Neurological Research
A Journal of Progress in Neurosurgery, Neurology and Neurosciences

ISSN: 0161-6412 (Print) 1743-1328 (Online) Journal homepage: https://www.tandfonline.com/loi/yner20

Bilateral common carotid artery occlusion with
minimal neurological deficit: Long term follow up
in 3 patients
Vera Zbornikova, Sissel Vorstrup & Erik Ryding
To cite this article: Vera Zbornikova, Sissel Vorstrup & Erik Ryding (1996) Bilateral common
carotid artery occlusion with minimal neurological deficit: Long term follow up in 3 patients,
Neurological Research, 18:2, 109-116, DOI: 10.1080/01616412.1996.11740388
To link to this article: https://doi.org/10.1080/01616412.1996.11740388

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Bilateral common carotid artery occlusion with
minimal neurological deficit: Long term follow
up in 3 patients
Vera Zbornikova, Sissel Vorstrup and Erik Ryding
Departments of Neurology University Hospital, Linkoping, Sweden and Rigshospitalet Copenhagen and Department of
Clinical Neurophysiology, University Hospital, Lund

Three patients, two women and one man, aged 56-70 year (mean 59 years) with modest
neurological deficits and bilateral occlusion of the common carotid arteries initially identified by
duplex scanning and angiography, were followed by repeated clinical and transcranial Doppler
examination (TCD) over 6.5 years. Vasomotor reactivity (VMR) was tested by combined
examination of TCD and xenon-133 cerebral blood flow (CBF) before and after intravenous
administration of 1 g acetazolamide. At follow-up CBF was measured using single photon
emission computerised tomography (SPECT). In two patients mean velocities in the middle
cerebral artery (MCA) were within the normal range at repetitive examinations with good VMR
rangin.f 30-111%, whereas CBF was reduced in MCA territories ranging 29-36 ml 100 g- 7
min- , but increasing 44- 69% after acetazolamide, indicating good VMR. These 2 cases had
anterograde flow in the ophthalmic artery and siphon. The third patient had very low MCA mean
velocities of 21-27 em sec- 1, increasing 26-33% after acetazolamide. This patient had
retrograde flow in the ophthalmic artery and siphon connected with bilateral prolonged
episodes of amaurosis fugax and transient ischemic attacks. In all three patients the posterior
cerebral arteries were major supplying co/laterals having high mean velocities of about
100 em sec~ 7 and high velocities in the bfisilar arteries of 85 em ~ec- 7 as well. During followup no patient had a new stroke, but all experienced orthostatic dizziness and chronic fatigue.
[Neural Res 1996, 18: 109- 1i 6]

Keywbfds: Common carotid artery; transcranial Doppler; cerebral blood flow

INTRODUCTION
Occlusion of the common carotid artery (CCA) is very
rare and obstruction of both CCA was previously
considered to be incompatible with normal life. However, if the external carotid .artery (ECA) ads as a
collateral to the internal carotid artery (ICA),the flow in
the ICA can be maintained in normal direction 1--4.
A reduction of regiol')al perfusion pr12ssure with
depressed vasomotor reactivi~ (VMR) · may follow
e disease ; We _have previously
extracranial obstructiv_
described the hemodynamic extracranial and intracranial features as estimated by duplex _scanning -· and
transcranial Doppler (TCD) in 18 patientswithunilater al
and 3 patients with bilateral CCA ocdusion 6 , ,Cerebral
blood flow (CBF) andTCD examinations including a test
of (VMR) was ·later performed in 12 of these patients 7 .
In this study we report the clinical course and the
Correspondence and reprint requests to: Vera Zbornikova, MD, PhD,
Department of Neurology, University of Health Science, S-581 85
Linkoping; Sweden. Accepted for publication October 1995.
© 1996 Forefront Publishing Group
0161-6412/96/020109-08

hemodynamic consequences including assessment of
VMR by repeated ultrasonic examination of extracranial
and intracranial vessels and CBF in 3 patients with
bilateral CCA occlusion .

PATIENTS
Three patients, 2 women and one ma:n, aged 56-70
(mean 59 years) . with long~standing qilateral CCA
occlusion, initially identified by duplex ·scanning and
angiography, were followed since J 987 (females) and
1989 (male) by repeated clini_cal andTCP _examination
for 38,---88 months, in average 6.5 years~ In 1989 a
s~quential examination of TCD and CBfiJsing xenon133 was done before and after intravenous administration of 1 g acetazolamide in patient nd. 1 and 2 7 .
Subsequently, CBF was measured after intravenous
administration of technetium-99m hexamethylpropylene
amine oxime (99 mTc-HMPAO) by single photon emission
tomography (SPECT) in all three cases.

Neurological Research, 1996, Volume 18, April 109

Common carotid artery occlusion with minimum neurological deficit: V. Zbornikova et al.

Repetitive TCD examinations were initially performed
by TC 64 Band since 1990 by 3-TCD scanner. The data
were compared to age-matched healthy controls 6 ,7.

MATERIALS AND METHODS
Ultrasonic examination
The extracranial vessels were examined by duplex
scanners with 7.5 MHz 2-D image and 5 MHz pulsed
Doppler (ATL Mark 600 and Acuson XP, USA), a method
described elsewhere 8 ' 9 .
Transorbital examination of the ophthalmic artery and
siphon was performed with a handheld probe using a
2 MHz transducer. The same transducer was used for
examination of intracranial vessels until 1990 10 . Since
1990 examination of intracranial vessels within the
whole circle of Willis was performed by 3-D transcranial
Doppler (TCD) scanner with a 2 MHz transducer (TransScan, EMI Germany). In the 3-D TCD scanner each focal
recording is stored as a combination of a directional
spectral Doppler recording and a colored dot in three

planes (frontal, horizontal and sagittal). A composite
display is built up by recording multiple spectra from
major cerebral arteries 11 .
Velocities from the middle cerebral artery (MCA) were
recorded at a depth of 5.0-5.5 em, anterior cerebral
artery (ACA) at depth of 6.5-7.0 em and posterior
cerebral artery (PCA) at a depth of 6.0-6.5 cm) 10 .
Recording from the vertebrobasilar system was performed with the patient lying on the side with
anteflexion of the head. One transducer was used
through the foramen magnum acoustic window (Figure
70). Maximal and mean velocities in em sec- 1 and
pulsatility index (PI) defined as (peak systole-end
diastole)jmean 12 were recorded. Pulse rise time (PRT)
was estimated as time in msec from the end diastole to
the peak systole 6 . The baseline TCD data were
compared with results from an age-matched controlgroup (n = 8), mean age 62 years.

CBF measurement
Three dimensional rCBF was measured by intravenous
injection of approximately 2 GBq 133 Xenon. The rCBF

B

A

05-07-93

Iru;a,o:; l·tlTT

05-07-93

Figure 1: Transcranial scan of the middle cerebral artery (MCA, A), anterior cerebral artery (ACA, B), posterior cerebral artery (PCA, C), basilar artery
(BA, D) in patient 2. The circular cursor indicates precisely location of the Doppler sample volume (white arrow) . Observe the prolonged PRT in MCA
and ACA and high velocities in PCA and BA

11 0

Neurological Research, 1996, Volume 18, April

Common carotid artery occlusion with minimum neurological deficit: V. Zbornikova et al.

was calcu Iated from the recorded 1 3 3 Xenon clearance
by the method of Kanno and Lassen 13 . Measurements
were done with the patient resting supine in a laboratory
that was quiet except for ambient noise at 1. rest, and 2.
20 min after i.v. administration of 1 g acetazolamide.
SPECT camera (Tomomatic 564), following 99 mTcHMPAO i.v. administration, was used for later flow
estimations.
Aortic arch angiography was performed at four
different angles, the sagittal and lateral view and at
45°right and left obl ique views.

Case reports

1. Female, born 1920, who at the age of 22 had
tuberculosis with lymphadenitis and was treated by x. ray radiation directed to her neck. In 1951 she awoke
with right-sided hemiparesis which resolved completely
within 2-3 days. Angiography 3 years later showed
bilateral CCA occlusion, probably .caused by the
previous radiation therapy, although p-ulseless disease
was considered as an alternative diagnosis at that time.
Hypertension was diagnosed in 1974 and treated with
betablockers .
Duplex examination in 1984 confirmed the occlusion
of both CCA, but revealed patent bifurcations on both
sides, with the ICA supplied in cephaled direction by the
ECA. The patient was admitted to hospital in 1985
because of intermittent right-sided hypoesthesia . Over
the following years the patient complained of intermittent dizziness and some impairment of memory.
Neurologica l examination and CT were normal. Current
med ication consists of Amilorid, Atenolol, Furosemid
retard, Allopurinol, Naproxen, Felodipin and Acetylsalicyl acid.
2. Female, born 1935, had a family history of
cardiovascular disease with two brothers having myocardial infarction . The patient was diagnosed as having
arterial hypertension, claudication of the lower extremities, angina pectoris and hyperlipidem ia. In 1984 'Y
graft' surgery was performed due to occlusion of the
distal aorta. In 1986 the patient was admitted with
vertigo and blurred vision provoked by head movement.
These symptoms were later provoked also by physical
work, particularly when raising her arms above the
horizontal line, and by postural changes. The neurological status revealed a rightsided hemianopia. CT scan
showed a left occipital infarct 4.4 x 3 em.
Duplex scanning revealed bilateral CCA occlusion
with patent left bifurcation where flow was directed from
ECA to ICA. On digital subtraction angiogram the right
vertebral artery was seen to be occluded as well. Her
neurologic symptoms gradually worsened over time, but
repeated aortic arch angiography and CT in 1992 were
unchanged .
She is now treated by lsradipin, Simvastin, Spironolacton and Dicoumarol.
3. Male, born 1921, smoker, with hyperlipid~mia since 1978, treated by diet. Hypertension was
diagnosed 1989. The same year the patient suffered from

vertigo and had a minor stroke with right-sided
hemiparesis.
CT showed a small subcortical ischemic infarct
(1.5 x 1.5 em) in the left carotid territory. Primarily,
duplex scanning showed bilateral occlusion of CCA with
patent bifurcation bilaterally. The aortic arch angiography showed occlusion of both CCA. Right ICA was filled
downstream to the siphon but the left ICA was patent
and filled by ECA. Subsequently, the patient complained
of blurred vision of the right eye and 2 years later
observed prolonged amaurosis fugax of the right eye
lasting about 30 min. In 1992 he was admitted with
blurred vision of the left eye and vertigo provoked by
physical work and postural changes and the same year
left-sided transient ischemic attack.
A by-pass anastomosing the left subclavian artery to
the patent ICA was attempted, but was not feasible due
to deep location of the subclavian artery. He is treated
by 75 mg dose acetylsalicyl acid.

Systolic and mean velocities and pulsatility index in
ophthalmic, siphon, vertebral a nd basilar artery at repetiti ve
examinations 1987-1993 in 3 patients

Table 1:

Left

Right
No

Artery

s

M

PI

s

M

PI

Ophtha lmic

32
50
60
83
61
-33
- 20
-38
-26
-54
-36
- 38
49
60
56
61
56
52
-27
-28
-35
-46

16
27
35
61
40
23
10
26
18
35
27
24
15
54
32
40
36
29
17
19
21
33
17
50
42
106
40
36
29

2.00
1.78
1.05
0.89
0.80
0.75
1.15
0.47
0.43
0.67
0.47
0.80
2.00
1.14
1.09
0.80
0.90
0.63
0.65
0.53
0.85
0.65
0.60
1.36
1.00
0.88
0.77
1.08
0.78

32
23
36
48
- 36
27
-48
- 23
-36
-44
-40
-58

23
71

12
12
27
32
23
12
28
19
24
30
29
31
12
36

2.6
3.33
0.96
0.90
0.80
1.15
0.98
0.57
0.63
0.75
0.79
0.75
3.33
1.14

-54
56
35
-25
-42
-24
-38
-15
165
103

26
36
25
17
30
20
27
11
103
65

0.88
0.93
0.69
0.76
0.58
0.57
0.55
0.55
1.00
1.06

56
46

46
36

0.60
0.63

2

3

Siphon
2

3

Vertebral
2
3
Basilar

2
3

-23
96
68
160
56
65
51

s

132
160
102
179
51
109

M
72
114
60
104
31
83

PI
1.27
0.83
0.81
0.80
1.00
0.72

S, systolic; M, mean velocity; PI, pulsatility index

Neurological Research, 7996, Volume 78, April 111

Common carotid artery occlusion with minimum neurological deficit: V. Zbornikova et al.
Table 2:

Velocities and pulsatility index in the middle cerebral artery
anterior cerebral artery and posterior cerebral artery at repetitive
examinations during 1987- 1993
Right
No

s

M

PI

s

M

PI

MCA

98
100
100
96
88
95
105

0.93
0.85
1.04
1.13
0.70
0.61
1.08
0.80
0.80
1.61
0.89
1.38
1.04

100
82
87
113
74
69
77
79
72
54
36
41
29
41

64
60
56
67
56

96
42
61
46
40

60
65
59
51
62
72
61
51
64
28
38
30
24

56
52
51
38
26
27
23
35

0.93
0.85
1.00
1.10
0.59
0.56
0.64
0.73
0.58
0.68
0.69
1.13
0.60
0.42

59
100
128
124
115
110
102
42
56

24
60
83
83
77
70
64
28
31

1.16
1.15
1.22
0.67
0.83
0.86
0.89
1.61
1.16

100
124
51

59
72
31

1.15
1.15
1.00

54

38

0.61

160

96

0.78

148
206
186
182
150
86
165
160
-77
64
160

100
1so
114
110
99
54
119
114
54
45
107

0.73
0.76
0.86
0.69
0.61
1.01
0.69
0.66
0.54
0.71
0.62

160
191
118
127
113
100
150
140
112
100
106
-150
108

100
1so
63
72
77
62
98
83
70
72
76
109
74

0.98
0.76
1.10
0.94
0.73
0.67
0.79
0.96
0.90
0.66
0.75
0.55
0.72

77

3

ACA

2

3
PCA

2

3

Table 3:

Transcranial Doppler
Five patent bifurcations were found. In 3, the flow
direction was from the ECA to the ICA, whilst in the
remaining 2, flow was reverted, from ICA to ECA. TCD
results are described in Tables 1 and 2, VMR in Tables 3
and 4.
In the ophthalmic artery and the siphon (Table 1),
velocities were in anterograde direction in patient 1 and
2. PI in patient 2 was < 1.0, which suggested low
perfusion pressure in the ICA bed (Figure 2b). In patient
3 the velocities in the ophthalmic artery and the siphon
were in retrograde direction with a blunted profile of the
pulse curve, i.e. delayed pulse rise time (PRT) as
compared to normals (0.113 s, Figure 2a) 6 •
MCA velocities at repetitive examinations (Table 2)
were within the normal range 6 and did not change
significantly during follow up in patient 1 and 2, and
both showed considerable increase after acetazolamide
administration (Table 2). In the third patient lower mean
velocities were observed with average values of
29±6cm sec- 1 and 30±6cm sec- 1 , on the right and
left side respectvely. After acetazolamide, increases in
mean velocities of about 26% and 33%, were seen, but
these values were still below the normal range (Table 3).
Anterior cerebral artery (ACA) velocities were high in
case 1 and 2, (72 ± 16 and 74 ± 8) although flow signals
were very weak in patient 2, except for the first study in
1987. In the case 3 ACA velocites were reduced and
weak (Table 2).
In all patients the PCA were the main supplying
collaterals with high average of mean velocities. In
patient 2 very high velocities were detected in both
posterior communicating arteries with turbulence (Figure 3). In patient 3 velocities varied between different
examinations, but during the second, third and the last

Left

Artery

2

RESULTS

so

Systolic and mean velocities and pulsatility index in the middle cerebral artery before (a) and after (b) acetazolamide, in three patients
Right

No

s

M

1a
b
2a
b
3a
b

98
136
64
79
42
58

56
90
40
56
27
35

Change

61%
40%
30%

Left
PI

PRT

s

M

1.12
0.88
0.75
0.55
0.89
0.86

272
272
180
180
200
210

86
122
64
74
30
37

38
80
40
58
21
28

Change

111 %
45%
33%

PI

PRT

1.26
0.90
0.65
0.76
0.67
0.57

242
181
180
181
290
250

Change=% increase of M from resting values. Pulse rise time (PRT) = time in msec from enddiastole to peak systole. S, systolic; M, mean; PI,

Table 4:

Regional CBF expressed in ml 100 g- 1 min- 1 in ACA, MCA and PCA at baseline (a) and after acetazolamide in patient 1 and 2
Right

No

ACA

1a
b
2a
b

28
48
36
54

Change

71

so

MCA
29
49
36
52

Left

Change

69
44

PCA
34
57
41
62

Change=% increase .from baseline values after acetazolamide

112

Neurological Research, .1996, Volume 78, April

Change

68
51

ACA
27
45
34
52

Change

67
53

MCA
29
49
35
53

Change

69
51

PCA
33
56
36
58

Change

70
61

Common carotid artery occlusion with minimum neurological deficit: V. Zbornikova et al.

Right

Left

Figure 2A-B: Records of spectra from ophthalmic artery (upper) and siphon (lower) in patient 3 (1 A) and 2 (1 B). Note reverse (1 A) and bidirectional
flow pattern of the pulse curves (left 1 B) in the ophthalmic artery. PRT is delayed in al l recordings

Figure 3: Posterior communicating arteries (PCoA) in the same patient recorded from the left temporal window. Left scan corresponds to the right
and right to the left PCoA

Neurological Research, 1996, Volume 18, April 113

Common carotid artery occlusion with minimum neurological deficit: \1. Zbornikova et al.

A
SPECT results in patients 1,2,3 . A: Patient 1. Hypoperfusion
parasagitally on the both sides in frontoparietal region, consistent with
cortical atrophy
Figure 4:

B: Patient 2. Lack of perfusion in the left occipital lobe, related to
previously described infarction

and right vertebral arteries, respectivel y. In patient 3
velocities are within the normal range. In the basilar
artery, patient 1 and 2 had increased mean velocities
(66 em sec- 1 ), with even higher levels at the second
examination (109 em sec- 1 , Figure 1) . Patient 3 had a
low level of 31 em sec - 1 initially, which increased to
83 em sec- 1 at follow up examination.

CBF
Patient 1 and 2 had both low global resting flow
levels, 30 and 37 ml100 g- 1 min - 1, as compared
to a level of 55±5 ml100 g- 1 min - 1 in age-matched
controls. In the MCA territories CBF ranged from 2936 ml 100 g- 1 min - 1 . Case 2 in addition had a marked
CBF reduction in the left occipital lobe, rel ated to the
infarct seen on CT.
Adequate global flow increases ranging from 44- 69%
were seen following acetazolamide, without change in
regional flow distribution (Table 4). SPECT exami nations
are described in Figures 4a-c.
C: Patient 3. Severely reduced flow level in the entire MCA territory on
the left side. On the right centrally in the MCA territory is seen a small,
well demarcated area of hypoperfusion

recording the velocities in the right PCA w ere
> 100 em sec. The patient suffered headache during
these registrations.
Increase of mean velocities in vertebrobasi lar territory
was observed. Patient 1 and 2 h ad values of
84±27 em sec - 1 and 79 ± 32 em sec - 1, in the left
114 Neurological Research, 7996, Volume 78, April

DISCUSSION
All three patients had only modest neurologial deficits
w hen referred to neurologic-evaluation, despite severe
obstructive extracranial disease. Transient neurological
symptoms, including dizziness related to orthostatic
changes, occurred during follow up, without residual
functional disability. This outcome is in concordance
with our previous study on CCA occlusion, where the
best prognosis was seen in the patients having patent
bifurcation andjor good co llateralization 6 . However
orthostatic dizz iness may be a conseq uence of flow

Common carotid artery occlusion with minimum neurological deficit: \1. Zbornikova et al.

redistribution as well as following ischemia and development of low perfusion infarction.
Retinal ischemia as prolongated amaurosis fugax or
blurred vision may depend on temporary insufficiency of
ophthalmic collateral during increased hemodynamic
demands within the anterior circulation 14 . Dominating
ophthalmic collaterals with retrograde flow direction is
generally not sufficient in occlusive carotid disease and
often accompanied by severe neurological deficits 15 •
This pattern was found in patient 3, who had ischemic
infarct in the left MCA territory.
Velocities in MCA did not change significantly during
the observations time. In patient 1 and 2 the values were
within the normal range reflecting adequate flow
increase in the collaterals as well functioning circle of
Willis. In the third patient the values were very low as a
possible consequence of inadequate function of the
collaterals and low regional perfusion pressure with
following permanent tissue damage.
Changes of wave form observed, with delayed PRT
generally and low PI on the both sides in patient 2 and
on the left side in patient 3 may reflect a post-occlusive
phenomena and a fall in pressure gradient as we found
in our previous study of patients with CCA occlusion.
These changes were reported also by others 16•17 .
ACA flow signals in patient 3 were difficult to estimate
because of a low Doppler shift.
Velocities in PCA and basilar artery were very high,
probably because vertebra-basilar circulation was a
feeding source to the MCA territory. PCA as dominating
collateral in extracranial bilateral severe atherosclerotic
lesion, eg. carotid stenosis> 75% lumen reduction or
occlusion was confirmed by us 7 . In normals the mean
velocity in BA is lower than in MCA, values between
31-40 em sec- 1 18 . Blood volume in BA is around
300 ml min - 1 ., eg smaller than in the ICA with amount
in each artery about 350 ml min - 119 . The basilar artery
is probably too small to maintain adequate amount of
the blood in bilaterally severely stenosed or occluded
internal carotid arteries. Increased velocities in BA as
well as reversed periorbital flow are signals of ineffective
collateral circulation with subnormal perfusion of
MCA 20 .
During follow up we observed the difference between
the first and second examination of BA, with higher
values at the last recording, which may be explained by
reduced peripheral cerebral resistance with precapillary
vessel dilatation and increased demands in brain tissue
within the MCA vascular territory.
Ischemic defects were presented in all patients, but
low perfusion was the possible cause of infarction in
patient 3, where we could not record Doppler signals
from the depth < 4.5 em on the left side. Low flow
infarction occurs mostly in the border zone between
posterior and anterior circulation 21 . VMR was excellent
in both female patients but impaired in the male no. 3,
where very low values in MCA were seen in resting
condition.
CBF measurement showed very low global flow and
in spite of very good response after acetazolamide, the

reached values were still below those for age related
normal population. This state can lead to development
of ischemic lesion e.g. chronic penumbra, defined as
reversible ischemic paralysis with impaired function of
neurons, which occurs, if flow decreases to interval 1823 ml 100 g- 1 min- 1 22 .
Our study suggests that despite good vasomotor
response these patients are chronically and increasingly
hypoperfused. Bypass operation with an anastomosis
between subclavian-patent ICA and in special selected
cases direct thrombendarterectomy in CCA, may possibly prevent retinal ischemia and enhance perfusion
within anterior circulation 23 •24

ACKNOWLEDGEMENT
We thank associate professor G6ran Granerus, Department of Nuclear Medicine, University Hospital Linkoping for evaluation of SPECT examinations. We also thank
associate professor Bengt Nilsson, Department of
Neurology, University Hopital Lund for valuable advice
in preparation of the manuscript.
Part of this work was presented at 'Joint meeting of the
Swiss and Swedish neurological and neurosurgical
societies' May 10-13, 1992 in Lund, Sweden .
The project was supported by grants from Swedish
Stroke Society and Heart and Lung foundation.
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