Neurological Applications in Diagnosis and Treatment

CT is useful in detecting structural abnormalities causing multifocal, focal, or subcortical cerebral dysfunction. Evaluation of the brain stem is generally limited to the midbrain and upper pons. CT has limited usefulness in the evaluation of the spinal cord and nerve roots. CT is not useful in the evaluation of neuromuscular disease.


Intra-axial Disorders. CT can often identify lesions responsible for cerebral dysfunction and is ordered in the acutely ill neurological patient with a history of trauma, stroke, "worst headache" of life, anticoagulation or bleeding diathesis, or seizure. In any case of suspected acute intracranial hemorrhage, intravenous contrast medium should not be administered because contrast medium enhancement and acute extravascular blood have similar attenuation characteristics. Likewise, evaluation for infarction should be performed without contrast medium enhancement to exclude hemorrhage and also because subacute infarction may show mild enhancement such that it is indistinguishable from normal cortex. Scans performed within the first 24 hours of clinical symptomatology of infarct may not reveal any detectable abnormality. Early signs of middle cerebral artery infarct include hyperdensity of the artery (thrombus, embolus), loss of differentiation of insular cortex and lentiform nucleus from adjacent capsular white matter structures due to edema, and effacement of the sylvian fissure and sulci.

Differential diagnosis of enhancing lesions includes primary brain neoplasm, metastasis, abscess, infarct, demyelinating disease, resolving hematoma, and vascular malformation. Abscesses, metastases, and high-grade primary neoplasms incite prominent vasogenic edema, whereas other enhancing lesions usually show less edema. Demyelinating disease shows ring or solid enhancement in the acute stage, commonly in a periventricular location. Resolving hematomas show ring enhancement 1 to 2 weeks after hemorrhage at the margin of the hematoma bed. Arteriovenous malformations demonstrate enlargement of feeding arteries and draining veins with central dense enhancement representing the nidus. Cavernous angiomas show enhancement in a solid pattern and are often hyperdense without contrast medium owing to calcification.

Intracranial calcifications are seen in a variety of disease processes. Arteriovenous malformations, aneurysms, and cavernous angiomas all may contain calcifications. Of the neurocutaneous disorders, tuberous sclerosis and Sturge- Weber show characteristic patterns. Patients with tuberous sclerosis demonstrate calcifications that are mainly periventricular in location ( Fig.J^.-Z ). Patients with Sturge-Weber syndrome show a gyriform pattern of calcification seen in the posterior temporal, parietal, and occipital cortex. Patients with neurofibromatosis may also demonstrate parenchymal calcifications in the basal ganglia and elsewhere. Excessive basal ganglia calcifications are seen in many metabolic disorders usually related to calcium metabolism. Neoplasms that calcify include gliomas (particularly oligodendrogliomas), meningiomas ( ..Fi.g,.23-8 ), ependymomas, craniopharyngiomas, and choroid plexus papillomas. The most common acquired intracranial infection to demonstrate intracranial calcification is cysticercosis.

CT plays a complementary role to MRI in evaluation of patients with cranial nerve palsies. CT excels in evaluation

Figure 23-8 Sixty-year-old woman with right parasagittal meningioma. Without contrast, the lesion is hyperdense and contains calcifications. Low-density white matter represents vasogenic edema.

of the bony skull base and can detect pathological processes such as tumor, infection, and primary bone lesions as they encroach upon, enlarge, or destroy foramina. Because all the cranial nerves have a close relationship to the skull base, bone detail thin-section scanning should be obtained in all patients with these palsies. Of the cranial nerves, only the optic nerve can be directly visualized by CT. Patients with monocular visual loss may demonstrate enhancement and/or enlargement of the optic nerve.


Magnetic resonance imaging is generally the test of choice for evaluating upper or lower motor neuron disease localized to the spinal cord, spinal roots, or plexi. In particular, CT should not be used as a primary imaging modality in suspected spinal cord compression because soft tissue lesions such as abscesses, hematomas, and sometimes disk herniations may be missed. CT serves a complementary role in defining bone lesions causing spinal cord compression once the level of interest has been identified by MR or myelography (if MR is contraindicated). Metastatic disease, discogenic disease with osteophyte formation and calcification of disc material/ligaments, infection, and primary bone tumors or metabolic lesions are examples of pathological processes in which CT can add information to MRI. CT can visualize nerve roots surrounded by low-attenuation fat particularly in the lumbar neural foramen and is useful in evaluating bone encroachment on the neural foramina from endplate osteophyte formation, facet degeneration, or uncinate process osteophytes of the cervical spine. CT myelography can visualize nerve roots and the spinal cord in the thecal sac and is particularly useful in the patient who cannot undergo MRI.


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