Magnetic resonance imaging
Magnetic resonance imaging is the imaging modality of choice for most neurologic conditions. MR images can be obtained rapidly, non-invasively and with no exposure to ionizing radiation. Images can be generated in any orientation. MRI has high soft tissue resolution and sensitivity to tissue edema.
MRI has a higher sensitivity than CT to brainstem and cerebellar ischemia, making it of particular use in the posterior fossa. MR images can be ‘weighted’ to augment contrast between tissue types.Furthermore, specialized pulse sequences have been developed to highlight specific tissue properties. A number of different sequences can be obtained at the same imaging session, providing more information than from any single sequence alone. For example, information provided by T1-and T2-weighted imaging can be augmented by that provided by susceptibility-weighted sequences (sensitive to hemorrhage), diffusion-weighted imaging (tissue destined to infarct without prompt intervention), MR angiography (vascular anatomy), MR perfusion imaging (cerebral perfusion), and MR spectroscopy (concentration of specific cerebral metabolites). The technical aspects and role of MRI in stroke will be discussed in later chapters.
However, MRI has a number of limitations in stroke (Table 2.2). First, MRI is approximately twice as expensive as CT. Claustrophobic patients may have difficulties tolerating the studies. MRI is contraindicated in patients with fragments of metal, for example within the eyes, and in patients with intracranial aneurysm clips, cardiac pacemakers or any other electrically or magnetically active implanted devices that could interact with the magnetic field.
Brain MRI of Early ischemic changes are subtle Ischemic changes may be seen in conventional MR studies within 1 to 2 hours of stroke onset. The earliest findings include loss of the normal flow void within major intracranial vessels and the presence of arterial enhancement if contrast has been used. The first morphological changes are due to the development of parenchymal swelling with effacement of cortical sulci and distortion of the ventricular system. These changes are first seen in T1-weighted sequences and may be present in up to half of patients within 6 hours. This early swelling occurs without signal change and is most likely related to the onset of cytotoxic edema, which can develop within minutes in experimental ischemia. Signal changes only appear with the development of vasogenic edema and are not usually found before eight hours on T2-weighted sequences or hours on T1-weighted sequences. As a consequence, the overall sensitivity of MRI for ischemia is low in the first few hours following the onset of symptoms. Conventional MRI is also subject to the same limitations as cerebral CT when it comes to delineating acute from chronic infarction, and stratifying patients according to infarct presence, location and size prior to therapy or randomization in acute stroke trials (Fig. Brain MRI below).
Conventional magnetic resonance imaging sequences may not differentiate acute from chronic infarction. Conventional T2-weighted imaging (T2-WI) (A) and diffusion-weighted imaging (DWI) (B) in three patients with subcortical infarction imaged at 11 hours (a), 10 hours (b) and 10.5 hours (c) after the onset of symptoms. Ischemic changes are seen in the periventricular and subcortical white matter on T2-WI but there is no way of distinguishing acute from chronic infarction. Hyperintense regions of acute infarction are clearly seen on DWI.
jurnal radiology Tags: brain MRI of chronic infarction
MRI has a higher sensitivity than CT to brainstem and cerebellar ischemia, making it of particular use in the posterior fossa. MR images can be ‘weighted’ to augment contrast between tissue types.Furthermore, specialized pulse sequences have been developed to highlight specific tissue properties. A number of different sequences can be obtained at the same imaging session, providing more information than from any single sequence alone. For example, information provided by T1-and T2-weighted imaging can be augmented by that provided by susceptibility-weighted sequences (sensitive to hemorrhage), diffusion-weighted imaging (tissue destined to infarct without prompt intervention), MR angiography (vascular anatomy), MR perfusion imaging (cerebral perfusion), and MR spectroscopy (concentration of specific cerebral metabolites). The technical aspects and role of MRI in stroke will be discussed in later chapters.
However, MRI has a number of limitations in stroke (Table 2.2). First, MRI is approximately twice as expensive as CT. Claustrophobic patients may have difficulties tolerating the studies. MRI is contraindicated in patients with fragments of metal, for example within the eyes, and in patients with intracranial aneurysm clips, cardiac pacemakers or any other electrically or magnetically active implanted devices that could interact with the magnetic field.
Brain MRI of Early ischemic changes are subtle Ischemic changes may be seen in conventional MR studies within 1 to 2 hours of stroke onset. The earliest findings include loss of the normal flow void within major intracranial vessels and the presence of arterial enhancement if contrast has been used. The first morphological changes are due to the development of parenchymal swelling with effacement of cortical sulci and distortion of the ventricular system. These changes are first seen in T1-weighted sequences and may be present in up to half of patients within 6 hours. This early swelling occurs without signal change and is most likely related to the onset of cytotoxic edema, which can develop within minutes in experimental ischemia. Signal changes only appear with the development of vasogenic edema and are not usually found before eight hours on T2-weighted sequences or hours on T1-weighted sequences. As a consequence, the overall sensitivity of MRI for ischemia is low in the first few hours following the onset of symptoms. Conventional MRI is also subject to the same limitations as cerebral CT when it comes to delineating acute from chronic infarction, and stratifying patients according to infarct presence, location and size prior to therapy or randomization in acute stroke trials (Fig. Brain MRI below).
Conventional magnetic resonance imaging sequences may not differentiate acute from chronic infarction. Conventional T2-weighted imaging (T2-WI) (A) and diffusion-weighted imaging (DWI) (B) in three patients with subcortical infarction imaged at 11 hours (a), 10 hours (b) and 10.5 hours (c) after the onset of symptoms. Ischemic changes are seen in the periventricular and subcortical white matter on T2-WI but there is no way of distinguishing acute from chronic infarction. Hyperintense regions of acute infarction are clearly seen on DWI.
jurnal radiology Tags: brain MRI of chronic infarction
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