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Transient ischaemic attacks are associated with increased rates of global cerebral atrophy
  1. R J L Walters1,
  2. N C Fox2,
  3. J M Schott1,
  4. W R Crum2,
  5. J M Stevens3,
  6. M N Rossor1,
  7. D J Thomas1
  1. 1Department of Clinical Neurology, St Mary’s Hospital, London W2, UK
  2. 2Dementia Research Group, Institute of Neurology, Queen Square, London WC1, UK
  3. 3Department of Neuroradiology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1, UK
  1. Correspondence to:
    Dr D J Thomas, Department of Clinical Neurology, St Mary’s Hospital, London W2 1NY, UK;
    dafydd.thomas{at}ic.ac.uk

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.

  • cerebral atrophy
  • transient ischaemic attacks
  • hypertension

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