1. Diffusion MR Imaging in Central Nervous System
Claudio de Carvalho Rangel, MD, L. Celso Hygino Cruz, MD, Tatiana Chinem Takayassu, MD, Emerson L. Gasparetto, MD, PhD, Romeu Cortes Domingues, MD 
Magnetic Resonance Imaging Clinics 
Volume 19, Issue 1, Pages (February 2011)
DOI: /j.mric
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2. Fig. 1
A 63-year-old female patient with a stroke with right facial palsy for 1 week. FLAIR (A) shows hyperintense lesions in the deep white matter. DWI (B) and ADC mapping (C) show a focal area of restricted diffusion, compatible with ischemic stroke (arrows).
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3. Fig. 2
A 67-year-old female patient with stroke with 2 hours of left hemiparesis. Axial CT (A) and axial FLAIR (B) show no abnormalities, but a small area of restricted diffusion (C and D arrow) suggests an infarct. Dynamic susceptibility contrast-MRI (DSC-MRI) maps, time to peak (E) and relative cerebral blood volume (F) show the penumbra area (demarcated line) with potential salvable ischemic tissue. Three dimensional time of flight MR imaging (G) reveals reduced flow in the right middle cerebral artery.
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4. Fig. 3
A 30-year-old pregnant woman with PRES with eclampsia, headache, and seizures. Axial FLAIR (A) shows confluent areas of edema and hyperintense signal in the basal ganglia and posterior parieto-occiptal regions. DWI (B) and ADC map (C) suggest that the major portion of the lesion correspond to vasogenic edema.
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5. Fig. 4
Transient global amnesia. Axial FLAIR (A), DWI (B), and ADC map (C) show a focal area of hyperintensity with restricted diffusion localized in the lateral aspect of the right hippocampus (arrows).
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6. Fig. 5
In case 1, axial contrast-enhanced T1-WI (A), T2-WI (B) and DWI (C) show a large extra-axial cystic lesion with signal intensity similar to the CSF, as well as high diffusion, corresponding to the arachnoid cyst. In case 2, axial T1-WI (D), T2-WI (E) and DWI (F) show an extra-axial lesion with same features of an arachnoid cyst on conventional MRI, but with high signal intensity on DWI, which corresponds to an epidermoid tumor.
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7. Fig. 6
Glioblastoma multiforme. Axial contrasted-enhanced T1-WI (A), coronal T2-WI (B), DWI (C), and ADC mapping (D) demonstrate a large necrotic mass with a central area of facilitated diffusion and a peripheral area of restricted diffusion.
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8. Fig. 7
A 56-year-old male with glioblastoma multiforme. Coronal T2-WI (A), tractography (B), DWI (C) and ADC map (D) show a heterogeneous mass located on the right parietal lobe. The peripheral area of the mass shows restricted diffusion, and the central area has a high diffusivity. The lesion seems to dislocate the corticospinal tract contralaterally.
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9. Fig. 8
Pyogenic abscess. Axial FLAIR (A), axial contrasted-enhanced T1-WI (B), DWI (C), and ADC map (D) show a round enhancing lesion surrounded by edema with a central area presenting high signal intensity on DWI and low ADC, probably due to the high viscosity of the pus.
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10. Fig. 9
Meningitis with pyogenic subarachnoid collection. Axial FLAIR (A, B) and DWI (C, D) demonstrate hyperintense signal on the subarachnoid space, which have restricted diffusion (arrows in B and D).
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11. Fig. 10
An 11-year-old female with frontal sinusitis and empyema. Axial T2-WI (A), axial T1-WI (B), axial and sagittal contrasted-enhanced T1-WI (C and D), DWI (E) and ADC map (F) show an extraaxial collection in the frontal region, with restricted diffusion. Note also the small subdural empyema along the right front-parietal region, better visualized by DWI (arrows).
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12. Fig. 11
In septic emboli, axial FLAIR (A) and contrasted-enhanced T1-WI (C) demonstrate bilateral contrast enhanced lesions with restricted diffusion (B and D).
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13. Fig. 12
In a case of herpetic encephalitis, axial T2-WI (A) and DWI (B) show areas of edema and hyperintense signal as well as restricted diffusion in both temporal lobes.
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14. Fig. 13
Creutzfeldt-Jakob disease (CJD). Case 1: 72-year-old female patient with behavioral changes for 2 weeks. Axial FLAIR (A) and DWI (B) show abnormal areas of hyperintensity with restricted diffusion in the caudate nucleus and putamen, as well as in the cortex of the parieto-occipital lobes, consisting with the classic form of CJD. Case 2: Axial FLAIR (C) and DWI (D) show abnormal areas of hyperintensity in the cortex of both occipital lobes (white arrows), indicating the variant form.
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15. Fig. 14
In a case of influenza encephalitis, axial FLAIR (A) shows no abnormal changes but DWI (B) reveals a focal area of restricted diffusion on the splenium of the corpus callosum.
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16. Fig. 15
Acute disseminated encephalomyelitis (ADEM). Axial FLAIR (A) and contrast-enhanced T1-WI (B) reveals a diffuse hyperintense non-enhancing lesions in the white matter of both hemispheres. DWI (C) demonstrates bilateral, diffuse areas of restricted diffusion. In a follow-up MRI performed 3 months later, FLAIR (D), contrast-enhanced T1-WI (E), and DWI (F) show significant improvement, with no areas of restricted diffusion.
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17. Fig. 16
Acute plaque of multiple sclerosis. Axial FLAIR (A), contrasted-enhanced T1-WI (B), DWI (C), and ADC map (D) show a focal hyperintensity, noncontinuous ring contrast enhancement lesion in the right parietal lobe. This peripheral area had restricted diffusion.
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18. Fig. 17
Multiple sclerosis. Axial contrast-enhanced T1-WI (A), DWI (B), FA measurement (C), and FA color map (D) reveal an acute plaque (arrows) with enhancement and restricted diffusion in the left frontal lobe. Note the reduced FA in the NAWM surrounding the plaque (2, 3 and 4). Normal FA value is seen in (1) (D).
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19. Fig. 18
Diffuse axonal injury. Multiple small hypointense lesions of the subcortical white matter and corpus callosum are better visualized by T2 GRE (C, D) than by FLAIR (A, B) images. DTI shows reduced FA values within the lesion and in the surrounding NAWM (E, F). Tractography (G) demonstrated reduced fiber density, mainly in the corpus callosum.
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20. Fig. 19
Alzheimer's disease. Coronal T2-WI (A) demonstrates slight and symmetric volume loss of hippocampi (arrows). A coronal FA color map shows reduced FA values on the splenium of the corpus callosum (B, 1), bilaterally on the posterior cingulate gyrus (B, 2 and 3), and on the superior longitudinal fasciculus (C, 1 and 2).
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21. Fig. 20
Hypoxic-ischemic encephalopathy. Axial T2-WI (A, B) shows areas of diffuse and excessive high signal intensity (DEHSI) in white matter of a premature asphyxiated newborn. FA map (C, D) shows areas of reduced anisotropy in posterior portions of the corpus callosum and left posterior limb of the internal capsule secondary to Wallerian degeneration of axons.
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22. Fig. 21
A 40-week-old newborn male patient with infarction, presenting with poor suckling and seizures. MRI obtained 72 hours after birth shows barely visible areas of hypointensity on T1-WI (A) and hyperintensity on T2-WI (B), corresponding to the “missing cortical sign” (arrows). DWI (C) shows a core area of reduced diffusion in the parieto-occipital cortex, with high relative cerebral blood volume (D), representing arterial infarction associated with reperfusion.
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23. Fig. 22
A 5-year-old female patient with congenital cytomegalovirus infection and polymicrogyria. Axial T2-WI (A) shows polymicrogyria and some foci of heterotopia. FA color map (B) at the same level shows a horizontally oriented pattern of subcortical white matter fibers (arrows). A normal control FA color map (C) is shown for comparison.
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24. Fig. 23
A 6-year-old male patient with Joubert syndrome. Axial and coronal T2-WI (A, B) show the molar tooth malformation with increased width of the superior cerebellar peduncle (arrows). The absence of the superior cerebellar peduncle decussation (arrow) was apparent in the FA color map (C). A control patient with normal superior cerebellar decussation at the pons (arrow) is shown for comparison (D).
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25. Fig. 24
Corpus callosum agenesis. Sagital T1-WI (A) and coronal T2-WI (B) demonstrate the absence of the corpus callosum and the characteristic ventricle shape. Axial (C, D) and coronal (E) FA color maps depict Probst bundles (C, E, arrows) as green bundles lying in an anteroposterior orientation. Tractography superimposed on the FA color map (F) shows that these fibers do not cross the midline.
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26. Fig. 25
Leigh syndrome. High signal areas on the putamen are visualized by T2-WI (A, arrow), whereas foci of high DWI signal intensity (B, arrows) and low ADC values (C, arrows) demonstrate an acute exacerbation of Leigh encephalopathy. Spectroscopy (D) shows metabolic peaks of lactate probably secondary to anaerobic glycolysis.
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27. Fig. 26
Mitochondrial encephalopathy with lactic acidosis (MELAS). DWI (A) shows hyperintense cortical and subcortical signals with low ADC values (B, arrows), corresponding to acute exacerbation of mitochondriopathy and atrophic changes.
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28. Fig. 27
In pontine myelinolysis and extrapontine myeinolysis, T2-WI shows foci of hyperintense signal on the pons (A) and bilateral and symmetric areas of high signal intensity on the putamen and thalami (B). DWI shows areas of restricted diffusion on the pons (C), putamen, and thalami (D).
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29. Fig. 28
Wernicke's encephalopathy. Areas of high signal intensity on FLAIR images (A, B) and restricted diffusion on DWI (C, D) are demonstrated bilaterally on the mammillary bodies, periaqueductal gray matter, and in the frontal cortex bilaterally.
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30. Fig. 29
Multiple sclerosis. Demyelinating plaques can be detected as diffuse hyperintense lesions on both T2-WI (B, F) and STIR (C, G) images. Contrast-enhanced T1-WI (A, E) does not demonstrate any abnormal enhancement. Sagittal DTI (D, H) shows reduced FA values within the lesion and in the surrounding normal-appearing spinal cord, suggesting a more extensive abnormality. STIR, short tau inversion recovery.
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31. Fig. 30
Ependimoma. Sagital T2-WI (A) and T2* GRE (B, C) demonstrate a hyperintense on expansive lesion located at the middle portio of the cervical spine, which does not cause disruption, but only a mild dislocation of the main fibers, demonstrated on tractography (D).
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32. Fig. 31
Cavernoma. Coronal (A) and axial T2-WI (B), and T2∗ GRE (B), show hyperintense expansive lesion on the posterior and right lateral aspects of the cervical spinal cord at C1-C2 level, which does not enhances after intravenous contrast administration on contrast-enhanced T1-WI (C). Axial T2∗ GRE (D) demonstrates a foci of hypointense signal intensity within the lateral aspect of the lesion. There is no disruption of the main fibers demonstrated on tractography (E). Gd, gadolinium.
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