Surgical treatment (excision or stereo-tactic radiosurgery) is reserved for patients with recurrent hemorrhage, intractable epilepsy, or progressive neurologic dete-rioration (Fig. 2.21).
◆Cavernous Malformation
Cerebral cavernous malformations (alsoknown as cavernous hemangiomas) arecompact vascular malformations consistingof thin-walled capillaries without interven-ing neuronal tissue. On gross examination,they are circumscribed, red, lobulated mass-es from less than a millimeter to several cen-timeters in diameter. Most are supratentorialand are found in the frontal and temporallobes. They are usually solitary, althoughsome patients can have multiple lesions andfamilies have been identified in which sev-eral members have multiple lesions.
Occasionally, cavernous malformations are associated with developmental venous anomalies. These are small clusters of ve-nules that drain a small segment of nor-mal brain via a single larger anomalous vein that leads to either a dural sinus or an ependymal vein. Usually seen only on postgadolinium MRI, venous angiomas re-semble an umbrella or palm tree.
Most patients are asymptomatic, and most cavernous malformations are found
Fig. 2.21a–fa–e Cavernous malformation with associated developmental venous anomaly. (a) NCCT. Vague, 1-cm rounded right frontal hyperdense lesion; no associated edema. (b) T2WI. “Mulberry-like,” mixed-signal-intensity lesion with surrounding low-signal rim on gradient echo imaging. No associated edema or other parenchymal abnormality. (c) GRE. Low signal intensity corresponds to hemosiderin within the malforma-tion. (d,e) T1-weighted postgadolinium images show an associated developmental venous anomaly: a small umbrella-like cluster of venules that drain a small segment of frontal lobe parenchyma adjacent to the cavernous malformation. A single draining vein courses along the ventricle and septum pellucidum to join the internal cerebral vein.
f Multiple cavernous malformations. Three large occulent parenchymal calcications, up to 4 cm in di-ameter, located in the right frontal lobe and left insula. Associated right frontal cortical encephalomalacia.
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geneous, low in attenuation, and diusely swollen, with sulcal and cisternal eace-ment. Because the meninges are supplied by branches of the external carotid artery (ECA), which are usually not compromised, they will often appear dense against adja-cent low-attenuation brain and can simu-late diuse subarachnoid hemorrhage.
The basal ganglia, cerebral cortex,thalami, cerebellum, caudate nuclei, andhippocampi are most sensitive to hy-poxic ischemic injury, and patients whosuer less severe hypoxia may show low-attenuation CT changes or high-signal T2-weighted MRI changes in these structures(Fig. 2.22).
◆Anoxic Injury
Anoxic (also known as hypoxic-ischemic) cerebral injury results from global lack of oxygen delivery to the brain for an ex-tended period. It is most frequently the consequence of cardiopulmonary arrest, respiratory failure, carbon monoxide poi-soning, near-drowning, or asphyxia. Pa-tients typically present to the Emergency Department with a history of prolonged resuscitation eorts.
CT findings in adults with prolonged anoxia, hypoxia, or global hypoperfusion include progressive loss of normal gray-white matter dierentiation, generalized cytotoxic edema, and sulcal and ventricu-lar eacement. The brain appears homo-
Fig. 2.22a–fa–d Anoxic injury following prolonged cardiorespiratory arrest. (a,b) Initial NCCT. Diminished gray-white dierentiation with normal ventricles and sulci. (c,d) Follow-up NCCT 24 hours later. Progressive decrease in parenchymal attenuation with complete perimesencephalic cisternal and convexity sulcal eacement. Both lateral ventricles are compressed. Increased apparent density within the subarachnoid space reects maintained meningeal perfusion rather than true subarachnoid hemorrhage.
e,f Less severe anoxic injury following cardiac arrest and resucutation. Immediate post-arrest CT is nor-mal. Four days later, low attenuation changes are limited to the caudate nuclei and lateral putamina.
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The primary role of CT in acute strokeis to exclude hemorrhage, which contrain-dicates the use of thrombolytic agents inthose patients who present within 3 hoursof symptom onset. If readily available, dif-fusion-weighted MRI is the most sensitiveexamination for identifying early cerebral in-farction, and it can do so within 30 minutes.
Cytotoxic edema increases during the first 3 days after cerebral infarction, and on CT itappears as a well-defined area of low atten-uation involving gray and white matter. Cor-responding hyperintensity is evident on T2and FLAIR MRI sequences at this stage. Afterapproximately 2 weeks, an evolving infarctmay become less obvious on CT because of a“fogging” eect in which microhemorrhage and cellular repair lead to pseudonormal-ization of brain density. Diusion-weighted MRI signal begins to fade around 1 weekand is usually nearly normal by 2 weeks.Hemorrhagic conversionis a term that refersto spontaneous bleeding within an area ofischemic brain, most commonly in patientswith large-territory (middle cerebral or in-ternal carotid artery) infarcts (Fig. 2.23).
◆ Cerebral Infarct Due to Arterial Occlusion
Ischemic cerebral infarcts result from acute compromise of arterial blood flow to a por-tion of the brain, with consequent cellular death. The neurologic deficit resulting from the infarct depends on the vessel occluded, the location and extent of the territory it supplies, and the available collateral circu-lation. For example, a left middle cerebral artery infarct would be expected to result in aphasia as well as contralateral hemipa-resis and sensory disturbance.
The sensitivity of nonenhanced CT is limited in the first 12–24 hours after symptom onset; however, subtle signs of early infarct can be seen even within the first 3 hours. A hyperdense cerebral vessel (known as the bright basilar artery or hy-perdense middle cerebral artery) indicates thrombosis. Early parenchymal changes are due to ischemic (cytotoxic) cellular swelling and include (1) focal loss of nor-mal gray-white matter dierentiation, (2) cortical sulcal eacement, (3) poor basal ganglia definition, and (4) nonvisualization of the “insular ribbon,” which is the nor-mally dense insular cortex.
Fig. 2.23a–fa,b Early infarct with dense middle cerebral artery and insular ribbon signs. The left middle cerebral artery is abnormally dense. The left insular cortex is isodense to adjacent white matter and hypodense compared with the normal cortex.
cSubacute left middle cerebral artery territory infarct. Cytotoxic edema with homogeneous low-attenu-ation change involving both gray and white matter in the distribution of theleft lenticulostriate vessels