Đánh giá tổn thương bó tháp và một số chỉ số của cộng hưởng từ khuếch tán liên quan với chức năng vận động của bệnh nhân nhồi máu não tt tiếng anh

MINISTRY OF EDUCATION & TRAINING

MINISTRY OF DEFENCE

108 INSTITUTE OF CLINICAL MEDICAL AND PHARMACEUTICAL SCIENCES

VU DUY LAM

ESTIMATING PYRAMIDAL TRACT LESIONS AND
SOME DIFFUSION TENSOR IMAGING INDEXS
RELATED TO MOTOR FUNCTION IN
ISCHEMIC STROKE PATIENTS

Speciality : Medical Imaging
Code

: 62.72.01.66

SUMMARY OF THE THESIS

HÀ NỘI - 2019


THIS THESIS IS FINISHED IN 108 INSTITUTE OF CLINICAL
MEDICAL AND PHARMACEUTICAL SCIENCES

Name of supervisor:
1. MD, PhD, Ass. Prof. Lam Khanh
2. MD, Ass. Prof. Vu Long

Reviewer 1: ……………………………………………..................

Reviewer 2: ……………………………………………..................

Reviewer 3: ……………………………………………..................

The thesis will be upholded by hospital council at:
h

date month

year 2018

Can find out more about this thesis in:
1.

National Library

2.

Library of 108 Institute of clinical Medical and
Pharmaceutical sciences.


1
POSITION OF THE PROBLEM
Importance of the problem:
Cerebral infarction is a severe diease which is the 3rd most
common cause of mortality in Viet Nam after cancer and myocardial
infarction. Ischemic stroke makes some serious sequelae, 50% alive
patients got paralytic symptoms and depended on the helping of the

community.
Motor paralysis is a symptom highly related to the damage of the
pyramidal tract. In the past, the diagnosis of the pyramidal injury
mostly depended on the Babinski sign (+). The medical imaging of
the pyramid was very difficult, because it had the same density and
signal with the white matter in CT and MRI imagings.
The invention of DTI can display the pathway of nervers in the
brain and applying this technique can evaluate the damage of the
tract, study the relationship between the pyramidal damage with
patient’s motor function recovery which help doctors to make a right
prognosis, have an effective treatment stratery and reduce patient’s
sequela. Therefor, we performed this research: “Estimating
pyramidal tract lesions and some Diffusion Tensor Imaging indexs
related to motor function in ischemic stroke patients” in 108 Institute
of Clinical Medical and Pharmaceutical Sciences, where had a
specialist stroke center and a MRI 3.0 Tesla with DTI sequence.
Aim of the thesis
1. Describe the imaging characteristics of the neural tract lesions
in DTI inischemic stroke patients compared to normal people.
2. Estimate the relation between some DTI indexs to motor
function in ischemic stroke patients.
Contribution of the thesis: This is the first research in Viet Nam
about the damage of pyramidal tract in MRI.
Contribution in radiology: Develop a new technique in radiology.
Contribution in treatment: Help to prognose the chance of
motor recovery to make an effective treatment strategy.


2
Presentation of the thesis

The thesis comprises 116 pages, dealing with 2 pages for Position
of the Problem, 30 pages for the Overview, 17 pages for the Subjects
and Research Method, 32 pages for the Study Results, 28 pages for
the Discussion, 2 pages for the Conclusions. There are 45 tables, 18
charts, 28 images of the study design. There are 114 references,
including 13Vietnamese documents and 101 English documents.
Chapter 1: OVERVIEW
1.1. Anatomy
The pyramidal tract is the most important motor pathway in the
human brain. The pyramidal tract includes both the motor cortex and
the motor pathways.
1.1.1. The motor cortex
Classically the motor cortex is an area of the frontal lobe located
in the anterior to the central sulcus. It contains the primary motor
cortex, the premotor cortex, the supplementary motor area.
1.1.1.1. The primary motor cortex
The primary motor cortex is located between the precentral sulcus
and central sulcus include central gyrus and the paracentral lobule.
Anatomically, the precentral gyrus can be divided into four
segments: the inferior segment, the middle segment, the superior
segment, the paracentral segment
In function, each the segment of the precentral gyrusis a functionl
unit control a partof the body. The inferior segment: functional unit
of the face; the middle segment: functional unit of the hand and arm;
the superior segmentfunctional unit of the trunk; the paracentral
segment: functional unit of the leg.
1.1.1.2. The premotor cortex: The premotor cortex is in front of the
primary motor cortex, patially locate in the mesial aspect of
hemisphere anterior to the paracentral lobule.
1.1.1.3. The supplementary motor area

The supplementary motor area (SMA) is located in the mesial
aspect of the first frontal gyrus, anterior to the primary motor cortex
of lower extremity and above the cingulate sulcus and behind the


3
premotor cortex. The SMA is linked with the contralateral SMA
through the commissural fibers of the corpus callosum.
1.1.2. Motor pathways
Motor pathways or the pyramidal pathwaysinclude two
components: the pyramidal tract or corticospinal tract and the
corticonuclear fibers. In function, the pyramidal tract controls muscle
of the trunk, the corticonuclear fibers control muscles of the head,
face and neck.
The pyramidal tract
The origins and pathways of the pyramidal tract are fully decribed
in the anatomy books, we would not repeat it. In general, the
pyramidal tract can be divided into two parts:Upper part (hemisphere
part) shaped like a fan and lower part (from cerebral stem
downwards) is cylinder in shape. At present, with the DTI we can see
the image of pyramidal tract from the cerebral cortex to the upper
part of the medulla oblongata.The pyramidal tract is composed of
approximately 1 million axons of motor neuron.
Each neuron consists of a cell body, one or more dendrites and an
axon. The axon is the primary structure part of the tract. Axons with
myelin sheath are called myelinated appear white, masses of such
axons form the fiber bundle. CNS axons are myelinate by oligodendrocytes, which do not provide a neurilemma. Consequently,
damaged CNS axon (the pyramidal tract) usually do not regenerate to
result Waller degeneration.
1.2. Pathology

1.2.1. Cerebral infarction
Acute stage: The necrosis process is formed, local edema of the
brain, initiation is intracellular cytotoxic edemathen there were
vasogenic edema and extracellularedema.
Subacute stage: In this stage, the process of repair and absorption
of necrotic tissue, it takes place from the periphery towards the
center of encephalomalacic area. The result of this process is the
formation of cyst with surrouding glial scars.
Chronic stage: The appearance of the fluid-filled cavity lined by
astrocystes and glial scars, the sulci and ventricle is dilated, the gyri
is shrinked.


4
Cerebral infarction in areas where the pyramid tract passes leads
to damage in each segment passing through. This process takes place
in several stages, the last and most severe consequence is Waller
degenerationin the far part of axon. Neurotransmitter ability of axon
is lost.
1.2.2. Damaged pyramid tract
The injury process will go through 4 stages.
Stage 1: Manifested by physical interruption of the myelin sheath
and axon.
Stage 2: Characterized by the destruction of the myelin sheath.
Stage 3: The myelin sheath almost disappeared, the glial tissue
replaced the myelin sheath and axon degeneration.
Stage 4: Characterized by cerebral volume lost and atropic the
white matter bundle (Waller degeneration).
Morphologically, it can only detect an axon degeneration at stage
4. Early manifestations of degeneration can only be detected by the

change of FA and ADC indexes on DTI.
1.3. Clinical diagnosis
Patient clinical nerve symptoms help doctors to direct the
diagnosis. Besides, evaluating the area of lesion, clinicians need to
measure the level of losing motion though patient muscle power and
the recovery by mRankin scales.
-Evaluate clinical muscle power by MRC scales 1976
Display from 0-5. 0 point: completely paralytic. 5 points: normal
power.
- Evaluate the patient recovery by mRankin scales.
Prognosis by Rosso (2011): good recovery if mRankin ≤ 2, bad if
6 > mRankin > 3.


5
Chapter 2: SUBJECTS AND RESEARCH METHODS
2.1. Subjects
2.1.1. Places and time
The thesis was performed in the 108 Institute of Clinical Medical
and Pharmaceutical Sciences from 2/1011 to 9/2016.
2.1.2. Subjects
* Selection criteria of patients
- Paralytic patients diagnosed as brain infarct by MRI 3.0 Tesla in
the 108 Institute of Clinical Medical and Pharmaceutical Sciences.
- Patients had one infarct lesion located in pyramidal tract in MRI.
- Patients was treated and had full records in the 108 Institute of
Clinical Medical and Pharmaceutical Sciences
- Non-resident patients were recovered motion function with the
stardard process over 1 year.
* Criteria of Comparation

- Adults with every genders, none paralytic, none clinical symptoms.
- Non-abnormal imagings in MRI.
* Exclusion criteria
- Patients is not available with selection criterias.
- Patiens with relapsed infart in clinical or CT scans.
2.1.3. The sample size
It is calculated by this formula:

n  

2
1 / 2

pq
d 2

With level of confidenceis 99% (Z1-/2= 2,58), precisionis 0,1, the
percentage of the damaged pyramidal tractis 44% according
toresearchAli (2012) with 57,1%. Following this formula, the
sample size in this reseach is:
N = 2,582 x 0,571 x 0,12/0,12 = 45.
2.2. Methods of study
2.2.1. Study design
Prospective studies, cross – sectional descriptive.


6
2.2.2. Means of research
- MRI Achieva 3.0 Tesla Phillips with 16 channel coils and DTI
sequences.

- Software: Extended MR Workspace.
2.2.3. The protocol of MRI examination
- Perform MRI scout viewthrough the head.
- Examination the brain: take the axial slides from the base to the vertex
along to the OM linewith these sequences T1W, T2W, FLAIR, DWI.
- Examination the pyramidal tract with DTI sequences 32 SENSE
(TR: 10172 ms, TE: 93 ms) with EPI technique,the number of
diffuse direction: 32; b: 1000s/mm2 ; matrix: 128 x 128, FOV: 230 x
230 mm; slide thickness 2 mm, voxel size: 1,8 x 1,8 x 2 mm.
- Tranfer data to the workstation.
2.2.4. Protocol of analyzing data and reconstruction imagings
- Build FA 2D color map.
- Reconstruction 3D of the pyramidal tract from FA color map.
2.3. The criteria used in study
2.3.1. General characteristics
- Comparation group:
- Infarction group
2.3.2. DTI of pyramid tract in the comparation group
- Departure of the tract, measurement of the tract in 3D.
- FA, ADC values of total pyramidal tract. FA, ADC values of each
tract: corona radiate, internal capsule, basal ganglia, thalamus, pons.
Corona radiata
Internal capsule
Midbrain
a
b
c

Pons infarct
Medulla oblongata

Hình 2.1. Illutration of brain shows ROIs of the CST for FA,
ADC measurements.
Pons infacrt; a: top, b: center, c: bottom. Source Zhang 2015


7
2.3.3. DT imagings in infarct patients
- Imagings of infarction area: location, median area, median
depth, FA, ADC.
- Imagings 2D, 3D of the pyramid tract on MRI.
- The degree of the damaged of the pyramid tract, relation
between tract lesions and the level of paralytic.
- Relation between the characteristics of diffusion tensor indexs
and the recovery after 1 year.
2.4. Collecting, handlingand analysis data
2.4.1. Collecting techniques
2.4.2. Tools to collect the information
2.4.3. Handling and analysis data
Data is analysed by biomedical statistics method. Analyse data by
software SPSS16.0, Epi 3.5.4, Epicalc 2000.Value p < 0,05 is
statistical significance.
Chapter 3: RESULTS
3.1. Clinical characteristics
- Comparation group
Age and gender: 52 people devided into 26 males and 26
females, the medium age is 41,4 ±15,4. No one is paralytic.
- Infarction group
3.1.1. General information
- Gender

The number of males are 45 people, account for 69,0% and 20
females, account for 31%. Male/female: 2,2.
-Age
The medium age in this research is 63,3±12,9. The minium is 32
years and the maximum one is 92 years. The median age is 65 years.
3.1.2. Clinical symptoms
3.1.2.1. Time admission and time of treatment
The medium time admission since having the first symptom. The
hyperacute is 5,1 ± 2,1 hours. The acute is 17,2 ± 6,4 hours. The
subacute is 83,5 ± 41,4 hours. The chronic is 384 ± 145,9 hours
The medium time of treatment is 17 ± 5,9 days


8
3.1.2.2. The recovery after 1 year
Table 3.3. mRankin scores after 1 year
mRankin scores
0
1
2
3
4
5
6
Total

Number (n)

Percentage %

3
11
17
11
5
3
7
57

5,3
19,3
29,8
19,3
8,8
5,3
12,3
100

3.2. Imagings characteristics in DTI
3.2.1. Pyramid tract DTI in comparation group
3.2.1.1. The size of the tract
Table 3.5. The size of the tract in the both sides
Side
Right
Left
Index
Voxel
818,8 ± 84,6
834,1 ± 82,2
Length (mm)

129,1 ± 11,4
127,8 ± 10,3
Number of fibres
498,9 ± 67,9
496,5 ± 35,8

p
0,35
0,54
0,82

3.2.1.2. DTI indexs of the tract
Table 3.6. FA and ADC in the whole pyramidal tract
Pyramidal tract

Right

Left

p

FA

0,530±0,089

0,512±0,070

0,25

ADC (10-3 mm2/s)

0,839±0,100

0,832±0,101

0,70

Indexs


9
3.2.2. Imagings of the infarct area in MRI
3.2.2.1. Distribution of the artery supplement
Table 3.7. The artery supplement
Number of
Area supplement
(%)
patients (n)
Anteriorcerebral artery
5
7,76
Middle cerebral artery
39
60,0
Posterior cerebral artery
7
10,8
Basilar artery
13
20,0

Vetebral artery
1
1,5
Total
65
100
3.2.2.2. Location of the infacrt
Table 3.8. Location of the infacrt
Number of
Location of the infacrt
(%)
patients (n)
Corona radiata
15
23,1
Internal capsule
5
7,7
Basal ganglia
9
13,8
Infacrtions Thalamus
4
6,2
Midbrain
3
4,6
Pons
13
20

Medulla oblongata
1
1,5
Area supplied by MCA
15
23,1
Total
65
100
3.2.2.3. Medium area of the infacrt
Table 3.9-10. Medium area and depth of the infacrt
Location
Medium
Medium
area (mm2)
depth (mm)
Corona radiata
384,4±319,5
15,6±8,1
Internal capsule
368,9±257,8
25,5±14,5
Basal ganglia
124±100,2
18,2±4,4
Infarction Thalamus
139,5±58,9
17±2,4
Midbrain
138,6±120,2

15±12,5
Pons
181,7±98,7
13,2±3,9
Medulla oblongata
57
10
Area supplied by MCA
2568,1±1513
44,3±17,3
p
0,00
0,00


10
3.2.2.4. Chracteristics of DTI indexs
Table 3.11. Compare the FA and ADC values in the infarction and
the opposite side in the hyperacute and acute stages
Opposite
Infarction
Value
side
p
(n=29)
(n=29)
FA
0,285±0,192
0,529±0,197
0,00

ADC
0,686±0,389
0,783±0,256
0,26
Table 3.12. Compare the FA and ADC values in the infarction and
the opposite side in the subacute stages
Opposite
Infarction(n
Value
side
p
=33)
(n=33)
FA
0,245±0,162
0,526±0,200
0,00
ADC
0,843±0,443
0,745±0,211
0,23
Table 3.13. Compare the FA values in the infarction and the
opposite side
Location
Infarct
Opposite side
p
Corona radiata
0,316±0,237
0,582±0,117

0,00
Internal capsule
0,204±0,183
0,400±0,170
0,03
Basal ganglia
0,262±0,089
0,680±0,239
0,00
Thalamus
0,226±0,111
0,594±0,239
0,03
Midbrain
0,202±0,176
0,620±0,263
0,08
Pons
0,276±0,170
0,523±0,212
0,00
Medulla oblongata
0,199
0,385
Area supplied by MCA
0,246±0,156
0,485±0,231
0,00
3.2.3. Imagings of the tract lesions in DTI.
3.2.3.1. Number of the tract lesions

Table 3.14. Number of the tract lesions
Number of
Pyramidal tract
Percentage (%)
patients (n)
Right

30

46,2

Left

35

53,8

Total

65

100


11
3.2.3.2. Relation between the location of tract and the infarction
Table 3.15. Relation between the location of tract and the
infarction
Involvement

No
(n)

Partial
(n)

Total
(n)

Total
(n)

Location
Corona radiata
1
6
8
15
Internal capsule
5
1
3
9
Basal ganglia
3
0
2
5
Thalamus
4

0
0
4
Midbrain
2
0
1
3
Pons
1
2
10
13
Medulla oblongata
0
0
1
1
5
3
7
15
Area supplied by MCA
Total
21
12
32
65
Table 3.16. Signal of the infarction in the tract showed in FA color
map.

Normal

Low
signal

Empty
signal

Total

2
3
1
2
0
1
0
3
12

5
3
2
2
2
7
1
6
28

8
3
2
0
1
5
0
6
25

15
9
5
4
3
13
1
15
65

Location

Corona radiata
Internal capsule
Basal ganglia
Thalamus
Midbrain
Pons
Medulla oblongata
Area supplied by MCA

Total


12
Table 3.17. Compare the FA and ADC values in the infarction and
the opposite side

Pyramid tract
FA
ADC(10-3 mm2/s)

The
infarction
(n=65)

The opposite
side (n=65)

p

0,491± 0,073
0,846 ± 0,119

0,527 ± 0,046
0,899 ± 0,095

0,00
0,00

Table 3.18. Compare theFA, ADC, voxel ratio and the length of

right pyramidal tract between the infarction group and
comparation group.
Right tract
Infarction
Comparation
group
group
p
(n=30)
(n=52)
Ratio
FA
0,506±0,06
0,530± 0,09
0,28
ADC
0,869±0,11
0,839±0,10
0,21
Voxel
477,1±61,38
818,8 ± 84,6
0,00
Length
118,5±21,7
129,1 ± 11,4
0,00
Number of fibres
121±116,2
498,9 ± 67,9

0,00
Table 3.19. Compare theFA, ADC voxel ratio and the length of left
pyramidal tract between the infarction group and comparation
group.
Left tract
Infarction
Comparation
group
group
p
(n=35)
(n=52)
Tỷ số
FA
ADC
Voxel
Length
Number of fibres

0,476±0,082
0,827±0,127
487,6±282,4
110,6±25,8
99,6±98,5

0,512±0,071
0,832±0,101
834,1 ± 82,2
127,8 ± 10,3
496,5 ± 35,8

0,03
0,83
0,00
0,00
0,00


13
3.2.3.3. Damaged in infarction pyramidal tract segments in the
hyperacute stage
Table 3.20-21. Compare FA, ADC values between infarction
pyramidal tract segments and the opposite side
The opposite
side
(n=9)

p

Values

Location

Infarction
(n=9)

FA

Center
Top

0,525±0,210
0,438±0,181

0,694±0,104
0,512±0,150

0,07
0,39

Bottom

0,478±0,152

0,648±0,210

0,08

Center

0,567±0,111

0,736±0,062

0,00

Top

0,546±0,216

0,850±0,150

0,00

Bottom

0,762±0,180

0,648±0,210

0,26

ADC

3.2.3.4. Damaged in infarction pyramidal tract segments in the acute
stage
Table 3.22-23. Compare FA, ADC values between infarction
pyramidaltract segments and the opposite side
The opposite
Infarction
Location
side
p
Values
(n=20)
(n=20)
FA

ADC

Center

0,488±0,204

0,608±0,176

0,04

Top

0,544±0,153

0,509±0,136

0,43

Bottom

0,556±0,162

0,617±0,172

0,24

Center

0,613±0,202

0,747±0,114

0,01

Top

0,673±0,172

0,785±0,096

0,01

Bottom

0,698±0,176

0,815±0,175

0,03


14
3.2.3.5. Damaged in infacrtion pyramidal tract segments in the
subacute stage
Table 3.24-25.Compare FA, ADC values between infarction
pyramidal tract segments and the opposite side
The
Infarction
opposite
Values
Location
p

(n=33)
side
(n=33)
0,680±0,132 0,00
Center
0,507±0,236
0,585±0,118 0,00
Top
0,445±0,194
FA
0,667±0,176 0,16
Bottom
0,601±0,205
Center
0,620±0,227
0,725±0,212 0,05
Top
0,724±0,214
0,725±0,137 0,98
ADC
Bottom
0,693±0,211
0,736±0,179 0,37
In this research, there were 3 patients in the chronic stage. The
number of patients aren’t enough to perform comparation.
3.2.4. Relation between the tract DTI indexs and the patient’s
motor function after 1 year
Table 3.26. The degree of the tract lesion followingNelles (2008)
Intact
(n)

Partial
disruption
(n)

Complete
disruption
(n)

Total

Corona radiate

2

5

8

15

Internal capsule

3

3

3

9

Basal ganglia

1

2

2

5

Thalamus

2

2

0

4

Midbrain

0

2

1

3

Pons

1

7

5

13

Medulla oblongata

1

0

1

Area supplied by MCA

0
3

6

6

15

Total

12

28

25

65

Statement
Location


15
3.2.4.1. Relation between the degree of the tract damaging and the
patient’s motor function after 1 year
Table 3.27. Relation between the degree of tract damaging and
mRankin score after 1 year
Statement
mRankin score

Intact
(n)

Partial
disruption(n)

Complete
disruption(n)

Total

2
4
3
0
0
0
2
11

0
6
11
5
2
0
1
25

1
1
2
6
4
3
4
21

3
11
16
11
6
3
7
57

0
1
2
3
4
5
6
Total

Table 3.28. Relation between the degree of the tract damaging and
the motor recovery after 1 year
Statement
Recovery

Good
Bad
Total
p

Intact
(n)

Partial
disruption(n)

9
2
11

Complete
disruption(n)

Total

4
17
21

30
27
57

17
8
25
0,005

Table 3.29. Comparing the recovery rate bettween the group intact
tract and disruption tract
Recovery
Good

Bad

Total

Intact

9

2

30

Disruption

21

25

27

Total

30

27

57

Statement

16
3.2.4.2. Relation between some clinical factors, DTI indexs and the
patient motor function after 1 year.
* Relation between some clinical factors and mRankin score after
1 year.
Table 3.30. Relation between some clinical factors and mRankin
score after 1 year.
Correlation
Factor
coefficient
p
Spearman (r)
Arm muscle power at the admission

-0,29

0,01

Arm muscle power at the discharge

-0,24

0,04

Leg muscle power at the admission

-0,31

0,01

Leg muscle power at the discharge

-0,18

0,09

* Relation between some tract damaged factors and mRankin
score after 1 year.
Table 3.32. Relation between some tract damaged factors and
mRankin score after 1 year.
Correlation
Factor
coefficient Spearman
p
(r)
rFA ratio
0,06
0,32
Virtual fibre ratio
-0,15
0,13
Length ratio
-0,39
0,001
Voxel ratio
-0,24
0,03
FA in the center

-0,40
0,001
ADC in the center
0,10
0,23
FA in the bottom
-0,23
0,04
ADC in the bottom
0,10
0,21
FA in the top
0,18
0,09
ADC in the top
-0,02
0,44


17
* Relation between FA, ADC values in the tract damaged segment
in the hyperacute and acute stages and the recovery after one year.
Table 3.33-37.Relation between FA, ADC values in the tract
damaged segment in the hyperacute and acute stages and the
recovery after one year.
Values

FA

ADC

Location

Good
recovery
(n=12)

Bad recovery
(n=14)

p

Center
Bottom
Top
Center
Bottom
Top

0,588±0,232
0,616±0,159
0,603±0,192
0,628±0,205
0,661±0,128
0,672±0,162

0,473±0,220
0,616±0,150
0,556±0,139
0,574±0,244

0,643±0,086
0,626±0,190

0,36
0,99
0,63
0,64
0,78
0,61

* Relation between FA, ADC values in the tract damaged segment
in the subacute stages and the recovery after one year.
Table 3.38-41. Relation between FA, ADC in the tract damaged
segment in the subacute stages and the recovery after one year.

Values

FA

ADC

Center
Bottom
Top
Center
Bottom

Good
recovery
(n=17)

0,538±0,266
0,713±0,135
0,448±0,209
0,564±0,215
0,612±0,182

Top

0,708±0,238

Location

Bad recovery
(n=12)

p

0,484±0,213
0,522±0,228
0,399±0,189
0,736±0,213
0,6165±0,214

0,62
0,01
0,17
0,07
0,96

0,741±0,203

0.69

In the good recovery, FA in the bottom is higher than the center,
it has statistical significance (p=0,01).


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* Prognose the motor recovery after 1 year.
Table 3.44. Multivariateregression logistic in the good recovery
following mRankin score after 1 year
mRS score after 1 year
Statistical
Confidence
significance
interval95% (CI)
(p)
0,75
0,355
4,209

Admission arm muscle power

Odds
Ratio
(OR)
1,223

Discharge arm muscle power

0,592

0,89

0,465

1,946

Admission leg muscle power
FA in the center lesion

1,439
14,284

0,51
0,14

0,481
0,392

4,304
521,136

FA in the bottom lesion

0,871

0,90

0,014

43,348

Lengthratio

5,881

0,005

2,399

14,420

Voxel ratio
Pyramid tract disruption

1,329
1,099

0,69
0,92

0,327
0,138

5,394
8,754

Prognosis factors

According to the multivariate regression model, among these
prognosis factors, the length ratio between the infarction side and the
opposite side is the only factor to evaluate the patient recovery after
1 year with OR=5,881; p<0,01. With the cut-off ≥ 0,86, the length
ratio can predict a good recovery ability after 1 year with the
sensibility Se= 83% and the specific Sp= 60%.
Chapter 4: DISCUSSION
4.1. Clinical characteristics
4.1.1. Infarction group
4.1.1.1. General characteristics
- Gender
Our sample size had 45 males, account for 69,8% and 20 females,
account for 31%. Male/female: 2,2.
4.1.1.2. Clinical symptoms
- Time admission
According to the stage, the soonest time admission is 3 hours in
the hyperacute stage, the latest time in the chronic stage is 480 hours,


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the medium time in the acute stage is 17,2 ± 6,4 hours and is 83,5 ±
41,4 hours in the chronic stage.
- The medium treatment time
Resident treatment time in this research are 17 ± 5,9 days.
- The recovery after 1 year
After 1 year, 57/65 patients were evaluated the mRankin score
again(Table 3.3). Almost patients (31 patients)accounts for 54,4%)
recovered after 1 year with 0 - 2 mRankin scores, the others (19
patients) who had3-6 mRankin scoresaccounted for 45,6%.
4.1.2. Comparation group

This group had 52 adults, the medium age is 41,4 years,
male/female = 1.
Comparation two sides of the tract (Table 3.5-6) about number
ofvoxels, length, virtual line,FA and ADC we haven't seen the differrent
(p>0,05). When analysing DTI indexs (FA, ADC) in the two sides of the
tract, we haven't seen the statistically significant (p>0,05).
4.2. MRI in the infarction area
4.2.1. Distribution according to the cerebral artery supplement.
Infarction in the middle cerebral artery supplement had the highet
figures, with 55,4% (36 patients). Table 3.7 show that, the lowest
percentage of infarct was in the area supplied by anterior choroidal
artery.
4.2.2. Location of infarct
Table 3.8 shows that, most of brain infarct located in
supratentorial with 73,8%.Pons infarction is often seen in the
infratentorial (13/65 patients, with 20%).
4.2.3. The area and depth of the infarction
The biggest medium infarction area supplied by MCA is 2568,1
mm2. The smallest area infarction is in medulla oblongata (57 mm2)
(Table 3.9-10). In our statistics, there is no relation between the
infarction area and the mRankin score after 1 year (r=0,12; p>0,05)
and it is also no relation between the infarction area and the level of
arm paralysed (r = -0,23; p > 0,05).


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In our research, the deapest infarction is located in area supplied
by MCA (44,3 mm) and the most shallow area is in the pons (13,2
mm). Table 3.9-10 shows that it has statistically significant (p<0,01,
F=10,5) in the infarction depth.

4.2.4. DTI indexs in the infarction
According to some authors Benedictus (2010), Jang (2010),Nael
(2015)and Werring (2000), in all stages in infarction, FA decreased
in the center. It shows thatFA in the hyperacute, acute and subacute
stageis significant lower than the opposite side (p<0,01) (Table 3.1112). Table 3.13 compares some pyramid tract segments,FA goes down
significantly than the opposite side (FA Infarction 0,2 - 0,3; The
opposite side 0,4 - 0,7), it has statistically significant with p<0,05. Our
research is the same with Sikio (2015), FA decreases in the infarction
than the opposite sideand the research of Werring (2000).
4.3. DT imagings of the tract lesion in ischemic stroke patients
4.3.1. Infarctside
The left pyramid tract has more damaged than the right
side,however it hasn't statistically significant (Table 3.14).
4.3.2. Relation between the pyramidal tract and the infarction area
In our research, the infarction area takes whole perimeter of the
tract in over a half of total patients (32/65). In this cases, infarction in
pons is the most popular with 10/32 patients (31,3%), the second
most popular is in corona radiate (25%) (Table 3.15).
4.3.3. The expression of the damaged pyramidal tract in the
FAcolor map
Table 3.16 shows some types of signal changes in pyramidal tract
in FA color map.None signal change is account for38,5%. Low
signal is the most popular with 43,1%, In most of cases, FA in the
infarct side is lower than the opposite side. In our research (Table
3.17), FA ininfarction area (0,491 ± 0,073) is lower than the opposite
side (0,527 ±0,046) (p<0,001). When comparing aboutlength,
voxelandnumber of fibresof infarction group withcomparation group,
these indexs is lower, it has statistically significantwith p<0,01
(Table 3.18-19), it means when the tract got infarction, it got smaller
than normal.

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4.3.4. Characteristics of pyramidal tract lesion according to
infarction stage
4.3.4.1. The hyperacute stage
In the hyperacute stage, in the damaged segment, FA decreases in
the top, middle and bottom of the infarction, but it hasn't statistically
significant (Table 3.20). In contrast, ADC values has astatistically
significantdecrease in the center and top of the segment comparing to
the opposite (p<0,001) (Table 3.21).
4.3.4.2. The acute stage
In the acute stage, FA and ADC values decrease. In our research,
FA value in the center is lower than the opposite, it has statistically
significant (p=0,04) (Table 3.22).Table 3.23 shows that ADC in the
top, bottom and center of the infarction has a significant
decreasethan the opposite sidewith p<0,05.
4.3.4.3. The subacute stage
According to the theory, in this stage, FA and ADC values
decrease.Table 3.24 shows that, FA value decreases in the along side
comparing to the opposite side, but it is significant decrease in the
center and the top (p<0,01). Intable 3.25, ADC value in the center is
lower than the opposite (p=0,05).
4.3.4.4. The chronic stage
There are only 3 patients in this group so we haven’t taken the
comparation.
4.4. The relation between DTI indexs and the patients motor
function
4.4.1. The level of damaging in the tract
According toNelles classification (2008), the tract lesionsare

divided into 3 levels in 3D imagings: intact, partial fiber
disruption, complete fiber disruption.In our research, thepartial
fiber disruption is the most frequently with 43%. Thecomplete
fiber disruption accounts for 38,5% (Table 3.26). The percentage
of thepartial fiber disruptionandcomplete fiber disruption in our
research is lower than these figures reported by Nakashima and
higher than these figures reported by Nelles and Ali.


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4.4.2. Relation between the damaged level of the tract and the
patient recovery after 1 year
Table 3.27-29comparing the percentage of 2 groups (no
disruption and disruption)we have seen that the percentage of the
recovery in no disruption group has 5,3 times higher than the figures
in the disruption group (OR:5,3; 95% CI:1,0-27,6; p<0,005). It
means there is a high relation between the damaged level of the tract
and the patients recovery after 1 year (p<0,05).
4.4.3. The relation between some clinical factors and DTI indexs
with the recovery of infarct patients after 1 year
4.4.3.1. The relation between some clinical factors and the infarction
patients mRankin scores after 1 year
According to the relation between some clinical factors and the
mRankin scores after 1 year (Table 3.30) we see 3 points: the arm
and leg muscle power at the admission and the arm muscle power at
the dischargehad a medium inverse correlation (r = -0,30) with
mRankin scores after 1 year (p<0,05).
4.4.3.2. The relation between some DTI indexs in the infarction area
andthe mRankin scores after 1 year
Intable 3.31we couldn’t see that the correlation between the area,

depth of the infarction with mRankin scores after 1 year and it is the
same with FA and ADC (p>0,01).
4.4.3.3. Relation between some damaged factors of the tract with the
mRankin scores after 1 year
Intable 3.32we can see a medium inverse correlation (r= -0,4)
between the length ratio, FA values in the center and the mRankin
scores after 1 year (p<0,01). Comparing the length ratio between 2
groups (good and bad recovery) by calculatingarea in ROCcurve
(AUC: 0,791, p<0,01) with the cut off values ≥ 0,86 it is seen that the
length ratio is usefull to prognose the good recovery after 1 year with
the sensitivity 83%, the specific 60%. FA in the center of the
infarctedsegments had AUC: 0,718, p<0,01. With the cut off point
FA ≥ 0,41 the FA recovery prognosis value in the center of
segmenthad the sensitivity of 87% and the specific of 63%.


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4.4.3.4. The relation between FA, ADC values in the infarctedsegments
in the hyperacute and acute stages and the patient recovery after 1 year
Table 3.33-3.37 FA and ADC values in the center, top and bottom
of the infarctedsegments in the good group is not different with the
bad one (p>0,05). Comparing FA and ADC values at the bottom and
center of the infarctedsegmentit can be seen that there has no
statistically significant different in the same group (p>0,05).
4.4.3.5. The relation between FA, ADC values in the infarcted segments
in the subacute stages and the patient recovery after 1 year
In the subacute stage (Table 3.38-41)shows that, in the subacute stage,
FA in the bottom of the infarcted segment in the good recovery group is
significantly higher than the bad one (FA values in the good group: 0,71 ±
0,14, FA values in the bad group: 0,52 ± 0,23, p<0,01), FA value in the

bottom of the infarcted segment rises higher than this figures in the center
(FA in the bottom 0,71 ± 0,14, FA in the center 0,54 ± 0,27,
p<0,05).Rising FA values means good recovery.Using the calculating
area in ROC curve method, it can be seen that FA value at the bottom of
the infarcted segment has the predicting value to the area below AUC
curve = 0,713 (p<0,05). With the cut off point FA ≥ 0,532, the predicting
sign has the sensitivity of Se=88%, the specific of Sp=59%.
4.4.3.6. Prognosis of the infarction patients
Analysing the clinical factors, the degree of the damaged tract and
some DTI indexs involved with the patient recovery after 1 year by
multiple regression logistic (Table 3.44) it can be seen that the length
ratio (infarction/the opposite side) is an independent factor to
prognose the patient recovery with OR=5,881; 95%CI 2,39 – 14,42;
p < 0,01.With the cut off pointof the pyramid tract length ≥ 0,86with
the sensitivity of 83% and the specific of 60%.
CONCLUSION
After one year researched of 65 infarction patients in other stages
by DTI, we have some summaries:
1. Imaging characteristics of pyramidal tract in the DTI
In the infarct, the left pyramidal tract got more often
damaged(53,8%). The lacunar infarct with complete disruption of the
tract dominates with 49,2%.