STROKE AND ITS MIMICS

Abstract

Background: Acute neurological deficit constitutes one of the most common emergency presentations. If acute ischemia represents the most common cause of acute neurological deficit, the diseases mimicking ischemic strokes represent upto one third of the cases. Ischemic stroke is usually a diagnosis of exclusion in the emergency room, usually supported by non-contrast computed tomography (NCCT), which is the first step in the evaluation of patients with acute stroke due to its widespread availability and relatively short imaging time. MRI has a better sensitivity in both identifying acute ischemia or other differential diagnosis to stroke.

 

Objective: To correctly identify stroke mimics, which will significantly affect patient’s management and long-term morbidity. 

Material and Methods:  Cases for this pictorial review were selected from imaging material collected at Radiology Department of Shifa cx xInternational Hospital during a 10-year period from Jan 2013 till Sep, 2023 who presented with acute neurological deficit.

Results: In addition to acute ischemia, following different mimickers were seen in these patients;
1. HYPOGLYCEMIA: In which MR showed T2 bright signal abnormality in bilateral basal ganglia.
2. PRIMARY BRAIN NEOPLASM: Usually having chronic subtle symptoms but can be confused with acute infarct with patient present suddenly. Gliomas can be easily differentiated by presence of surrounding vasogenic edema, mass effect and post contrast enhancement. Low grade glioma without any significant vasogenic edema can be confused with an infarct however lack of diffusion restriction favor glioma in this case.
3. ENCEPHALITIS: MRI typically shows bilateral asymmetrical involvement of frontotemporal lobe often with internal hemorrhage.
4. PRESS: on MR we see bilateral symmetrical vasogenic edema within parieto-occipital lobes. PRESS changes are reversible as well.
5. DEMYLEINATING DISEASE: MS is most common demyelinating disease mimicking as stroke. MR show multiple oval fingers like T2 and FLAIR post contrast enhancement in periventricular location and deep white matter with active lesion showing solid, complete or C shaped ring enhancement.
6. HEPATIC ENCEPHALOPATHY:  MR being a problem-solving tool and showing hyperintensity on T1 pre-contrast in bilateral globus pallidus and MRS showing increase glutamine peak with choline and myoinositol peaks.
7. INTRACERBERAL AND SUBDURAL HEMORRHAGE: MR features depend on the age of blood.
8. CEREBERAL VENOUS THROMBOSIS:  MR shows T2 and FLAIR hyperintense lesion in non-arterial distribution often with a hemorrhagic component and sometimes presenting with isolated subarachnoid hemorrhage.   
9. EPILEPSY: There maybe area of cortical diffusion restriction on MRI with swelling on T2 and FLAIR. Sometimes, post ictal stage is seen on MR with bilateral pulvinar lesions and lesion of splenium of corpus callosum.
10. OTHERS: tuberculosis, Mets. reversible splenial lesion.

Conclusion: In case of acute neurological deficit, main aim of MRI reporting should not only to confirm or exclude the diagnosis of acute ischemia but also to correctly identify various stroke mimics.

Keywords: Stroke, thrombolysis, computed tomography, magnetic resonance imaging.