Welcome to the WSC 2021 Interactive Program

Abstract Body

TIAs are difficult to diagnose since the diagnosis relies mainly on the patient's account of their symptoms.The differential diagnosis is wide, including migraine, seizures and structural brain lesions. The neurological examination is usually normal unless the symptoms are ongoing. Diagnostic tests may confirm a mimic, offer supporting evidence for the diagnosis but even diffusion weighted magnetic resonance imaging (DWI) will demonstrate acute focal ischaemia in only a third of patients. Importantly there are no tests which exclude the diagnosis of TIA. Because of this inter rater reliability for the diagnosis is modest.

Many models of TIA care have been described including those based on assessments in general practice, emergency departments, specialist telephone hotlines, specialist ambulatory/outpatient clinics and stroke unit admissions. However, the key requirements are to provide immediate, or at least same day, access to:

1. a clinical assessment and interpretation of the patient's symptoms by an experienced clinician

2. an explanation of the symptoms for the patient and advice regarding activities such as driving

3. investigations to help confirm or refute the diagnosis and to determine the likely underlying cause and

4. most importantly early initiation of secondary prevention with antithrombotic medication, sometimes even before investigations have been completed, and other interventions such as statins, blood pressure lowering and carotid sugery based on the assessment of cause(s).

The preferred model(s) of care will vary depending on many local factors but whichever are chosen should be monitored to ensure they promptly and reliably deliver these essential elements of TIA care.

Abstract Body

The two goals of the diagnostic workup in transient ischemic attack (TIA) are first, to demonstrate that the experienced symptoms were actually caused by a TIA and second, to identify the etiology of the TIA to start personnalized secondary prevention. Recent progress in imaging and bioengineering could change the way we approach the diagnosis of TIA. For instance, preclinical studies demonstrated that we can detect cerebral endothelial activation resulting from a TIA by molecular MRI, even in the absence of cerebral infarction. Other approaches aiming at detecting atherosclerotic plaque rupture or left atrial appendage thrombosis are also under investigation. The most recent developments in preclinical and clinical diagnostic tools will be presented.

Abstract Body

Transient neurological symptoms are due to acute ischaemia (TIA-Transient Ischaemic Attacks) or other non-ischaemic conditions (TIA mimics-migraine aura, focal seizure, amyloid spell, etc.). About 50% of patients with a suspected TIA/minor stroke have atypical TIA or TIA-mimic diagnosis. The evidence base for diagnosis of TIA is limited. Since acute ischaemic lesions on diffusion-weighted imaging are present in relatively few patients with a definite TIA, symptomatic diagnosis remains the mainstay of clinical practice. However, the widely accepted high level definition of a TIA as sudden onset, focal neurological deficit of presumed vascular origin lasting less than 24 hours provides no guidance on which symptoms are likely to be vascular in origin. It is crucial that patients with transient neurological symptoms have a correct diagnosis as it has fundamental implications for their investigation and treatment. Patients with isolated focal, negative non-progressive symptoms (non-consensus TIA) have a similar short and long-term risk of stroke as patients with classic-TIAs. Furthermore, non-consensus TIA patients have similar baseline investigation findings (atrial fibrillation, intracranial or extracranial vascular stenosis, patent foramen ovale, etc) as classic-TIAs. Although there is some evidence that non-specific transient neurological symptoms (transient neurological attacks) are associated with an increased risk of vascular events, there is still uncertainty about the risk of strokes after transient neurological symptoms that are non-focal or positive or progressive. The diagnosis of ischaemic and non-ischaemic transient neurological symptoms, their investigation and prognosis will be discussed.