Imaging findings of demyelination on computed tomography (CT)

Check out this case-based article to learn about the expected CT and MRI findings of brain demyelination.
Last update4th Jan 2021

Computed tomography (CT) is not a regular part of the assessment of the brain for patients with multiple sclerosis (MS) since magnetic resonance imaging (MRI) is much more sensitive to changes in the white matter. However, in some cases, the white matter abnormalities of MS may be first evident on a CT scan before a definitive diagnosis is made. When you see white matter abnormalities on CT, you should consider demyelination as a cause, especially when they are homogeneously low in attenuation and limited to the white matter.

Case 1: Tumefactive demyelination

In our first case, the patient’s MRI scan demonstrated typical imaging findings of tumefactive demyelination. You should notice that there is less mass effect on the ventricle in the magnetic resonance (MR) fluid-attenuated inversion recovery (FLAIR) scan than what you might expect for a mass of this size (Fig. 1). As well, the enhanced scan shows only a partial ring of enhancement. These two findings are frequently seen in cases of tumefactive demyelination.

Figure 1. Magnetic resonance (MR) fluid-attenuated inversion recovery (FLAIR) scan showing findings typical of tumefactive demyelination with less mass effect on the ventricle than expected. The enhanced magnetic resonance imaging (MRI) scan also shows typical findings of a partial ring of enhancement.

While MRI shows abnormalities associated with tumefactive demyelination very well, a CT scan can still be helpful because these abnormalities often resemble a brain tumor. In most patients with tumefactive demyelination, their non-contrast CT scan will show that the mass has homogenous low attenuation. This differs from the appearance of neoplasms since they will usually have areas of high attenuation that are visible on non-contrast CT, which is most likely from the regions of dense cellularity that are typical for most neoplasms.

Magnetic resonance perfusion can also help distinguish tumefactive demyelination from neoplasms. High-grade tumors should (at minimum) have elevated cerebral blood volume, while tumefactive demyelinating lesions (TDLs) usually show low cerebral blood volume.

Figure 2. A computed tomography (CT) scan showing homogenous low attenuation in the region of the mass in a patient with tumefactive demyelination.

Keep in mind that you shouldn’t expect to establish a diagnosis of TDL based on the patient’s prior history of MS, or expect to see other white matter lesions. In most cases, tumefactive demyelination is the first manifestation of demyelination.

Not all patients with TDLs will go on to develop MS. In many cases, TDLs are part of a monophasic disease called acute disseminated encephalomyelitis (ADEM). Fortunately, TDLs will respond to steroids, but follow-up imaging is prudent to confirm that the lesion regresses over six to eight weeks (as expected).

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Case 2: Acute toxic encephalopathy

While confluent white matter lesions can be evident with multiple sclerosis, sometimes CT will demonstrate diffuse white matter involvement in patients with no prior neurological deficits. For example, a young patient was brought to the emergency room (ER) unconscious and his CT demonstrated diffuse white matter abnormalities (Fig. 3).

His MRI diffusion sequence also demonstrated a corresponding restricted diffusion throughout the white matter of both hemispheres. Based on the CT and MRI findings, along with the clinical presentation, MS was an unlikely diagnosis. In fact, these findings are more consistent with acute demyelination.

The patient had a positive drug screen in the ER, and further history indicated that the patient had been using heroin. This history suggests the diffuse white matter changes were a complication of heroin use called acute toxic encephalopathy, and these changes were not reversible.

Figure 3. A computed tomography (CT) scan demonstrating diffuse white matter abnormalities, and magnetic resonance imaging (MRI) diffusion sequence scan demonstrating a corresponding finding of restricted diffusion consistent with acute demyelination of the white matter of both hemispheres. These findings are typical of acute toxic encephalopathy.

Case 3: Metabolic insult

Diffuse white matter abnormalities in both hemispheres can also occur secondary to a metabolic insult such as anoxia, shown next on an MRI from a different patient (Fig. 4). Drug overdose and anoxia frequently occur together.

Figure 4. Magnetic resonance imaging (MRI) scan of white matter abnormalities in both cerebral hemispheres secondary to anoxia.

Case 4: Multiple sclerosis

The next CT scan shows two homogeneously low attenuation lesions in the brain without focal high attenuation within or nearby the lesions. While the patient’s CT scan is not diagnostic for demyelination, it should lead you to strongly consider MS in your differential, which is the correct diagnosis in this case. But, in nearly all cases of suspected or evident white matter abnormalities on CT, MRI with contrast enhancement is usually of value.

Figure 5. Computed tomography (CT) findings of two homogeneously low attenuation lesions, without focal high attenuation within or nearby the lesions. These findings should lead to further investigation to rule out a diagnosis of multiple sclerosis (MS).

Compared to CT, MRI is much more sensitive to changes in the white matter. However, you may see white matter abnormalities on CT first. If these findings are homogeneously low in attenuation, and limited to the white matter, you should consider demyelination that could be due to multiple sclerosis, tumefactive demyelination, or even acute toxic encephalitis.

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Recommended reading

 

  • Kim, DS, Na, DG, Kim, KH, et al. 2009. Distinguishing tumefactive demyelinating lesions from glioma or central nervous system lymphoma: added value of unenhanced CT compared with conventional contrast-enhanced MR imaging. Radiology. 251: 467–475. PMID: 19261924

About the author

Alexander Mamourian, MD
Professor Emeritus of Radiology at the University of Pennsylvania and Professor of Radiology, Neurosurgery, and Neurology at Penn State, Hershey Medical Center, USA.
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