Stroke differential diagnosis and mimics: Part 1

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An estimated 9% to 30% of patients with suspected stroke and 2.8% to 17% of patients treated with IV-tPA have stroke mimics.1-7 The majority of stroke mimics are due to seizures, migraines, tumors and toxic-metabolic disturbances.3,8 Imaging usually facilitates diagnosis, as stroke has typical imaging features at different stages and follows typical topographic patterns. However, most of these features, even restricted diffusion (Table 1), are not unique to stroke.9-17 In this article we present stroke and its mimics based on 7 main patterns of topographic distribution (Figure 1). Although overlap exists, these patterns are helpful in narrowing the differential diagnosis.

Imaging features of ischemic stroke at different stages

Acute (less than 24 hours)

Computed tomography findings are initially subtle and include a hyperdense vessel, decreased gray-white matter differentiation, and sulcal effacement.18-20 Diffusion weighted imaging is highly accurate and can detect stroke as early as 15 minutes after onset.21 The T2/FLAIR hyperintensity takes hours to become apparent.22

Subacute (24 hours to 2 months)

The CT hypodensity becomes more apparent and ADC values gradually increase and pseudo-normalize at 4 to 10 days.23 Gyriform enhancement appears at 6 days and persists for as long as 2-3 months. Edema peaks in 3-4 days and decreases after 7 days. Hemorrhagic transformation usually occurs 2 to 7 days after ictus.

Chronic (more than 2 months)

This phase is characterized by volume loss, cavitation and gliosis. The gliosis surrounding the cavitation is hypodense on CT and hyperintense on T2WI and FLAIR. DWI shows variable signal, typically with increased ADC values.

Distribution patterns of ischemic stroke and its mimics

Regional gray and white matter

Single vascular distribution stroke

Ischemic infarctions in a single vascular distribution are most often a consequence of emboli arising from atherosclerotic plaques or dissection of the large craniocervical arteries, most commonly the carotid bifurcation. These emboli most frequently occlude the middle cerebral arteries or internal carotid terminus, followed by posterior cerebral arteries, vertebrobasilar system and the anterior cerebral arteries and results in regional cortical and subcortical pattern of involvement.24


One-third of stroke mimics are due to seizures or postictal deficits.25,26 Sometimes, seizure may cause restricted diffusion (Figure 2).27 The distinguishing features are nonvascular distribution, earlier edema and gyral enhancement, normal or elevated perfusion, absence of vascular occlusion, and sometimes simultaneous restricted cortical and elevated subcortical diffusion.28-38


Migrainous aura and hemiplegic migraine are the cause of 5-10% of stroke mimics and may show restricted diffusion.25,26,39-41 The distinguishing factors are a long history of migraines, involvement of multiple arterial territories and absence of vascular occlusion.40,42,43 Perfusion decreases in acute-onset aura and is normal or elevated in prolonged episodes.40,42,43 The lesions are usually reversible,40,42,43 but 15% of strokes in patients younger than 45 years of age are due to migraine.44

Brain tumors

A primary brain neoplasm may present with acute neurologic deficits. Occasionally a low-grade glial tumor with mild mass effect and cortical involvement may be confused with a subacute infarction (Figure 3).45 It can, however, be easily differentiated based on nonvascular distribution and lack of significant restricted diffusion or gyral enhancement. Nevertheless, both subacute infarcts with hemorrhage and high-grade hemorrhagic gliomas can show areas of restricted diffusion, heterogeneous enhancement and mass effect that can be indistinguishable.

Herpes simplex encephalitis

Herpes simplex is the most common cause of viral encephalitis and presents with a combination of fever, headache, confusion, seizures and neurologic deficits. 46-48 It has a predilection for the limbic system (medial temporal and inferior frontal lobes, insula and cingulate gyri) (Figure 4).49,50 DWI is superior to other sequences for detection and usually shows concurrent areas with decreased and increased diffusivity.51,52 Restricted diffusion is observed in early stages and leads to irreversible neuronal damage.51,53 The glutamate excitotoxic pathway is believed to be the cause of restricted diffusion. Lesions are typically also hyperintense on FLAIR images and frequently undergo hemorrhagic transformation.10


Hypoglycemia can present with focal neurologic deficits.54-59 Restricted diffusion may be seen in the cerebral cortex (particularly the occipital lobes), corona radiata and centrum semiovale.11,60-63 Involvement of the basal ganglia, hippocampi, internal capsules and splenium has also been reported.64-66 The cerebellum, brain stem and hypothalamus are usually spared due to more active glucose transport mechanisms.67,68 The cause of diffusion restriction is thought to be energy failure due to lack of glucose, excitotoxic edema, and/or asymmetric cerebral blood flow.

Transient global amnesia (TGA)

TGA is diagnosed by sudden onset of transient antegrade memory loss.69,70 The pathogenesis is unclear, but ischemia, seizures, and migraine have been considered.71-73 It typically appears as punctate foci of restricted diffusion in the hippocampus (Figure 5).15,74,75 In one report, the frequency of positive DWI findings increased from 5% to 85% when ictus-to-imaging time increased from 8 hours to 48 hours.74

MELAS (Mitochondrial encephalopathy, lactic acidosis, and stroke-like events)

MELAS presents with nausea, vomiting, seizures, muscle weakness and abrupt neurological deficits, usually by age 40.76 MRI shows T2 hyperintensity, swelling and restricted diffusion in the cortex and subcortical white matter.45 The distinguishing factors are multifocal lesions in various stages of evolution, simultaneous areas of restricted and elevated diffusion in acute lesions, nonvascular distribution and a predilection for the posterior parietal and occipital lobes (Figure 6).77,78

Venous infarctions

Venous thrombosis is uncommon and accounts for 1% of all strokes.79 It may show normal parenchyma, lesions characterized by vasogenic edema with elevated diffusion, lesions characterized by cytotoxic edema with restricted diffusion and/or hemorrhagic lesions, all in a non-arterial distribution.80 Restricted diffusion may be reversible, particularly when it is associated with seizures.81,82 Dural venous sinus thrombosis has a cortical and subcortical pattern and thrombosis of the internal veins and straight sinus causes bilateral thalamic involvement.

Cortical and deep gray matter

Hypoxic-ischemic encephalopathy

HIE is the result of global hypoxia.83 The most common causes are cardiac arrest, respiratory failure and shock. In severe cases, the cortex and deep gray nuclei are affected (Figure 7).84,85 In mild cases, a border zone infarction pattern may be seen.86 Rarely, a pure white matter pattern may be seen as global ischemia may induce demyelination.85,86 The cerebellum is usually spared.85,86

Wernicke’s encephalopathy

Wernicke’s encephalopathy occurs in alcoholics and other malnourished patients with thiamine deficiency. Patients present with altered mental status, memory impairment, ophthalmoplegia or ataxia. Typically, MRI shows symmetric T2/FLAIR hyperintensity in the mammillary bodies, hypothalami, medial thalami, tectal plate and periaqueductal area, but the cerebral cortex may also be involved.87-91 In early stages, restricted diffusion can be seen due to cytotoxic edema (Figure 8).

Hepatic encephalopathy

The typical imaging finding in milder cases is symmetric T1 hyperintensity in globus pallidus.92,93 In more severe cases, MRI may show T2 hyperintensity and restricted diffusion in the cortex (especially the cingulate gyri and insula), and basal ganglia (Figure 9).45,92,94,95 The thalami, periventricular white matter and brainstem may also be involved.96 Diffuse cortical involvement can be reversible, but is associated with an increased risk of permanent neurologic sequela. 96 The decrease in ADC values is attributed to the excitotoxic injury and osmotic disturbance in astrocytes due to ammonia.97,98

Creutzfeldt-Jakob disease

Patients present with a rapidly progressive, transmissible and fatal neurodegenerative disease caused by a misfolded prion protein.99,100 DWI is more sensitive than FLAIR or T2WI and is associated with decreased ADC.101,102 In CJD there is symmetric involvement of the basal ganglia and either symmetrical or asymmetrical involved of the cortex (Figure 10).103-107

Eastern equine encephalitis

The agent is a mosquito-borne arbovirus, and presentation ranges from flu-like symptoms, confusion and somnolence to neurological deficits, seizures and coma. Approximately 5% of infections lead to encephalitis, 1/3 of patients die, and the survivors are left with significant morbidity. The lesions typically appear as T2-FLAIR hyperintense lesions in the basal ganglia, thalami and brainstem (Figure 11).108, 09 Less commonly cortex and the periventricular white matter are involved.108,109

Deep gray matter diffusion abnormality

Small vessel stroke/penetrating vessel stroke

Small vessel strokes comprise 20–25% of all strokes110 and are located in the distribution of small penetrating arteries, including the lenticulostriate, anterior choroidal, thalamoperforator, and paramedian basilar artery branches. These strokes are usually caused by arteriolosclerosis due to hypertension and are typically less than 15 mm, but a subset are caused by thrombi at the site of arterial occlusion or embolism111,112 and cause infarction in multiple adjacent deep penetrating artery territories.

Carbon monoxide poisoning

In mild cases, there is a predilection for symmetric restriction diffusion and T2 hyperintensity in the bilateral globus pallidi (Figure 12).113,114 In more severe cases the remainder of the basal ganglia, thalami, hippocampi, supratentorial white matter, corpus callosum, and less often the cerebral cortex may be involved.115 Following a period of transient clinical improvement, a delayed encephalopathy may occur with bilateral confluent periventricular white matter T2 hyperintensity and areas of restricted diffusion.116 Restricted diffusion in the acute phase is likely secondary to cytotoxic edema. In the delayed phase, it may be related to demyelination.116

Osmotic myelinolysis

Osmotic myelinolysis is most often due to rapid correction of hyponatremia, but it can be seen with malnourishment, chronic alcoholism, hyperosmolar conditions, such as hyperglycemia, and in liver transplant patients. Patients typically present with pseudobulbar palsy and spastic quadriplegia. It can present with central pontine and/or extrapontine myelinolysis (Figure 13).117 The pontine lesion is centrally located and spares the corticospinal tracts.118 The extrapontine lesions are symmetric and involve the thalamus, basal ganglia and lateral geniculate body and cerebellar white matter.118 The T2 hyperintensity may lag up to 2 weeks, but restricted diffusion appears within the first 24 hours and may persist up to 3 weeks. 118-120 The pathogenesis of diffusion restriction in is not fully elucidated, but it may be related to the shift of the extracellular water into the cells or intramyelin splitting, vacuolization, and rupture of myelin sheaths due to osmotic effects. 118

Vigabatrin toxicity

Vigabatrin is used for treatment of infantile spasms and refractory complex partial epilepsy and is associated with asymptomatic transient MRI abnormalities (Figure 14) especially in younger ages.121,122 Toxicity is characterized by symmetric T2 hyperintensity and restricted diffusion in the basal ganglia, thalami, anterior commissure, corpus callosum and midbrain.122,123 The MRI abnormalities typically resolve even without cessation of treatment.122-124 The cause for the T2 and diffusion abnormalities is unclear, although it is suggested that it may be related to intramyelin edema.125

Nonketotic hyperglycemia

Nonketotic hyperglycemia occurs in patients with diabetes mellitus type 2 and is associated with new-onset chorea, seizures and focal neurologic deficits.126-129 The findings on imaging studies can be either unilateral or bilateral130 and maybe mistaken for a lenticulostriate ischemic stroke (Figure 15). On CT, the basal ganglia appear dense. The MRI findings are T1 hyperintensity, T2 hypointensity, and restricted diffusion with no associated susceptibility effect. The T1 hyperintensity may be related to manganese in reactive astrocytes.130 The pathophysiologic mechanisms for restricted diffusion remain controversial and include protein desiccation, myelin breakdown, hyperviscosity, microcalcification, and microhemorrhage.130-132


Stroke mimics are common in the emergency department and some of these patients may be treated with intravenous tPA. Despite many clinical and imaging overlaps, a pattern-based approach provides a reasonably accurate method to diagnose of many of these conditions and facilitate appropriate and timely management.

Part 2 of this article may be found online at


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Kamalian S, Kamalian S, Boulter DJ, Lev MH, Gonzalez RG, Schaefer PW.  Stroke differential diagnosis and mimics: Part 1.  Appl Radiol.  2015;44(11):26-39.

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About the Author

Shahmir Kamalian, MD; Shervin Kamalian, MD; Daniel J. Boulter, MD; Michael H. Lev, MD; R. Gilberto Gonzalez, MD, PhD; Pamela W.

Shahmir Kamalian, MD; Shervin Kamalian, MD; Daniel J. Boulter, MD; Michael H. Lev, MD; R. Gilberto Gonzalez, MD, PhD; Pamela W.

Dr. Shahmir Kamalian is Assistant Professor, Department of Radiology at University of Massachusetts Medical School, Worcester, MA; Dr. Shervin Kamalian is Radiology Resident, Department of Radiology at Mount Auburn Hospital, Cambridge, MA; Dr. Boulter is Assistant Professor, Department of Radiology at The Ohio State University, Columbus, OH; Dr. Lev is Director of Emergency Imaging and Professor of Radiology, Dr. Gonzalez is Director of Neuroradiology and Professor of Radiology, and Dr. Schaefer is Associate Director of Neuroradiology and Associate Professor of Radiology, all at Massachusetts General Hospital/Harvard Medical School, Boston, MA.

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