Difference between revisions of "Magnetic resonance imaging (MRI)"

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There are many sequences to review, and given time constraints, you will need to prioritize. One recommendation would be:
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There are many sequences to review, and given time constraints, you will need to prioritize. Here is one approach in cognitive neurology and neuropsychiatry clinic:
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# Look for white matter changes on T2 FLAIR
 
# Look for white matter changes on T2 FLAIR
 
# Distinguish between areas of focal atrophy and global atrophy on T1 axial (also coronal view for medial temporal lobe).  
 
# Distinguish between areas of focal atrophy and global atrophy on T1 axial (also coronal view for medial temporal lobe).  
 
# Check SWI for potential microbleeds
 
# Check SWI for potential microbleeds
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'''Atrophy patterns'''
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''Global cerebral atrophy'' (symmetric atrophy of the entire supratentorial brain) (Pasquier et al, 1996)
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* None: normal sulci and gyri
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* Mild: sulcal widening with preservation of gyral thickness
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* Moderate: sulcal widening with gyral volume loss
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* Severe: severe “knife blade” atrophy, sulcal widening is larger than gyral thickness
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** How to interpret moderate to severe global cerebral atrophy:
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*** It is a reliable (though non-specific) marker of cognitive and functional impairment in advanced age; it may be caused by age, Alzheimer’s disease, and/or white matter hyperintensities (Al-Janabi et al, 2018)
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*** Degree of global cerebral atrophy is correlated (negatively) with MMSE scores, even independent of age (Al-Janabi et al, 2018)
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''Regional atrophy'' (using the same assessment and description as above for global atrophy)
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* Frontal
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* Temporal
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* Parietal
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* Occipital
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* Limbic structures
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** Medial temporal atrophy descriptions:
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*** None: no CSF visible around the hippocampal body
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*** Mild widening of choroidal fissure
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*** Moderate widening of choroidal fissure, mild enlargement of anterior temporal horns, mild loss of hippocampal height
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*** Severe widening of choroidal fissure, moderate enlargement of anterior temporal horns, moderate loss of hippocampal height
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*** Severe widening of choroidal figure, severe enlargement of anterior temporal horns, severe hippocampal atrophy
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''White matter disease'': common and nonspecific, most commonly related to microvascular disease. Fazekas scale ranked 0 – 3: (Fazekas et al, 1987)
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*0: No or few nonspecific punctate foci of signal abnormality
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*1: Scattered punctate foci of signal abnormality
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*2: Scattered, partially confluent areas of signal abnormality
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*3: Large, confluent areas of signal abnormality
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== References ==
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Al‐Janabi, O. M. et al. Global Cerebral Atrophy Detected by Routine Imaging: Relationship with Age, Hippocampal Atrophy, and White Matter Hyperintensities. J. Neuroimaging 28, 301–306 (2018). https://pubmed.ncbi.nlm.nih.gov/29314393/
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Fazekas, F., Chawluk, J. B., Alavi, A., Hurtig, H. I. & Zimmerman, R. A. MR signal abnormalities at 1.5 T in Alzheimer’s dementia and normal aging. AJR Am. J. Roentgenol. 149, 351–356 (1987). https://pubmed.ncbi.nlm.nih.gov/3496763/
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Pasquier, F. et al. Inter- and intraobserver reproducibility of cerebral atrophy assessment on MRI scans with hemispheric infarcts. Eur. Neurol. 36, 268–272 (1996). https://pubmed.ncbi.nlm.nih.gov/8864706/

Revision as of 09:00, 13 June 2021

There are many sequences to review, and given time constraints, you will need to prioritize. Here is one approach in cognitive neurology and neuropsychiatry clinic:

  1. Look for white matter changes on T2 FLAIR
  2. Distinguish between areas of focal atrophy and global atrophy on T1 axial (also coronal view for medial temporal lobe).
  3. Check SWI for potential microbleeds


Atrophy patterns

Global cerebral atrophy (symmetric atrophy of the entire supratentorial brain) (Pasquier et al, 1996)

  • None: normal sulci and gyri
  • Mild: sulcal widening with preservation of gyral thickness
  • Moderate: sulcal widening with gyral volume loss
  • Severe: severe “knife blade” atrophy, sulcal widening is larger than gyral thickness
    • How to interpret moderate to severe global cerebral atrophy:
      • It is a reliable (though non-specific) marker of cognitive and functional impairment in advanced age; it may be caused by age, Alzheimer’s disease, and/or white matter hyperintensities (Al-Janabi et al, 2018)
      • Degree of global cerebral atrophy is correlated (negatively) with MMSE scores, even independent of age (Al-Janabi et al, 2018)


Regional atrophy (using the same assessment and description as above for global atrophy)

  • Frontal
  • Temporal
  • Parietal
  • Occipital
  • Limbic structures
    • Medial temporal atrophy descriptions:
      • None: no CSF visible around the hippocampal body
      • Mild widening of choroidal fissure
      • Moderate widening of choroidal fissure, mild enlargement of anterior temporal horns, mild loss of hippocampal height
      • Severe widening of choroidal fissure, moderate enlargement of anterior temporal horns, moderate loss of hippocampal height
      • Severe widening of choroidal figure, severe enlargement of anterior temporal horns, severe hippocampal atrophy


White matter disease: common and nonspecific, most commonly related to microvascular disease. Fazekas scale ranked 0 – 3: (Fazekas et al, 1987)

  • 0: No or few nonspecific punctate foci of signal abnormality
  • 1: Scattered punctate foci of signal abnormality
  • 2: Scattered, partially confluent areas of signal abnormality
  • 3: Large, confluent areas of signal abnormality


References

Al‐Janabi, O. M. et al. Global Cerebral Atrophy Detected by Routine Imaging: Relationship with Age, Hippocampal Atrophy, and White Matter Hyperintensities. J. Neuroimaging 28, 301–306 (2018). https://pubmed.ncbi.nlm.nih.gov/29314393/

Fazekas, F., Chawluk, J. B., Alavi, A., Hurtig, H. I. & Zimmerman, R. A. MR signal abnormalities at 1.5 T in Alzheimer’s dementia and normal aging. AJR Am. J. Roentgenol. 149, 351–356 (1987). https://pubmed.ncbi.nlm.nih.gov/3496763/

Pasquier, F. et al. Inter- and intraobserver reproducibility of cerebral atrophy assessment on MRI scans with hemispheric infarcts. Eur. Neurol. 36, 268–272 (1996). https://pubmed.ncbi.nlm.nih.gov/8864706/

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