Basilar artery blood flow during head rotation in vertebrobasilar ischemia.

PATIENTS AND METHODS: Forty-six patients with vertebrobasilar ischemia and 40 control subjects were examined during head rotation using transcranial Doppler ultrasonography. RESULTS: In the control group, no difference in blood flow velocity through the BA was found between the neutral and rotated positions. Based on these data, a blood flow reduction in the BA of more than 20% was considered to be significantly abnormal (p < 0.01). In three of 46 patients no signal was detectable in the BA using TCD. The reduction in blood flow velocity through the BA during head rotation was strongly dependent on the condition of the VA; none of 23 patients without atherosclerotic lesions or hypoplasia of the VA developed a significant reduction in blood flow through the BA. Two of 11 patients with unilateral VA lesions had significantly reduced blood flow in the BA (27% and 31%), although both were asymptomatic. Five of nine patients with bilateral VA lesions showed a significant reduction in blood flow through the BA (mean = 52%, minimum = 30%), and four of these developed clinical symptoms such as vertigo or diplopia during the rotation maneuver. CONCLUSION: These data suggest that patients with uni- or bilateral lesions of the VA are at risk for developing clinically relevant reductions in blood flow through the BA during head rotation. Because not all patients with VA lesions developed reduced blood flow velocity, we conclude that individual vascular mechanisms must play an important compensatory role.

[Acute therapy and prevention of ischemic cerebral infarct]. / Akuttherapie und Prophylaxe des ischämischen Hirninfarktes.

The acute therapy of the cerebral infarct necessitates the fast evaluation of the favorable risk factors and the assessment of its pathogenetical mechanisms to facilitate a specific treatment as early as possible. Acute treatment procedures like the rheologic therapy, anticoagulation, thrombolysis, application of calcium antagonists, and antiedematous therapy are discussed. Recommendations for the secondary prophylaxis with drugs like acetylsalicylic acid or triclopidine after transitory ischemic attacks or manifest brain infarctions are given. The indications for the surgical therapy of stenoses of the extracranial vessels supplying the brain are discussed and rules for the emergency management of the transitory ischemic attack are introduced.

Ultrasound for the assessment of the embolic risk of carotid plaques.

In a prospective study we compared duplex-ultrasound characteristics of symptomatic internal carotid artery (ICA) stenoses with cranial computerized tomographic (CCT) findings in 82 patients suffering from completed or transient middle cerebral artery symptoms. The aim was to assess the pathogenic role of ICA plaque morphology and the potential embolic risk of ICA plaques. The degree of carotid stenosis was estimated by spectral analysis of the pulsed Doppler signal. The CCT findings were classified as being either normal, lacunar lesions, hemodynamically induced low-perfusion infarctions, or territorial embolic infarctions. According to their ultrasonic features we characterized the ICA plaque surface as smooth or irregular and their structure as homogeneous or heterogeneous. Plaques with an irregular surface and heterogeneous echogenicity dominated significantly in CCT-territorial infarctions (p < 0.01), whereas hemodynamically induced low-perfusion infarctions showed no relationship with any plaque characteristic. High degree ICA stenoses (> 50%) dominated in both territorial infarctions and low-perfusion infarctions, as compared to ipsilateral normal CCT or lacunes (p < 0.05). Normal CCT and lacunar infarctions were associated with homogeneous and smooth plaques (both p < 0.05). We conclude that > 50% ICA stenoses can cause both hemodynamically induced low-perfusion infarctions as well as thromboembolic territorial infarctions, whereas ulcerated and heterogeneous plaques constitute a high risk factor for arterio-arterial embolic stroke. Furthermore, carotid ultrasound may help to estimate the clinical significance of carotid lesions.

[CO2 test with transcranial Doppler sonography in cerebral ischemia]. / CO2-Test mit der transkraniellen Dopplersonographie bei zerebralen Durchblutungsstörungen.

We evaluated the CO2-induced vasomotor reactivity of the cerebral vasculature in 48 patients with high degree stenosis or occlusion of the internal carotid artery by transcranial Doppler ultrasonography measuring changes of flow velocities in the middle cerebral artery. Further, the vasomotor reactivity of the basilar artery was measured in 48 patients with vertebro-basilar ischemia. These results were compared with the findings in normal individuals. The vasomotor reactivity was significantly reduced in patients with stenosis or occlusion of the internal carotid artery as compared to normal controls. In patients with high degree ICA stenoses, undergoing to carotid surgery, CO2-test showed a significant improvement of the pathological vasomotor reactivity 6 month after the operation. In the group of patients with vertebro-basilar ischemia, the vasomotor reactivity measured in the basilar artery, was significantly reduced in patients with completed brainstem infarctions but not in patients with transient brainstem ischemia or infarctions in the posterior cerebral artery territory. We conclude that evaluation of the cerebral vasomotor reactivity by transcranial Doppler ultrasound is able to identify an inadequate cerebral blood supply and may help to estimate the hemodynamic effect of stenosis or occlusion of the extracranial brain supplying arteries.

Doppler CO2-test in patients with vertebrobasilar ischemia.

The pathogenesis of vertebrobasilar ischemia (VBI) is still uncertain. Embolism and systemic hypotension have been discussed as possible causes. We evaluated the basilar arteries of 35 VBI-patients by transcranial Doppler-sonography at rest and under hypercapnic conditions and compared these findings with the basilar flow velocities in 10 healthy volunteers matched by age. We found no difference between the controls and the VBI-patients for the basilar flow velocities at rest. Under hypercapnia (end-tidal CO2-concentration 8.5%), the basilar blood flow velocities in the healthy controls increased by an average of 53.0% but only by 32.3% in the VBI-patients (p less than 0.005). The reduction of CO2 dependent vasomotor reactivity was observed in all VBI-patients, except in patients with infarction in the posterior cerebral artery area, possibly indicating a different pathogenic mechanism of stroke. The results in all other patients revealed no obvious correlation to the clinical course or angiographic or dopplersonographic findings. As CO2 dependent vasomotor reactivity and brain perfusion pressure dependent cerebral autoregulation have similar mechanisms, we conclude that systemic hypotension might play an important part in VBI.

Clinical relevance of intraplaque hemorrhage in the internal carotid artery.

In this study the correlation between hemispherical ischemic symptoms and the presence of intraplaque hemorrhage in carotid plaques has been evaluated. 38 patients who had undergone carotid endarterectomy were examined clinically and the specimens obtained from operation were studied morphologically. The patients were divided into two groups, asymptomatic and symptomatic regarding the territory of the supplying carotid artery. The presence of intraplaque hemorrhage, shown by Ladewig's Trichrom stain, as well as evidence of iron, immunohistochemical stain of hemoglobin and native fluorescence microscopy was noted, and, according to their extension, classified into three degrees. As a result, there was neither a correlation between history of ischemic brain symptoms and the presence of intraplaque hemorrhage, nor between clinical symptoms and extension of hemorrhage. The plaques were high degree stenotic (greater than 80%) in most of the patients and showed various degenerative changes. In 97% of all plaques with hemorrhages surface defects were seen. Our results confirm that intraplaque hemorrhage is one out of a series of pathological events which occurs during advanced atherosclerosis. Blood inflow from the lumen through an already damaged plaque surface is a common event and a correlation with the onset of symptoms is unlikely.

Colour Doppler flow imaging of the carotid arteries.

53 patients with carotid artery atherosclerosis were examined by colour Doppler flow imaging. These results were compared with real time duplex sonography and continuous wave Doppler sonography. In 48 low degree stenoses (less than 50%) the B-mode showed 36 smooth and 12 ulcerated plaque surfaces. In 24 high degree stenoses (greater than 50%) 10 plaques were smooth and 14 ulcerated. In the low degree stenoses, which exhibited smooth surfaces in B-mode examination, colour flow Doppler showed nine additional cases with turbulences in the area of the stenotic site. This indicates that plaque ulcerations in low degree stenoses are underestimated. In contrast, in nearly all cases with high degree stenoses marked turbulences could be demonstrated by colour Doppler flow imaging independent of the B-mode, showing regular or ulcerated plaque surfaces. Additionally, the duplex ultrasound diagnosed a carotid artery occlusion in 11 cases, but the colour coded Doppler was able to assess a remaining blood flow in two out of these 11 cases. Our results suggest that the colour Doppler flow imaging as a noninvasive technique is an advantage in diagnosing plaque ulcerations and it is more precise in diagnosing carotid occlusions than duplex-sonography is.

Correlation of lactic acid level, cell count and cytology in cerebrospinal fluid of patients with bacterial and non-bacterial meningitis.

The relation between lactate concentration and cell count was determined in 394 CSF samples from unselected patients. In addition, a similar analysis was performed in 156 CSF samples from patients with bacterial and non-bacterial meningitis. The correlation between cell type and lactate level was also examined. The analysis demonstrated a significant linear increase in lactate showing high lactate levels at cell counts above 350 cells per microliter. Since the lactic acid concentration in bacterial meningitis increases linearly with the number of lactate-producing cells, it may be concluded that the increased lactate concentration results from CSF pleocytosis. If lactate levels are higher than the normal distribution, additional sources of lactate production such as cerebral hypoxia must be assumed.