WHITE MATTER SCALING. Brain White Matter. Axon 3/19/2012. Susanne Müller MD, PhD
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1 WHITE MATTER SCALING Susanne Müller MD, PhD Department of Clinical Science, Intervention and Technology at Karolinska Institutet Division of Medical Imagingand Technology, Stockholm, Sweden and Department of Radiology, Karolinska University Hospital in Huddinge Brain White Matter contains: - fibres(axons) - neuroglial cells (astrocytes, oligodendrocytes) - vascular structures - interstitial space Axon -elongated fiber that extends from the cell body (cortex) to the terminal endings -transmits the neural signal at speeds up to 90 metres per second -the larger the axon, the faster it transmits information -may or may not have a myelin covering (myelinatedtransmits much faster) -most neurons have only one axon -transmits information away from the cell body 1
2 Myelin - produced/ maintained by oligodendrocytes - if destroyed remyelinisation(often incompletely) if oligodendrocytes intact - damage decrease in velocity or conduction block Myelinated axon All nerve cell processes in the central nervous system (CNS) peripheral nervous system (PNS) have one or more sheaths or coverings. Myelinatedprocesses in the PNS have a sheath of Schwann cells around a myelin wrapping. The myelin is produced by the Schwann cells. Neuron dendrite node of Ranvier axon terminal (synapse) nucleus myelin Swann cell Wikipedia 2
3 DTI Diffusion Tensor Imaging - red: left- right - blue: up-down - green: forth-back CT MRI FLAIR T2 WM CHANGES CT - hypodens - ill- defined MRI (Flair/T2) - hyperintens - well- defined 3
4 WM changeson MRI - caps: adjacent to frontal horns - Periventricular: caps frontal/ posterior horns, bands along lateral ventricles, confluent with changes in deepwm - Deep WM: punctuate, patchy, confluent WM changeson MRI MULTIPLE SCLEROSIS 4
5 ENLARGED PERIVASCULAR SPACES STRATEGIC INFARCTIONS = infarctions in areas crucial for normal cognitive functioning of the brain Strategic infarcts and small vessel disease Cognitive dysfunction in VaDcan be the result of : 1. Large vessel infarctions: -Bilateral in territory of anteriorcerebral artery. -Parietotemporal-and temporo-occipital association areas of the dominant hemisphere (angular gyrusincluded) -Posteriorcerebral artery occlusion with infarction of the paramedianthalamic region and inferior medial temporal lobe of dominant hemisphere 2. Watershedinfarctions in the dominant hemisphere (superior frontal and parietal) 3. Small vessel disease: -Multiple lacunarinfactionsin frontal white matter (>2) and basal ganglia(>2) -WMLs (at least more than 25% of WM) bilateral thalamic lesions 5
6 IDEAL RATING SCALE - simple - reliable - includes anatomical distribution - includes severity of WM changes DIFFERENT SCALES Fazekas PVHI and DWHMI DISTINCT - PVHI: 0: absence 1: caps or pencil-thin lining 2: smooth halo 3: irregular extending into WM - DWHM: 0: absence 1: punctate foci 2: beginning confluence of foci 3: large confluent areas Wahlund PVHI and DWHMI COMBINED (frontal, temporal, parietooccipital regions; infratentorial/ basal ganglia excluded) - no WM changes - small solitary WM changes - multiple discrete or large solitary WM changes - multiple, partly confluentwm changes - multiple, largeconfluentwm changes FAZEKA SCALE (1987) - MRtool - provides an overall impression on the occurrence of white matter hyperintensities for the complete brain - best scored on transverse FLAIR (or T2-weighted) images. - Score: Fazekas0: No or a single punctatewmh lesion Fazekas1: Multiple punctatelesions Fazekas2: Beginning confluencyof lesions. Fazekas3: Large confluent lesions. 6
7 FAZEKAS Fazekas0: No or a single punctate WMH lesion Fazekas1: Multiple punctate lesions Fazekas2: Beginning confluencyof lesions. Fazekas3: Large confluent lesions. FAZEKAS Fazekas1 is normal in elderly. Fazekas2 and 3 are pathologic, but can sometimes be seen in normal functioning people. They are however at high risk for disability. In 600 normal functioning elderly the Fazekasscore predicted disability within one year (table). In the Fazekas3 group 25% was disabled within one year (10). CASE 1 Female 53 yrs Fazekas:? 7
8 CASE 1 Female 53 yrs Fazekas: periventricular: thin caps, punctate lesions, thin bands: 1 DWHM: 1 CASE 2 Male64 yrs Fazekas? CASE 2 Male64 yrs Fazekas: DWHM: 2 periventricular: 3 8
9 WAHLUND SCALE (1990) - on CTWM lesions = hypodensareas 5mm - takesonlydeepwm lesions intoaccount - doesnot considerrims or subtlecapsaround lateral ventricles - no total score - separate scoresfor regions: frontal, temporal, parietooccipital; basal ganglia* (infratentorial excluded¹) * striatum, pallidum, int/ext caps., thalamus, claustrum ¹due to difficulties in well visualising CASE 3 Male77 yrs Wahlund:? CASE 3 Male77 yrs Wahlund: lesions in frontallob: 1 and 2 external capsule: 1 9
10 CASE 4 Female 81 yrs Wahlund:? CASE 4 Female 81 yrs Wahlund: large confluent lesions in frontal-, parietal-, occipitallobe: 3 external capsule: 2 CASE 5 Female 93 yrs Wahlund:? 10
11 CASE 5 Female 93 yrs Wahlund: large confluent lesions in all lobes: 3 basal ganglia: confluent lesions: 3 Wahlund:? Wahlund: Ø Status post contusion with parenchymloss 11
12 Remember the differentialdiagnosis!! Thank you! 12
13 13
14 MRI T2weighted Försörjningsområden av a cerebri anterior (ACA) a cerebri media (MCA) a cerebri posterior (PCA) samt deras grenar 14
15 CASE 2 Male74 yrs Fazekas? CASE 2 Male74 yrs Fazekas: DWHM: 2 periventricular: 3 15
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