Discussion
These 3 cases of BADE had different patterns of presentation. In
case 1, BADE was diagnosed by MRI showing an infarct in the left
MCA deep territory, in case 2 it was identified due to a recent history
of isolated severe headache, and in case 3 it had caused a right paramedian pontine infarct. The clinical course also differed considerably between our 3 cases. Patient 1 died a year later due to a sudden
subarachnoid hemorrhage while the 2 other patients improved or
remained stable during the same length of follow-up. These results
are in accordance with the reported death rates (varying from 55% at
1 year [2] to 40% at 3 years [10] in small series of patients).
We observed that the patient who deceased 1 year after subarachnoid hemorrhage initially had the smallest wall thickness and the
smallest diameter of BADE but later had the largest and fastest
increase in diameter. The BADE expansion was also important in the
second patient, who developed ventricular enlargement secondary to
brainstem compression. The third case, who initially had both the
largest BADE diameter and the largest wall thickness (including the
thrombus) had no ischemic or hemorrhagic events during the 1-year
follow-up. These data suggest that the initial diameter of the arterial
ectasia is not the only prognostic parameter and that the combination
of a thin wall and a rapid, important expansion may be more pejorative and predictive of rupture. In contrast, the height of the BADE
bifurcation or its lateral displacement do not change before arterial
rupture. These data are in line with those reported for aortic aneurysms often associated with BADE [11, 12], in which the risk of rupture is related not only to the size of the ectasia but also to the rate of
expansion [13, 14].
References
1 Smoker WR, Corbett JJ, Gentry LR, Keyes WD, Price MJ, Mc-Kusker S:
High-resolution computed tomography of the basilar artery 2. Vertebrobasilar dolichoectasia: Clinical-pathological correlation and review. Am J
Neuroradiol 1986;7:61–72.
2 Haddad GF, Haddad FS: Cerebral giant serpentine aneurysm: Case reports
and review of the literature. Neurosurgery 1988;23:92–97.
3 Yu YL, Moseley IF, Pullicino P, McDonald WI: The clinical picture of
ectasia of intracerebral arteries. J Neurol Neurosurg Psychiatry 1982;45:
29–36.

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4 Inanasu J, Suga S, Stao S, Onozuka S, Kawase T: Long-term outcome of 17
cases of large–giant posterior fossa aneurysm. Clin Neurol Neurosurg 2000;
102:65–71.
5 Nagahiro S, Takada A, Goto S, Kai Y, Ushio Y: Thrombosed growing
aneurysm of the vertebral artery: Growth mechanism and management. J
Neurosurg 1995;82:796–801.
6 Nakatomi H, Segawa H, Kurata A, Shiokawa Y, Nagat K, Kamiyama H,
Ueki K, Kirino T: Clinicopathological study of intracranial fusiform and
solichoectatic aneurysms. Insight on the mechanisms of growth. Stroke
2000;31:896–900.
7 Anson JA, Lawton MT, Spetzler RF: Characteristics and surgical treatment
of dolichoectatic and fusiforms aneurysms. J Neurosurg 1966;84:185–
193.
8 Little JR, St Louis P, Weinstein M, et al: Giant fusiform aneurysm of the
cerebral arteries. Stroke 1981;12:183–188.
9 Passero S, Filosomi G: Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998;29:653–659.
10 Milandre L, Bonnefoi B, Pestre P, Pelissier JF, Grisoli F, Khalil R: Vertebrobasilar arterial dolichoectasia. Complications and prognosis. Rev Neurol (Paris) 1991;147:714–722 [in French].
11 Gautier JC, Hauw JJ, Awada A, Loron P, Gray F, Juillard JB: Dolichoectatic intracranial arteries. Association with aneurysms of the abdominal
aorta. Rev Neurol (Paris) 1988;144:437–446 [in French].
12 Sacks JG, Lindenburg R: Dolicho-ectatic intracranial arteries: Symptomatology and pathogenesis of arterial elongation and distention. Johns Hopkins Med J 1969;125:95–106.
13 Limet R: Determination of level of expansion and incidence of rupture of
abdominal aortic aneurysms. Bull Mem Acad R Med Belg 1992;147:253–
264 [in French].
14 Powell JT, Brown LC: The natural history of abdominal aortic aneurysms
and their risk of rupture. Acta Chir Belg 2001;101:11–16.
Hugues Chabriat, Service de Neurologie, Hôpital Lariboisière
2 rue Ambroise Paré, FR–75010 Paris (France)
Tel. +33 1 4995 2593, Fax +33 1 4995 2595
E-Mail hugues.chabriat@lrb.ap-hop-paris.fr

Cerebrovasc Dis 2004;17:264–266
DOI: 10.1159/000076964

Diffusion MRI in Pure Transient Global Amnesia
Associated with Bilateral Vertebral Artery
Dissection
D. Michel a, P. Garnier a, F. Schneider b, A. Poujois a,
F.G. BarraI b, C. Thomas-Antérion a
Departments of a Neurology and b Neuroradiology, University
of Saint-Etienne, Saint-Etienne, France

Introduction
The clinical criteria for the diagnosis of transient global amnesia
(TGA) have been well established [1]. TGA is characterized by an
abrupt onset of massive anterograde amnesia accompanied by repetitive questioning and generally resolves within 24 h. Retrograde
amnesia variable in extent is also present. During the attack, the
patient appears perplexed, disoriented in time and place but remains
alert and communicative with preservation of self-identity. Cognitive impairment is limited to amnesia (e.g. no aphasia or apraxia).
Other focal neurological symptoms are absent.
Though pure TGA is a well-documented clinical entity, there is
still uncertainty concerning the mechanism of neuronal dysfunction.

Case Reports
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disturbances but had a normal neurological examination. The second
MRI showed that both the largest diameter and the maximal wall
thickness had increased by 22.2 and 13.3 mm, respectively (fig. 1d),
associated with a moderate ventricular enlargement.
Case 3. This 54-year-old man had a long history of hypertension
and hypercholesterolemia. He was admitted after sudden onset of
dizziness and dysarthria. Neurological examination performed 6 h
later showed bilateral moderate distal upper limbs weakness, a left
cerebellar ataxia and a bilateral Babinski sign. Ultrasound examination revealed an enlargement of right and left MCA associated with
BADE. ECG was normal. MRI 1, performed on day 1, showed a
recent right paramedian pontine infarct with a large BADE and
brainstem compression. The BADE had an initial largest diameter of
23.5 mm and a maximal wall thickness of 13.5 mm including a mural
thrombus (fig. 1e). After administration of aspirin the patient recovered and no further event occurred. A second MRI performed 7
months later showed an increase in both the diameter (now 26.9 mm)
and the wall thickness (now 18.3 mm) of the BADE (fig. 1f). At 12
months, the clinical status was unchanged.

1

2

3

4

Fig. 1. The axial T2-weighted images (TE/TR: 119/

5,340 ms, FOV 17.2 ! 23 cm, matrix 240 ! 512, 6-mm
slices, 3 NEX) obtained during the TGA show no abnormalities.
Fig. 2. On DWI, a hyperintensity was seen in the left thalamus corresponding to an ADC ratio decrease of 33%.

Fig. 3, 4. The cerebral angiography shows a tapered occlu-

sion on the V2, V3 segment of the right vertebral artery (arrow in 3) and a false channel on the V2 segment of the left
vertebral artery (arrow in 4).

Case Report
A 27-year-old right-handed man was admitted to the hospital for
an abrupt memory loss. He had no medical history of migraine headache, seizures or recent head injury. Over the previous 15 days, he
had gone for several rides on a mountain bike. Moreover, he had
been painting his ceiling during 1 day. During this period, he complained of an unusual cervical pain. In the course of his last mountain
bike excursion, he repetitively queried about the bicycle pump, the
cyclometer, the score of a recent football match, his job. His friend
noted that he was not bewildered but abnormally quiet. He could
easily drive his bike, then his car.

Case Reports

On admission at 1 a.m., about 10 h after onset, a senior neurologist noted a dense anterograde amnesia. The cognitive impairment
was limited to amnesia. He had no behavioural manifestations. He
was oriented to place but not to time and had no loss of personal
identity. No accompanying neurological focal signs or symptoms
were noted. The attack lasted about 13 h. The patient’s amnesia was
present throughout the MRI imaging procedures. T1- and T2weighted images were normal (fig. 1). The diffusion-weighted images
(double-spin echo, single-shot echo planar using two bipolar diffusion gradients in 3 orthogonal directions, b value: 1,000 s/mm2, TE/
TR: 166/4,712 ms, FOV 27.5 ! 27.5 cm, matrix 128 ! 128 zero
filled to 256 ! 256, 6-mm slices, 1 NEX) show a hyperintense signal
in the left thalamus (fig. 2) corresponding to an ADC decrease of 33%
compared to the mirror thalamus region. The following day, a vertebral angiography showed a dissection of the right (V2–V3 segments)
and left (V2 segment) vertebral arteries (fig. 3, 4). The basilar artery
was well injected. The echocardiography was normal. Anticoagulation was administered during the next 3 months.
Clinical evolution was favourable. At this time, neuropsychological tests were normal, except for the amnesia of the events and a very
short retrograde amnesia (1 h). Two months later, T2-weighted MRI

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Pure TGA has been shown to be associated with migraine, epilepsy
and various precipitating events. We report a case of a young patient
with a TGA, fulfilling the clinical criteria of Hodges and Warlow [1].
Diffusion-weighted imaging (DWI) with evaluation of the apparent
diffusion coefficient (ADC) was performed during the active phase of
the TGA. At the same time, a bilateral vertebral artery dissection was
shown. So, this case raises the hypothesis that a pure TGA in a young
subject could have the meaning of a vertebrobasilar transient ischaemic attack.

Discussion
Although ischaemia has been proposed as a potential cause of
pure TGA, there is still uncertainty concerning this hypothesis. In the
cases related to a cerebrovascular event, the observed signs and
symptoms were not consistent with a pure TGA. Focal neurological
symptoms and signs like a blurred vision [2] or an alteration of the
consciousness were present [3]. The impairment of memory did not
resolve within 24 h and occurred 1 year before an acute thalamic
infarct [4] or could be a coincident event [5]. Moreover, neither CT
scan nor standard magnetic resonance studies were able to establish a
temporal or causal relation between the cerebrovascular event and
symptoms [4, 6]. A case of pure TGA, really due to a vascular cause,
was reported in association with a simultaneous haemorrhage of the
lentiform nucleus [6]. In SPECT studies during the attack [7], the
distinction between flow reduction caused by a vascular disease and
flow reduction secondary to neuronal dysfunction is difficult.
In our case, an exact temporal relation between TGA and the left
thalamic abnormalities noted on DWI is established. Only a few
magnetic resonance DWI studies have previously investigated pure
TGA without evidence of cerebrovascular disease. In these studies,
DWI was performed in the active or in the recovery phase. Images
were normal [8, 9] or showed regressive elevated signals [10–13] in
neuronal networks implicated in memory: the splenium of the corpus
callosum, the right or left hippocampus and the medial basal temporal lobe. In our patient, a hyperintense signal on DWI was seen in the
left thalamus during the active phase of the ictus. The corresponding
ADC reduction (33%) was similar to that observed in long TIAs and
less pronounced than in stroke patients [14].
Furthermore, the association with a bilateral vertebral artery dissection argues in our case also in favour of a transitory ischaemia
even if pure TGA has not been published in vertebral artery disease
[15]. Moreover, such DWI/ADC changes were also reported in a case
report of TGA precipitated by cerebral angiography with a non-ionic
contrast agent [11]. The authors concluded to an ischaemia due to
emboli.
Some authors have proposed spreading depression as the underlying mechanism in TGA [10] like in migraine aura [16]. However, a spreading depression has never been proven in usual TGA.
Although the underlying mechanism of pure TGA remains uncertain, we conclude to a relationship between transient ischaemia and
pure TGA in our case. A pure TGA, particularly in a young subject,
requires a search for a cerebrovascular disease.
References
1 Hodges JR, Warlow CP: The aetiology of transient global amnesia: A casecontrol study of 114 cases with prospective follow-up. Brain 1990;113:
639–657.
2 Howard RS, Festenstein R, Mellers J, Kartsounis LD, Ron M: Transient
amnesia heralding brain stem infarction. J Neurol Neurosurg Psychiatry
1992;55:977.
3 Laterra J, Gebarski S, Chris Sackellares J: Transient amnesia resulting
from vertebral artery dissection. Stroke 1988;19:98–101.
4 Gorelick PB, Amico LL, Ganellen R, Benevento LA: Transient global
amnesia and thalamic infarction. Neurology 1988;38:496–499.
5 Kushner MJ, Hauser WA: Transient global amnesia: A case controlled
study. Ann Neurol 1985;18:684–691.

266

6 Bogousslavsky J, Regli F: Transient global amnesia and stroke. Eur Neurol
1988;28:106–110.
7 Goldenberg G, Podreka I, Plaffelmeyer N, Wessely P, Deeke L: Thalamic
ischemia in transient global amnesia: A SPECT study. Neurology 1991;41:
1748–1752.
8 Gaas A, Gaa J, Hirsch J, Schwartz A, Hennerici MG: Lack of evidence of
acute ischemic tissue change in transient global amnesia on single short
echoplanar diffusion-weighted MRI. Stroke 1999;30:2070–2072.
9 Budson AE, Schlaug G, Briemberg HR: Perfusion and diffusion weighted
magnetic resonance imaging in transient global amnesia. Neurology 1999;
53:239–240.
10 Strupp M, Brüning R, Wu RH, Deimling M, Reiser M, Brandt T: Diffusion-weighted MRI in transient global amnesia: Elevated signal intensity in
the left mesial temporal lobe in 7 of 10 patients. Ann Neurol 1998;43:164–
170.
11 Woolfenden AR, O’Brien MW, Schwartzberg RE, Norbash AM, Tong DC:
Diffusion-weighted MRI in transient global amnesia precipitated by cerebral angiography. Stroke 1997;28:2311–2314.
12 Ay H, Furie KL, Yamada K, Koroshetz WJ: Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;
51:901–903.
13 Matsui M, Imamura T, Sakamoto S, Ishii K, Kazui H, Mori E: Transient
global amnesia: Increased signal intensity in the right hippocampus on diffusion-weighted magnetic resonance imaging. Neuroradiology 2002;44:
235–238.
14 Kidwell CS, Alger JR, Di Salle F, Starkman S, Villablanca P, Benston J,
Saver JL: Diffusion MRI in patients with transient ischemic attacks. Stroke
1999;30:1174–1180.
15 Mokri B, Houser WH, Sandok BA, Piepgras DG: Spontaneous dissections
of the vertebral arteries. Neurology 1988;38:880–885.
16 Hadjikhani N, Sanchez Del Rio M, Wu O, Schwartz D, Bakker D, Fischl B,
Kwong KK, Cutrer FM, Rosen BR, Tootell RBH, Sorensen AG, Moskowitz MA: Mechanisms of migraine aura revealed by functional MRI in
human visual cortex. Proc Natl Acad Sci USA 2001;98:4687–4692.
Daniel Michel, MD
Department of Neurology, Hôpital Bellevue
FR–42055 Saint-Etienne Cedex (France)
Tel. +33 4 7712 7805, Fax +33 4 7712 0543
E-Mail daniel.r.michel@free.fr

Cerebrovasc Dis 2004;17:266–268
DOI: 10.1159/000076965

Crescendo Transient Ischemic Attacks due to
Middle Cerebral Artery Stenosis
Konstantinos Spengos a, Marios Panas a, Georgios Tsivgoulis a,
Konstantinos Vemmos b, Konstantinos Sfagos a,
Demetris Vassilopoulos a
a Department of Neurology, University of Athens Medical

School, Eginition Hospital, and b Department of Clinical
Therapeutics, Acute Stroke Unit, University of Athens Medical
School, Alexandra Hospital, Athens, Greece

Crescendo transient ischemic attacks (TIAs) are defined as disabling, recurrent transient cerebral ischemic episodes, which are
characterized by an increasing frequency, duration, or severity of
events [1, 2] indicative of a critical narrowing of the lumen of the
involved artery by an atherosclerotic plaque with superimposed
thrombus [3].

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was normal. Magnetic resonance angiography showed a recanalization of the right vertebral artery and a small aneurysm on the left.
The patient remained asymptomatic 18 months after his TGA.