Medical history, diagnostic criteria and pathophysiology
Migraine with aura: the criteria for typical migraine with aura have high sensitivity and high specificity (5). Migraine with aura is defined as visual, somatosensory, speech, motor (hemiplegic migraine) or brainstem symptoms (migraine with brainstem aura) associated with a migraine attack. The symptoms typically develop gradually (usually over 5–20 minutes) and the maximum duration is 60 minutes for each individual symptom (5).
Migraine with aura is likely caused by a specific neurophysiological phenomenon called cortical spreading depression, a slow-spreading wave of cortical electrical discharges (2–3 mm/min) and hyperperfusion (1–2 minutes), followed by hypoperfusion lasting 1–2 hours (6). Around 30 % of migraine sufferers experience migraine with aura. Visual disturbances are the most common (> 90 %), but many also experience episodes of sensory phenomena (approximately 30 %) and language disturbances (approximately 20 %), usually accompanied by another aura symptom (Figure 1) (5). Headache tends to immediately follow the aura, but it can also occur simultaneously, be delayed by more than an hour, or be absent or mild. In cases of paresis or monocular vision loss, other conditions than migraine should initially be considered.
The neurological symptoms that occur during the migraine aura are thus not caused by hypoperfusion and ischemia but rather a primary discharge of nerve cells, resulting in transient positive neurological symptoms such as blurring, light flashes and paraesthesia. Such symptoms may be followed by transient negative neurological symptoms (loss of function), such as hemianopsia and numbness, which very rarely cause permanent damage (migrainous infarction). The role of migraine as a risk factor for stroke is not well understood, but a tendency to generate both cortical spreading depression (aura) and microemboli may be a causal link (7). Cortical spreading depression can also be induced by damage to brain tissue (8), in other words, migraine aura does not rule out cerebral ischemia.
Transient ischemic attack (TIA) can be defined as a transient episode of neurological dysfunction caused by focal brain ischemia, but where no ischemic lesion can be detected by appropriate brain imaging (1, 9).
When trying to differentiate between TIA and other causes of transient neurological symptoms, agreement on different clinical assessments, including by stroke specialists, is quite poor (10). Specificity is low, especially when tested against the criteria for migraine aura (11). Radiological evidence will point to focal cerebral damage in many patients with a clinical TIA diagnosis (1, 12, 13), and this is now defined as a minor stroke.
TIA symptoms usually start suddenly, decrease gradually, and typically last seconds or minutes, rarely exceeding an hour (Figure 2). If a patient experiences multiple symptoms, they occur simultaneously and are usually negative. Repeated stereotypical TIA most often represents lacunar syndromes (small vessel disease), but can also be caused by haemodynamic changes as a result of large artery stenosis. Isolated transient loss of vision in one eye (amaurosis fugax) is a classic symptom of ipsilateral significant carotid stenosis. Central vision loss, eye motility disorders, visual field defects and visual neglect are the most common visual disturbances in acute cerebral ischemia (14). The most dramatic lacunar TIA cases involve recurring hemiparesis due to poor circulation in a region of the internal capsule. Vertigo, dysphagia and diplopia generally occur in combination with other focal neurological symptoms, but can also be seen in isolation. Loss of consciousness is very rarely seen in TIA. Headaches can occur during TIA, and were experienced by 13 % of patients in a recent study (15), typically in women with a history of migraines. Table 1 summarises the main differences between TIA and migraine.
Table 1
How to differentiate between TIA and migraine (1)
| | TIA | Migraine |
|---|
| Demographic | Older adults, vascular risk factors | Young people, more common in women |
| Neurological symptoms | Negative symptoms, maximum intensity at onset, no spread.
Probable TIA
Motor weakness or sensory deficit in arm and leg on the same side. Motor weakness or sensory deficit in one limb and in the face on the same side. Hemianopsia or monocular blindness. Aphasia or dysarthria.
Possible TIA
Unsteady gait
Diplopia
Vertigo
Dysphagia
Probably not TIA
Amnesia, confusion, sensory deficit in one limb or only in the face, unusual cortical visual phenomena (total vision loss, afterimages, visual hallucinations, flashes of light etc.), loss of consciousness, headache. | Positive symptoms with gradual spread, but which can be followed by negative symptoms from the same region. Symptoms may spread sequentially from one modality to another, typically visual disturbances followed by somatosensory phenomena. |
| Onset and development | Acute onset of symptoms that gradually subside (minutes), almost always within an hour. Recurrence within days, possibly weeks, but usually not over months or years. | Symptoms develop over minutes and typically last 20–30 minutes, but can last much longer. May recur over a period of several years. |
| Associated symptoms | Headaches may occur, normally during the episode with neurological symptoms. | Headaches typically follow neurological symptoms, often accompanied by migrainous symptoms such as nausea, vomiting, sensitivity to light and sound, and are exacerbated by movement. |
| MRI findings | Up to half will show acute changes on diffusion MRI. | Normal findings on diffusion MRI. |
In many ways, TIA represents the opposite of migraine with aura (Table 1), and based on this, researchers have tried to create new TIA criteria (known as explicit diagnostic criteria for TIA) in order to make a clearer distinction between the two (11). These have not been validated in Norwegian. The criteria have been shown to have high sensitivity (98–99 %) and specificity (74–96 %) (11, 16). Diagnostic tools and risk stratification systems have proven to be less accurate and have not, therefore, been adopted widely. Whether the new criteria are useful for general practitioners in determining whether a patient has had a migraine with aura or TIA, and for making decisions about thrombolytic therapy, is still unclear.