From the Guidelines
Bilateral caudate nucleus strokes are primarily caused by small vessel disease, particularly affecting the lenticulostriate arteries that supply the caudate nuclei, as well as large vessel atherosclerosis, cardioembolic events, vasculitis, hypercoagulable states, or drug-induced vasospasm. These strokes can result from various etiologies, including small vessel disease, large vessel atherosclerosis of the internal carotid arteries or middle cerebral arteries, cardioembolic events (such as atrial fibrillation, valvular heart disease, or cardiomyopathy), or less commonly, vasculitis, hypercoagulable states, or drug-induced vasospasm (particularly cocaine or amphetamines) 1.
Etiology and Evaluation
The etiology of bilateral caudate nucleus stroke is complex and multifactorial. Evaluation should include:
- Brain imaging (MRI with diffusion-weighted imaging is preferred over CT) to confirm the diagnosis of symptomatic ischemic cerebrovascular disease 1
- Vascular imaging (carotid ultrasound, CT angiography, or MR angiography) to screen for stenosis in patients with symptomatic anterior circulation cerebral infarction or TIA 1
- Cardiac assessment (echocardiogram and prolonged cardiac monitoring) to evaluate for possible cardiac sources of or transcardiac pathways for cerebral embolism 1
- Laboratory tests for hypercoagulable states or vasculitis to gain insight into risk factors for stroke and to inform therapeutic goals 1 ### Treatment and Secondary Prevention Treatment focuses on secondary prevention with:
- Antiplatelet therapy (aspirin 81-325mg daily, clopidogrel 75mg daily, or combination therapy depending on risk factors) 1
- Statins (atorvastatin 40-80mg or rosuvastatin 20-40mg daily) to reduce the risk of recurrent stroke 1
- Blood pressure control (target <130/80 mmHg) to reduce the risk of recurrent stroke 1
- Anticoagulation if a cardioembolic source is identified to prevent recurrent stroke 1 Addressing modifiable risk factors such as smoking cessation, diabetes management, and lifestyle modifications is essential for preventing recurrence.
From the Research
Etiology of Bilateral Caudate Nucleus Stroke
The etiology of bilateral caudate nucleus stroke can be attributed to various factors, including:
- Cardioembolic stroke associated with a variant circle of Willis, as seen in a case study where an 81-year-old man with atrial fibrillation presented with bilateral caudate nucleus infarction 2
- Small-artery disease, which was diagnosed in 59% of patients with caudate infarct in a study analyzing demographic features and risk factors of patients with acute caudate stroke 3
- Cardiac embolism, which was identified as the cause of caudate infarct in 20% of patients in the same study 3
- Other potential causes, such as patent foramen ovale (PFO), which may be associated with cryptogenic stroke or embolic stroke of undetermined source 4
Risk Factors
Risk factors for bilateral caudate nucleus stroke may include:
- Hypertension, which was present in 64% of patients with caudate infarct in one study 3
- Hypercholesterolemia, diabetes mellitus, and previous myocardial infarct, which were also identified as risk factors for caudate infarct 3
- Atrial fibrillation, which was present in the case study of an 81-year-old man with bilateral caudate nucleus infarction 2
Clinical Presentation
The clinical presentation of bilateral caudate nucleus stroke may vary, but common neurological abnormalities include: