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[page 30] [Emergency Care Journal 2013; 9:e11]

Transient global amnesia: 
an atypical presentation 
of acute aortic dissection
Monica Masoero, Giannina Leotta,
Federico Vischia, Antonio Sechi
Emergency Department, San Giovanni
Bosco Hospital, Torino, Italy

Abstract 

Aortic dissection (AD) is a cardiovascular
emergency whose most frequent symptom is
chest pain. However, clinical presentation can
also be varied and atypical. In the present
study we report a case of painless AD, which
resulted in a sudden memory loss at presenta-
tion. Physical examination and laboratory tests
regarding the patient did not show any abnor-
mal findings and a benign transient global
amnesia was diagnosed. The day after being
discharged, the patient came back to the emer-
gency department because a recurrent episode
of severe memory impairment occurred. This
time, additional clinical and laboratory signs
suggested clinical suspicion of AD. A chest
computed tomography angiogram was per-
formed and an extensive AD type A involving
carotid and iliac arteries was found. Our case
report shows that acute aortic dissection diag-
nosis can be difficult if clinical presentation is
atypical and must be assessed in the light of
various clinical signs and laboratory data.

Introduction

Aortic dissection (AD) is a cardiovascular
emergency whose most frequent symptom is
chest pain. However, clinical presentation can
be different and atypical.1

Not only are neurological symptoms at the
onset of aortic dissection frequent (17-40% of
the patients), but they are often dramatic and
may conceal the underlying pathological condi-
tion. Especially in pain-free dissections
(occurring in 5-15% cases) with predominant
neurological symptoms, diagnosis of AD can be
difficult and delayed.2,3

Despite major advances in diagnostic imag-
ing and progress in therapy, the diagnosis of
aortic dissection still remains unsuspected in
a high number of patients (up to 28%), and
mortality rate is still high.2,4

In literature, only few cases of transient
global amnesia (TGA) have been reported in
association with acute aortic dissection
(AAD).5-16

Hence, with the case reported below, we

want to emphasize AD as a rare cause of pure
TGA. Indeed, TGA itself often has a benign nat-
ural history, but AAD can be life-threatening if
it remains undiagnosed. 

Case Report

A 46-year-old man was admitted for the first
time to the emergency department (ED) of San
Giovanni Bosco Hospital because of an evi-
dent, sudden memory loss. His wife witnessed
the onset of the episode and reported that
since that morning his husband was mentally
confused and unable to remember what she
had said only few minutes before. 

His past medical history was unremarkable.
He had a family history of hypertension and
diabetes. He denied any known allergy and was
not taking any medications at home. At the
time of admission the patient was conscious
but mentally confused and continously asked
questions. He had no other symptoms than
headache, chest, neck or abdomen pain. His
physical examination was inexpressive and
appeared in general good conditions.

The vital parameters showed slight hypoten-
sion and the patient complained of a sense of
general weakness. There were no signs of
trauma or seizure-like activity and the neuro-
logical exam was completely normal except for
a severe memory impairment.

Electrocardiogram, chest radiography and
computed tomography (CT) scan of the head
did not reveal any abnormal findings. Few
hours after his admission, his ability to form
new memories started to improve suggesting a
benign pathology. During the period of obser-
vation the patient fully recovered; neverthe-
less, he continued to have difficulties remem-
bering the chronological order of events.

The patient was discharged about after 30 h
from admission with the diagnosis of TGA.
However, in order to exclude other differential
diagnoses, he was addressed to a further out-
patient neurologic evaluation and imaging
studies [electroencephalography (EEG), brain
magnetic resonance imaging (MRI) and ultra-
sonographic Doppler examination of carotid
and vertebral arteries].

The day after, his wife took him again to the
ED because of a recurrent episode of severe
memory loss. The patient was conscious, ori-
ented and co-operative, and his neurological
examination was still normal with no focal
neurological signs.

Upon clinical examination, he presented
blood pressure difference between his upper
extremities (128/41 mmHg on the left arm vs
98/43 mmHg on the right arm), his heart rate
was 110/min, regular, and pulse oximetry was
92%.

Chest x-ray and blood gas analysis were nor-

mal, while electrocardiography (ECG) revealed
signs of myocardial ischemia with ST-segment
depression in leads V3-V4-V5-V6.

Lab results showed increased levels of car-
diac enzymes (Troponine T 0.26 ng/mL), ele-
vated white blood cell count (16,000 cells/mm
Neutrophils 84.6%), stable creatinine (1.0
mg/dL) and marked positive D-dimer (4.93
mcg/mL). Levels of electrolytes were normal,
while lactate dehydrogenase (LDH) and C
reactive protein levels were 544 UI/L and 12.3
mg/dL, respectively.

Since D-dimer test result was positive, chest
CT angiogram was performed and confirmed
the suspected aortic disease. A Stanford type A
dissection involving the arch and the thoracic
aorta up to the abdominal tract and iliac arter-
ies was found. The dissection involved the
common and internal carotid artery on the left,
sparing the right common carotid artery
(Figures 1 and 2).

The patient was immediately transferred to
a cardiovascular thoracic surgery facility
where an endovascular repairing procedure
was successfully performed.

Discussion

Transient global amnesia is a neuropsycho-
logical syndrome in which a sudden, temporary
loss of the capacity of creating new memories
and a retrograde amnesia of variable intensity
occur, whereas consciousness, personal identi-
ty and attention are preserved. Patients usual-
ly have repetitive questioning and may be con-
fused.5

Emergency Care Journal; volume 9:e11

Correspondence: Monica Masoero, Emergency
Department, San Giovanni Bosco Hospital, piazza
Donatore del Sangue 3, 10124 Torino, Italy.
Tel./Fax: +39.011.4271099.
E-mail: raerte@yahoo.it

Key words: aortic dissection, transient global
amnesia, atypical presentation.

Contributions: the authors contributed equally. 

Conflict of interests: the authors declare no
potential conflict of interests.

Received for publication: 5 April 2013.
Revision received: 28 May 2013.
Accepted for publication: 29 May 2013.

This work is licensed under a Creative Commons
Attribution 3.0 License (by-nc 3.0).

©Copyright M. Masoero et al., 2013
Licensee PAGEPress, Italy
Emergency Care Journal 2013; 9:e11
doi:10.4081/ecj.2013.e11

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[Emergency Care Journal 2013; 9:e11] [page 31]

Generally, the typical duration of amnesia in
TGA is 12 h, and it never lasts more than 24 h.
Diagnostic criteria of TGA are purely based on
patient’s clinical features (Table 1).

Classical AAD has been described as pre-
senting with sudden, severe chest, back, or
abdominal pain characterized as ripping or
tearing in nature.1

Carotid dissection (CD) may represent a
threatening complication of AD or may be an
isolate disorder. The disease presents most
commonly with headache, Horner’s syndrome,
stroke, and cranial nerve palsies.7

Depending on the extent of the dissection
and any involvement of aortic branches,
patients with AD may present with a wide
range of symptoms and signs that may be com-
mon in other conditions as well, such as
ischemic stroke, myocardial infarction or other
neurological syndromes including TGA. Our
patient had no significant predisposing factors
for AD, such as a history of trauma, prior car-
diac surgical intervention, or known connec-
tive tissue disease, and at the time of admis-
sion, none of the most common manifestations
of AAD or CD occurred. To our knowledge, lit-
erature reports only four other cases of pure
TGA syndrome in association to AAD.10,12,13,15 In

two further cases, focal neurological symptoms
were associated (anysocoria, motor deficits)
and investigated.8 Our patient initially pre-
sented with a pure TGA without pain,
headache or focal neurological deficits. Still,
retrospectively, the sense of general weakness
with hypotension, and the slightly prolonged
duration of the episode (>12 h) were atypical
of classical TGA. In fact, the patient came back
to the ED again with the same amnesic disor-
der. This time, though, additional clinical and
laboratory signs such as difference in blood
pressure between the two arms, leukocytosis,
elevated D-dimer, LDH and C reactive protein

with concomitant increase of cardiac enzymes
(Troponine T) and ECG findings of myocardial
ischemia aroused the clinical suspicion of AD.
Moreover, in benign TGA recurrence is rare as
the reported risk of a recurrent attack within 5
years varies between 3 and 20%.3 For this
patient, thoracic CT scan was performed,
because the positive D-dimer test was inter-
preted together with the clinical features and
imaging or laboratory tests mentioned above.

D-dimer measurement is helpful for physi-
cians to order imaging tests. However, our case
showed that other important signs should lead
to suspect AAD as well as increased D-dimer

Case Report

Table 1. Transient global amnesia diagnostic criteria.

Attack must be witnessed
Acute onset of anterograde amnesia must be present
No alteration in consciousness must be present
No cognitive impairment other than amnesia must be present
No loss of personal identity must be present
No focal neurology or epileptic features must be present
No recent history of head trauma or seizures must be present
Attack must resolve within 24 h

Figure 1. Computed tomography angiography of the dissected
aortic arch showing an intimal flap separating the two lumens
(right arrow). The dissection involved the left carotid artery
(upper-middle arrow).  

Figure 2. Computed tomography angiography showing the extent
of the dissection up to the abdominal tract of the aorta and the
iliac arteries (arrow).

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[page 32] [Emergency Care Journal 2013; 9:e11]

levels. In literature, pulse deficits and differ-
ence of blood pressure have been described as
initial manifestation of AAD. Even if they are
not frequent (from about 10% to 30%), they
could suggest the diagnosis of AD and lead to
further diagnostics. In AAD, Troponine T may
be increased in up to 18% of patients at pres-
entation and is reportedly associated with a 3-
to-4-fold increased risk of delayed in-hospital
diagnosis.9

Colotto et al. provided a practical diagnostic
algorithm for a new approach to TGA patients
admitted to the ED. The first step is to collect
information about the onset of amnesic attack.
The second step is to carefully check the pres-
ence of the clinical and laboratory signs that
were described in previously reported cases
(Table 2).8,10,12-15 If none of the findings in Table
2 is registered, a pure TGA syndrome can be
suspected. Otherwise, if any of these abnor-
malities is present, ED physicians have to sus-
pect the possibility of AAD and urgent angio-
CT scan of the aorta must be considered.10 As
previously reported, the first thing to investi-
gate when examining a TGA patient in ED is
whether anyone witnesses the onset of amne-
sia attack: asking relatives, colleagues or any
other possible witness is recommended. 

Amnesic patient probably cannot recall the
onset of symptoms or even pain because the
memory of the episode is lost in amnesia.10

In literature, sudden paleness, syncope,
acute chest or back pain immediately preced-
ing the amnesic disorder have been described
as clues of AAD.10,12-14 

The pathophysiology of TGA remains
unknown; there are different hypotheses, but
the general consensus is that the amnesic dis-
order results from transient dysfunction in the
hippocampal structures, crucial to memory for-
mation. The dysfunction is often related to
idiopathic TGA, but epileptic or vascular origin
is also possible.15

The relationship between AAD and TGA is
still uncertain. In AD patients, the propagation
of the dissection and false lumen to the cere-
bral arteries could transiently reduce cerebral
blood flow and entail an ischemic stroke with
focal signs or a hypoxic encephalopathy with
syncope, seizure, or global amnesia. In two 

case reports, authors postulated that the acute
pain of AD triggered the stress reaction
responsible for TGA.12,13 In our case there was
no pain but neurological signs could also be
explained by systemic hypotension and related
cerebral perfusion deficit. 

Interestingly, neurological findings are fre-
quently evanescent and often fully remitted
before admission to the emergency room.3

They usually appear at or soon after the onset
of dissection. Rapid improvement in such
cases is probably the result of only transient
arterial occlusion at the moment of propaga-
tion of the dissection.2

In a recent study, Imamura et al. reported
that more than half of the patients with pain-
less AD were hypotensive. Hypotension
occurred in more than 25% of patients with
AAD and was associated with a higher rate of
in-hospital mortality and adverse events. It is
possible that hypotension reduces pain
because of low wall stress on the aorta.16 Also,
approximately half of all patients who did not
report pain showed neurological symptoms
only.3

Conclusions

In conclusion, our case report shows that
AAD diagnosis can be difficult and delayed
when clinical presentation is atypical.
Neurological symptoms are observed in one
third of patients with AD type A but the
absence of the important cardinal symptom
pain may misdiagnose AAD. Therefore, ED
physicians must have a high index of clinical
suspicion for this condition.

Although a pure TGA syndrome in associa-
tion with AAD is rare, AD should be considered
in the differential diagnosis of patients who
are admitted to the ED with a severe memory
impairment and the following clinical and lab-
oratory signs: hypotension/hypertension or dif-
ference in blood pressure between the two
arms, syncope or paleness, chest, neck or lum-
bar pain, fever, leukocitosis, and increased D-
dimer, myocardial enzymes, LDH or serum cre-
atinine levels. 

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Case Report

Table 2. Clinical and laboratory signs already described in previously reported cases.

Hypotension/hypertension or difference blood pressure between the arms10,12,13

Syncope, paleness12,13,14

Chest/back/lumbar pain8,13

Fever14

Leukocytosis10,14,15

Increase of D-dimer levels10

Unexplained increase of serum creatinine levels14,15

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