title: Transient ischaemic attacks are associated with increased rates of global cerebral atrophy.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Clinical Neurology, St Mary's Hospital, London W2 1NY, UK.
authors.forename: R J L
authors.initials: RJ
authors.lastname: Walters
authors.forename: N C
authors.initials: NC
authors.lastname: Fox
authors.forename: J M
authors.initials: JM
authors.lastname: Schott
authors.forename: W R
authors.initials: WR
authors.lastname: Crum
authors.forename: J M
authors.initials: JM
authors.lastname: Stevens
authors.forename: M N
authors.initials: MN
authors.lastname: Rossor
authors.forename: D J
authors.initials: DJ
authors.lastname: Thomas
mesh_terms: D000368:Aged; D001284:Atrophy; D001794:Blood Pressure / Q000502:physiology; D001921:Brain / Q000473:pathology*; D002544:Cerebral Infarction / Q000175:diagnosis / Q000503:physiopathology; D017352:Echo-Planar Imaging; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D020343:Hypertensive Encephalopathy / Q000175:diagnosis / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D002546:Ischemic Attack, Transient / Q000175:diagnosis* / Q000503:physiopathology; D008297:Male; D008609:Mental Status Schedule; D008875:Middle Aged; D012016:Reference Values; D012307:Risk Factors