Outline

• Basic information

• Materials

• Methods

• Result

• Discussion

• Inference

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fMRI and its principle

• fMRI is a functional neuroimaging procedureusing MRI technology .

• It measures brain activity by detectingassociated changes in blood flow.

• fMRI uses the blood-oxygen-level dependent(BOLD) contrast.

ref: wikipidea

fMRI of visual cortex

Ref: Wikipedia

Definitions

• Population receptive field mapping:

pRF model estimates the region of the visualfield that effectively elicits a response in a smallregion of the visual cortex (i.e., voxel).

Blood Oxygen Level dependence (BOLD) is used to estimate response in an region of interest (ROI).

Visual field defect

Ref: clinical junior.com

Objective

• After V1 injury recovery to some extent is wellknown. A recent study suggested, large scalereorganization occur in V1. But so far therewas no quantitative study.

• So, this study was meant look into the rangeof reorganization and its mechanism.

Research question

1. Does visual cortex (V1) really has plasticity?

2. If have then to what extent?

3. How does that work?

Materials and methods

• Control: 8 male + 1 female (age: 26-65 y)

ID Sex Age t Defect

P1 M 49 7 LUQ

P2 F 27 10 RUQ

P3 M 33 0.5 RUQ

P4 M 54 7 RUQ

P5 F 64 9 LUQ

Materials and methods (cont.)

• Visual field tests: Humphrey type

• Scanning: Structural and functional MRI

• Stimuli: moving square checker board bars (radius 11.25 degree)

• Infrared eye movement tracker

Anatomic Location Of the Lesion and Retinotopic Mapping.Anatomy Polar Angle Eccentricity Map Explained Variance

Perimetry maps Vs visual field coverage maps of spared area V1

Discussion

• Pattern 1: visual field coverage maps overlapped with perimetric scotoma.

• Pattern 2: visual field coverage maps didn’t cover the sighted quadrant of perimetricmaps.

• So , does the spared V1 changes after lesion?

• Does the position of pRF centre reorganise?

Primary assumptions Pattern

observation assumption

1 (P1+P2+P3)

activation Invisual mapping> perimetry

-visually driven activityin spared V1 was not enough.- BOLD signal is lower.

2(P4+P5)

activation Invisual mapping< perimetry

- pRFs partially surviving island in V1 enlarged/ V1 bipassing pathways

• After talairach coordiantes at an eccentricityof 8 deg along horizontal meridian of V1shows retinotropic representation of sparedV1 remained grossly unafffected (fovealrepresentation was in occipital pole,incresingly anterior location responded toincreasingly ant. Stimuli).

• Minor reorganization?

Methods (cont.)

• Methods to find minor degree reorganization:

1. pRF centre distribution as a function of distance from the scotoma

2. population receptive field size

pRF centre distribution as a function of distance from scotoma border

pRF size in spared V1 areas

pRF size of the contra lesional V1

Conclusion

1. Area V1 displays a limited degree ofreorganization in adult humans withhomonymous visual field defects

2. Reorganization is manifested in some patientsby a small shift(1-2 degree) in the pRF centerstoward the border of the scotoma and by aslight increase in V1 pRF sizes near the border ofthe scotoma.

3. Two different patterns of mismatch betweenresponses

Evaluation

• The paper is precise and relevant for answering questions about plasticity in adult V1.

• Patient selection could have been better. (P3)

• Some hypotheses are still unexplained.

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• After injury adult V1 displays palsticity.

• Reorganisation occurs through 1-2 deg shift ofpRF centre towards the border of scotomaand slight increase in the size of sparedcortical area on both hemisphere.

• A lot more has to explore –

-regarding optimal time window of plasticity.

-the mechanism and connection of V1bypass pathway.