Lack of hemispheric dominance for consciousness in acute ischaemic stroke.

BACKGROUND: Previous reports have suggested left hemispheric dominance for maintaining consciousness, although there is controversy over this claim. OBJECTIVE: To compare early impairment of level of consciousness between patients with right and left hemispheric stroke. METHODS: Data from 564 patients with ischaemic stroke enrolled in the placebo arm of a trial of a putative neuroprotectant were analysed. All patients had major hemispheric stroke with cortical dysfunction, visual field deficit, and limb weakness, with symptom onset within 12 hours of enrolment. Patients were prospectively evaluated on a predefined scale (1-6; 1 = fully awake, higher scores representing greater impairment) to measure level of consciousness at multiple time points over the initial 24 hours after presentation. The National Institutes of Health (NIH) stroke scale score at presentation and infarct volume at 30 days were determined. RESULTS: Some degree of impairment in level of consciousness was observed in 409 of the 564 patients (73%). Median maximum sedation score was 2 for both right and left hemispheric stroke (p = 0.91). Mean sedation score over 24 hours was 1.5 for both right and left stroke (p = 0.75). There was no difference between level of consciousness scores in right and left stroke at any individual time point during the 24 hour monitoring period. No association between side and impairment in level of consciousness was seen after adjustment for stroke severity and infarct volume. CONCLUSIONS: In contrast to previous reports, there was no evidence for hemispheric dominance for consciousness in the setting of a major hemispheric stroke.

Carotid Doppler high-intensity transient signals in dilated cardiomyopathy.

BACKGROUND: Thromboembolism is an infrequent but serious complication in dilated cardiomyopathy (DCM), and the role of primary preventive antithrombotic or anticoagulation therapy is undetermined. High-intensity transient signals (HITS) by Doppler ultrasound representing microemboli have been described in various clinical settings associated with increased risk of stroke. This study assessed the feasibility, reproducibility, and prevalence of HITS in patients with DCM. METHODS: Thirty patients with severely reduced left ventricular ejection fraction (< or = 35%, mean 25%) and New York Heart Association class II to III who were not receiving antithrombotic or anticoagulant therapy and 20 age-matched normal subjects were prospectively examined. Patients with atrial fibrillation, significant cardiac valvular heart disease, a history of cerebrovascular disease, and those who otherwise required antithrombotic or anticoagulation therapy were excluded. One-hour pulsed-wave Doppler recordings over the common carotid artery (CCA) were performed on 3 separate days in each subject by a single, experienced, blinded sonographer with a 4-MHz probe (TC-2000, Nicolet/EME) with a specially designed probe holder. Studies were read in a blinded, random fashion by 2 independent, experienced HITS Doppler recording readers. RESULTS: HITS in the CCA were detected in 6 (20%) of 30 patients with DCM and in 3 (15%) of 20 volunteers. This difference was not statistically significant. Intrareader and interreader reproducibility were high (kappa = 0.91 and 0.84, respectively; P <.001), whereas intrasubject reproducibility over the 3 visits was moderate to low (kappa = 0.22). There was no significant difference between HITS characteristics, that is, intensity and duration, in patients versus controls. CONCLUSIONS: The prevalence of CCA HITS in patients with clinically stable heart failure who are not receiving anticoagulation/antithrombotic therapy and are not in atrial fibrillation is low and not significantly different from normal patients. These data suggest that HITS monitoring is not a viable surrogate marker for increased thromboembolic risk in such patients with DCM.

Transcranial 3D B-mode imaging in a case of cerebral hemorrhage.

The case of a patient with temporal lobe hemorrhage is presented. This is the first report of use of a new three-dimensional data acquisition system that entails free-hand scanning with three-dimensional transcranial duplex sonography. Three-dimensional image reconstruction reduced the spatial asymmetry inherent in oblique two-dimensional ultrasonography, making evaluation of the precise location, size, and anatomic relations of intracranial hemorrhage easier.

Vagus nerve imaging with ultrasound: anatomic and in vivo validation.

To provide the anatomic basis and demonstrate the reproducibility of ultrasound studies for the identification of the vagus nerve within its course in the carotid sheath in the neck, cadaveric and in vivo imaging studies were conducted. On transverse B-mode images of the neck, there is a centrally hypoechoic and peripherally hyperechoic structure between the common carotid artery and the jugular vein inside the carotid sheath. This structure was also identified in a fresh, nonpreserved cadaver and was marked with a hypodermic needle by means of a transdermal approach. Neck dissection was performed leaving the carotid sheath intact. B-mode imaging yielded detailed anatomic information about the structures in the carotid sheath. Further dissection showed the vagus nerve as the target of the needle. One hundred consecutive transverse carotid scans were reviewed, and the characteristic echo patterns of the vagus nerve were identified in 97 instances. A distinct and reproducible, round, hypoechoic structure was defined adjacent to the common carotid artery and jugular vein as the vagus nerve. On the basis of this study, a new, noninvasive, and highly reproducible method to locate the vagus nerve in the carotid sheath is introduced. This may lead to further clinical application such as presurgical localization or ultrasound-guided needle studies. Stimulation of the vagus nerve has been proposed for seizure therapy. The diagnosis of vagus nerve tumors may be improved.

[Volume flow in carotid occlusion. Measurement using ultrasound time domains and color M mode analysis]. / Volumenfluss bei Karotisobstruktionen. Messung mittels Ultraschall-Zeit-Domänen- und Farb-M-Mode-Analyse.

AIM: To quantify the volume flow rate- (VFR-) effects of internal carotid disease on the common carotid artery both ipsi- and contralaterally for various degrees of stenosis. METHOD: A non-invasive ultrasonic time domain processing (M-mode) was used. This proved to be reproducible in vivo and accurate in vitro. 109 patients (mean age 66.7 yrs.) having at least 50% stenosis of the internal carotid artery or a cerebral ischaemia were studied. The haemodynamic effect of the stenosis on the entire anterior brain circulation supplied by the carotid artery was assessed. Stenoses were graded in 4 groups. RESULTS: Significant VFR reduction occurred ipsilaterally in high grade (75-94%) stenosis and occlusion of the internal carotid artery, but not with moderate (50-74%) stenosis (p < 0.05). Ipsilaterally to stenoses there was a decrease in VFR, which was more marked in higher than in lower grade stenoses. Contralaterally there was an increase in VFR. These groups differed in a statistically significant way (p < 0.05). CONCLUSION: This ultrasonic VFR method demonstrates the flow effect of carotid stenoses both ipsi- and contralaterally and adds to the understanding of the haemodynamics in individual patients.

Middle cerebral artery velocity correlates with nitroglycerin-induced headache onset.

Headache often accompanies treatment with nitroglycerin, but the cerebral hemodynamic effects and the exact mechanism of the headache are incompletely understood. Transcranial Doppler monitoring allows evaluation and monitoring of changes in blood flow velocity in the large intracranial arteries. The objective of this study was to assess middle cerebral artery (MCA) blood flow velocities with transcranial Doppler monitoring in subjects receiving continuous low-dose nitroglycerin intravenously or by patch, and correlate these with clinical headache. Twenty-eight normal adult men received nitroglycerin (0.12 micrograms/kg/min intravenously [n = 14] or 0.6 mg/min by transdermal patch [n = 14]), for up to 120 minutes, with monitoring of clinical headache status (standard 4-point scale), blood pressure, heart rate, end-expiratory PCO2 (CO2), and right MCA velocity. All subjects developed headache (mean time to onset, 34 min), reaching moderate or severe levels in 20. There were no differences in age, weight, mean blood pressure, mean heart rate, or resting end-tidal CO2 between those whose headache reached a moderate to severe level and those whose headache remained mild. MCA velocity decreased from baseline values at all levels of clinical headache (onset, -17%; moderate, -18%; severe, -16%; nitroglycerin stopped, -19%) (p, 0.0001 by t test for each stage of headache). MCA velocity remained decreased at the time of headache resolution (-14%; p < 0.001). Blood pressure, heart rate, and CO2 did not change significantly. There were no differences related to route of nitroglycerin dosing. These data show that continuous low doses of nitroglycerin by patch or intravenously produce headache in normal male subjects. MCA velocities were significantly decreased at headache onset and at all levels of headache severity. Changes in MCA velocity persisted beyond the clinical headache. These results suggest a direct MCA vasodilatory effect of nitroglycerin. This method may also be used to evaluate the intracranial hemodynamic effects of other vasoactive drugs, even in clinical settings.

Clinical cerebrovascular applications of arterial ultrasound volume flow rate estimates.

A variety of disorders affect cerebral hemodynamics. Volume flow rate (VFR) estimates now allow accurate quantification of the effect of cerebrovascular lesions on the conduit vessels, with excellent in vivo and in vitro correlation. Four selected cases with VFR data and angiographic correlation are presented to illustrate potential clinical uses of this method. The VFR estimates were obtained with a color M-mode-based velocity imaging technique, which uses time-domain processing (P-700 Color Velocity Imaging System, Philips Ultrasound International, Irvine, CA). In a patient awaiting coronary artery surgery, with unilateral internal carotid artery occlusion and contralateral angiographic stenosis (50-80%, reader variation), the baseline and acetazolamide-challenged common carotid artery VFRs showed excellent conduit function ipsilateral to this stenosis. Thus, the angiographic stenosis did not have significant hemodynamic effects and endarterectomy was avoided. In a patient with an arteriovenous malformation fed by the left vertebral and left external carotid arteries, high in the left cervical region, VFR estimates of two to three times normal predicted the feeding vessels, influenced management, and proved helpful in follow-up. In a patient with subclavian steal syndrome, VFR estimates quantified the steal after brachial hyperemia. Finally, in a patient with delayed vasoconstriction after subarachnoid hemorrhage, very low VFR estimates preceded clinical deterioration. Quantification of hemodynamic changes with VFR estimates was useful for the diagnosis, management, and follow-up of these patients with four types of cerebrovascular disease, and should be applicable in many others.

Control for carbon dioxide-related changes in flow velocity by transcranial Doppler monitoring.

Transcranial Doppler ultrasonography can monitor changes in intracranial blood flow velocity over time in a variety of experimental and clinical settings with excellent temporal resolution. Alterations in arterial carbon dioxide pressure exert a profound influence on blood flow velocity. Such changes exhibit important individual fluctuation depending on respiratory status. This limits the ability of transcranial Doppler to accurately study subtle changes in blood flow velocity, independent of the respiratory state of the subject. Suggested here is a method to control for the respiration artifact on blood flow velocity. The middle cerebral artery of 7 healthy male volunteers was studied with transcranial Doppler under resting conditions, monitoring end-tidal carbon dioxide concentration and blood flow velocity. Hyperventilation was performed both voluntarily and with pharmacological induction by human corticotropin-releasing hormone. These studies were carried out both with and without the use of counterregulation of the end-tidal carbon dioxide concentration via a respiration unit, with an adjustable carbon dioxide-oxygen gas supply preventing significant changes in end-tidal carbon dioxide. The blood flow velocity in the middle cerebral artery during maximal voluntary hyperventilation decreased from baseline values of 100% to 44.4 +/- 4.3% (a 55.6% decrease), and with human corticotropin-releasing hormone-induced involuntary hyperventilation, to 65.1 +/- 5.3% (a 34.9% decrease). With the control method, blood flow velocities during voluntary and pharmacological hyperventilation were 100 +/- 1.6% and 100 +/- 2.8%, respectively. This method allows for control of respiration-induced artifacts during transcranial Doppler monitoring, and can be used to assess the effect of direct or indirect blood flow velocity stimuli independent of respiratory status.

Intra- and extracerebral blood flow changes and flushing after intravenous injection of human corticotropin-releasing hormone.

To study facial flush after systemic administration of human corticotropin-releasing hormone (hCRH) we injected 100 micrograms hCRH intravenously to ten healthy young men. The increase in facial temperature was measured by infrared camera. A significant increase in facial temperature of 1.39 degrees C +/- 0.3 was found within 7 min in all patients, which lasted up to 60 min, although facial flushing was visible in only 50% (5/10) of the probands. In a second experiment 100 micrograms hCRH was then administered to seven other healthy young men. Intra- and extracerebral blood flow velocity changes in the medial cerebral artery (MCA) and external carotid artery (ECA) were measured after hCRH administration by use of Doppler sonography. We found a decrease of intracerebral blood flow which was caused by hyperventilation and was reversible following 6% CO2 hyperventilation during a second injection of 100 micrograms hCRH. Blood flow velocity in the ECA increased by 111.5 +/- 32.9% (compared to baseline level), lasted up to 60 min after hCRH injection, and was not reversible by 6% end-tidal CO2 ventilation. We thus demonstrated that the direct vasodilatory effect of hCRH involves the ECA-supplied vascular territory only. The intracerebral vasoconstrictory effect represents the result of hyperventilation following hCRH injection. The data thus clearly suggest an interaction of hCRH and the vascular endothelium of the ECA, causing a marked blood flow velocity increase and facial flushing.