Joanna Lovett, Consultant Neurologist - Southern Stroke Forums

Joanna Lovett, Consultant Neurologist
Wessex
Neurological
Centre

20-30% patients labelled as “stroke” in an A/E
setting have alternate diagnoses
P.J. Hand, J. Kwan, R.I. Lindley, M.S. Dennis and J.M. Wardlaw,
Distinguishing between stroke and mimic at the bedside: the Brain
Attack Study. Stroke 2006:37 ;769–775.
Up to 50% patients attending TIA clinics do not
leave with a diagnosis of TIA
OCSP and OXVASC data, Rothwell group

Causes of stroke mimic in the
case series studied by P
Hand et al, Stroke 2006
(109 patients from a total of 336
patients presenting with a diagnosis
of stroke)

Recent CVA (1)
Previous bleed (1)
Persistent
hypertension (1)
Over 80 (3)
Seizure (4)
Resolved or
resolving (4)
CT > 1/3 (3)
NIH SS < 4 (3)
Functional (2)
Haemorrhage (1)
> 3 hours (1)
Time unclear (3)
N = 27

Out of 56 new referrals (recent SUHT audit):
Diagnosis Number (%)
Migraine 6 (11%)
Syncope / bradycardia 5 (9%)
Transient Global Amnesia 4 (7%)
Seizure 3 (5%)
Vestibular 1 (2%)
Psychological 1 (2%)
Other non-cerebrovascular or unexplained 7 (13%)
TIA / Minor Stroke 29 (52%)

Transient focal weakness following a focal motor seizure or a
secondary generalised tonic seizure
Suggestive features:
Loss of consciousness and post ictal drowsiness
Stiffening, Limb jerking/twitching
tongue biting, incontinence
Previous history of epilepsy, intracranial pathology or neurosurgery
Note: these seizures are frequently due to underlying pathology and need
brain imaging if the diagnosis is new

Systemic sepsis
If the patient has had a previous neurological event (eg stroke) the
symptoms may re-emerge transiently with sepsis
CNS infections
Atypical CNS infections may cause acute focal neurology via focal
inflammation, vasculitis, haemorrhage, abscess, venous thrombosis,
seizures etc
E.g. HSV encephalitis, HIV, Lyme, Syphilis, TB, Listeria
There are usually additional clues such as a non-sudden onset, signs of
meningitis, drowsiness, prodromal illness, raised CRP etc

Clues to diagnosis:
Normal objective clinical signs – reflexes, plantars, tone
Non anatomical distribution of findings
Inconsistent and variable findings on examination – for
example:
“give way” weakness which improves with encouragement and
gradually increasing resistance
Improved function on distraction
Hoover’s sign
Old notes show previous similar presentations with normal
investigations

Hoover’s Sign

Clues to diagnosis:
But Normal objective clinical signs – reflexes, plantars, tone
Non anatomical sensory disturbance – e.g. over face
Inconsistent many patients and with variable signs findings of psychogenic on examination disease – for have
an example: underlying organic disease
give way” weakness which improves with encouragement and
gradually increasing resistance
it may be less risky to give a patient with functional
weakness Improved thrombolysis function on distraction than not treat a patient with true
stroke
Hoover’s sign
Old notes show previous similar presentations with normal
investigations

Acute hemiparesis and even aphasia can occur with
hypoglycaemia
They may only have mild drowsiness
Pathophysiology is unclear
Causes include diabetic medication (own or others), alcohol
or occasionally an insulinoma
Should reverse quickly (up to a few hours) once identified
and corrected
Note: hyperglycaemia, hepatic encephalopathy and
hyponatraemia have also produced a similar picture

Suggestive features
Accompanied by unilateral throbbing headache, photo and
phonophobia, or nausea
Previous history of migraine, especially if aura present
Family history of migraine – especially if hemiparesis present
Diagnosis clinchers
Hemi-motor or sensory features have a progressive onset: symptoms
“march” down arm/leg/face over seconds / minutes
Additional focal neurological features in a non-anatomical distribution
(dysphasia with left hemisensory disturbance)
Typical visual aura of migraine

Typical visual aura of
migraine

Typically develops over 5 mins and lasts < 60 mins
Can occur without headache
Visual aura
Homonymous
Often hemianopic, crescent, ragged edges, kaleidoscope effect.
Scintillating, bright, photopsia, or phosphenes.
Scotomas
Sensory aura (usually face and arm) and dysphasia also
common
Weakness, brain stem symptoms and altered consciousness
are less common

Migraineurs have a 2x increased risk of stroke and often have
small white matter lesions on MRI
A migraine can, under rare circumstances, progress to
established stroke
Familial migraine and stroke are linked in the hereditary
disorder CADASIL (cerebral autosomal dominant arteriopathy with
subcortical infarcts and leucoencephalopathy)

Investigate further
if not resolving
If objective focal neurological signs
if the diagnosis remains unclear
if there is a strong family history of young
stroke/dementia/death
Advice for migraine with focal auras
Avoid the OCP and smoking
Avoid triptans if hemiplegic aura

Suggestive features:
Gradual onset over hours/days
Clues that there may have been previous or other CNS
lesions, for example:
Previous optic neuritis, pale optic disc or RAPD
Previous trasnverse myelitis / spinal syndrome
Bladder instability – frequency / urgency
Bilaterally brisk reflexes / increased tome/ extensor plantars
Cerebellar and brainstem features, including INO and nystagmus
Not usually found in MS:
Sudden onset, headache, dysphasia, altered consciousness

Helpful investigations to differentiate between inflammatory
and vascular lesions:
MRI: distribution of lesions and acute appearance on DWI
LP: CSF oligoclonal bands
Visual evoked potentials: looking for evidence of optic nerve disease
(optic neuritis)

A brain stem stroke or TIA is likely to present with at least
some of:
Diplopia or other cranial neuropathies
Cerebellar symptoms / signs
A Horner’s syndrome
Hemiparesis or sensory loss, occasionally quadriparesis
An episode of loss of consciousness or isolated “dizziness” or
light headedness without focal neurological symptoms or
signs is not likely to be stroke or TIA

Features suggestive of a vestibular pathology
Profound vertigo +/- vomiting and nystagmus at the time of attack
Positive Rhomberg’s test
Precipitated by head movement e.g. turning in bed
especially BPPV : benign paroxysmal positional vertigo
May have tinnitus or hearing loss (e.g. Meniere’s disease)
Gradual onset +/- infective symptoms (e.g. Labyrinthitis)
Features suggestive of a cerebellar / brainstem stroke
Presence of dysarthria or cerebellar ataxia on examination
Negative Rhombergs test
Nystagmus persisting even after vertigo has subsided
Nystagmus may be complex, inlcuding rotatory or vertical
Other signs of posterior circulation ischaemia

The Dix-Hallpike
Manoeuvre
for BPPV
Precipitates vertigo after a
delay of several seconds lasting
30-60 seconds
Visible rotatory nystagmus
during the symptoms
NB cerebellar lesions may also produce
nystagmus with this test

Tumour
Abscess
Intracranial haemorrhage including
Subarachnoid haemorrhage
Subdural haematoma
Cerebral venous sinus thrombosis

Metastasis with secondary
haemorrhage and oedema
Subacute subdural haematoma

Non-aneurysmal SAH

Normal MRV Sagittal venous sinus thrombosis

For example:
Common peroneal nerve (foot drop)
Bells palsy (facial palsy)
Radial nerve (wrist drop)
A radial nerve palsy
Often comes on overnight
Often has little sensory loss
Is often mistaken for a more profound weakness because the loss of
finger and wrist extension inhibits testing of other movements

Transient loss of the ability to lay down new memories
Patients >50 years
Lasts a few hours – up to 24 hours
Characterised by
Unable to retain new information or recall recent events
May repeated ask, for example, “what day is it?”, “where are we?”.
Other mental functions are preserved (concentration, speech,
visuospatial etc)
Loss of recollection of the event
Aetiology is unknown – no proof for vascular, migrainous or epileptic cause
Prognosis is good – a few recur (~25%) and risk of stroke is not significantly
raised

To conclude.........

Most useful predictors of stroke are
History of sudden onset
Positive and
negative predictors
Focal signs or symptoms lateralizing to one for side stroke of versus the brain
mimics in P Hand et
al Stroke 2006
Poor predictors of stroke are
Confusion or altered consciousness without focal signs
Abnormal metabolic (especially glucose) or septic markers
CT imaging is required to exclude other intracranial
causes