TIAs in a Spontaneously Dissecting Aneurysm of the
Internal Carotid Artery—A Case Report

Shuzo Shintani, M.D.*
Tatsuo Shiigai, M.D. **
Shin Tsuruoka, M.D.†
and
Hiroshi Tsukagoshi, M.D.‡

IBARAKI and TOKYO, JAPAN

Abstract
A spontaneous internal carotid artery dissection of an aneurysmal form is
reported. The patient, a fifty-eight-year-old man, had manifested recurrent
transient left hemiparesis, dysesthesia of the left upper limb, and dysarthria for
three months. After administration of ticlopidine, the transient ischemic attacks
completely disappeared. Three months later, the follow-up angiographic study
revealed the same form of dissection in the same portion as compared with the
initial study. Conservative therapy was successful.
Introduction

Since Jentzer’ reported a case of a spontaneously dissecting aneurysm of the internal carotid artery (ICA) in 1954, an increasingly large number of reports have found a higher
incidence than had initially been thought.’-5 We encountered a spontaneous ICA dissection of
an aneurysmal form, and three months later a follow-up angiographic study was done. The
clinical symptoms, serial angiographic studies, and the management of this condition are discussed.
CASE REPORT
A fifty-eight-year-old man had manifested recurrent transient left hemiparesis, dysesthesia
of the left upper limb, and dysarthria since April, 1990. He suffered from these transient
ischemic attacks (TIAs) several times a day and was admitted to our hospital on June 20, 1990.
He had no history of head trauma but did have a history of hypertension for several years.
On admission, physical and neurologic examinations revealed no abnormalities except for
From the Departments of *Neurology, **Internal Medicine, and †Neurosurgery, Toride Kyodo General Hospital, Ibaraki,
Japan; and the ‡Department of Neurology, Tokyo Medical and Dental University, Tokyo, Japan

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mild hypertension (blood pressure was 160/90 mmHg) . Results of the laboratory examinations
were as follows: Blood cell counts indicated 471 x 104/mn~ of red blood cells (RBCs), 12.9
g/dL of hemoglobin, 40.4 % hematocrit, 23.9 x 104/mm3 of platelets, and 7900/mm3 of leukocytes. Urinalysis gave normal results. Serum biochemical analysis results were normal except
for 328 mg/dL of triglyceride (TG)(normal values: between 30 and 150 mg/dL). A chest x-ray
revealed no abnormality with the exception of 59% cardiothratic ratio (CTR) . ECG showed
ST depression in I, II, aVL, aVF, and giant negative T with ST depression in VS-V6 leads.
Cardioultrasonography revealed a marked concentric left ventricular hypertrophy (LVH).
EEG and brain single photon emission computed tomography (SPECT) appeared normal.
Brain computed tomography (CT) showed calcifications of the bilateral basal ganglia and a
small low-density lesion beside the right lateral ventricle (Fig. 1. A. B . ) .
Right carotid angiography by transbrachial method revealed an ICA dissection of an aneurysmal form in the near portion of the bifurcation of the common carotid artery (CCA) (Fig.
2). After administration of ticlopidine, 200 mg daily, the TIAs completely disappeared.
Three months later, he was readmitted to our hospital, and the follow-up angiographic
study was done on September 10, 1990. The right carotid angiography showed the same form
of dissection in the same portion as compared with the initial study of three months before

(Fig. 3).
Discussion
We studied repeat angiography of an ICA dissection. The follow-up study revealed no

progressive dissection of ICA, and an expansion of the aneurysm was not seen. Administration
of ticlopidine was effective in preventing the recurrent TIAs. Conservative therapy was successful.
The point of view in the present case is the morphologic feature of the dissection. The
carotid angiograms in our case showed the simple aneurysmal dilatation of ICA with double
contour (Figs. 2,3). Segmental stenoses or fusiform and saccular aneurysms were not seen.
The simple aneurysmal dilatation type of dissection without stenosis above and below is rare in
the previously reported spontaneous ICA dissections. Sellier et al reported 46 cases of spontaneous dissection of the internal carotid artery ; 33 cases were stenotic form dissections in the
angiographic features. The other 13 cases were aneurysmal form dissections, which included 8

FiG. 1.A.B. Brain CT showed the bilateral calcifications of the basal ganglia and a small low density lesion (arrow head)
beside the right lateral ventricle.

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FIG. 2. Serial right carotid angiogram showing a simple
aneurysmal dilatation with double contour in the near portion of the bifurcation of the common carotid artery (arrow

heads). Neither segmental stenoses nor string signs were

FIG. 3. Repeat arteriography three months later: The
simple aneurysmal dilatation of the carotid artery (arrow
heads) neither dissected nor expanded as compared with the
initial study of three months before.

seen.

of wide-base saccular aneurysm, 4 cases of fusiform aneurysm, and only 1 case of
simple aneurysmal dilatation with double contour. The ICA dissection of simple aneurysmal
dilatation without segmental stenoses was seen in only 1 case out of the 46 cases.
cases

Conclusions
The lesions detected by arteriography usually regress under medical treatment, such as
with anticoagulants, platelet inhibitors, and so on.6 Surgery should be reserved to progressively dissecting aneurysms and to patients who do not respond to anticoagulants or platelet
inhibitors. The administration of platelet inhibitor, ticlopidine 200 mg daily, was effective in
our case. The TIAs have completely disappeared after the administration. Some authors have
recommended repeat arteriography after two or three months&dquo;’ or even earlier9 in order to
decide the indication for surgical operation. We studied the repeat angiography three months
later, and the angiography showed neither enlargement of the aneurysm nor stenosis of ICA.
S. Shintani, M.D.

Department of Neurology
Toride Kyodo General Hospital
5901-1 Terada, Toride City
302 Ibaraki, Japan

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