This document discusses stroke mimics and chameleons. It begins by introducing stroke mimics, which account for 20-25% of suspected stroke cases. Common mimics include seizures, hypoglycemia, sepsis, migraines, and tumors. Functional disorders and delirium can also mimic strokes. The document then discusses stroke chameleons, which imitate other diseases due to their gradual onset or non-specific symptoms. Examples given include vertigo, monoparesis, and delirium. Several case studies are presented to illustrate specific mimics and chameleons. The document emphasizes the importance of thorough clinical assessment to distinguish strokes from mimicking conditions.

2. Introduction
 The clinical presentation of stroke varies.
 It is common to mistake other diseases for strokes (stroke mimics) and
strokes for other diseases (stroke chameleons).
 Different approaches to assessment ,different diagnostic skills, & occasional
difficulty distinguishing stroke from its mimics very soon after onset, may
affect eventual diagnosis of stroke
.

3. The proportion of suspected stroke patients with an eventual diagnosis of stroke or transient ischaemic
attack (TIA), from a systematic review and meta-analysis of case series, stratified by the context of
assessment (emergency department, primary care, stroke unit/neurovascular clinic, ambulance or other
referral sources).
The width of each diamond represents the 95% CI of the pooled proportion.

4.  Rapid recognition of stroke is important:
 The sooner ischaemic stroke patients receive thrombolysis3 or
 Are investigated and given secondary prevention to avoid further vaso-occlusive
events,
 The better the outcome.
 The correct diagnosis for patients without stroke leads to appropriate treatment
and avoids the potentially harmful effects of secondary stroke prevention
 therapies.

5. MIMICS
 Stroke mimics account for 20–25% of suspected stroke presentations, depending
on the context (figure 1).
 There is a diverse array of mimics (figure 2), and we will deal with a small selection
of them.
 Unfortunately, brain imaging is not the simple answer to distinguishing stroke
from its mimics.
 The reference standard for the diagnosis of stroke can only be clinical history and
examination, supported by brain imaging (which may be normal).

6. The 20 most common stroke mimics, identified in a systematic review and
meta-analysis of case series

7. Seizures
 Postictal Todd’s paresis can be difficult to differentiate from stroke
 Accounts for almost 20% of stroke mimics .
 The diagnosis is more readily apparent if patients have recurrent focal motor
seizures (which can be subtle).
 There may be a history of epilepsy, although this may not necessarily have been
diagnosed before admission.
 The substrate for the seizure is often an old ischaemic or haemorrhagic stroke,
easily mistaken for an acute stroke when brain imaging is reviewed.

8. T1-weighted axial MR brain scan showing cavitation in the left centrum semiovale
(arrow), in keeping with an old infarction, and an old cortical infarction.
Seizure mimic

9. Hypoglycaemia
 Hypoglycaemia normally presents with autonomic symptoms but can present with focal
neurological symptoms and signs alone.
 There may be episodes of focal neurological disturbance at the same time each day,
associated with diabetic medication.
 Although blood glucose measurement at the time of onset of neurological deficit can help,
it may be normal at the time of assessment
 Brain MRI may show transient DWI high signal in the context of hypoglycaemia.
 The ‘airway, breathing, circulation, don’t ever forget glucose’ (ABC-DEFG) approach is
important: blood sugar should always be measured before thrombolysis is given

10. Hypoglycaemia mimic – case
 A 75-year-old right-handed man woke with severe left-sided hemiparesis. Capillary blood
sugar in the ambulance was 1.8 mmol/l, successfully treated with intravenous dextrose.
 Neurological examination was normal by the time of arrival in the emergency unit, as was
brain CT. Full blood count showed an elevated mean corpuscular volume.
 The patient did not take any hypoglycaemic agents but did admit to alcohol excess,
including a heavy intake of gin the evening before presentation.
 Diagnosed hypoglycaemic hemiparesis and the patient was counselled over his alcohol
intake.

11. Sepsis
 Sepsis accounts for 12% of stroke mimics , so a thorough systemic examination is
always necessary.
 Raised inflammatory markers and fever support a diagnosis of sepsis, although
sepsis may itself be a risk factor for stroke: the risk from mycotic emboli is well
established and severe sepsis can induce a hypercoagulable state.
 Differentiating sepsis and stroke is difficult when patients have both conditions
simultaneously, for example, aspiration pneumonia secondary to stroke.
 Collateral histories from relatives or the general practitioner may help to
distinguish exacerbation of an old deficit from new stroke.

12. Migraine and other headache disorders
 Headache is a common feature of acute ischaemic stroke: 27% of patients
experience a headache at stroke onset.
 Primary headache disorders are responsible for 10% of stroke mimics
 Severe neurological deficits associated with headache—including familial
hemiplegic migraine and headache with associated neurological deficits
and lymphocytosis are difficult to disentangle from strokes

13. Migraine and other headache disorders
 A family history may help to identify cases of familial hemiplegic migraine, which is an
autosomal dominant disorder with high penetrance.
 Patients with this condition are typically young (average age of onset 17 years), female (70%)
and tend to have fewer attacks as they age.
 Patients with headache with associated neurological deficits and lymphocytosis (HaNDL)
report recurrent neurological deficits and headache, and have cerebrospinal fluid abnormalities
(lymphocytosis, elevated protein and high opening pressures)
 The neurological deficits typically last for hours and may include dysphasia, focal weakness or
confusion. CT and MRI are normal, although perfusion imaging may show focal deficits

15. Functional disorders
 Functional disorders often manifest as acute weakness or sensory disturbance, mimicking
stroke.
 There is frequently a trigger, such as a panic attack or dissociative episode.
 When diagnosing functional disorders, the positive features of functional disease are more
important than the absence of features of organic disease—for example, a positive Hoover’s
sign is more important than a normal brain CT.
 The key finding in the examination of functional weakness is inconsistency. Inconsistency
in the extent of impairment is illustrated by task-dependent weakness—the patient who
walks into the room but cannot move their leg at all when examined on the couch.

16. Brain tumours
 Tumours typically cause slowly progressive deficits but 5% of tumours have
a stroke-like presentation.
 Acute deficits are commonly due to haemorrhage into the lesion but may
also be secondary to extrinsic compression of vascular structures by
oedema, obstructive hydrocephalus or Todd’s paresis.
 The presence of very early mass effect suggests a tumour, as large artery
strokes usually take 24–48 h to develop cerebral oedema.

17. Characteristics of Common Stroke Mimics

18. CASE
 An 82-year-old woman was seen by the acute stroke intervention team for the
sudden onset of speech difficulty 90 minutes earlier. She had been working with a
physical therapist at home when she became unable to speak. There was no
associated weakness, alteration of consciousness, or headache. Per report, she had
experienced a minor ‘‘stroke’’ approximately 2 weeks earlier but had made some
improvement.
 The woman was afebrile, her initial blood pressure was 142/72 mm Hg, and the
finger-stick glucose level was 188 mg/dL. She was awake, alert, and appropriate.
Language examination was remarkable for impaired fluency with the ability to say
only fragments of words. She was able to follow simple midline commands but was
unable to follow complex commands. She was unable to repeat, read, or name
objects. There was no limb weakness or sensory disturbance. Her NIHSS score was 6.

19. Noncontrast head CT demonstrated a subtle
hyperdense lesion with mass effect involving
the left temporoparietal region (Figure 1-4, top,
arrows). Given the radiographic findings
suggestive of an underlying structural lesion,
the patient did not receive thrombolytic
therapy. Follow-up MRI demonstrated an ill-
defined enhancing lesion involving the white
matter and cortex of the left parietal lobe
suggestive of a low-grade neoplasm

20. Comments
 This case is an example of a stroke mimic.
 The abrupt onset of symptoms might not prompt initial consideration of an
underlying structural lesion as a potential etiology.
 However, one study found that 6% of patients with brain tumors presenting to an
emergency department had symptoms of less than 1 day’s duration (Snyder et al,
1993).
 Sudden onset of focal symptoms in patients with either diagnosed or undiagnosed
tumors may result from seizures, hemorrhage into the tumor, or obstructive
hydrocephalus caused by increasing mass effect.

22. CHAMELEONS
 Stroke chameleons imitate other diseases due to their tempo of onset (eg,
gradual progression or stuttering) or have symptoms that do not necessarily
implicate an arterial territory.
 It is uncommon to consider these patients for thrombolysis, but their
recognition enables patients to benefit from secondary prevention.

23. Vertigo
 Stroke is rarely the cause of dizziness: only 3% of patients presenting with
dizziness and additional symptoms have had a stroke or TIA
 The presence of new or worsened unilateral hearing loss, headache,
tinnitus or neurological symptoms is uncommon in isolated vestibular
neuronitis.
 Lateral medullary, lateral pontine and inferior cerebellar patterns of
infarction may mimic the clinical features of vestibular neuronitis.

24. The differences between central lesions and peripheral
lesions following a Dix–Hallpike manoeuvre

25. Vertigo chameleon- case
 A 75-year-old woman presented to the emergency unit with a 1-day history of dizziness, vertigo
and vomiting.
 She had a history of sick sinus syndrome with permanent pacemaker and also of Ménière’s
disease.
 On examination, she had atrial fibrillation, an ataxic gait, nystagmus (fast phase to the left) and
marked unsteadiness.
 The initial diagnosis was recurrent Ménière’s disease and she was prescribed prochlorperazine.
 However, the symptoms, signs and lack of improvement with vestibular suppressants prompted a
neurologist to organise a brain CT, which showed a subacute left cerebellar hemisphere infarction.

26. Monoplegia
 Isolated monoparesis is a rare presentation of stroke, comprising fewer than
5% of all strokes.
 Monoparetic stroke most commonly affects the arm, where the causative
lesion is often a middle cerebral artery stroke.
 Most strokes presenting with monoparesis are subcortical or deeper,
although about 30% are caused by cortical lesions.

27.  A 70-year-old woman had an episode of
right leg weakness of sudden onset,
fully resolving within an hour. The right
leg weakness recurred the next day,
prompting admission to hospital. She
had a history of rheumatoid arthritis.
On examination, there was weakness of
the right leg. The initial diagnosis was
of a myelopathy. Brain MRI showed
acute ischaemia in the territory of the
left anterior cerebral artery
Acute infarction in the left parasagittal
frontal lobe shown by high signal on
fluid-attenuated inversion recovery MRI
brain (arrow).
Acute infarction in the left parasagittal
frontal lobe shown by restricted
diffusion on diffusion weighted MRI
brain (arrow).

28. Delirium
 Non-dominant anterior circulation strokes affecting the temporoparietal region
may cause visual agnosia, prosopagnosia, loss of spatial orientation and
disinhibition of speech.
 The excessive speech production and difficulty in path finding often lead to a
diagnosis of delirium, with a search for an underlying infective or metabolic cause.
 Patients with non-dominant hemisphere deficits may have problems with
attention, lack of usual expression of emotion, lack of empathy with others, lack of
prosody of speech, lack of judgement of time and inability to comprehend non-
verbal communication or to recognise familiar sounds

29. Delirium chameleon
 A 79-year-old man went for his usual local walk. On
his way home he could not recognise his house,
despite his wife standing at the window waving. He
was brought to the hospital where he was very
talkative and would frequently get lost in the ward.
There were no other symptoms and no focal
neurological deficit. He had a past history of
paroxysmal atrial fibrillation and hypertension.
Brain CT showed a right frontal infarction
Recent right frontal cortical infarction on plain brain
CT (arrow).

30. Cauda equina syndrome chameleon
A 75-year-old woman presented at midnight with
bilateral leg weakness and
numbness. She had a history of hypertension and of type
2 diabetes mellitus. One month previously she had an
episode of haematuria. Her symptoms had started at
midday with back pain radiating down both calves. By
14:30 she had pain, numbness and paraesthesia affecting
both legs, and difficulty walking. Her general
practitioner assessed her at 18:00, at which point she
could only move her toes. There was reduced tone
strength and reflexes in both legs. In the emergency unit,
she had a flaccid paraplegia, areflexia, sensory level at
T11 and painless urinary retention. She was admitted
under the neurosurgical team with a diagnosis of cauda
equina syndrome. Urgent MR scan of the spine showed a
cord infarction from T9 to the conus , with an additional
left renal cell carcinoma.
Acute infarction of the spinal cord from T1 to
conus shown by high signal on sagittal T2-
weighted MRI (arrow). Acute infarction of the spinal cord at T12
shown by high signal on axial T2-weighted
MRI (arrow).

31. Examples of stroke chameleons

33.  Up to 60% of patients referred to a TIA clinic do not have a final diagnosis
of TIA, but this will depend on how patients are referred and the method
of diagnosis.
 Of 1532 consecutive patients attending our TIA service, 1148 (75%) had
either definite or possible TIA, 46 (3%) had minor stroke and the remaining
338 (22%) had one of 25 alternative diagnoses

34. Frequency of transient ischaemic attack (TIA) mimics from 1532 consecutive suspected
TIA referrals to the University College London comprehensive stroke service

35. Frequent causes of transient neurological symptoms
that can mimic TIA
 Frequent causes of transient neurological symptoms that can mimic TIA
include:
 ▸ Migraine aura
 ▸ Seizure
 ▸ Syncope
 ▸ Functional or anxiety related

36. Clinical features of transient ischaemic attack (TIA) and some common mimics

38. Limb-shaking TIAs
 Rhythmic, involuntary jerky limb movements can occur in haemodynamic TIAs, which
may thus be mistaken for focal motor seizures.
 The presence of limb shaking is a well-established sign of hemisphere hypoperfusion, due
to severe carotid or middle cerebral artery disease.
 The episodes tend to be brief (<5 min), recurrent and avoid the face. They can be
precipitated by activities that may reduce cerebral blood flow (such as postural change,
coughing and exercise).
 MRI, including DWI sequences, can help in showing a classical ‘borderzone’ pattern of
established or recent ischaemia, especially if symptoms are prolonged or recurrent

39. Imaging from a patient who presented with recurrent attacks of rhythmic jerking of the left arm, related to
changing from a sitting to standing position. (A) MR angiogram showing critical right middle cerebral artery
stenosis. (B) Fluidattenuated inversion recovery (FLAIR) MRI showing high signals in the right hemisphere
white matter in a ‘borderzone’ distribution.

40. Capsular warning syndrome
 The capsular warning syndrome is one of the most dramatic presentations in
stroke medicine.
 In this striking phenomenon, in situ disease of a single penetrating artery is
thought to cause fluctuating ischaemia and neuronal dysfunction limited to the
internal capsule.
 The early stroke risk is high.
 Many attacks can occur in a short period of time (eg, 24–48 h) leading to
suspicions of seizures or functional disorder in some patients.
.

41. Citations
1. Fernandes PM, Whiteley WN, Hart SR, et al. Pract Neurol 2013;13:21–28
2. Nadarajan V, et al. Pract Neurol 2014;14:23–31
3. Continuum: Lifelong Learning Neurol 2008;14(6)