• stroke is a medical emergency presenting with focal neurological deficits; stroke mimics are non-vascular conditions that present with symptoms similar to those of stroke.
  • incidence of stroke mimics is ~3-10% [Okano, 2018]   [Winkler, 2009]   [Scott, 2003]   [Tsivgoulis, 2011]
    • most common are epileptic seizures, migraine, brain tumors, functional disorders, TGA, hypoglycemia and other metabolic disorders, syncope, or intoxication
  • the existence of mimics causes troubles in the acute setting (should we initiate thrombolysis?) but also in the chronic stage (was it a recurrent stroke? Should we change secondary prevention? Is CEA indicated for carotid stenosis?)
    • incorrectly administered IVT may harm the patient, although available data show the relative safety of thrombolysis in stroke mimics [Tsivgoulis, 2011]
    • on the other hand, failure to provide adequate treatment to unrecognized stroke patients reduces their chances of recovery
  • it is essential to consider stroke mimics in the differential diagnosis of every patient with suspected stroke; however, potential candidates for thrombolytic therapy should not be excluded based on the sole concern that their neurological symptoms may be due to stroke mimics
  • several features (red flags) may help differentiate the stroke mimics from an actual stroke (see table)
Characteristic Probable stroke Probable mimics
age and sex older age (male = female) younger age  (females > males)
level of consciousness usually awake at the onset (except for extensive vertebrobasilar occlusion)
altered level of consciousness
onset and progress acute and sudden gradual
symptoms severity severe at onset fluctuations are common, usually milder deficit
risk factors vascular risk factors history of migraine, seizure, systemic illness, cognitive impairment
vascular territory vascular syndromes symptoms not corresponding to a single vascular territory
blood pressure at presentation increase blood pressure is common blood pressure usually not increased
signs and symptoms focal deficit
(limb paresis, gaze deviation, aphasia, or visual field defects)
sensory symptoms, vertigo, and visual symptoms,
often an absence of focal neurologic signs
involuntary movements uncommon may be present
 ischemic lesion or vessel occlusion, perfusion mismatch on CTP or MRI
(dense sign on NCCT, occlusion on CTA)
lesions not respecting the vascular territories
EEG EEG may show slowing over the affected area spikes and waves in seizures, PLEDS


  • the re-emergence of the previous stroke-related deficits in the settings of metabolic, infectious, and toxic dysfunction
  • may develop within weeks to years after the previous stroke
  • MRI shows the old stroke without any DWI lesion
  • symptoms are mostly short-lived and improve within 24 hours in most subjects

Nontraumatic convexal (focal) SAH

  • a rare cause of transient symptoms
  • more commonly occurring in older patients (> 60 years) [Beitzke, 2011]
  • MRI confirms the diagnosis (with almost 100% sensitivity); thin-sliced multiplanar CT is also a valuable emergency diagnostic tool (however, MRI remains crucial and mandatorily and has to be completed within the next 24–72 hours)  [Ertl, 2014]

→ more here

Non-traumatic convexal SAH

Transient symptoms in CAA (amyloid spells)

Stroke-like episodes in Sturge-Weber syndrome

Epileptic seizure

  • an epileptic seizure may mimic a stroke, and the patient may be mistakenly treated with thrombolysis after the seizure
    • the real problem is posed by conditions such as Todd’s hemiparesis, complex partial seizures mimicking symbolic dysfunction, etc.
    • epileptic seizures can also occur in the terrain of previous ischemia (poststroke epilepsy) and transiently worsen the previous deficit
  • however, epileptic seizures can also occur during an acute stroke (~1-6%), and the patient may not receive appropriate recanalization therapy if misdiagnosed as an isolated seizure  [Sylaja, 2006]  [Killpatrick, 1990]
    • an epileptic seizure at the onset of stroke is not a contraindication to thrombolytic therapy, provided that imaging demonstrates stroke (occlusion on CTA, perfusion mismatch, etc.)
Patient with a generalized epileptic seizure at the onset of acute stroke. NCCT shows early signs of ischemia, CTA occlusion in the right MCA

Clinical presentation

  • symptoms indicative of a seizure  → classification of seizures
    • focal seizures
      • positive motor or sensory symptoms
      • gradual spread (march)
      • uniform attacks
      • sometimes a therapeutic test with AE can help with repeated seizures
    • generalized seizures
      • tonic-clonic convulsions
      • impaired consciousness
      • postictal confusion
      • lost bladder control
      • tongue and/or cheek injury
  • objective history
    • a typical course of seizure, and a history of similar seizures in the past
    • in general, any initial transient disturbance of consciousness must raise suspicion of another etiology

Diagnostic evaluation

  • in unclear cases, imaging methods can help:
    • demonstration of arterial occlusion on CTA
    • demonstration of early ischemia on CT (ASPECTS)
    • demonstration of fresh ischemia on DWI with the corresponding hypointensity in the ADC map
    • positive CT perfusion
  • prolactin may already be normal at the time of arrival at the hospital (peak around 30 minutes), and the result is not available acutely


  • a frequent stroke mimic
  • migraine aura without the headache and the first attack of basilar or hemiplegic migraine represent the main problem
  • symptoms usually develop more slowly, spread or migrate, and are typically followed by headache with nausea/vomiting and photo/phonophobia (see table)
  • migraine is likely:
    • in younger patients with a history of similar recurrent attacks and absence of vascular risk factors
    • with positive symptoms developing within minutes or tens of minutes (gradual onset)
      • flashes, bright lines, and scintillations that begin in part or half of the visual field and may extend to the entire visual field or often move across the visual field
      • paresthesias, usually spreading or moving over half the body (march), including the head, over minutes to tens of minutes
    • with subsequent development of headaches
  • history of repeated uniform attacks with a slow onset may be helpful
  • if symptoms resolve quickly, DDx of TIA can be problematic (mainly if the condition occurs for the first time)
  • imaging, including MR-DWI or CT perfusion, is normal
  • dissection should be ruled out in new-onset hemicrania with focal findings!
 Migraine characteristics (must meet at least 2 of the following):

  • unilateral localization
  • throbbing character
  • moderate or high intensity (limiting or preventing normal daily activities)
  • aggravated by walking up stairs or simple normal daily activity
  • duration of 4-72 hours
  • concurrent nausea/vomiting and/or photophobia and phonophobia
TIA Migraine aura
personal history
usually no history of a similar attack
repeated attacks
symptoms onset
sudden (seconds) gradual (> 5 min)
duration mostly minutes
approx. 20-30 min (<  60 min)
timing focal symptoms with concurrent headache focal symptoms precede the headache
visual disorders
monocular disorders
positive scintillating scotomas, gradually spreading across the entire visual field
negative scotomas
headache migraine headache criteria see above
headache most commonly follows focal symptoms but may be absent
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Stroke-like migraine attacks after radiation therapy (SMART) syndrome

  • stroke-like migraine attacks after radiation therapy (SMART) syndrome is a delayed complication of brain radiotherapy (usually associated with doses of 50 Gy or more)
  • onset of symptoms varies widely from 1 to 40 years after initial radiation therapy
  • symptoms last from several hours to several weeks and typically consist of:
    • recurrent headaches with migraine-like aura
    • seizures
    • stroke-like symptoms referable to a unilateral cortical region (motor deficits, paresthesia, aphasia, and visual disturbances)
  • full recovery in most patients was reported
  • imaging findings may include unilateral increased T2 signal with associated gyral thickening and transient cortical enhancement in the temporal, parietal, and occipital lobes; the process spares the white matter
  • the pathogenesis is not as well understood as with other complications of radiation, such as leukoencephalopathy and radiation necrosis
    • proposed endothelial dysfunction may lead to disruption of the blood-brain barrier with subsequent marked cortical enhancement
    • some case reports have reported nonspecific gliosis without inflammation or no identifiable histopathologic abnormality

Metabolic and toxic encephalopathies

  • mental status changes and epileptic seizures with possible Todd’s hemiparesis predominate in the majority of encephalopathies (renal, hepatic failure)
    • impaired level of consciousness may progress
    • complications may occur even after hemodialysis (see below)
  • neuroglycopenia and Wernicke’s encephalopathy, in particular, may present with focal symptoms, posing the greatest difficulty in distinguishing a true stroke
  • most common in type 1 DM ( insulin-dependent)
  • usually with a glycemia < 2.2 mmol/l
  • clinical presentation
    • general symptoms (fatigue, mental changes, and sweating)
    • focal symptoms (hemiplegia, usually transient)
  • rapid resolution of symptoms usually occurs after glucose administration
  • severe hypoglycemia is a contraindication to thrombolysis without radiological signs of acute stroke (intracranial artery occlusion, ASPECTS < 10, positive DWI, etc.)
Wernicke encephalopathy
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Renal encephalopathy
  • clinical presentation of renal encephalopathy
    • apathy, personality changes
    • dysarthria, uncertainty in walking
    • asterixis, intention tremor, multifocal myoclonus
    • tetany, sensory disturbances, restless legs syndrome (RLS)
  • hemodialysis leads to the resolution of symptoms
  • neurological complications may occur after dialysis (due to fluctuations in urea and ion levels and from the persistence of brain tissue hyperosmolality after dialysis) :
    • dialysis disequilibrium syndrome
      • most commonly cephalea, nausea, vomiting, restlessness or drowsiness,  rarely epileptic seizures or delirium may occur
    • central pontine myelinolysis
      • manifested by pseudobulbar paralysis and rarely quadriparesis
      • caused by a sudden increase in osmolality
      • MRI confirms the diagnosis  Central pontine myelinolysis
    • non-traumatic subdural hematoma  (2-3% of patients)
      • caused by anticoagulants and coagulation abnormalities associated with chronic kidney disease (CKD)

Hypertensive encephalopathy

  • may accompany decompensated hypertension (usually with SBP > 220 mmHg/DBP  > 120 mmHg)   → hypertensive crisis
    • the rate of BP increase seems to be more important than its absolute value
  • failure of autoregulation leads to cerebral edema
  • clinical presentation:

Multiple sclerosis

  • DDx of a first attack of multiple sclerosis (MS) from a stroke and recognition of the coincidence of MS and acute stroke may pose problems
    • the most difficult decision is whether to administer IVT or not
    • age and the presence or absence of risk factors cannot be relied upon (stroke is increasingly seen in young patients without vascular risk factors)
    • in addition, MS can manifest at older ages (40-50 years) when patients may already have multiple vascular risk factors present
  • findings of occlusion on CTA, perfusion disturbances on CTP, or early signs of ischemia (ASPECTS<10) are helpful
  • MR DWI
    • even in acute plaque, there may be diffusion restriction on DWI ⇒ small lesions cannot be reliably distinguished radiologically from lacunar infarct   DWI, ADC, and FLAIR - MS attack with diffusion restriction on DWI in the plaque region
    • the demonstration of postcontrast lesion enhancement may help
    • in larger ischemic lesions can be distinguished by the typical shape and localization corresponding to some arterial territory

Benign paroxysmal positional vertigo (BPPV)

  • typical association with change of position → see here
  • provocation of dizziness and nystagmus during positional tests (Dix-Hallpike, Seemont, Log-roll, etc.)

Transient global amnesia (TGA)

  • a sudden, temporary (< 24h) episode of memory loss with the absence of other neurological signs that can’t be attributed to a more common neurological condition, such as epilepsy or stroke  → more here


  • tetany is usually manifested by involuntary muscle cramps or spasms due to abnormal alterations in the body’s electrolytes (especially calcium)
  • difficulties can cause isolated paresthesia associated with tetany → see here

Brain disorders with structural lesions

  • these disorders can be differentiated by neuroimaging (CT/MRI)
  • intracerebral or spinal hemorrhage
    • differentiate hemorrhagic infarction (arterial and venous)  Venous infarction due to thrombosis of the superior sagittal sinus, transverse sinus, and sigmoid sinus
  • tumor – acute deterioration may be caused by bleeding into the tumor due to decompensation of edema or epileptic seizure Malignant non-Hodgkin B-cell lymphoma Malign melanoma Glioblastoma multiforme
  • neuroinfectious diseases  Brain abscess Otogenous brain abscess 
    • fever, cephalea, the elevation of inflammatory markers, alteration of mental status, epileptic seizures
  • autoimmune encephalopathy
    • gradual onset
    • typical MRI presentation with a propensity to temporal lobes
    • EEG finding
    • autoantibodies (not available in the acute stage)
  • PRES

→ more here

  • no reaction in surrounding tissue, the lesion is hypointense on FLAIR (contains liquor), DWI/ADC, and GRE are negative
  • mostly asymptomatic; isolated cases with hydrocephalus, blepharospasm, etc., were reported
  • typical localizations:
    • basal ganglia
    • on the convexity
    • mesencephalon-pons junction
Enlarged Robin-Virchow spaces
  • history of trauma is unreliable or negative in up to 50% of cases; there may be no external signs of injury
  • furthermore, it is often unclear whether the patient fell due to hemiparesis induced by the stroke or whether the stroke was caused by the fall (e.g., due to dissection, artery rupture, etc.)
  • when trauma is suspected, search for:
    • the fracture in the bone window   Skull fracture
    • soft tissue swelling in the scalp   Traumatic subgaleal hematoma
    • associated contusion   Traumatic brain injury with contusion
  • don’t miss chronic SDH as it is isodense on CT between 1-3 weeks (look for signs of edema, add MRI in doubts)  Acute and chronic subdural hematoma
  • traumatic changes (contusions):
    • do not correlate with vascular territories
    • are typically localized in temporal and frontobasal brain regions
    • often contain a hemorrhagic component and edema and may be accompanied by minor SAH
Subdural hematoma

Psychosomatic disorders

  • first attack and conversion disorders with a focal deficit (paresis, etc.) pose the biggest problem; the situation is easier with anxiety disorders
  • a simplified classification can be made:
    • panic attacks, anxiety
    • conversion somatomorphic disorders
    • simulation
  • in the first attack, an organic cause must always be carefully ruled out (negative imaging, incl. DWI)
  • how to proceed during clinical examination:
    • assess the signs while distracting the patient’s attention (fluctuations in the severity of paresis)
    • objectify the findings using EMG, EP, brain imaging
    • look for discrepancies and fluctuations in motor impairment (e.g., rapid fall in Minagazzini in a walking patient, seeing a paretic patient walking in a hospital park, etc.)
    • investigate the exact borders in hemihypesthesia (in psychosomatic disorders, the border is usually in the middle)
    • search for the provoking moment and potential benefit of the current condition (partner’s interest, financial motivation, etc.)
    • note emotional inertia to severe deficits (e.g., a smiling patient who has suddenly “gone blind”)
      • exclude rare Anton (denies blindness) and inverse Anton syndrome (sees but thinks he is blind)!
    • look for psychiatric history
  • clinical presentation
    • in somatomorphic disorder or simulation, it is not uncommon to have impaired mobility of one or more limbs, impaired hearing or blindness, and bizarre gait
    • there is a long history of difficulties, repeated hospitalizations in various departments with negative findings
    • a vivid depiction of polymorphic difficulties, extensive documentation, keeping a diary of difficulties, etc.
    • absence of pyramidal phenomena, trophic changes in paresis, etc.
  • purposeful, deliberate action for specific gain (e.g., compensation, pension, etc.)
  • disorders in which physical symptoms are present without an obvious organic cause, have a presumed psychogenic cause and are not consciously produced or simulated
  • mechanisms:
    • reactivation of past emotions by a relatively recent provoking stressor
    • reactions to a serious current trauma (e.g., rape, recent history of physical or psychological abuse)
    • chronic suppression of anger followed by a series of frustrations in adulthood
  • panic disorder without or with agoraphobia
  • acute stress disorder
  • post-traumatic stress disorder
  • often accompanied by hyperventilation, strong feelings of fear (must be actively questioned), shortness of breath, palpitations
  • the typical triggering factor usually occurs
  • attacks tend to be uniform (typically paresthesias and dysesthesias, but there may also be motor manifestations)
  • a test with anxiolytic drugs can be performed

Peripheral neurogenic lesions

  • usually can be distinguished by history, typical areal distribution of sensory and motor impairment, and usually present pain
  • a detailed neurological examination should differentiate peripheral from central symptoms
  • small pre- or postcentral infarcts may be problematic, causing isolated motor or mixed deficits involving only specific muscle groups (e.g., cortical hand syndrome)
Patient with severe right acral monoparesis. IV thrombolysis was ineffective. MRI was performed 36 hours later
  • may cause a problem in the case of sudden manifestation, for example, due to infection or drugs, and with asymmetric presentation
  • in particular, sudden onset bulbar involvement with diplopia may raise suspicion of a vascular etiology, but if bilateral ptosis is present, it is more likely to be a manifestation of myasthenia gravis
  • in the event of an acute diagnostic emergency, the effect of injectable neostigmine can be tested

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Stroke mimics
link: https://www.stroke-manual.com/stroke-mimics/