TIA mimic

Unlike TIA patients with infarction on DWI, it is not obvious that patients with normal DWI have suffered from ischemia as the cause of their transient symptoms. In these patients, TIA mimics should also be considered (see Chap. 19). However, an ischemic etiology for transient symptoms cannot be excluded by the lack of an associated hyperintense lesion on DWI. A short-lasting episode of ischemia without DWI changes, or with reversible DWI changes as demonstrated in animals (Minematsu et al. 1992 Mintorovitch et al. 1991), might have occurred at the time of symptoms. In addition, DWI may occasionally miss very small infarctions, especially in the brainstem location (Ay et al. 1999 Kuker et al. 2002 Lovblad et al. 1998). This is most likely due to susceptibility artifacts induced by surrounding bones at the skull base. New multi-array head coil systems and parallel imaging techniques promise to overcome this limitation and improve the detection rate of small infarctions in the brainstem. 

Anything that causes a TIA may, if more severe or prolonged, cause a stroke (Sempere et al. 1998). There are many non-vascular conditions that may cause symptoms suggestive of TIA or stroke, and these are referred to in this book as TIA mimics or stroke mimics. The separation of TIA from stroke on the basis of a 24-hour time limit is useful since the differential diagnosis of the two syndromes is different to some extent (i.e. the spectrum of TIA mimics differs from that of stroke mimics). 

Some conditions and syndromes are particularly frequently misdiagnosed as TIA (Table 8.2), but features in the history are often helpful in distinguishing TIA and minor stroke from mimics (Table 8.3). 

Sylaja PN, Coutts SB, Subramaniam S et al (2007). Acute ischemic lesions of varying ages predict risk of ischemic events in stroke/TIA patients. Neurology 68 415-419 UK TIA Study Group (1993). Intracranial tumours that mimic transient cerebral ischaemia lessons from a large multicentre trial. Journal of Neurology, Neurosurgery and Psychiatry 56 563-566... 

Accurate estimation of the early risk of stroke after TIA or minor stroke requires particular study methods. First, potential patients must be recruited as rapidly as possible after the event so that strokes following very early after TIA are included. Second, patients should be assessed initially by an expert stroke physician to ensure that the diagnosis is made reliably and mimics are excluded. Third, follow-up should be in person and outcome events should be independently adjudicated to ensure correct identification of subsequent strokes. Lastly, patients should ideally be recruited from a defined population as opposed to a particular clinical setting in order to reduce selection bias. 

Due to the narrow time window available for the initiation of thrombolytic treatment, speed is of the essence. The rationale in the work up for acute stroke is, therefore, to identify as quickly as possible those patients who may benefit from lA or IV thrombolysis or other available acute stroke therapies. Importantly, CTA excludes from treatment patients with occlusive stroke mimics (e.g., transient ischemic attack [TIA], complex migraine, seizure) who will not benefit from, and may be harmed by, such therapies. 

---