Differentials
Stroke
SIGNS / SYMPTOMS
Sudden-onset, focal neurological deficit that cannot be explained by another condition such as hypoglycaemia.[9] An ischaemic brain lesion on brain imaging, even if a patient's episode of focal neurological dysfunction rapidly resolves, signifies an ischaemic stroke.[3]
INVESTIGATIONS
Clinical diagnosis: CT may be normal, or may show signs of infarction or haemorrhage.
Hypoglycaemia
SIGNS / SYMPTOMS
Most commonly seen in a patient who takes hypoglycaemic medications.
Can cause syncope, generalised weakness, or confusion, but also is reported to cause focal deficits, especially if old cerebral insults are present.
INVESTIGATIONS
Blood glucose <3.33 mmol/L (<60 mg/dL).
Seizure with post-seizure (Todd's) paralysis
SIGNS / SYMPTOMS
One of the most frequent mimics of cerebral ischaemia.
Patients will frequently have pre-existing epilepsy.
Witnesses will report positive motor symptoms (such as tonic-clonic activity) prior to onset of weakness.
Symptoms may have 'jacksonian march' across the affected area.
Incontinence, tongue biting, and post-event altered mental status suggest seizure rather than TIA.
INVESTIGATIONS
The distinction is frequently made based on the clinical history.
Electroencephalogram can be done to evaluate for seizures or for postictal slowing.
Elevated prolactin level has a secondary role to suggest seizure.
Complex migraine
SIGNS / SYMPTOMS
Usually occurs in patients with prior history of migraine headaches.
Aura or scotomata may precede onset of weakness.
Presence of headache and nausea along with neurological symptoms suggest complex migraine.
INVESTIGATIONS
Clinical diagnosis: no differentiating tests.
Space-occupying lesion (intracranial haemorrhage, abscess, or mass)
SIGNS / SYMPTOMS
Preceding trauma or anticoagulation predisposes to haemorrhage.
Fever or leukocytosis would suggest central nervous system (CNS) infection rather than ischaemia.
Headache and vomiting may occur with increased intracranial pressure.
May have a relatively gradual onset compared with ischaemic neurological deficits.
Rapid complete resolution of symptoms would be atypical of an irreversible structural lesion.
INVESTIGATIONS
Non-contrast head CT rules out presence of acute haemorrhage.
CT with contrast or MRI can be done if continued suspicion for CNS abscess or mass.
Elevated WBC count in an infection.
Functional neurological and somatic symptom disorder
SIGNS / SYMPTOMS
Deficits may not fit a single vascular territory.
Physical examination may demonstrate inconsistencies such as demonstrating 'breakpoint' weakness. Some patients will have had adverse life events but, importantly, these are neither necessary nor sufficient for the diagnosis.[57] Psychological comorbidities (especially anxiety, panic, and depression) are common, affecting over 50% of patients.[58]
INVESTIGATIONS
Clinical diagnosis: no differentiating tests.
Labyrinthine disorders
SIGNS / SYMPTOMS
Benign positional vertigo may be mistaken for posterior circulation infarct.
Hearing loss and tinnitus suggest Meniere's disease.
Labyrinthitis can cause vertigo and disequilibrium but motor function and other cranial nerves should be normal.
INVESTIGATIONS
Clinical diagnosis: no differentiating tests.
Multiple sclerosis (MS)
SIGNS / SYMPTOMS
New MS lesions or a pseudoexacerbation might be mistaken for TIA, but MS will tend to cause reversible neurological deficits lasting longer than those of TIA.
History of symptoms (vision loss, in particular) suggestive of MS is very helpful.
INVESTIGATIONS
MRI can reveal MS plaques.
Lumbar puncture in MS may demonstrate slightly elevated cerebrospinal fluid (CSF) cell count but never above 50/microlitre; glucose and protein should be normal; oligoclonal bands and elevated CSF immunoglobulin G (IgG) and IgG synthesis rates are present in 80% of MS cases.
Peripheral neuropathy
SIGNS / SYMPTOMS
Bell's palsy may be mistaken for ischaemic insult. Unlike central ischaemia, Bell's palsy does not spare the forehead.
Visualising the tympanic membrane and surrounding skin can be helpful to rule out a similar condition, Ramsay Hunt, which is a herpes infection of the geniculate ganglion. Vesicles are present in the canal or as the canal meets pinna.
Peripheral neuropathies with the exception of transient compression neuropathy tend to last longer than 24 hours.
INVESTIGATIONS
For peripheral neuropathy with transient symptoms, no testing is generally needed.
Global hypoperfusion/syncope
SIGNS / SYMPTOMS
Syncope caused by basilar TIA is almost always associated with focal neurological signs/symptoms in addition to the syncope itself.
Systemic illness is suspected based on fever, tachycardia, or hypotension.
Systemic illness, especially with hypotension, may mimic TIA by causing pre-existing CNS injuries such as MS plaques or old strokes to have more pronounced symptoms.
BP may be low or orthostatic vital signs may be positive in the patient with hypotension as cause of syncope/weakness.
INVESTIGATIONS
If underlying infection, may have an elevated WBC count.
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