncomplicated mitral valve prolapse (MVP), is a possible source of cardiac embolism to the brain. There are only a few reports on the frequency of clinically silent circulating microemboli in these two conditions. We performed I-hour recordings of one middle cerebral artery in 4 patients with MVP and 14 patients with PFO to detect circulating microemboli. For the identification of microembolic signals we used blinded off-line evaluation and bigated transcranial Doppler sonography (sampling from two different depths in the vessel). Microembolic signals were detected conventionally in 3 out of 14 patients with PFO (3, 8, and 14 microembolilh), and in none out of the 4 patients with MVP. The absence of microembolic signals in patients with MVP and the low frequency of microemboli in patients with PFO reflect the different embolic potential of these two cardiac abnormalities. [Neural Res 1998; 20: 499-503]

Spontaneous cerebrospinal fluid (CSF) pressure oscillations with a wavelength of 0.5-2/min (B-waves) are used as a criterion for shunt insertion in hydrocephalic patients. We describe CSF pressure oscillations in two nonhydrocephalic patients with normal baseline CSF pressure. Intracranial pressure was recorded via a ventricular drainage in a 54-year-old male who had a lumber CSF leak after surgery for lumbar spinal stenosis and disc herniation after the leak was closed. In the second patient, a 42-year-old male, CSF pressure was monitored via a lumbar drainage which was placed for treatment of a subcutaneous CSF effusion after resection of a recurrent temporal meningioma. CSF pressure oscillations of a wavelength of 0.5-2/min were observed with a relative frequency of 50% (patient 1) and 60% (patient 2) of the recorded time. Also longer waves were observed. Our data suggest that CSF pressure oscillations are not confined to hydrocephalic patients with raised intracranial pressure.

In a prospective series of symptomatic adult hydrocephalus characterized by gait disturbance, cognitive impairment, and/or urinary incontinence, 88 of 118 patients (75%) had additional akinetic, tremulous, hypertonic, or hyperkinetic movement disorders. Their prevalence was highest in patients with idiopathic normal pressure hydrocephalus (NPH) of the elderly (56/65 patients, 86%), and they were less frequent in patients with secondary NPH (10/15, 66%), with nonhydrodynamic atrophic/other hydrocephalus (20/33, 61%), and with obstructive hydrocephalus/aqueductal stenosis (2/5, 40%). Akinetic symptoms were found in 73 of 118 patients (62%), and the most frequent movement disorder was upper extremity bradykinesia (55%). Akinetic, tremulous, hypertonic, and hyperkinetic movement disorders were exclusively secondary to causes not related to hydrocephalus in 24 of 118 patients (20%). The proportion of patients with movement disorders not attributable to only such causes was highest in the idiopathic NPH group (44/65, 68%). Thirteen of 118 patients (11%) presented with a parkinsonian syndrome. There was evidence for coexistent Parkinson's disease in four of these patients. Parkinsonism was found to be secondary to NPH in five patients and was found improved after shunting. Akinetic symptoms in patients with NPH generally responded favorably to CSF diversion, which was evident in 80% of a subset of this group. Various other movement disorders did not show definite improvement. The high prevalence of bradykinesia and other akinetic symptoms in NPH and the beneficial effect of shunting on such symptoms suggest that NPH may cause a more generalized disorder of motor function.

Aspirin and ticlopidine are two commonly used drugs in the prevention of cerebral embolic ischemic events. No direct comparisons in a cross-over design of the effects of ticlopidine and aspirin on asymptomatic circulating cerebral microemboli are available. We investigated 53 patients with cerebrovascular disease. Twenty-six patients were dosed for 2 weeks, 300 mg aspirin once daily and then for 2 weeks, 250 mg ticlopidine twice daily. In 27 other patients the scheme was reversed. Transcranial Doppler monitoring (both middle cerebral arteries simultaneously for 1 h were performed at the end of the two weeks. The signal was recorded on digitalised audio tapes and analyzed blinded off-line. The number of embolic signals per hour and vessel was 15.7 under aspirin and 11.7 under ticlopidine (difference not significant). The correlation between the number of emboli under the two medications was high. The highest number of embolic signals was found in high grade carotid stenosis. In patients with a low number of embolic signals, reproducibility was low. A minimum of 7 embolic signals in one treatment group is required for further therapeutic drug trials to allow reasonable comparisons. This study may help to plan further therapeutic trials using emboli detection.

Albeit still unproven, it is supposed that the presence and number of asymptomatic circulating cerebral microemboli detected by transcranial Doppler ultrasound (TCD) may be an indicator of stroke risk. Little research has been done to assess the reproducibility of these data and the required time for recording. We examined one middle cerebral artery in 7 subjects with carotid, aortic or cardiac embolic source for 24 h by TCD. Analysis for embolic signals was done off line completely blinded to the diagnosis and the time of the day during the recording. Embolic signals were found in all 7 subjects varying from 0 per h to 13 per h. Embolic signals occurred throughout the day with a nonsignificant tendency towards higher values in the early morning hours. Half an hour recording would not have been suitable to rule out or to confirm the presence of embolic signals as there were too many gaps between embolic signals of more than 1/2 h. One hour is the required minimum. Concerning the number of embolic signals, even a recording of four hours yielded variabilities of 0.25 and 8 embolic signals per hour in the same person. We recommend to perform follow-up studies the same time of the day. In patients with a low number of embolic signals longer recordings or a lower detection threshold with a higher number of detected embolic signals are necessary to compare frequencies of embolic signals.