Which noncontrast CT scan findings are characteristic of stroke?

Updated: Nov 30, 2018
  • Author: Andrew Danziger; Chief Editor: L Gill Naul, MD  more...
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On noncontrast CT scan, early findings (within 6 hours) include subtle loss of gray-white differentiation corresponding to increased water content from early cytotoxic edema. [46, 47, 2, 48, 49, 50] Loss of definition of cortex and obscuration of deep gray matter structures may exist.

In middle cerebral artery infarction, obscuration of lateral margins of the insula, (the insular ribbon sign) and loss of density of the basal ganglia nuclei, such as the lentiform nucleus (vanishing basal ganglia sign), may exist (see the images below).

Noncontrast CT was obtained to evaluate this 64-ye Noncontrast CT was obtained to evaluate this 64-year-old male who awoke with aphasia and right-sided weakness. Loss of the normal gray-white differentiation between the normally denser insular cortex and the less attenuating subinsular white matter is seen; this is consistent with loss of the "insular ribbon."
Follow-up noncontrast CT scan obtained approximate Follow-up noncontrast CT scan obtained approximately 12 hours after the initial study in the same patient demonstrates further evolution of the infarction, which is now extensive and spans most of the left middle cerebral artery (MCA) territory.
Noncontrast CT scanning was performed to evaluate Noncontrast CT scanning was performed to evaluate this 70-year-old female with a history of acute onset of right-hand weakness and aphasia. Loss of gray-white differentiation in the left insular cortex and in the immediately adjacent cortical and subcortical portions of the left temporal operculum is seen; this is strongly suggestive of an acute infarction.

Hyperattenuation of vessels may be seen (dense vessel sign or dot sign); these are believed to represent acute thrombus or embolus and has been described in the MCA, basilar artery, and venous sinuses (see the images below).

Noncontrast CT scan in an 80-year-old female who p Noncontrast CT scan in an 80-year-old female who presented with acute onset of right-sided weakness. The left middle cerebral artery (MCA) trunk appears highly attenuated (the dense MCA sign), suspicious for acute thrombosis or embolism. A follow-up noncontrast CT demonstrated an evolving infarct of the lentiform nucleus.
Dense middle cerebral artery (MCA) sign: Noncontra Dense middle cerebral artery (MCA) sign: Noncontrast CT in another patient with strokelike symptoms demonstrates a hyperdense appearance of the right MCA with subtle loss of gray-white differentiation of the anterior right temporal lobe.
Dense basilar artery: Axial noncontrast CT scan de Dense basilar artery: Axial noncontrast CT scan demonstrates a hyperdense basilar artery in a patient with pontine infarction who was later found to have basilar artery thrombosis. Other large vessels besides the middle cerebral artery (MCA) can produce a dense vessel sign when occluded.

After approximately 12-24 hours, a more well-defined area of hypodensity, which may have associated mass effect with sulcal or ventricular effacement, may be seen. The hypodensity is usually irreversible and is felt to correlate with minimum final infarct size. [8, 13]

Mass effect typically peaks by about 5 days post ictus and disappears over the next several weeks. [8]

In roughly one half of cases, the infarct may change from hypodense to isodense. This has been termed the "fogging effect" on CT and is usually seen 2-3 weeks post ictus during the subacute phase of infarction and should resolve on subsequent imaging. IV contrast may make the infarct more conspicuous. The phenomenon is believed to be due to influx of lipid-laden macrophages, decreased water content, proliferation of capillaries, reperfusion, and petechial hemorrhage (see the image below). [51, 52]

CT fogging effect: Axial noncontrast CT scan demon CT fogging effect: Axial noncontrast CT scan demonstrates focal low density, loss of gray-white differentiation, and mild sulcal effacement in the right parietal region (left image, arrow) in a 62-year-old female presenting with acute stroke. A follow-up noncontrast CT scan obtained 10 days later demonstrates diminished sulcal effacement and isodensity with a near-normal appearance (middle image), thought to be secondary to the CT "fogging effect" that may be seen during the evolution of an infarct. The axial diffusion-weighted image (right) confirms the right parietal infarct.

After approximately 6-8 weeks, a well-defined cavity may be seen, corresponding to encephalomalacia. Evidence of volume loss, such as ex-vacuo dilatation of the adjacent ventricle, may exist. Cortical laminar necrosis may be seen in chronic infarcts with gyriform cortical calcification (see the images below).

Noncontrast CT of the brain in a patient with hist Noncontrast CT of the brain in a patient with history of remote CVA demonstrates low density in the right frontal and anterior temporal regions in the MCA distribution. Evidence of parenchymal volume loss with ex-vacuo dilatation of the right lateral ventricle is present, indicating chronicity infarction.
Chronic infarction: Noncontrast CT scan demonstrat Chronic infarction: Noncontrast CT scan demonstrates a well-defined area of volume loss in the right temporal lobe with a low-density appearance consistent with encephalomalacia. No mass effect exists.

Lacunar infarcts appear as small, 5-15 mm areas of low density initially. After approximately 4 weeks, lacunar infarcts should appear as well-defined, cystic low-density areas. Typical locations include the subinsular regions, basal ganglia, thalami and capsular regions, and corona radiata.

Findings on NCCT during the hyperacute phase may be extremely subtle, and a high index of suspicion should be maintained when interpreting the examination. The characteristic findings, namely parenchymal hypodensity, obscuration of gray-white differentiation, and sulcal effacement, are strongly suggestive.

The previously held concept that most studies obtained within 6-12 hours are generally negative was likely related to the limited capabilities of early equipment. In one study, imaging done within 4-6 hours of acute stroke onset showed changes of early infarct in approximately 70% of patients. Another study performed on patients within 5 hours of angiographically proven acute MCA occlusion showed evidence of infarction in 81%. [53, 54, 55]

Soft copy image review using variable window width and center level settings may further facilitate detection of parenchymal hypodensity and acutely ischemic tissue. [56]

In a study of 252 patients presenting with atypical stroke symptoms in the ED and negative findings on head CT, subsequent MRI identified acute to subacute infarct in 29 of those patients. The mean age of the MRI-positive group was 74 years. The study authors noted that in elderly patients with a history of prior stroke or transient ischemia attack, a lower threshold should be maintained for ordering a head MRI despite a negative head CT. [57]

False-positive areas of hypoattenuation may be seen due to beam hardening artifact from bone along the cerebral convexities from the adjacent calvaria and in the posterior fossa due to the skull base. Streak artifacts may also cause parenchymal hypodensity adjacent to aerated sinuses. The typical location and appearance, linearity, and extension beyond brain parenchyma should all help identify these artifacts.

Artifactual hypodensity may be seen when the cortex is volume-averaged with adjacent cerebrospinal fluid in a sulcus, fissure, or cistern.

Various other lesions may produce focal areas of hypodensity both with and without mass effect, including perivascular spaces, infiltrative tumors with vasogenic edema, and encephalitis.

The CT “fogging” effect may transiently produce isodensity of an infarct that always resolves on follow-up imaging.

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