Venous Microembolic Signals Detected in Patients With Cerebral Sinus Thrombosis
Background and Purpose We sought to assess the usefulness of the Doppler technique in the monitoring of microembolic signals in the main venous outflow pathways in superior sagittal sinus thrombosis.
Methods Transcranial Doppler ultrasound was performed with a range-gated 2-MHz transducer in 6 patients with superior sagittal sinus thrombosis, in 5 subjects with platelet hyperaggregability, and in 20 healthy volunteers. Emboli monitoring was performed mainly in one distal internal jugular vein for 10 to 15 minutes.
Results Three of the six patients (50%) with superior sagittal sinus thrombosis had microemboli. None of the patients with platelet hyperaggregation or healthy volunteers revealed microemboli.
Conclusions Microemboli can be found in superior sagittal sinus thrombosis by Doppler ultrasound. Their prognostic significance remains to be determined.
Transcranial Doppler ultrasound has been broadly used in the evaluation of intracranial arteries and their diseases. Recently, MES have been found in the basal cerebral arteries in stroke, prosthetic heart valves, and atrial fibrillation, and during carotid and cardiac surgery.1 Emboli monitoring has also been applied recently in deep vein thrombosis of the legs.2 In SSST, Doppler studies have been performed for the evaluation of the cerebral venous collaterals.3 4 5 Emboli detection technique in the cerebral venous system has not been applied until now. The purpose of this study was to examine the prevalence of venous MES in SSST by means of the ultrasound technique and to study the relationship to anticoagulation treatment.
Subjects and Methods
Venous Doppler studies were performed in 6 consecutive patients with SSST (5 women, 1 man) confirmed by either cerebral angiography or MR angiography (median age, 26.5 years), in 5 subjects revealing PH (median age, 42 years), and in 20 healthy volunteers without central nervous disorders (median age, 39 years). Informed consent was obtained from all subjects. Doppler ultrasound was performed with a range-gated 2-MHz transducer (Multidop-X, Firma Elektronische Systeme GmbH, DWL). With the use of the submandibular approach and a sample volume of approximately 10 mm, the distal internal jugular vein was identified with a flow toward the probe based on its proximity to the internal carotid artery. The probe was handheld during the examination at a depth of 50 to 60 mm. The gain was lowered to facilitate visual recognition of MES. In the patient group venous emboli monitoring was performed in the dominant internal jugular vein for 10 to 15 minutes. The examination was repeated in the first 2 weeks every 2 or 3 days on the same side. Later, the frequency of examination was dependent on the clinical course and Doppler findings. The number of examinations ranged between 10 and 20 for each patient. MES frequency was calculated as the number of emboli per 15 minutes. In the healthy subjects and patients with PH, venous emboli detection was performed for 15 minutes at each internal jugular vein. MES were identified by the investigator on-line during the recording by their characteristic high-frequency sound and marked unilateral power increase (Fig 1⇓). For arterial emboli monitoring, both middle cerebral arteries were insonated for 30 minutes in all patients with PH, including the 1 patient with PH and SSST. Platelet function was evaluated on the basis of the platelet reactivity index by means of previously described methods.6 Platelet reactivity index values >1.2 were considered pathological.
All patients with SSST, except 1, were women. Affliction of the transverse sinus was observed in 5 of our 6 patients. A complete occlusion of one of them was seen in three instances. The clinical manifestation appeared acutely in 4 patients and chronically in 2. All patients suffered from headache and visual disturbances, 2 from epilepsy and hemiparesis, and 1 from fluctuations in consciousness. Risk factors included oral contraceptives in 1 patient. Factor V Leiden mutation, PH, and neoplasia were found as an underlying thrombophilic condition in 1 patient. No patient developed heparin-associated thrombocytopenia in the course of treatment. Four had complete recovery, and 2 had mild sequelae.
All patients underwent heparin therapy at least 48 hours before the first emboli monitoring was performed. Heparin was followed by warfarin for several months. MES were detected in 3 of 6 patients (50%) with SSST. The rate of MES and the duration of their occurrence, however, varied greatly. MES were found ranging from 3 to 150 per 15 minutes. The emboli subsided during anticoagulation treatment with high-dose heparin in 2 patients after 2 and 11 days, respectively. Both revealed a low rate of MES (3 per 15 minutes and 9 per 15 minutes, respectively). The third patient revealed the most interesting findings. The last MES were observed after 110 days. Initially, the MES rate decreased during heparin treatment within 1 week from 90 to 30 per 15 minutes. During insufficient anticoagulation, the embolic frequency transiently increased to 150 per 15 minutes (Fig 2⇓). Perfusion scintigraphy of the lung performed at this time revealed no evidence for pulmonary embolism. Warfarin was given for 4 months without recurrence of MES. This patient also had PH. To rule out a different cause of the MES, the subject revealing the platelet disorder and 5 patients with PH, most of whom suffered from tinnitus, underwent arterial emboli detection in both middle cerebral arteries. No MES were found in any instance. Venous monitoring in the 5 patients with PH and in 20 healthy subjects was normal. The platelet reactivity index of all patients with PH was ≥1.4.
SSST is still a poorly understood disease with a quite variable prognosis. The severity of the clinical course seems to depend mainly on the acuity of thrombus formation and the capacity for compensation due to major venous vessels. High-dose heparin followed by oral anticoagulation is usually recommended.7 The duration of oral anticoagulation, however, is still open to discussion, since no clinical or technical parameter is known for determining the point when oral anticoagulation can be discontinued. The detection of MES indicates a new approach in the assessment of anticoagulation treatment. This method is now well established in arterial disorders. The predictive value is still debatable; however, one recently published prospective study indicates a positive correlation between the risk of ischemia and the rate of MES.8
Venous emboli have been detected with the use of duplex scanning in deep vein thrombosis of the legs. In a recently published report, 26 of 60 patients (43%) had MES. The emboli rate ranged from 5 to 800 per minute. After anticoagulation with heparin, MES were abolished within 72 hours.2 Clinically silent MES also seem to be a common finding in patients with SSST. In our study 3 of 6 patients (50%) revealed MES. Two of them showed a fast regression within a few days of heparin treatment. This may suggest that in the other 3 patients without MES detection, rapid anticoagulation prevented fragmentation of the thrombus. Emboli monitoring during the first 2 days and off-line analysis of the signals will probably increase the detection rate and number of MES. It is also conceivable that longer monitoring times will lead to more positive findings. In normal subjects and in patients with PH, no MES were found, indicating that we had observed a specific finding related to the fragmentation of thrombotic material in the cerebral sinus independent of PH. Other possibilities, eg, a general activation of the coagulation system as a consequence of the thrombotic process, however, cannot be excluded. The limited number of observations also impeded a clear differentiation between the effect of anticoagulation and the natural history of MES.
In conclusion, our study has shown that the TCD method is a valid technique for detecting and monitoring venous MES in SSST. The prognostic significance of the relationship to anticoagulation therapy, however, remains to be determined.
Selected Abbreviations and Acronyms
|SSST||=||superior sagittal sinus thrombosis|
|TCD||=||transcranial Doppler ultrasound|
Reprint requests to José Manuel Valdueza, MD, Department of Neurology, University Hospital Charité, Humboldt University, Schumannstraße 20/21, 10117 Berlin, Germany.
- Received February 5, 1997.
- Revision received May 12, 1997.
- Accepted May 15, 1997.
- Copyright © 1997 by American Heart Association
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