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Brain Imaging : Inflammatory, Infectious, and Vascular Diseases
1
How is multiple sclerosis (MS) diagnosed?
MS is the most common cause of acquired demyelinating disorders. The disease has a characteristic relapsing-remitting course and usually manifests between the third and fifth decades of life with a female predominance. On magnetic resonance imaging (MRI), the demyelinating lesions of MS are ovoid and hyperintense (bright) in signal intensity on T2-weighted images and occur predominantly in the white matter, especially in the periventricular location (usually perpendicular to the ventricular surface) ( Figure 41-1 ). The corpus callosum, white matter around the temporal horns of the lateral ventricles, and middle cerebellar peduncles are other favored locations of MS plaques. There may be enhancement of the plaques (ringlike or solid) that denotes active disease. Occasionally, MS plaques can be large and masslike (tumefactive MS), in which case differentiation from a tumor may be difficult.
2
What is the differential diagnosis of MS based on imaging findings?
The diagnosis of MS is a clinical one (neurologic symptoms spaced over time and in multiple distributions), with supporting radiologic findings. The diagnosis cannot be made on imaging findings alone because other inflammatory and vascular processes can manifest with similar imaging findings. White matter lesions similar to MS can be seen with a spectrum of inflammatory conditions, including Lyme disease, sarcoidosis, and vasculitis.
3
What are the clinical and imaging features of acute disseminated encephalomyelitis (ADEM)?
ADEM is an acute monophasic demyelinating disease seen most commonly in the pediatric population. It is characterized by acute demyelination following a recent viral infection or vaccination. The white matter lesions in the brain are bilaterally asymmetric and usually demonstrate enhancement ( Figure 41-2 ). Involvement of the basal ganglia, brainstem, and spinal cord may also occur. Tumefactive MS can mimic this entity radiologically although the diffuse bilateral pattern of involvement with lesions in the gray matter (basal ganglia) and preferential involvement of the subcortical white matter in ADEM may help distinguish the two entities.
4
What are the causes of intracranial abscesses?
Infectious agents gain access to the central nervous system (CNS) by direct spread from a contiguous focus of infection, such as sinusitis, otitis media, mastoiditis, orbital cellulitis, or dental infection. Infection from these locations may also spread to the intracranial compartment by retrograde venous reflux. Hematogenous spread of infection can also occur from a distant nidus of infection, such as the lung. Polymicrobial infection is common with brain abscesses. Four stages have been described in abscess evolution: early cerebritis, late cerebritis, early capsule formation, and late capsule formation. A mature abscess is characterized by a “ring-enhancing” lesion on cross-sectional imaging.
5
What is the imaging differential diagnosis of a ring-enhancing lesion in the brain?
The following disease processes can have an imaging presentation identical to brain abscess: metastatic disease, primary CNS glioma, resolving hematoma, and demyelinating disease. Interpretation of the radiologic findings in conjunction with the clinical history is usually helpful to differentiate between these possible etiologies.
6
What advanced MRI techniques may be useful in distinguishing brain abscess from neoplasm?
Differentiating a subclinical brain abscess from a cystic or necrotic tumor with conventional computed tomography (CT) or MRI can be difficult. 1 H magnetic resonance spectroscopy and diffusion-weighted imaging (DWI) can be useful in this regard ( Figure 41-3 ). Typically, on DWI, an abscess is hyperintense (bright) due to presence of pus.
7
What anatomic location in the brain is preferentially involved by herpes simplex encephalitis?
In adults, type 1 herpes simplex virus is responsible for fulminant, necrotizing encephalitis. The virus preferentially involves the temporal lobes, but involvement of the frontal lobes (especially the cingulate gyrus) is common. Often, there is bilateral temporal lobe involvement, although this is usually asymmetric. On MRI, there is T2-weighted hyperintensity in the temporal and frontal lobes with enhancement ( Figure 41-4 ). Clinically, the patient presents with acute confusion, disorientation, or seizures progressing to stupor and coma. Most cases are a result of reactivation of dormant virus in the trigeminal ganglion. There is commonly asymmetric temporal lobe involvement. Hemorrhage in the affected area is also common.
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