Reminder of important clinical lesson

‘Fogging’ resulting in normal MRI 3 weeks after ischaemic
stroke
Philip Choi, Velandai Srikanth, Thanh Phan
Department of Neurosciences, Monash Medical Centre, Melbourne, Australia
Correspondence to Dr Philip Choi, philip.choi@gmx.com

Summary
CT of the brain is often negative in acute stroke. The absence of changes suggestive of infarction on MRI of the brain in the setting of a
recent stroke is unusual. An otherwise fit and well 69-year-old Caucasian man presented to the hospital with a 26-h history of acute mild
right hemiparesis. CT brain on arrival showed no abnormality. MRI brain was also normal 3 weeks post stroke with abnormality seen only at
11 weeks. Stroke remains a clinical diagnosis. The time of the stroke must be taken into consideration when interpreting MRI brain images.
Infarct may be ‘invisible’ on MRI in the subacute phase of ischaemic stroke.

BACKGROUND

OUTCOME AND FOLLOW-UP

Physicians often assume MRI is the ‘definitive’ test to
see whether a patient’s stroke-like symptoms was due
to stroke or not. It is now well recognised that CT may
be normal in the acute phase of stroke. It is important to
note that MRI, even with all the different sequences, can
be negative in the subacute phase of stroke as well. Patient
may be misdiagnosed as stroke mimics if the MRI is not
interpreted or reported with the time of onset of symptom
in mind.

Patient’s symptoms gradually improved over 10 days. MRI,
including diffusion weighted imaging (DWI), apparent diffusion coefficient and fluid-attenuated inversion recovery
images of the brain 3 weeks after the index stroke was
normal (figure 1A–D). Interestingly, a repeat study 8 weeks
after the first MRI confirmed a left paramedian pontine infarct on T2-weighted sequence (arrow on figure 1H) but not
on the DWI sequence. The patient reported no new neurological symptoms in between the first and second MRI
studies.

CASE PRESENTATION
A 69-year-old Caucasian man with no significant medical
history presented with 26 h of occipital headache, mild
right facial, arm and leg weakness.

INVESTIGATIONS
CT of the brain 30 h and again 58 h after symptom were
normal.

DISCUSSION
Our case illustrates that the combination of pseudonormalisation1–3 and ‘fogging’ in the subacute phase of ischaemic stroke may cause an infarct to be invisible on MRI.
Signal intensity on DWI for acute infarct is maximal within
24 h of onset and may become invisible after 2 weeks post
stroke.4 During the time of DWI normalisation, the infarct

Figure 1 (A–D) The initial apparent diffusion coefficient, diffusion weighted imaging, fluid-attenuated inversion recovery and high
resolution T2 images show no abnormality. (H) The follow-up MRI scan shows abnormality best seen on the high resolution T2 image.

BMJ Case Reports 2011; doi:10.1136/bcr.04.2011.4110

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is usually visible on T2-weighted image but in this patient,
it was normal as well. This may be explained by a less wellrecognised phenomenon termed ‘fogging’.5 Typically fogging is used to describe the reduced infarct extent between
initial and subsequent scans. In this instance, fogging rendered the infarct invisible. A decrease in apparent infarct
extent on serial DWI scans after stroke in the presence of
haemorrhagic transformation has been shown previously.6
Thus fogging is thought to be related to mild haemorrhagic
transformation or neocapillary growth with some minor
leakage of red cells from friable capillaries. The true extent
of an infarct may not be apparent until at least 7 weeks
post stroke.5

Learning points
Stroke remains a clinical diagnosis.
MRI brain must be interpreted with the stroke onset
timing in mind, as MRI may be negative in the
subacute phase of stroke.
▶ Repeated imaging may be necessary to locate infarct
territory in order to guide secondary prevention
therapy (symptomatic carotid stenosis vs posterior
circulation disease).
▶
▶

Competing interests None.
Patient consent Obtained.

REFERENCES
1. Sylaja PN, Coutts SB, Krol A, et al. When to expect negative diffusionweighted images in stroke and transient ischemic attack. Stroke
2008;39:1898–900.
2. Pereira AC, Doyle VL, Clifton A, et al. Case reports. The transient
disappearance of cerebral infarction on T(2)Weighted MRI. Clin Radiol
2000;55:725–7.
3. Axer H, Grässel D, Brämer D, et al. Time course of diffusion imaging in acute
brainstem infarcts. J Magn Reson Imaging 2007;26:905–12.
4. Burdette JH, Ricci PE, Petitti N, et al. Cerebral infarction: time course
of signal intensity changes on diffusion-weighted MR images. AJR Am J
Roentgenol 1998;171:791–5.
5. O’Brien P, Sellar RJ, Wardlaw JM. Fogging on T2-weighted MR after acute
ischaemic stroke: how often might this occur and what are the implications?
Neuroradiology 2004;46:635–41.
6. Jager HR, Soh C, Beric V, et al. Haemorrhagic transformation of acute
ischaemic infarcts: a pitfall in the interpretation of diffusion-weighted images
and maps of apparent diffusion coefficients. Annual Scientific Meeting
of the British Society of Neuroradiologists. Guildhall, Winchester 2002.
Neuroradiology 2003;45:119.

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Choi P, Srikanth V, Phan T. ‘Fogging’ resulting in normal MRI 3 weeks after ischaemic stroke. BMJ Case Reports 2011;10.1136/bcr.04.2011.4110,
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BMJ Case Reports 2011; doi:10.1136/bcr.04.2011.4110