MRI Guides Diagnostic Approach for Ischaemic Stroke

M A Kumar; H Vangala; D C Tong; D M Campbell; A Balgude; I Eyngorn; A S Beraud; J M Olivot; A W Hsia; R A Bernstein; C A Wijman; M G Lansberg; M Mlynash; S Hamilton; M E Moseley; G W Albers

Background and aim Identification of ischaemic stroke subtype currently relies on clinical evaluation supported by various diagnostic studies. The authors sought to determine whether specific diffusion-weighted MRI (DWI) patterns could reliably guide the subsequent work-up for patients presenting with acute ischaemic stroke symptoms.
Methods 273 consecutive patients with acute ischaemic stroke symptoms were enrolled in this prospective, observational, single-centre NIH-sponsored study. Electrocardiogram, non-contrast head CT, brain MRI, head and neck magnetic resonance angiography (MRA) and transoesophageal echocardiography were performed in this prespecified order. Stroke neurologists determined TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification on admission and on discharge. Initial TOAST stroke subtypes were compared with the final TOAST subtype. If the final subtype differed from the initial assessment, the diagnostic test deemed the principal determinant of change was recorded. These principal determinants of change were compared between a CT-based and an MRI-based classification schema.
Results Among patients with a thromboembolic DWI pattern, transoesophageal echocardiography was the principal determinant of diagnostic change in 8.8% versus 0% for the small vessel group and 1.7% for the other group (p<0.01). Among patients with the combination of a thromboembolic pattern on MRI and a negative cervical MRA, transoesophageal echocardiography led to a change in diagnosis in 12.1%. There was no significant difference between groups using a CT-based scheme.
Conclusions DWI patterns appear to predict stroke aetiologies better than conventional methods. The study data suggest an MRI-based diagnostic algorithm that can potentially obviate the need for echocardiography in one-third of stroke patients and may limit the number of secondary extracranial vascular imaging studies to approximately 10%.

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The Clinical Use of Structural MRI in Alzheimer Disease

Giovanni B. Frisoni; Nick C. Fox; Clifford R. Jack; Philip Scheltens; Paul M. Thompson

Structural imaging based on magnetic resonance is an integral part of the clinical assessment of patients with suspected Alzheimer dementia. Prospective data on the natural history of change in structural markers from preclinical to overt stages of Alzheimer disease are radically changing how the disease is conceptualized, and will influence its future diagnosis and treatment. Atrophy of medial temporal structures is now considered to be a valid diagnostic marker at the mild cognitive impairment stage. Structural imaging is also included in diagnostic criteria for the most prevalent non-Alzheimer dementias, reflecting its value in differential diagnosis. In addition, rates of whole-brain and hippocampal atrophy are sensitive markers of neurodegeneration, and are increasingly used as outcome measures in trials of potentially disease-modifying therapies. Large multicenter studies are currently investigating the value of other imaging and nonimaging markers as adjuncts to clinical assessment in diagnosis and monitoring of progression. The utility of structural imaging and other markers will be increased by standardization of acquisition and analysis methods, and by development of robust algorithms for automated assessment.

Introduction

Clinical and neuropathological studies have greatly advanced our knowledge of the pathophysiology and progression of Alzheimer disease (AD). This disease is associated with progressive accumulation of abnormal proteins (amyloid-β [Aβ] and hyperphosphorylated tau) in the brain, which leads to progressive synaptic, neuronal and axonal damage. Neurobiological changes occur years before symptoms appear, with a stereotypical pattern of early medial temporal lobe (entorhinal cortex and hippocampus) involvement, followed by progressive neocortical damage.[1,2] The delay in emergence of the cognitive correlates of these changes suggests that the toxic effects of tau and/or Aβ progressively erode ‘brain reserve’ until a clinical threshold is surpassed and amnestic symptoms develop. For example, amnestic mild cognitive impairment (MCI)—memory disturbance in the absence of dementia—is followed by more-widespread cognitive deficits in multiple domains until a disability threshold is reached and traditional diagnostic criteria for probable AD are fulfilled.[3] The prospect of disease-modifying drugs that can slow or prevent disease progression has prompted increased interest in identifying individuals with AD earlier and more accurately.

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