What is a watershed infarct and how does it appear on a non‑contrast CT scan?

Watershed Infarct on CT

A watershed infarct is an ischemic stroke occurring at the border zones between major cerebral arterial territories, appearing on non-contrast CT as areas of hypodensity in characteristic locations—either at cortical junctions between major arteries or in subcortical regions between superficial and deep vascular territories. 1, 2

Definition and Anatomic Location

Watershed (or border zone) infarcts are ischemic lesions that develop at the junction between two main arterial territories, constituting approximately 10% of all brain infarcts. 2 These vulnerable regions exist where blood supply from different arterial sources meets but does not anastomose, making them susceptible to ischemia when cerebral perfusion decreases. 1, 2

Types of Watershed Infarcts

External (Cortical) Watershed Infarcts

• Located at junctions between superficial territories of major cerebral arteries, most commonly between the anterior and middle cerebral arteries (ACA-MCA) or between the middle and posterior cerebral arteries (MCA-PCA). 1, 2
• Appear as wedge-shaped hypodense areas on CT in these marginal zones. 3
• Present with characteristic neurological deficits: hemiparesis, transcortical motor aphasia, and dementia when involving ACA-MCA borders; mild hemiparesis and apathy when involving MCA-PCA borders. 1, 3

Internal (Subcortical) Watershed Infarcts

• Located between superficial and deep territories of the middle cerebral artery or in periventricular white matter regions, particularly in the basal ganglia and posterolateral frontal areas. 1, 2
• Appear as long-line or triangle-shaped hypodense areas on CT in these subcortical locations. 3
• Result primarily from hemodynamic compromise rather than embolism. 2

CT Imaging Characteristics

Non-Contrast CT Findings

• Small areas of hypodensity in cortical watershed zones, basal ganglia, deep white matter, or periventricular regions are the hallmark findings. 4
• Hypodensity may not be visible in the first 6 hours after symptom onset, as CT is relatively insensitive for detecting acute ischemic changes early. 4
• Ischemic lesions that cross usual arterial boundaries (particularly with hemorrhagic components) or in close proximity to venous sinuses should raise suspicion for alternative diagnoses like cerebral venous thrombosis. 4

Important Caveats

• CT is the essential first-line test to exclude hemorrhage before any thrombolytic therapy, but it has limited sensitivity for small cortical or subcortical infarctions, especially in the posterior fossa. 4
• Frank hypodensity on CT within the first 6 hours, involvement of one-third or more of the MCA territory, and early midline shift are CT findings that predict cerebral edema and poor outcomes. 4
• Serial CT scanning in the first 2 days is useful to identify patients at high risk for developing symptomatic swelling. 4

Pathophysiology and Clinical Context

Hemodynamic Mechanism

• Internal watershed infarcts are caused mainly by hemodynamic compromise from decreased cerebral blood flow in distal vascular territories. 1, 2
• 75% of patients have internal carotid artery occlusion or tight stenosis associated with hemodynamically significant cardiopathy, increased hematocrit, or acute hypotension. 5
• Syncope at onset (37%) and focal limb shaking (12%) are frequent clinical presentations suggesting hemodynamic etiology. 5

Embolic Mechanism

• External watershed infarcts are believed to result from embolism, though not always with associated hypoperfusion. 2
• Multiple small cortical infarcts in watershed and MCA territory areas are typical findings in embolic stroke from carotid disease. 6

Diagnostic Approach

MRI with diffusion-weighted imaging is superior to CT for detecting watershed infarcts, particularly in the acute phase, but CT remains the essential initial test in emergency settings to exclude hemorrhage. 4, 1, 6

When CT is Appropriate

• Emergency evaluation to exclude hemorrhage before thrombolytic therapy—this is mandatory. 4
• Rapid assessment when MRI is not readily available or in patients with contraindications to MRI (pacemakers, claustrophobia). 4
• Serial monitoring for complications like hemorrhagic transformation or cerebral edema. 4

Limitations Requiring Advanced Imaging

• CT alone is inadequate for confirming the diagnosis of watershed infarcts, particularly small or early lesions. 4
• CTA of the head and neck should be added to rapidly assess for large vessel occlusion and carotid stenosis, which are critical for treatment decisions and surgical planning. 4, 1
• MRI with DWI and FLAIR sequences is the gold standard for assessing ischemic core and identifying watershed patterns more sensitively than CT. 6, 2

Management Implications

Treatment must address the underlying mechanism—optimization of cerebral perfusion and carotid stenosis management for hemodynamic watershed infarcts, versus anticoagulation or antiplatelet therapy for embolic watershed infarcts. 1

• Blood pressure management is crucial: avoid aggressive lowering in patients with arterial stenosis to prevent hypoperfusion, but target systolic BP <140 mmHg for nondiabetics and <130 mmHg for diabetics in the chronic phase. 1, 6
• Duplex ultrasound or CTA should be performed to identify carotid stenosis >50-70%, which may require endarterectomy or stenting. 6
• Antiplatelet therapy is uniformly recommended for secondary prevention unless cardioembolic source (like atrial fibrillation) is identified, in which case anticoagulation is preferred. 1, 6