Asymmetry is often the first and most obvious sign of the presence of an abnormal mass or parenchymal injury. When an abnormal mass or fluid collection is identified, it is critical to discern whether the lesion is intra- or extra-axial in location, in order to generate an accurate differential diagnosis. This should be done before evaluating the lesion's other imaging characteristics. Intra-axial (intraparenchymal) lesions arise from within the brain parenchyma itself. They are within and may expand brain parenchyma, and may also efface adjacent subarach-noid/CSF spaces. Primary brain tumors, such as gliomas and parenchymal metastases are common examples of intra-axial masses. Extra-axial (extraparenchymal) masses displace adjacent brain parenchyma, and a plane or cleft between the mass and brain is often identifiable; adjacent subarachnoid spaces are typically enlarged. Extra-axial masses can be extradural, dural, meningeal or intraventricular in their origin. Examples include meningiomas, nerve sheath tumors, arachnoid cysts, epidermoids, dural metastases, and epidural and subdural hematomas.
Cerebral edema leads to abnormal areas of low attenuation on CT or T2 hyperintensity on MR due to increased local tissue water content. Cerebral infarction, tumors and inflammatory processes can all incite edema and also disrupt the normal differentiation of gray and white matter. Cortex is normally seen as a superficial ribbon of gray matter that is denser (or brighter) than the underlying white matter on CT. Generalized loss of this gray-white differentiation is typically seen in diffuse cerebral edema. In a related fashion, the integrity of the deep gray nuclei (caudate, lenti-form and thalamic) can be assessed by ensuring that they can be distinguished clearly from the surrounding deep white matter. Causes of injury to the deep gray nuclei include focal infarcts, hypoxic or anoxic injury, and metabolic or toxic insults.
Abnormal masses, fluid collections and cerebral edema can all cause mass effect and elevated intracranial pressure, and result in abnormal shift or herniation of brain parenchyma. All of the six main types of herniation—subfalcine, uncal,
Table 6. Suggested sedation protocols used to perform diagnostic studies in children
Midazolam (Versed) PO
Sodium pentobarbital PR (Nembutal)
Sodium pentobarbital IM
Sodium pentobarbital IV
Sodium pentobarbital IV and Morphine sulfate
Fentanyl citrate IV
Propofol (Diprivan) IV
75-100 mg/kg for first 10 kg body weight. Followed by 50 mg/kg, up to maximum of 2000 mg. May give additional incremental doses if child is still awake after 20 minutes.
Administer 30-45 minutes before imaging. 0.3-0.5 mg/kg
Administer 30-45 minutes before imaging. 25 mg/kg via urinary catheter attached to syringe. May give second dose of 15 mg/kg if child is still awake after 20 minutes. Avoid if child has hepatic or metabolic disease.
Administer 30 minutes before imaging. 6 mg/ kg for first 15 kg body weight. Followed by 5 mg/kg, up to total of 200 mg.
2.5 mg/kg push over 30-40 seconds. If not sufficient for initial sedation, additional doses of 1.0 mg/kg , up to total of 6 mg/kg. Repeat 1.0 mg/kg doses as needed to maintain sedation during study.
Pentobarbital 1-2 mg/kg, alternating with morphine 0.05 mg/kg, until child is adequately sedated.
1 vg/kg slow push every 5-7 minutes as needed, up to maximum of 4 vg/kg. For adult-sized patients, 25-50 vg lV per dose.
0.02-0.05 mg/kg slow push. If not sufficient for initial sedation, give 50% of original dose every 2-4 minutes, up to total of 0.6 mg/kg within an 8 hour period. Reduce dose if child has hepatic dysfunction.
2.5 mg/kg for induction. 200 vg/kg/min infusion.
Requires anesthesiologist or nurse anesthetist.
Sedative Antagonists Route Dosing
Naloxone hydrochloride IV (Narcan)
Flumazenil (Romazicon) IV
0.01-0.1 mg/kg, titrate to reversal by repeating dose every 2-4 minutes, up to total of 2 mg.
0.01 mg/kg with maximum single dose of 0.2 mg. Titrate to reversal, by repeating dose every 3-5 minutes, up to total of 1 mg.
downward, tonsillar, upward and external herniation—can be identified by imaging. Subfalcine herniation describes the medial displacement of the cingulate gyrus beneath the falx cerebri. Uncal herniation occurs with medial displacement of the medial temporal lobe (uncus), causing effacement of the ipsilateral perimesencephalic cisterns, and if severe, direct mass effect on the midbrain. Downward herniation manifests as caudal displacement of the diencephalic structures (e.g., deep gray nuclei) with consequent effacement of the suprasellar and perimesencephalic cisterns. Tonsillar herniation is characterized by downward her-niation of the inferior cerebellar tonsils through the foramen magnum. Upward herniation is caused by a posterior fossa mass, and refers to superior displacement of the cerebellum through the tentorial incisura, resulting in mass effect on the dorsal midbrain. External herniation is the outward "extrusion" of brain parenchyma through a defect in the calvarium, such as a prior craniectomy, skull fracture, or congenital encephalocele.
Evaluation of ventricular size and configuration must also be performed. As mentioned above, asymmetry assists in the detection of abnormalities but may not be helpful in the case of midline structures. The following structures should always be assessed on a sagittal MR sequence: corpus callosum, hypothalamic-pituitary axis, pineal/tectal region, brainstem, cerebellum, foramen magnum, superior sagittal and straight dural venous sinuses, upper cervical spine, clivus and nasopharynx. MR sequences also offer the opportunity to confirm the patency and caliber of the major intracranial vessels, since they normally display a signal void due to the rapid flow and movement of protons in blood. An absent flow void signifies either slow flow in or occlusion of a vessel.
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