Transient ischaemic attacks are associated with increased rates of global cerebral atrophy

Abstract

Objectives: To determine whether patients presenting with a first transient ischaemic attack (TIA) subsequently show increased rates of brain atrophy compared with age matched controls; and to assess potential risk factors for brain atrophy in this group. Methods: 60 patients with a first, isolated TIA and 26 age and sex matched controls were recruited. None had evidence of cognitive impairment. Vascular risk factors were treated appropriately. All subjects had volumetric imaging at the start of the study and one year later, when they were clinically reassessed. TIA patients also had serial dual echo brain imaging. Rates of whole brain atrophy were calculated from the registered volumetric scans, as was the incidence of new ischaemic lesions. In the TIA group, the degree of white matter disease was assessed. Atrophy rates and blood pressure were compared between patients and controls. Results: 22 patients (37%) developed new "clinically silent" infarcts during follow up. The mean (SD) annualised percentage atrophy rate in the TIA group was significantly higher than in the controls, at 0.82 (0.39)% v 0.33 (0.3)% (p < 0.0001). In the TIA group, diastolic blood pressure (p = 0.004) and white matter disease severity (p < 0.001) were correlated with cerebral atrophy rate. Increased white matter disease was found in patients in whom new ischaemic lesions developed (p < 0.001). Conclusions: Patients presenting with a first TIA have excess global brain atrophy compared with age matched controls over the subsequent year. Increased atrophy rates following a TIA may be directly or indirectly related to increasing white matter disease and diastolic hypertension. Future studies should assess whether this atrophy inevitably leads to cognitive decline, and whether aggressive treatment of risk factors for cerebrovascular disease (particularly hypertension) after a TIA can influence outcome. C erebrovascular disease is associated with both cognitive decline and dementia. Cerebrovascular dementia may result from infarction of clinically eloquent cortical sites subserving specific cognitive functions or small, strategic subcortical infarcts (in the thalamus, caudate nucleus, or anterior internal capsule) that disrupt cortico-subcortical pathways.

White Matter Lesions and Brain Atrophy: More than Shared Risk Factors? A Systematic Review

“…The characteristics and results of the 4 studies [68,69,70,71] performed in patients with vascular risk factors are presented in table 3a and the characteristics and results of the 4 studies [72,73,74,75] performed in patients with symptomatic cerebrovascular disease are given in table 3b. Of these 8 studies, 5 examined the cross-sectional and 3 the longitudinal relation between WML and atrophy.…”

“…The studies that investigated patients with manifest cerebrovascular disease included stroke survivors 3 months after discharge [72, 74], patients with a transient ischemic attack [75], and patients with a lacunar stroke [73]. …”

“…In the patients with stroke or TIA, cross-sectional associations were found between more WML and more cortical, central and medial temporal lobe atrophy [72,73,74,75]. The relation between WML and ventricular enlargement was also found in the longitudinal study [74].…”

Relationship between Retinopathy and Cognitive Impairment among Hypertensive Subjects

“…Microcirculation disorders and endothelial dysfunctions are also responsible for impaired cognitive functions in hypertension [7]. Some studies have reported that transient ischemic attacks seen in hypertensive patients are associated with diastolic hypertension and white matter disease and that they cause global cerebral atrophy [8, 9]. The mechanisms for negative relations between hypertension and cognitive impairment do not seem to be limited to the cerebrovascular events; thus, further studies are needed.…”

Evidence of brain atrophy detected on magnetic resonance imaging is associated with failure of acquisition of the ability for insulin self-injection

“…on the progression of brain atrophy [6][7][8]. Generalized cerebral atrophy has been shown to be associated with the development of cognitive impairment after stroke [9][10][11][12].…”