Clinical
Presentation: A 36-year-old quadriplegic male with a history of hypertension and drug abuse presented with altered mental status.
Imaging Findings: Initial non-contrast CT showed subtle loss of gray-white differentiation and effacement of the sulci in the left frontal lobe near the vertex. MRI performed 2 months later shows post-contrast enhancement of the left frontal and temporoparietal gyri, consistent with a subacute infarct. Non-contrast CT performed 3 months after the onset of symptoms, shows focal encephalomalacia and volume loss within the affected left frontal region. This is the expected evolution of a cerebral infarct.
Figures 1 and 2 show the initial axial non-contrast head CT images. Notice subtle loss of gray-white differentiation and sulcal effacement in the left frontal lobe near the vertex.
Figures 3 and 4 show T1-weighted post-contrast axial MR images from 2 months later. There is gyral enhancement within the corresponding left frontal region.
Figure 5 shows an axial non-contrast CT image from 3 months after the initial study. There is focal low-attenuation encephalomalacia and volume loss within the corresponding left frontal region.
Diagnosis: Acute infarct on CT
Discussion: Stroke is the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. Stroke or cerebrovascular accident (CVA) is a nonspecific term encompassing a variety of pathophysiologic conditions, including thrombosis, embolism, and hemorrhage. The incidence for first-time strokes is more than 400,000 per year. This number is projected to increase to one million per year by the year 2050. Strokes are broadly classified as as either hemorrhagic or ischemic. Acute ischemic stroke refers to strokes caused by thrombosis or embolism and accounts for 85% of all strokes. Ischemic strokes are most often due to extracranial embolism (from the heart, neck vasculature, or paradoxical) or intracranial thrombosis, but they may also be caused by global decreases in cerebral blood flow.
A stroke can cause a multitude of physical symptoms. These commonly include abrupt onset of hemiparesis, monoparesis, quadriparesis, visual loss,visual field deficits, diplopia, dysarthria, ataxia, vertigo, aphasia or altered level of consciousness. Establishing the time of onset of these symptoms is of utmost importance as it is a primary determining factor in whether the patient may receive thrombolytics. Current AHA/ASA guidelines for the administration of rt-PA includes onset of symptoms less than 3 hours before beginning treatment.
An emergent non-contrast head CT scan is the mandatory initial imaging work-up for a presumed stroke. It is obtained to diagnose or exclude intracranial hemorrhage as well as to identify any underlying tumor, AVM, abscess or extra-axial hematoma that could mimic stroke symptomatology. It is important to note that the main goal of the initial non-contrast CT is not to definitively diagnose a CVA. Approximately 60% of patients with confirmed strokes will have negative initial CT scans. The lesion will become more apparent as time passes. The changes in the CT appearance of a cerebral infarct over time must be understood. It is not usually until 6-12 hours after symptom onset that sufficient edema is recruited into the stroke area to produce a regional hypodensity on a CT scan. A large hypodense area present on CT scan within the first 3 hours of symptom onset should prompt careful requestioning regarding the time of stroke symptom onset.
Despite frequently being negative, several early signs of acute stroke are occasionally identified within the first 4-6 hours. These signs include a high attenuation middle cerebral or other artery (dense MCA sign). Other very early signs include obscuration of the lentiform nucleus, loss of gray-white differentiation particularly along the lateral insula, (insular ribbon sign) and asymmetry/effacement of cortical sulci. See Table 1 for CT findings of cerebral infarcts by age.
Table 1: Timeline of CT findings in cerebral infarct.
Hyperacute < 12 hrs
Acute 12 – 24 hrs
1 – 3 days
4 – 7 days
1 – 8 weeks
Months to Years
60% are completely normal
Low density basal ganglia
Increasing mass effect
Gyral enhancement
Contrast enhancement persists
Encephalomalacia
Hyperdense artery (dense MCA sign)
Loss of gray/white differentiation
Wedge-shaped area of low density
Mass effect
Resolving mass effect
Volume loss
Obscuration of lentiform nuclei (insular- ribbon sign)
Sulcal effacement
Hemorrhagic transformation
Edema
Transient calcification
Rare calcification
Loss of gray/white differentiation
Sulcal effacement
More sensitive imaging modalities can be employed to identify acute cerebral infarcts. Currently, magnetic resonance with diffusion-weighted imaging (DWI-MRI) is being utilized to demonstrate infarcts early after symptom onset. Additional modalities commonly utilized include CT angiography of the head and neck and MR angiography. Despite imaging advances in early identification of strokes, a non-contrast head CT is still the standard initial study performed. The oftentimes subtle appearance of a hyperacute stroke on CT therefore becomes important.
Osborn AG: Diagnostic Neuroradiology. St. Louis:Mosby, 1994:330-397.
Siskas N, Lefkopoulos A, Ioannidis I, Charitandi A, Dimitriadis AS. Cortical laminar necrosis in brain infarcts: serial MRI . Neuroradiology. 2003 May;45(5):283-8. [Medline]