Management of Bilateral Anterior Cerebral Artery (ACA) Infarct
Bilateral ACA infarcts should be managed with the same acute reperfusion protocols as other large vessel strokes, with immediate IV thrombolysis if presenting within 4.5 hours and consideration for endovascular therapy, while anticipating severe frontal lobe dysfunction including akinetic mutism, primitive reflexes, and profound disability that will require intensive rehabilitation. 1, 2
Immediate Assessment and Acute Reperfusion
Administer IV tissue plasminogen activator (rtPA) if the patient presents within 3-4.5 hours of clearly defined symptom onset and has no contraindications (contraindications include current anticoagulant use with elevated INR >1.7, extensive hypodensity on CT, or bleeding risk factors). 1, 3
Perform immediate neuroimaging with CT or MRI to confirm diagnosis, exclude hemorrhage, and assess extent of infarction—frank hypodensity on CT within 6 hours or MRI diffusion-weighted imaging volumes ≥80 mL predict rapid deterioration. 2, 4
Consider endovascular thrombectomy for bilateral ACA occlusions if treatment can be initiated within 6 hours of symptom onset, though evidence is more limited than for MCA territory strokes—patients with A1 or A2 segment occlusions were included in major thrombectomy trials. 2
Delay aspirin administration for 24 hours if thrombolytic therapy is given; otherwise, initiate aspirin 160-325 mg daily within 24-48 hours of stroke onset. 1, 3
Monitoring and Supportive Care
Admit to a specialized stroke unit or neurocritical care unit with capabilities for managing acute stroke complications and monitoring for neurological deterioration. 2, 4
Monitor blood pressure closely—maintain ≤180/105 mmHg if mechanical thrombectomy performed; for patients not receiving reperfusion therapy, avoid aggressive blood pressure lowering unless >220/120 mmHg. 2
Implement prophylaxis for venous thromboembolism with intermittent pneumatic compression devices beginning on day of admission, as bilateral ACA infarcts cause severe lower extremity weakness and immobility. 3
Conduct formal dysphagia screening before initiating oral intake to reduce aspiration pneumonia risk, as bilateral frontal damage impairs swallowing coordination. 5
Management of Cerebral Edema
Monitor closely for cerebral edema development, which typically peaks 3-4 days post-infarct but can accelerate within 24 hours—bilateral ACA infarcts involving deep white matter carry particularly high risk. 4, 6
Medical management includes: elevating head of bed 20-30 degrees, restricting free water, avoiding excess glucose administration, treating hyperthermia, minimizing hypoxemia and hypercarbia, and avoiding antihypertensive agents that cause cerebral vasodilation. 4
For increased intracranial pressure refractory to medical management, consider hypertonic saline, osmotic diuretics (mannitol), hyperventilation, and neurosurgical consultation for potential decompressive surgery. 4
Anticipated Clinical Syndrome and Rehabilitation
Expect severe frontal lobe dysfunction including akinetic mutism (inability to initiate speech or movement despite being awake), primitive reflexes (grasp, suck, glabellar tap), parkinsonian features (rigidity, akinesia, hypophonia), and profound urinary incontinence—these occur even without direct prefrontal cortex involvement due to disconnection of medial prefrontal-subcortical circuitry. 6, 7
Bilateral lesions produce more severe disability than unilateral ACA infarcts: left-sided infarcts cause transcortical motor aphasia and right leg weakness; right-sided infarcts cause acute confusional state and motor hemineglect; bilateral infarcts cause akinetic mutism and dependent functional status. 7
Initiate early intensive rehabilitation assessment focusing on mobility training, speech therapy for mutism/aphasia, and bladder management, recognizing that recovery is often prolonged and incomplete. 2
Secondary Prevention
Investigate stroke etiology thoroughly—in isolated ACA territory infarcts, arterial dissection is the most common cause (43% in one series), particularly in younger patients with physical exertion preceding stroke onset or headache. 8
Other etiologies include cardioembolism, large-artery atherosclerosis, and small-artery disease affecting Heubner's artery—perform MRA, CTA, or conventional angiography to identify vascular lesions. 8, 7
Initiate appropriate secondary prevention based on etiology: antiplatelet therapy (aspirin 50-325 mg daily, aspirin/extended-release dipyridamole 25/200 mg twice daily, or clopidogrel 75 mg daily) for atherothrombotic or lacunar stroke; anticoagulation (INR 2.0-3.0) for cardioembolic stroke. 3
Critical Pitfalls to Avoid
Do not delay reperfusion therapy while waiting for complete etiologic workup—every 30-minute delay decreases chance of good outcome by 8-14%. 2
Do not assume patients with bilateral ACA infarcts will have good outcomes even with successful reperfusion—the frontal lobe damage and white matter disconnection often result in severe persistent disability requiring long-term care planning. 6, 7
Do not overlook arterial dissection as the underlying cause, especially in younger patients without traditional vascular risk factors—three-dimensional rotational angiography may be needed for diagnosis. 8
Avoid administering full-dose anticoagulation with IV or subcutaneous heparin in the acute phase, as this does not improve outcomes and increases bleeding risk. 3