Related Experiment Videos
Cerebral Embolism as a Cause of Stroke and Transient Ischemic Attack
John Stirling1, Kazuhiro Muramatsu, Toshitaka Shirai
1CBF Laboratory, Veterans Affairs Medical Center, 2002 Holcombe Boulevard-151A, Houston, TX 77030.
Insights
Cerebral embolism, often from atrial fibrillation (AF), causes stroke. Advanced imaging like CT and MRI can identify embolic strokes and their origins, enabling timely treatment.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Cerebral embolism is a primary cause of stroke and transient ischemic attacks.
- Cardiogenic cerebral embolization is prevalent in atrial fibrillation (AF), especially with rheumatic or arteriosclerotic heart disease.
Purpose of the Study:
- To highlight the diagnostic capabilities for cerebral embolic infarctions and their sources.
- To emphasize the importance of early identification for effective prophylactic therapies.
Main Methods:
- Utilized various invasive (I) and noninvasive (NI) diagnostic procedures.
- Included computerized tomography (CT) scanning, magnetic resonance imaging (MR), angiography, Doppler ultrasound, and echocardiography.
- Transcatheter Doppler monitoring and Holter monitoring were employed for emboli and arrhythmia detection.
Main Results:
- Diagnostic tests visualize embolic occlusions, infarctions, arterial plaques, and cardiac thrombi.
- CT or MRI effectively identify cerebral infarctions from large emboli.
- Transcranial Doppler detects cerebral emboli and cardiac shunting; Holter monitoring identifies arrhythmias.
Conclusions:
- Early recognition and precise identification of cerebral embolism types are crucial.
- Effective prophylactic therapies are available, underscoring the need for timely diagnosis.
Abstract:
The most frequent cause of stroke and transient ischemic attacks is cerebral embolism. Cardiogenic cerebral embolization is common among patients with any cause of atrial fibrillation (AF) but particularly in AF resulting from rheumatic and arteriosclerotic heart disease. Rare causes of cerebral embolism include fat entering the bloodstream after trauma, tumor cells arising from atrial myxomata, and gas embolism. Cerebral embolic infarctions and their sources of origin can now be confirmed during life by many invasive (I) and noninvasive (NI) procedures including computerized tomography (CT) scanning (NI), magnetic resonance imaging (MR) (NI), contrast angiography (I), digital subtraction angiography (I), magnetic resonance angiography (NI), carotid Doppler and transcranial Doppler (NI), and echocardiography (NI) without and with contrast. These tests visualize the following: embolic occlusions of small and large cerebral arteries, resultant cerebral infarctions in appropriate vascular territories, plaques within the aorta, subclavian, vertebral, and carotid arteries, and mural thrombi located within the heart and aortocephalic arteries. Transcranial Doppler monitoring of the middle cerebral artery detects both small (asymptomatic) and large (symptomatic) cerebral emboli, as well as transseptal cardiac shunting, which is a cause of paradoxical embolization. Holter monitoring detects episodic cardiac dysrhythmias not apparent during routine ECG. CT or MRI identify cerebral infarctions resulting from virtually all large cerebral emboli. Early recognition and identification of types of cerebral embolism are important because of the availability of effective prophylactic therapies. (ECHOCARDIOGRAPHY, Volume 13, September 1996)