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
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
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
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
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
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 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
Cortical and deep gray matter
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 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).
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
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
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.
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 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 www.appliedradiology.com.
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