e,f Tension pneumocephalus due to temporal bone fracture. Bifrontal subdural air collections with mild compression of the frontal parenchyma. Opacied left mastoid air cells are consistent with an acute tem-poral bone fracture. Air in the cisterns and left sylvian ssure indicate arachnoid injury.
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cerebral compartment can cause subfal-cine, transtentorial, or central herniation; vascular compromise; and ischemia.
CT findings in both traumatic and non-traumatic swelling include global sulcal eacement, small ventricles, and com-pressed perimesencephalic and suprasellar cisterns. In head trauma, swelling is usu-ally associated with other findings includ-ing extra-axial hematomas, contusions, subarachnoid hemorrhage, and ventricular trapping (Fig. 2.14).
◆Cerebral Swelling
Cerebral swelling may be due to traumatic injury or one of many nontraumatic etiolo-gies, including intracranial neoplasm, in-fection, various metabolic derangements, and hypoxic-anoxic injury.
In severe head trauma, cerebral tissue damage, often associated with systemic hypovolemia, hypoxia, and hypercarbia, disrupts normal cerebral autoregulation and leads to a toxic cycle of elevated in-tracranial pressure, ischemia, and further tissue damage. Swelling localized to one
Fig. 2.14a–fa,bTraumatic cerebral swelling. Small right frontal extra-axial hematoma and diuse traumatic subarach-noid hemorrhage. Global cisternal and sulcal eacement with poor gray-white dierentiation. Associated right frontal scalp soft tissue swelling, orbital roof fracture, intraorbital hematoma, and intraorbital air.
c,d Traumatic cerebral swelling in another patient. Poor gray-white dierentiation, sulcal and perimes-encephalic cisternal eacement, right frontal subacute subdural hematoma/hygroma, and traumatic con-vexity subarachnoid hemorrhage.
e,f Cerebral swelling due to anoxic injury. Complete loss of gray-white dierentiation. No visible sulci or cisterns.
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and dilated. Further compression forces the contralateral cerebral peduncle against the tentorial dural reflection and injures descending motor fibers, causing ipsilat-eral hemiparesis. The posterior cerebral artery can also be compressed in uncal herniation, causing an ipsilateral temporal/occipital infarct with visual field defects opposite the injured hemisphere.
Downward (central) herniation occurs in severe bilateral hemispheric injuries. Inferior brainstem displacement com-promises its vascular supply and can lead to ischemic or reperfusion injury. Cross- sectional imaging findings include cister-nal eacement, compression of the cere-bral peduncles, and ventral or ventrolateral brainstem hemorrhage (Duret hemor-rhage) located near the midline at the pon-tomesencephalic junction.
Upward transtentorial herniation can occur with cerebellar hemorrhage, low oc-cipital trauma, or infratentorial masses. Like downward transtentorial herniation, it can result in brainstem ischemia and hemorrhage.
Signs and symptoms of herniation often develop rapidly and include somnolence or stupor, agitation, neurologic deficits, cranial nerve palsies, and “Cushing triad” (hypertension, bradycardia, and irregular respiration) (Fig. 2.15).
◆Cerebral Herniation
Cerebral herniation is defined by displace-ment of swollen or compressed brain acrossthe falcine and tentorial dural reflections, through a calvarial defect, or through theforamen magnum. Causes include subduralor epidural hematomas, parenchymal hem-orrhage, tumors, and focal cerebritis or ab-scess. Depending on location, direction, andseverity, herniated brain can compress cra-nial nerves and descending and ascendingbrainstem fiber tracts, obstruct intraventric-ular CSF flow, and occlude cerebral arteries.
The most common pattern is subfalcine herniation, in which the cingulate gyrus herniates under the falx. Contralateral hy-drocephalus (ventricular trapping) results from obstruction of the lateral ventricle at the foramen of Monro. Compression of the anterior cerebral artery branches, when displaced across the falx, can cause an ip-silateral superior frontal or cingulate gyrus infarct, which may manifest clinically as contralateral leg weakness.
Brain herniation through the tentorial notch can be either downward (central), upward (due to posterior fossa hemor-rhage), or lateral (uncal). Uncal herniation is more common than other transtentorial herniations. As the herniating medial tem-poral lobe compresses parasympathetic fi-bers on the periphery of the third cranial nerve, the ipsilateral pupil becomes fixed
Fig. 2.15
a,b Acute subdural hematoma with subfalcine and uncal herniation. Hyperdense, crescentic left ho-lohemispheric SDH with hemorrhagic temporal contusion. Uncal herniation with complete cisternal ef-facement, displacement of the left lateral ventricular temporal horn to the midline, and trapping of the left lateral ventricle. Left posterior cerebral artery and anterior cerebral artery occlusion with traumatic cerebral infarcts involving the left occipital lobe (PCA distribution) and left superior frontal gyrus (ACA distribution).
c,d Downward transtentorial herniation with Duret hemorrhage. Diuse cerebral swelling with cisternal eacement, poor gray-white dierentiation, and large central pontine hemorrhage.
e,f Upward transtentorial herniation due to traumatic cerebellar hemorrhage. Diuse cerebellar swelling with upward transtentorial herniation, complete cisternal eacement, multiple pontine hemorrhages, and low-attenuation brainstem change.
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mote head injury include prior craniotomy, facial fractures, and burr