Abstract
Nonfocal transient neurological attacks (TNAs) are episodes with an acute onset of unexplained nonfocal symptoms that cannot be attributed to a specific territory of the brain, such as unsteadiness or bilateral weakness. These attacks are considered benign, possibly because the etiology of TNAs is still unknown. However, recent publications show that TNAs are not at all benign as they are associated with an increased risk of stroke, cardiac events and dementia. This thesis has tried to gain more insight in the etiology and cognitive consequences of TNAs.
Given the nonfocal nature of TNAs, it was first hypothesized that they result from global brain hypoperfusion. Our results showed that TNAs are related to the presence of carotid artery occlusion. However, subsequently, we found no difference in 24-hour blood pressure characteristics between patients with and without TNAs, nor did we find a relation between TNAs and total brain perfusion. Therefore, our results do not support the hypothesis that TNAs are caused by global brain hypoperfusion.
An alternative hypothesis is that TNAs are the result of focal brain ischemia. We investigated which mechanisms are involved in this process. We found that TNAs are related to lacunes and white matter hyperintensities on brain MRI, which suggests that a disease of the small brain vessels plays a role in the etiology of TNAs.
Furthermore, we found that patients with a recent TNA are more often cognitively impaired than patients without TNAs.
Given the nonfocal nature of TNAs, it was first hypothesized that they result from global brain hypoperfusion. Our results showed that TNAs are related to the presence of carotid artery occlusion. However, subsequently, we found no difference in 24-hour blood pressure characteristics between patients with and without TNAs, nor did we find a relation between TNAs and total brain perfusion. Therefore, our results do not support the hypothesis that TNAs are caused by global brain hypoperfusion.
An alternative hypothesis is that TNAs are the result of focal brain ischemia. We investigated which mechanisms are involved in this process. We found that TNAs are related to lacunes and white matter hyperintensities on brain MRI, which suggests that a disease of the small brain vessels plays a role in the etiology of TNAs.
Furthermore, we found that patients with a recent TNA are more often cognitively impaired than patients without TNAs.
Original language | English |
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Awarding Institution |
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Award date | 4 Jul 2019 |
Place of Publication | [Utrecht] |
Publisher | |
Print ISBNs | 978-94-028-1507-8 |
Publication status | Published - 4 Jul 2019 |
Keywords
- transient neurological attacks
- nonfocal symptoms
- etiology
- cerebral perfusion
- cerebral small vessel disease
- cognition