What are the radiologic signs of cerebral edema on a non‑contrast computed tomography (CT) brain scan?

Radiologic Signs of Cerebral Edema on Non-Contrast CT Brain

Cerebral edema on non-contrast CT manifests as loss of gray-white matter differentiation, sulcal effacement, compression of cerebrospinal fluid spaces, and hypodensity of brain tissue, with these findings appearing as early as 6-10 hours after acute injury. 1

Primary CT Signs of Cerebral Edema

Loss of Gray-White Matter Differentiation

• The most sensitive early sign is loss of the normal gray-white matter interface, particularly visible at the lateral margins of the insula (insular ribbon sign) and in the lentiform nucleus. 1
• This finding reflects cytotoxic and vasogenic edema causing decreased X-ray attenuation in gray matter structures. 2
• Gray matter becomes hypodense and approaches the attenuation of adjacent white matter, creating a blurred boundary. 1

Sulcal Effacement and Mass Effect

• Sulcal effacement represents compression of the subarachnoid spaces due to brain swelling and appears as loss of the normal cortical sulci. 1, 3
• Focal or diffuse brain swelling causes compression of cerebrospinal fluid spaces, including the basal cisterns and ventricles. 1
• Liquoral space asymmetry between hemispheres indicates unilateral edema with mass effect. 3

Hypodensity of Brain Parenchyma

• Brain tissue appears darker (hypodense) on CT due to increased water content from edema. 1, 3
• Hypodensity may be focal (localized to infarct territory) or diffuse (global cerebral edema). 1
• In severe cases, the entire affected hemisphere shows decreased attenuation compared to the contralateral side. 1

Quantitative Assessment

Gray-White Matter Ratio (GWR)

• The GWR quantifies edema severity by measuring Hounsfield unit attenuation in gray matter (caudate nucleus, putamen, thalamus, cortex) relative to white matter (internal capsule, corpus callosum, centrum semiovale). 2
• A GWR below 1.20 indicates severe cerebral edema and is associated with extremely poor survival, with only 2 of 58 patients surviving in one study. 2
• Lower GWR values correlate with decreased consciousness and worse neurological outcomes. 2

Territory-Specific Patterns

Middle Cerebral Artery Territory

• Early signs appear in 80% of middle cerebral artery infarctions within 6-10 hours, including hyperdense vessel sign (32%), sulcal effacement (12-16%), and gray matter hypodensity (12%). 3
• Edema in frontal, parietal, and occipital lobes corresponds to superior sagittal sinus thrombosis. 1

Deep Structures

• Thalamic edema or hemorrhage with intraventricular extension suggests deep venous thrombosis (vein of Galen or straight sinus). 1
• Temporal lobe parenchymal changes correspond to lateral transverse and sigmoid sinus thrombosis. 1

Secondary Signs of Elevated Intracranial Pressure

Midline Shift and Herniation

• Displacement of midline structures (septum pellucidum, third ventricle) indicates significant mass effect from edema. 1
• Effacement of basal cisterns signals impending transtentorial herniation. 1
• Flattening of the posterior globes and empty sella are secondary signs of chronically elevated intracranial pressure. 1

Ventricular Compression

• Compression or effacement of the lateral ventricles, particularly asymmetric narrowing, reflects hemispheric swelling. 1
• Hydrocephalus may develop if edema obstructs cerebrospinal fluid pathways. 1

Timing and Evolution

Acute Phase (0-24 Hours)

• Early infarct signs may be subtle, with sensitivity of only 57% in the first 6-10 hours. 3
• Detection improves with time as edema progresses, with most signs becoming evident by 24 hours. 1

Subacute Phase (24-72 Hours)

• Edema volume peaks between 24-72 hours after injury. 4
• Mass effect and herniation risk are highest during this period. 1

Predictive Features for Malignant Edema

Extent of Early Changes

• Involvement of more than one-third of the middle cerebral artery territory on initial CT predicts increased risk of hemorrhagic transformation and poor outcome. 1
• Patients with both hyperdense middle cerebral artery sign and sulcal effacement have particularly high mortality from transtentorial herniation. 3

Postinterventional Hyperdensities

• After endovascular thrombectomy, postinterventional cerebral hyperdensities (contrast staining or hemorrhage) predict malignant brain edema. 5
• A Hyperdensity on CT Score greater than 3 has 73% sensitivity and 87% specificity for predicting malignant edema. 5

Critical Pitfalls to Avoid

• Do not dismiss subtle early signs: Loss of gray-white differentiation may be the only finding in the first few hours, and missing this can delay critical interventions. 1
• Do not confuse acute blood with edema: Hyperdense areas may represent hemorrhage rather than edema; correlation with clinical presentation is essential. 1
• Do not rely solely on CT in the first 6 hours: Sensitivity is limited early, and MRI with diffusion-weighted imaging is more sensitive for acute ischemia and subtle edema. 1
• Do not overlook posterior fossa edema: CT is relatively insensitive for detecting posterior fossa pathology, where even small amounts of edema can cause life-threatening brainstem compression. 1

When CT Findings Warrant Urgent Intervention

• Presence of widespread early infarct signs with mass effect requires neurosurgical consultation for possible decompressive craniectomy. 1
• GWR below 1.20 indicates severe injury with minimal chance of meaningful recovery and should guide goals-of-care discussions. 2
• Progressive edema on serial CT scans despite medical management necessitates escalation of therapy or surgical decompression. 4