From the Department of Neurology, Barmbek Hospital, Hamburg, Germany.
Correspondence to Dr Christian Arning, Abteilung Neurologie, Allgemeines Krankenhaus Barmbek, D-22291 Hamburg, Germany. E-mail christian.arning{at}t-online.de
Case Description—A 32-year-old woman presented after
multiple episodes of left monocular visual impairment and right-sided
focal signs. MRI revealed a low-flow infarction on the left;
color-coded duplex sonography (CCDS), however, showed normal vascular
findings. During the inpatient rehabilitation, a renewed visual
impairment occurred; an immediate CCDS examination now demonstrated a
filiform stenosis of the left internal carotid artery (ICA) 4
cm above the origin and indirect signs of a severe stenosis of
the right ICA. Results of a follow-up examination 18 hours later were
again normal. Six weeks later, on reoccurrence of visual impairment, a
reversible stenosis of the left ICA was again demonstrated. A
search for possible causes of vasospasm was unsuccessful. After
treatment with calcium antagonists the patient was free of
complaints (with the exception of 3 very short attacks of visual
impairment) during the following 12 months.
Conclusions—Cervical carotid artery vasospasms can apparently
occur spontaneously without a mechanical trigger. Because their
detection is difficult, vasospasms may go undetected.
The symptoms recurred 5 weeks later with an additional dysarthria, and
the patient was admitted to hospital immediately. On admission a slight
vascular murmur was detected in the left side of the neck. Again, the
symptoms regressed rapidly. In addition to the previous
diagnostic investigations, MRI of the head was carried out
but results were not significant; the vascular sonography was not
repeated. In the following 12 months similar symptoms occurred
temporarily (about 5 times at irregular intervals); in these episodes
the patient was not seen by a physician.
Approximately 13 months after the first episode, the patient was again
admitted. The symptoms were now more strongly pronounced than in
earlier episodes, and there was also a neuropsychological syndrome,
with lack of drive and mental slowness, as well as an aphasia. This
time the symptoms did not disappear rapidly but remained, at first,
constant. Intensive diagnostic examinations were performed
in the next few days but did not produce any etiologic clarification.
Vascular sonography was again without pathological findings. MRI showed
an extensive subcortical increase in signal intensity in the left
parietal region. This finding was best interpreted as a low-flow
infarction of hemodynamic origin, and because of the
negative vascular findings on Doppler sonography and MR
angiography, the possibility of an inflammatory lesion was considered.
Treatment with prednisone for 3 weeks was begun. The cerebrospinal
fluid was analyzed twice (on days 4 and 19); results were
without significance both times. Also, no indications for a possible
inflammation were found in the blood. Virology (including a test for
human immunodeficiency virus) was also negative, as were
bacteriological-serological diagnoses (including tests for
Borrelia burgdorferi and Treponema pallidum),
blood count investigations, and extensive immunologic diagnoses
(including tests for antinuclear antibodies, immunoelectrophoresis,
C-reactive protein, and lysozyme). Furthermore, no coagulation disorder
was found.
Under rehabilitation measures with physical therapy, ergotherapy, and
logopedics, the deficiency symptoms improved slowly, although a slight,
right-side hemiparesis remained. At 31/2 weeks after admission,
the patient complained of a sudden recurrence of the known
visual impairment in the left eye. Vascular sonography was performed
immediately and revealed a filiform stenosis of the left
internal carotid artery (ICA) 4 cm cranial of its origin (Figure 1
The prednisone treatment was continued, with the dose being very slowly
reduced. At a dose of 30 mg/d, the known visual impairment occurred
again, 6 weeks after the preceding episode. Color-coded duplex
sonography again revealed a filiform stenosis of the left ICA
in the same position (Figure 3
The further course with the renewed occurrence of a reversible
stenosis of the left ICA at the same site again supports the
interpretation of these findings as vasospasm. The detection of
repeated spasm of the carotid artery in combination with the patient's
ipsilateral visual disorders supports the suggestion that a vasospasm
had also occurred at the time of her earlier symptoms but had not been
detected due to its short duration. However, the cause of this
functional narrowing remains unclear, because none of the usual causes
of spasm could be found. Apparently the patient benefited from
treatment of the symptoms: in a follow-up period of more than 12
months, 3 short-duration visual impairments have occurred but were not
accompanied by further neurological deficit symptoms.
Another important aspect is the temporary change in the ECG, which may
be interpreted as the effect of a coronary artery spasm.
Findings of this type have been described in migraine
patients.11 The diagnostic problems
in the detection of vascular spasms in coronary arteries are
well known: at the moment of investigation the arteries appear to be
normal—the vasoconstriction has already disappeared. Vasospasms of
carotid arteries can be so short lived that they cannot be seen with
the usual diagnostic examinations, as in the present
case. But they may also last for several days (like the second
stenosis documented in this case) and may then be mistakenly
interpreted as dissections.
In light of the above-mentioned diagnostic difficulties, it
is possible that vasospasms may not be recognized in all patients. It
remains to be determined whether this is a functional syndrome (eg, a
migraine variant) or whether the spasms result from an as-yet
unidentified angiopathy.
Received January 29, 1998;
revision received March 2, 1998;
accepted March 5, 1998.
© 1998 American Heart Association, Inc.
Case Report
Cervical Carotid Artery Vasospasms Causing Cerebral Ischemia
Detection by Immediate Vascular Ultrasonographic Investigation
Abstract
Top
Abstract
Introduction
Case Report
Discussion
References
Background—The etiology of cerebral
ischemic accidents in young adults often remains
unclarified.
Key Words: carotid arteries • cerebral ischemia • ultrasonics • vasospasm • young adults
Introduction
Top
Abstract
Introduction
Case Report
Discussion
References
Vasospasms of the
cranial arteries are a well-known cause of cerebral ischemia in
cases of subarachnoidal hemorrhage and have also been
reported in isolated cases of migraine,1
vasculitis,2 and
eclampsia.3 Extracranial vasoconstrictions may
arise from mechanical manipulations during operative
interventions,4
vasopuncture,5 and catheter
examinations,6 as well as in cases of ergot
poisoning.7 It was previously suspected that
extracranial vasospasms could be of some importance in the pathogenesis
of migrainous strokes,8 but this possibility
could not be confirmed until now.
Case Report
Top
Abstract
Introduction
Case Report
Discussion
References
In September 1995, a 32-year-old woman experienced acute visual
impairment with light flashes and dark spots in the left eye and later
a 1-sided hemiparesis and sensory impairment on the right side followed
by bilateral forehead pain. The symptoms disappeared within 2 hours.
All examinations, including cranial CT and extracranial and
intracranial vascular sonography carried out 2 days later, were
negative. Apart from a moderate consumption of nicotine (nonsmoker
since the beginning of November 1996), no vascular risk factors were
present. The patient was otherwise healthy, and there was no
history of migraine-like headaches. She was not taking oral
contraceptives or any other drugs. 
). On the right, a severe flow
impediment of the ICA was detected; there was an ophthalmic collateral
with rapid, unambiguous retrograde flow in the supratrochlear artery.
Direct signs of a stenosis were not seen in the examined
section of the right ICA. The patient was given an infusion of saline
for circulatory support and heparin for embolus prophylaxis as well as
prednisone. This time no further deficiency symptoms occurred. The next
day, visual impairment was no longer present, and results of a
sonographic follow-up (18 hours after the previous examination) were
once again normal (Figure 2). To avoid
the possibility of provoking a vasospastic reaction, angiography was
not attempted.
View larger version (81K):
[in a new window]
Figure 1. (Views of the same vascular sections appear in
Figures 1 through 4 
.) Color-coded duplex sonography taken on December
3, 1996, at 7:30 PM. Top, Color Doppler mode shows
evidence for a filiform stenosis in the internal carotid artery
(ICA) 4 cm cranial of the bifurcation. Bottom, Pulsed-Doppler mode
shows reduction in flow rate in the starting section of the ICA.
(System: Acuson 128 XP10, linear scanner L538.)
View larger version (86K):
[in a new window]
Figure 2. Color-coded duplex sonography performed on
December 4, 1996, at 1:30 PM. Top, Normal findings in color
Doppler mode. Bottom, The flow rate is normal. ). This
time, however, the findings for the right carotid and supratrochlear
arteries were inconspicuous. Treatment comprised infusion of saline and
heparin. The visual impairment lasted 2 days, during which other
symptoms did not appear. On follow-up examinations on succeeding days,
the stenosis was still detectable, albeit to varying extents,
but finally normalized after 3 days (Figure 4). A routine ECG at this time showed
slight recovery disorders over the posterior wall; later ECG
measurements were inconspicuous. On the assumption of a recurrent
vascular spasm, the patient was treated with vasodilators (first
molsidomin and nifedipine, then nitrendipine). At the
12-month follow-up, the patient was free of complaints, with the
exception of 3 very short attacks of visual impairment. A vascular
sonographic follow-up was inconspicuous.
View larger version (83K):
[in a new window]
Figure 3. Color-coded duplex sonography performed on January
18, 1997. Top, Renewed evidence for a filiform stenosis of the
internal carotid artery (ICA) at the same site as before. Bottom,
Considerable reduction in flow rate in the starting section of the ICA,
even more pronounced than in the previous episode (Figure 1 ).
View larger version (78K):
[in a new window]
Figure 4. Color-coded duplex sonography performed on January
22, 1997. Normal findings in color Doppler (top) and
pulsed-Doppler modes (bottom).
Discussion
Top
Abstract
Introduction
Case Report
Discussion
References
Despite intensive diagnostic efforts, the etiology of
cerebral ischemic accidents in young adults often remains
unclear.9 It is worthy to note that in this case,
even after the occurrence of a cerebral infarction of
hemodynamic origin, the cause of the perfusion disorder
was not recognized. Only during the ninth attack, which occurred in the
hospital, very severe bilateral vascular stenoses of the ICAs
were detected by immediate sonography. If the examination had been
carried out after an interval of more than 1 day, it would have shown
normal findings. The rapid regression of the stenoses within
less than 18 hours excludes the possibility of a vascular
stenosis due to arteriosclerosis or
dissection; even so, the degree of stenosis, according to the
usual hemodynamic criteria,10
amounted to at least 90%.
References
Top
Abstract
Introduction
Case Report
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  W. G. Janzarik, P. A. Ringleb, M. Reinhard, and S. Rauer Recurrent Extracranial Carotid Artery Vasospasms: Report of 2 Cases Stroke, August 1, 2006; 37(8): 2170 - 2173. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. H. Benninger, D. Georgiadis, J. Gandjour, and R. W. Baumgartner Accuracy of Color Duplex Ultrasound Diagnosis of Spontaneous Carotid Dissection Causing Ischemia Stroke, February 1, 2006; 37(2): 377 - 381. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||