Diffusion-negative MRI in acute ischemic stroke: a case report
© Rathakrishnan et al; licensee BioMed Central Ltd. 2008
Received: 28 May 2008
Accepted: 29 July 2008
Published: 29 July 2008
Diffusion-weighted magnetic resonance imaging is a very sensitive tool for the early diagnosis of acute ischemic stroke. This is employed in some stroke centers as the primary screening tool to select patients eligible for thrombolysis.
We present the case of a 49-years old Chinese man whose diffusion-weighted magnetic resonance imaging performed 12 hours of symptom onset was negative.
Although the initial diffusion-weighted magnetic resonance imaging was negative, the imaging repeated after 4 days despite static neurological symptoms and signs, could demonstrate an acute medullary infarction.
Diffusion-weighted imaging may not be100% sensitive in very early stages, especially in posterior circulation strokes. Our case serves as a reminder that clinical assessment still retains priority until a diagnostic modality offering 100% sensitivity and specificity is discovered.
Diffusion-weighted magnetic resonance imaging (DWI-MRI) is considered to be a very sensitive tool for the early diagnosis of acute ischemic stroke. This is employed in some stroke centers as the primary screening tool to select patients eligible for thrombolysis. However DWI may not be100% sensitive in very early stages, especially in posterior circulation strokes. We present a patient in which DWI-MRI was negative even after 12 hours of symptom onset and only the imaging repeated after 4 days could demonstrate an acute infarction.
A 49-year old Chinese man, office clerk by occupation was admitted with sudden vertigo and unsteady gait. The vertigo was unremitting with eye closure and not posturally related. There was no trauma, neck pain or illness. There was no significant medical illness in past and accordingly, he was not on regular medication and did not smoke. Clinical examination revealed right lateral gaze-evoked nystagmus, right upper limb dysmetria and ataxic gait. Sensation to pain and temperature was intact and there was no evidence of a Horner's syndrome.
Our patient demonstrates that DWI-MRI performed early may fail to demonstrate an acute infarct especially if it is small and located in territory supplied by posterior circulation. This may have an impact on the clinical decision making process in centres using DWI-MRI as a tool to guide aggressive therapy in patients with acute stroke . Our case did not develop any new neurological signs and neuroimaging was repeated to ascertain if DWI would remain persistently negative despite static neurological deficits consistent with a cerebrovascular event.
In acute cell death, failure of sodium-potassium ATPase pumps result in the shift of water from extracellular to intracellular compartments, reflected as a hyperintense lesion on DWI . DWI provides the earliest imaging evidence of ischemic injury  and can reveal abnormalities before other conventional MR sequences, even in transient ischemic events [4, 5]. However DWI as an isolated sequence may fail to demonstrate an acute stroke in up to 20% cases . Infarcts involving the medullary region yield highest false negative rates . This becomes clinically relevant if MRI-DWI is employed as the imaging modality to determine attempts at recanalization during the acute treatment of ischemic stroke .
Technical reasons have been postulated for the occasional failure of DWI-MRI to demonstrate an acute infarction including poor spatial resolution, high signal-to-noise ratio and magnetic susceptibility artefacts around the brain stem . Another important factor is the time elapsed from ictus at which the scan is performed. While positive DWI-MRI has been observed within 2.5 minutes of arterial occlusion in animal models, a longer duration (within 3 hours) in humans may not be sufficient for DWI changes despite a fixed neurological deficit [9, 10]. Contrary to the previous reports of false-negative MRI-DWI within 3 hours of symptom-onset, our patient had a prolonged fixed neurological deficit for 24 hours and yet DWI failed to demonstrate an infarct despite flow-void abnormality in the right vertebral artery. We hypothesize that the point at which the reversible ischemia transforms into irreversible infarction and impaired diffusibility had not been crossed [7, 9] when our patient had the initial MRI and thus the DWI remained negative. DWI abnormalities may be reflective of dynamic disturbances along different points of the ischemic cascade [3, 7]. While 'restricted-diffusion' on DWI can occur with prolonged tissue hypoxia, the changes may be reversible if early reperfusion is achieved [3, 7]. This indicates that MRI-DWI changes are not 'per se' absolute markers of ongoing or established ischemia and conversely, the absence of a DWI-lesion does not completely rule out an ischemic state.
This may be argued that the first MRI could have missed the particular section of the brain that underwent the ischemic infarct. This possibility, although very unlikely, can not be completely excluded. Another explanation for DWI-negative MRI could be an interval infarction between the two MRI scans performed in our case. However, our patient did not develop any new symptoms or signs suggestive of a new neurological injury.
In conclusion, if there is a high index of suspicion for an acute cerebrovascular event especially involving the posterior circulation with an unremarkable initial MRI-DWI, a repeat study after 24 hours of a fixed neurological deficit may be more demonstrative. Our case serves as a reminder that clinical assessment still retains priority until a diagnostic modality offering 100% sensitivity and specificity is discovered.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Magnetic resonance imaging
- Oppenheim C, Stanescu R, Dormont D, Crozier S, Marro B, Samson Y, Rancurel G, Marsault : False-negative diffusion-weighted MR findings in acute ischemic stroke. AJNR Am J Neuroradiol. 2000, 21: 1434-1440.PubMedGoogle Scholar
- Lovblad KO, Laubach HJ, Baird AE, Curtin F, Schlaug G, Edelman RR, Warach S: Clinical experience with diffusion-weighted MR in patients with acute stroke. AJNR Am J Neuroradiol. 1998, 19: 1061-1066.PubMedGoogle Scholar
- Guadagno JV, Warburton EA, Jones PS, Day DJ, Aigbirhio FI, Fryer TD, Harding S, Price CJ, Green HA, Barret O, Gillard JH, Baron JC: How affected is oxygen metabolism in DWI lesions?: A combined acute stroke PET-MR study. Neurology. 2006, 67: 824-829. 10.1212/01.wnl.0000233984.66907.db.View ArticlePubMedGoogle Scholar
- Wang W, Goldstein S, Scheuer ML, Branstetter BF: Acute stroke syndrome with fixed neurological deficit and false-negative diffusion-weighted imaging. J Neuroimaging. 2003, 13: 158-161. 10.1177/1051228403251632.View ArticlePubMedGoogle Scholar
- Inatomi Y, Kimura K, Yonehara T, Fujioka S, Uchino M: Hyperacute diffusion-weighted imaging abnormalities in transient ischemic attack patients signify irreversible ischemic infarction. Cerebrovasc Dis. 2005, 19: 362-368. 10.1159/000085203.View ArticlePubMedGoogle Scholar
- Kitis O, Calli C, Yunten N, Kocaman A, Sirin H: Wallenberg's lateral medullary syndrome: diffusion-weighted imaging findings. Acta Radiol. 2004, 45: 78-84. 10.1080/02841850410000692.View ArticlePubMedGoogle Scholar
- Engelter ST, Wetzel SG, Radue EW, Rausch M, Steck AJ, Lyrer PA: The clinical significance of diffusion-weighted MR imaging in infratentorial strokes. Neurology. 2004, 62: 574-580.View ArticlePubMedGoogle Scholar
- Albers GW: Expanding the window for thrombolytic therapy in acute stroke. The potential role of acute MRI for patient selection. Stroke. 1999, 30: 2230-2247.View ArticlePubMedGoogle Scholar
- Lefkowitz D, LaBenz M, Nudo SR, Steg RE, Bertoni JM: Hyperacute ischemic stroke missed by diffusion-weighted imaging. AJNR Am J Neuroradiol. 1999, 20: 1871-1875.PubMedGoogle Scholar
- Linfante I, Llinas RH, Schlaug G, Chaves C, Warach S, Caplan LR: Diffusion-weighted imaging and National Institutes of Health Stroke Scale in the acute phase of posterior-circulation stroke. Arch Neurol. 2001, 58: 621-628. 10.1001/archneur.58.4.621.View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.