Tohoku

J. Exp.

Med.,

1990, 161, Suppl.,

Occipital

Lobe

Emission

Tomography

139-153

Infarction

and

Positron

KOICHI TAGAWA,Ken NAGATAand FUMIO SHISHIDO*
Division of Neurology and* Radiology Research institute for
Brain and Blood Vessels, Akita 010

TAGAWA,
K., NAGATA,K. and SHISHIDO,F. Occipital Lobe Infarction and
Positron Emission Tomography. Tohoku J. Exp. Med., 1990, 161, Suppl., 139-153
Even though the PET study revealed a total infarct in the territory of the left
PCA in our 3 cases of pure alesia, it is still obscure which part of the left occipital
lobe is most closely associated with the occurence of the pure alexia. In order to
elucidate the intralobar localization of the pure alexia, it is needed to have an ideal
case who shows an pure alexia due to the localized lesion within the left occipital
lobe. Furthermore, high-resolution PET scanner will circumvent the problem in
detecting the metabolism and blood flow in the corpus callosum which plays an
important role in the pathogenesis. We have shown that the occlusion of the right
PCA also produced a left unilateral agnosia which is one of the common neurological signs in the right MCA infarction. To tell whether the responsible lesion
for the unilateral spatial agnosia differs between the PCA occlusion and the MCA
occlusion, the correlation study should be carried out in a greater number of the
subjects. Two distinctive neuropsychological manifestations, cerebral color blidness and prosopagnosia, have been considered to be produced by the bilateral
occipital lesion. The PET studies disclosed reduction of blood flow and oxygen
metabolism in both occipital lobes in our particular patient who exibited cerebral
color blindness and posopagnosia.
posterior cerebral artery occlusion;
positron emission CT; pure alexia; visual and visuo-spatial agnosia

Lesions in the occipital lobe are known to cause the particular neuropsychological features in addition to the visual field defects. The dominant hemisphere lesion causes a pure alexia and color agnosia, whereas the bilateral involvement causes prosopagnosia, cerebral color blindness and/or object agnosia. The
lesion in the non-dominant occipital lobe often causes a unilateral spatial agnosia.
The occipital lobe is supplied by the posterior cerebral artery. By means of
quantitative measurements of cerebral blood flow and metabolism utilizing the
positron emission tomography (PET), the present study was endeavored to elucidate the pathophysiological mechanisms underlying the neuropsychological features due to the occlusion of the posterior cerebral artery.

Preseit
address and reprint requests to: Koichi
Fukuoka-higashi
Hospital,
1612 Kubo, Koga-machi,
139

Tagawa,
The Stroke Center, National
Kasuya-gun,
Fukuoka
811-31, Japan.

140

K. Tagawa

SUBJECTS
The

study

included

ages

ranged

between

57

occluded

in

4 patients,

the

right

Three

out

of

4

patients

with

the

right

PCA

occlusion

One

of

was

PCAs

were

occluded

PCA

showed

a pure

neglect

both

PCAs
The

bral

blood

ing

as

PET

method.

to

the

(CBF),

oxygen
alexia.

In

a pure

alexia

(alexic

in

spite

Five

patients

of
with

artery

(MCA)

region.

Their

mean

analyze

group)

were

as a control

group

included

studies
in

Fig.

1,

3 slices

at

42.5,

50.0

and

57.5mm

respectively.

We

may

call

respectively.

The

regional

the

mean

value

and

mean

spatial

the

was
cerebral

regions

in

the

were

regional

exhibited

a left

was

established

for

the

unilateral

with

those

occlusion

of

obtained
the

Prosopagnosia

and

demonstrated

by

color

blindness.

the

the

pixels

the

left

occlusion

of

1978).
oxygen-15
this

steady

system:

cerebral

cere-

blood

volume

for

the

plane

data

upper
by

(rCBF)
by

1985).

the

the

left

middle
occipital

measured

for

left

occipital

lobe.

The

of

the

the

of

the
pixel

onset).
in

print-out

the

regional

al.

were

established

parts

averaging

in

were

averaging
and

of

1 month

on

a pure

et

values
the

than

exhibit-

exhibit

arteries

PET

in

(later

and

not

group)(Tagawa

(18•~30mm)

calculated

3 patients

did

perforating

orbitomeatal

middle

alexia,

regional

stage

regional

PET

spatial

agnosia

right

posterior

agnosia"

on

from

middle

),

the

PET

left

As
each

occipital

data

at

lobe,
each

ROI

CMRO2,(rCMRO2).
the

3 regional

of

images,

The
values;

mean

(mCMRO2).

unilateral
at

the

the

who

(ROIs)

calculated

The

spatial

135

CBF

was

CMRO2,

interest

the

a lower,

lobe

with

by

pure

(non-alexic

of

chronic

above
as

PCA

the

Quantitative

of

agnosia.

ROI

compared

the

slices;

(mCBF)

who

years.

values

Unilateral

lesion

to

PET

57.6

consisting

occipital

patient

for

ROIs

the

CBF

The

performed

3 different

2 patients

of

shown

the

for

with

territory

placing

of

both

a unlilateral

(Tagawa

(CMRO2

data

the

PET

were

PET

compared

in

and

occlusion

to

The

and

displayed

provided

artery

years.

(OEF).
the

infarct

was

the

according

oxygen

left

were

by

of

66.6

1 patient,

patients

were

the

age

two

cerebral

was
in

blindness
III

of

CBF

on

CMRO2

rate

posterior
age

occluded

the

color

the

mean

was

occlusion
an

cerebral

to

PCA

parameters

metabolic

of
the

HEADTOME

fraction

order

an

the

occlusion

years;

cerebral

circulatory

extraction

Pure

alexia

with

cerebral

73

field.
and

different

an

and

with

visual

out

with

patient

right

carried

Four

and

A

a prosopagnosia

was

flow

2 patients.

alexia.

showed

state

(CBV)

in

7 patients

METHODS

Their
PCA

spatial

and

present

(PCA).
left

et al.

the

cerebral

artery

cerebral

color

blindness.

PET

studies

in

were

due

parietal
the

patients

data

to

analyzed
the

lobe

quantitatively

occlusion
which

print-out

PET

exhibiting

a unilateral

of
is

right

called

images.

The
spatial

in

the

"a

PCA.
classical

results

were

agnosia

due

(MCA).

a

The
patients

distribution
who

exhibited

of

the
a

ischemic

lesions

prosopagnosia

and

Fig. 1. Location of the regions of interest (ROIs) on the print-out PET data.
The mean of the ROI values from the 3 slices served the occipital regional
values.

a

Occipital

Lobe

Infarction

and PET

141

RESULTS AND DISCUSSION
Pure

alexia
Table

izes

1 shows

the

PET

occipital
The

the

data

mCBF
left

mCMRO2

mCBF

mCBF

mCBF

and

alexic

group

was

ml/min)
and

than
were

were

significance

in

of

in

40.8•}3.6

and

was

for

found

among

the

the

left

alexic

group
3.17•}0.58

3.00•}0.15

the

rCBF

In

and

were

<0.01).

in

the

the

control

groups.

the

control

group,

left
Both

lower

occipital

in

the

mCBF

alexic

group,

control

group,

respectively.

or

mCMRO2

between

in

the

part
of

mCBF

was
the

respectively.

right

left

mCMRO2

significantly

The

the

occipital

the

2 summer-

between
and

and

3.10•}0.18,

lobe

in

Table

nonalexic

group.

(p

group.

relationship

ml/min)

43.0•}3.5

and

right

alexic
the

alexic,

occipital

the

the

(ml/100

control

36.0•}9.0

in

2 illustrates

were,

the

the

rCMRO2
Fig.

18.4•}2.2

mCMRO2

mCMRO2

mCMRO2
they

and

(ml/100

occipital

and

3 groups.

occipital

1.68•}0.11

rCBF

in

and

respectively,

while
No
the

two

of

the

left

the

middle

group.
In

the

occipital

lobe

part

were

41.6•}

6.2

for

the

or

group,

the

16.6•}3.4

38.1•}4.4

42.6•}2.7

and

lobe.

rCBF

1.77•}0.51,

and

the
rCMRO2

1.49•}0.25,

and

respectively.

Relationship

Both

CBF

without
occlusion

The

and

pure

was

no

the

regional
were

alexia. •œ,

without

pure

left
alexia; •¡,

predirection

for

the

the

control
of

the

the

middle
part

were

the

upper

rCMRO2

of

the

CMRO2

in

CBF

and
in

those

occlusion
control

with
with

left

basal

group.
left

of

In

the

the

alexic

occipital

lobe

were

part

18.8•}1.6

were,

19.7•}7.0

and

of

right

part

the

left

occpital

lobe.

alexia

than

those

a lexia; •›,
ganglia

were

obtained

lower

pure
pure

part

were

distribution

of

of

upper

data

part

lower
PCA

the

lower

and

between

of

regional

in

those

CMRO2

those

similar

Those

rCBF

Those

lobe

respectively.

respectively,

2.

in

and

The

occipital

lower

respectively.

respectively

There

within

rCMRO2

2.82•}0.26,

respectively.

occipital

rCMRO2

1.79•}0.21,

and

and

3.08•}0.34,

3.10•}0.38,

and

Fig.

group,

were

and

right

rCBF

and

control

infarction.

left

the

PCA

142

K. Tagawa

et al.

Occipital
occipital

lobe

part

were

were

35.5•}9.8

36.9•}8.1

and

One
the

of
left

group

the

rCBF

or rCMRO2

two

patients

who

those

their

of

the

a visual
the

field

x-ray

left

CT

temporal

as

showed

that

the

with

mCMRO2

of

the

left

alexia,
occipital

there

They

51.1%

and

53.0%

of

of

the

group,
lobe

and

54.2%
tendency

was

extracted

or

rCMRO2

within

the

One

either

of

the

occlusion
those
as

of
high

to

the

left

the

two

patients

showed

his

the

control

as

The

within

those
pure

mCBF

and

group.

The

which

the

ability
the

by

the

left

occlusion

of

the

left

cause

the

pure

with

occlusion

of

lesion

and

the

ischemic

an

important

role

results

of

the

aspects

of

blood

were

markedly

with

those

group
that

a

in

generally

thought
of

Therefore,
The

alexia.
left

PCA

the

development

genesis

of

study

with

and

metabolism,

reduced

in

the

left

normal

reading

in

including

those

with

complete

occlusion

has

with

the
of

may

produce

a

been

accepted

that

is

the
the

spite

is

the

As

mCBF

and

mCMRO2

the

alexic

PCA

group

and

mCMRO2

disturbed

relative

the

lesions

in

areas
seen

present

or

upon

the

et

al.

with

the
not
in

1978).

play
In

which

blood

flow

and

oxygen

metabolism

the

alexic

group

as

the

in
PCA

ganglionic

left

PCA

severe

form

of

pure

the

lesion

of

the

occlusion
small

at

provided

its

or

with

the

quantitative

with

infarcts.

origin

the

extension
may

studies

lobe

the
were

does
not

circulation

(Tagawa

group.
the

however,

depend

or

and

frequently

is

rCBF

of

which

alexia

alexia

the

control

spite

by

PCA,

to

of

side.

distribution

mCBF

left

collateral

occpital

of

caused

of

PET

and

other

and

in

severely

considered

pure

the

mCBF

the

of

callosum,

the

the

part

in

of

the

be

pure

both

basal
the

the

both
of

with

alexia

of

lower

studies

mCBF

those

to

the

decrease

alexia

was

pure

Whether

the

the

the

in

intra-lobar

pure

corpus

occlusion

this

respectively.

showed

the

did

In

distribution

ability

splenium

PCA.

present

reading

flow

circulation
It

PCA.

patient

right

group.

respectively.

compared
a

a

lobe,

occipital

as

alexic

control

the

between

other

in

and

or
exhibit

mCMRO2

alexia

irrigated

of

not

the

the

only

of

severe

group,

occlusion

of

who

those

group;

intra-lobar

group,

did

a

study.

the

patient

PET

occipital

control
from

group.

lobe

alexic

alexic

control

writing

was

the

the

the

intact

patient

of

alexic

who

there
in

in

occipital

always

those

right

the

other

the

those

control

rCMRO2

by

with

occipital

specific

derived

were
for

territory.

reduction

left

rCBF

data

middle

part

this
of

localized

PCA

compared

the

No

was
left

significant

the

the

area
the

the

a

with

of

in

as

of

of

those

within

in

spite
those

the

was

mCMRO2
42.8%

as

upper

exhibited
in

the

tendency

between

lobe

compared

were

in

of

the

lobe

alexia

patient

infarct

was

of

specific

occipital

mCMRO2

high

quantitative

patients

were

pure

which

those

an

This
and

Those

no

mCMRO2

group.
mCBF

were

the

the

display

and

defect

lobe

Summarizing

not

mCBF

The

and
was

within

control

hemianopsia.

have

the

showed

respectively.

There

did

143

and PET

respectively,

of

and

patient,
of

3.21•}0.61,

the
PCA

Infarction

3.12•}0.72,

respectively.

homonyous
not

and

and

3.17•}0.51,

distribution

of

35.8•}10.0

Lobe

compared
the

control

This

indicates

a

poor

collateral

in

addition

alexia.
callosal

splenium

to

the

K. Tagawa

144

et al.

lesion of the inferior medial aspect of the left occipital lobe causes a pure alexia.
Based on the pathological findings of 17 cases who exhibited this syndrome,
Benson and Geschwind (1969) reported that, in addition to the callosal lesions, the
occipital lesions located at the left lingual gyrus and/or the left fusiform gyrus
with an expansion to the left cuneus and the left calcarine cortex by a various
degree. Although they did not asserted that the callosal lesion was indespensable
for the ocurrence of the pure alexia, they concluded that there had been so far no
other reported lesion than the left occipital lobe lesion and the callosal splenium
that could cause a pure alexia. Greenblatt (1983) confirmed the same lesions
responsible for the pure alexia in 10 autopsied cases. Recently, on the other
hand, Greenblatt (1976) reported that subcortical lesions adjacent to the left
angular gyrus caused a pure alexia. There is still a controversy about the
responsible lesion for the pure alexia. It should be clarified with new diagnostic
devices whether a even localized lesion can produce a severe form of pure alexia
or extensive lesion can only cause a severe form of this syndrome. However, the
results of the PET studies could not bring a conclusion to this question because
the detection of the blood flow or metabolism in the corpus callosum was still
beyond of the resolution of PET studies. Until now it is difficult to detect the
regional values of CBF or CMRO2,in the lingual gyrus or in the fusiform gyrus by
the present precedure. It is needed to elucidate the intra-lobar localization with
the PET studies in respect to the severity of pure alexia by accumulating of the

Fig. 3.

CT findings

is shown

of a patient

in the territory

with

pure alexia.

of the left

PCA.

An extensive

low density

area

Occipital

Lobe

Infarction

and PET

Fig. 4. PET findings of a patient with pure alexia.
CBF images (a); CMRO2
images (b). Corresponding to the CT lesion, both CBF and CMRO2 were
reduced markedly in the territory of the left PCA.

145

146

K. Tagawa

et al

cases and improving of in ROI setting.
Illustrative case report. A 67-year-old right-handed man noticed a numbness
in his right hand on March 3, 1982. There had been a progression in his neurological deficits and he became right hemiparetic with a right hemihypesthesia in
a week. Then he complained of difficulty in seeing thing on his right side. He
was hospitalized on March 18. On admission, he exhibited a right homonymous
hemianopsia and a mild right hemiparesis with a right hemihypesthesia accompanied by a paresthesia. He also showed a severe impairment in reading, a
mild sensory aphasia and color naming difficulty. Vertebral angiography
revealed an occlusion of the left PCA at the crural segment. The x-ray CT
showed a extensive low density area in the territory of the left PCA. After
admission, he showed a rapid improvement in the aphasia and the motor and
sensory disturbance.
The neuropsychological evaluation performed after the
recovery from the aphasia disclosed a severe form of pure alexia and a color
agnosia. The reading was severely impaired for both Kanji and Kana at the level
of letter, word and sentence and he was unable to carry out practical reading.
Although his spontaneous writing or dictation were normal, the copying was

Fig. 5. PET findings of a patient exhibiting a left unilateral spatial agnosia due
to the infarct in the territoy of the right MCA. CBF images (top), CMRO2
(middle) and OEF images (bottom). Both CBF and CMRO2,were reduced at
the junctional area among the temporal, parietal and occipital lobes on the
right hemisphere.

Occipital

Lobe

Infarction

and PET

147

severely impaired. There was no significant effects from the motor facilitation in
reading (kinesthetic reading). The color naming difficulty disappeared within 3
months of onset. There was no change in the right homonymous hemianopsia
throughout. His neuropsychological features has been followed for 4 years but
the practical reading had not improved yet and he still exhibited a severe pure
alexia. The PET studies performed 21 months after the onset disclosed a reduction of CBF and CMRO2 in the territory of the left PCA, which corresponded to
the lesion on the x-ray CT (Figs. 3, 4).
Left unilateral spatial agnosia

Fig. 5 shows the PET findings in a patient with left unilateral spatial agnosia
due to the infarct in the right MCA territoy. There was a reduction of CBF and
CMRO2at the junctional area among the temporal, parietal and occipital lobes on
the right hemisphere, which is known to be the classical lesion responsible for the
left unilateral spatial agnosia. Fig. 6 shows a distribution of rCBF and rCMRO2
measured at the posterior part of the right parietal lobe in 16 occasions in 11
patients with left unilateral spatial agnosia (Tagawa et al. 1986). When they
were compared with those without left unilateral agnosia, the distribution of the
two groups overlapped between 25 and 35 ml/100 ml/min for rCBF, and between
1.8 and 2.2 ml/100 ml/min for rCMRO2. The values around these levels were
considered to be the threshold for the ocurrence of the left unilateral spatial

Fig.

6.

Relationship

the

right

unilateral
two

between

regional

parietal

lobe.

Both

spatial

agnosia

than

patient

groups

between

1.8

spatial

agnosia.

and

coexisted
2.2

ml/100

CBF

and

CBF

and

in

the

CMRO2

CMRO2

in
were

control

group.

between

25

and

35

ml/min

for

CMRO2. •›,

ml/100

The

the

posteior

lower

in

part
those

distribution

ml/min
control: •œ,

for

of
with

of
CBF,
unilateral

the
and

K. Tagawa

148

et al.

agnosia. Since the CBF values may vary according to the stage of cerebral
infarction because of the luxury perfusion phenomenon, the CMRO2 that is stable
in the course of cerebral infarction can be the reliable indicator for brain function.
The CMRO2, below 2.0 ml/100 ml/min is considered to cause a left unilateral
spatial agnosia. These results were compared with the PET findings in a patient
who exhibited a left unilateral spatial agnosia due to the occlusion of the right
PCA in respect to the pathogenetic mechanism of the left unilateral spatial
agnosia.
Illustrative case report. A 61 year-old rigth-handed man became unable to
return to his bedroom when he went to the restroom on October 4, 1983. He was
hospitalized on Octchober 7. On admission, the neurological examination
revealed a left homonymous hemianopsia, a topographical disorientation and a
left unilateral spatial agnosia The vertebral angiography disclosed an occlusion
of the right PCA at the ambient segment. Extensive infarct was seen at the right
occipital lobe on x-ray CT (Fig. 7). The PET studies performed 13 days after
onset showed a marked reduction of both CBF and CMRO2,is the territory of the
right PCA (Fig. 8). At the junctional area among the temporal, parietal and
occipital lobes on the right hemisphere, the rCBF was 31.3 ml/100ml/min, which
was included in the threshold range for the occurrence of the unilateral spatial
agnosia, whereas the rCMRO2 was 2.61 ml/100 ml/min, which was above the

Fig. 7.

CT findings

occlusion

of the

occipital

lobe.

of a patient
right

PCA.

with

a left unilateral

An extensive

spatial

infarct

was

agnosia
seen

due to the
in

the

right

Occipital

Lobe

Infarction

and PET

Fig. 8. PET findings in a patient with a left unilateral spatial agnosia due to the
occlusion of the right PCA. CBF images (a); CMRO2 imges (b). Both
CBF and CMRO2 were markedly reduced in the territory of the right PCA .

149

150

threshold

K. Tagawa

et al.

level.

The responsible lesion for left unilateral spatial agnosia has been believed to
be located at the junctional area among the temporal, parietal and occipital lobes
or the area between the parietal and occipital lobes on the right hemisphere (Brain
and Domasio 1941; Paterson and Zangwill 1944). Since these areas are included
in the right MCA territory, those patients who has an infarct is the territory of the
right MCA frequently develope a left unilateral agnosia. In addition, a subcortical hemorrhage at the junctional area also may causative of the left unilateral
spatial agnosia and even a right putaminal hemorrhage which has an effects on the
junctional area also causes a left unilateral spatial agnosia. Furthermore, a right
frontal lobe lesion, an occlusion of the rigth PCA, a right thalamic hemorrhage
and an occlusion of the right anterior choroidal artery were reportedly causative
for the left unilateral spatial agnosia.
We previously reported a patient who displayed a left unilateral spatial
agnosia due to the occlusion of the right PCA (Tagawa et al. 1978). The single
photon emission CT (SPECT) was carried out on another patient with reference
to the pathogenetic mechanism of the left unilateral spatial agnosia in the right
PCA occlusion (Tagawa et al. 1982). Although the junctional area among the
temporal, parietal and occipital lobe is in general considered to belong to the
territory of the posterior branch of the MCA, this area can be also regarded as a
border zone between the MCA territory and the PCA territory. Even if the MCA
was occluded, the junctional area can be preserved and the left unilateral spatial
agnosia does not occur when the collateral blood flow is sufficient from the PCA.
In those with left unilateral spatial agnosia due to the occlusion of the right MCA,
an occlusion of the MCA is the crucial factor in causing the left unilateral spatial
agnosia but the poor collateral circulation from the PCA can be also the important
factor from the hemodynamic point of view. In case with an occlusion of the
PCA, the area supplyed by the cortical branch can be preserved when the
collateral blood flow is sufficient from the MCA. There is a possibility that the
junctional area between the MCA and PCA became ischemic in a case with an
occlusion of the PCA when the collateral blood flow is poor from the MCA. The
SPECT study revealed an ischemic lesion at the border zone area between the
right MCA and the right PCA territory in the patient who showed a left unilateral
patial agnosia with an occlusion of the right PCA. If it can be substantiated that
an infarct occurrs at the junctional area among the temporal, parietal and occipital lobes when the collateral blood flow is poor from the MCA in a case with
an occlusion of the PCA, the classical lesion may account for the left unilateral
spatial agnosia in a patient with an occlusion of the right PCA. In the prenent
results with PET studies, however, the rCBF decreased as the threshold level
whereas the rCMRO2 was still preserved above the threshold level at the junctional area among the right temporal, parietal and occipital lobes. The left
unilateral spatial agnosia due to the occlusion of the right PCA may differ from

Occipital

Lobe

Infarction

and PET

151

that due to the right MCA occlusion in the deeper lesion involving the connecting
fibers. The reduction of CBF at the classical region might participate at least in
the genesis of the left unilateral spatial agnosia in our patient.
Further systematic study is needed with a larger number of the subjects to elucidate the
pathophysiological differences of the left unilateral spatial agnosia between the
right PCA and the right MCA.
Cerebral

color

blindness

and

prosopagnosia

Illustrative case report. A 67-year-old ambidextrous man complained of
difficulty in recognizing the faces of the familiar person and he often lost his way
to his home when he went out in April, 1983. He complained of a visual
disturbance and he was hospitalized on July 4, 1983. On admission , close examination disclosed a concentric restriction of the whole visual field and his visual
acuity was mildly decreased in both fields. He exhibited a severe memory
disturbance, prosopagnosia, color blindness and topographical disorientation .
Color naming, color sorting and color matching were severely impaired. He also
showed difficulties in coloring of outline drawings. lshihara screening test and
hue discrimination were severely abnormal. The cerebral angiography revealed a
complete occlusion of the right PCF and the left PCA territory was poorly
visualized. There were low density areas in both occipital lobes on CT (Fig . 9).

Fig. 9.
CT findings of a patients
with cerebral color blindness
and prosopagnosia
due to the infarction
of both
PCA territories.
Low density
areas were
demonstrated

in both

occipital

lobes.

152

Fig. 10.

PET

findings

of

a

K. Tagawa

et al.

patients

with

cerebral

color

blindness

and

prosopagnosia.
CBF images (top), CMRO2 images (middle) and OEF images
(bottom).
Reduction of CBF and CMRO2 was marked in both PCA territories.

The PET was performed

9 day after onset.

Both CBF ane CMRO2 were marked-

ly reduced in both PCA territories corresponding
to the CT lesions (Fig. 10).
It has been speculated based on the clinicopathological
investigations
that
the bilateral occipital lesion is responsible for the prosopagnosia and cerebral
blindness
(Damasio and Damasio
1983). In this case, color blindness
prosopagnosia are considered
PCA territories.

to be related

to the severe ischemic

damage

color
and

in both

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