Embolus is produced as a result of endogenous fibrinolytic system within a clot, so embolus may dissolve on its own. Hence embolic events can present as TIA if clot dissolves rapidly before causing neuronal death and does not need Thrombolytic therapy. This is why if a patients neurology is resolving, we don’t use thrombolysis. If emboli doesn’t dissolve in time then leads to neuronal death.
Vasospasm such as migraine aura, hypoglycaemia or hypotension etc can also cause TIA like features. Focal Seizures with Post Ictal phase can also cause TIA like presentation. Any clue for gain of neuronal functions such as stiffness, heaviness or shakiness etc favour seizures. Migraine can present with aura alone without headache so absent headache doesn’t exclude migraine (classically migraine aura starts from occipital and more toward frontal lobe, so giving visual symptoms n sensory symptoms before motor ).
Embolic stroke is sudden onset in seconds (as it’s preformed blood clot n takes no time to reach to reach to brain). That sudden onset is also seen in haemorrhagic stroke too but the later causes headache or symptoms of raised ICP or brain irritation (seizures etc). Ischemia causes loss of neuronal function and seizures being gain of function are less likely in ischemia. Sudden onset neurological deficit helps differentiates it from Thrombotic stroke where neurological deficit is progressive and evolves over minutes or hours depending on speed of thrombus formation in major arteries such as Internal Carotid. Emboli usually occluded smaller arteries such MCA /ACA whereas thrombus usually occluded major arteries such as carotids / Internal carotid where atherosclerosis is common.
Blood can be seen on CT scan but remember CT can miss bleeding if it’s done within first few hours. So CT negative in first few hours doesn’t surely exclude bleeding.
Embolic source is either heart or carotids. Atrial Fibrillation, valvular lesions with blood clot formation, metallic valves, poor LV function with blood clot in LV are common cardiac causes. Sometimes patients may have right to left shunt such as PFO where systemic veinous clots or fat emboli or air emboli can also cause stroke. Arch of Aorta or Carotids with atherosclerotic plaque or vasculitis can produce clot to break off as emboli.
Other types of emboli such as fat or air emboli can also cause stroke and should be kept in mind in patients with PFO or patients with interventional vascular procedures especially with carotid etc. So imaging the heart with Echo, checking it’s rhythm with monitoring (holter, loop recorder etc), imaging carotid with Doppler or CT angiography), bubble echo especially on young patients to exclude PFO etc is important workup.
Embolic stroke is more common in anterior circulation than posterior circulations (verterobasilar territories) likely because of anatomical features such as origin of vertebral, diameter etc.
Embolic stroke can be multi focal and in that case it’s can be confused with multifocal neurology such as small vessel vasculitis, endartritis seen in chronic meningitis cases, Metastatic disease, MS etc.
Treatment depends on cause and presentation.
AF or LV thrombus needs anticoagulation. Immediate start of anticoagulation in patient with large size infarction increases risk of bleeding within the infarct. So if infarct size is large then one may have to wait for 10-15 days for the gliosis to establish before starting anticoagulation.
Thrombus or Embolus in major vessels not responding to initial thrombolysis will need thrombectomy / embolectomy by clot retrieval if patient presents within window period. Carotid revascularisation will be needed if stenosis / blockage is 70% or more or with appropriate neurological findings.
Thrombolysis for acute presentation depends on prior functional status of patient, exclusion of contraindications to thrombolysis , clinical neurological deficit, ischemic pnembra on CT perfusion and NIHSS score. Clinical deficit is a major guide to decide about thrombolysis. Eg a singer with aphasia means a major deficit. Similarly posterior stroke may have major deficit but low NIHSS score. So NIHSS score doesn’t always correlate well with severity of deficit.