Letter to the Editor
Received: February 24, 2006
Accepted: May 16, 2006
Published online: August 17, 2006

Eur Neurol 2006;56:54–56
DOI: 10.1159/000095145

Transient Global Amnesia Associated with Acute
Intracerebral Hemorrhage at the Cingulate Gyrus
Bora Yoon Ji-Yeon Yoo Yong-Soo Shim Kwang-Soo Lee Joong-Seok Kim
Department of Neurology, The Catholic University of Korea, Seoul, Korea

Case Report
A 57-year-old right-handed man was
admitted via the emergency room because
of an acute memory disturbance and repetitive questioning. He asked his friend the
same questions repeatedly, e.g. ‘What am I
doing here?’, ‘How did I get here?’. When
his friend gave him an answer, he then said
‘Yes, I see’, but then repeated a similar
question again. He did not complain of any

other neurological symptoms such as headache, dizziness or focal weakness. There
was no history of hypertension, diabetes,
transient ischemic attacks, stroke, epilepsy,
migraine, psychiatric illness, head trauma
or alcohol abuse.
On examination, the patient was alert,
with a blood pressure of 130/80 mm Hg, a
regular heart beat of 75 beats/min and a
temperature of 36.7 ° C. Physical examination demonstrated no pathologic findings.
On cognitive function evaluation, comprehension was intact and the patient was fully conscious; however, he immediately forgot what was heard and continued repetitive questioning regarding what he was
doing here. Except for memory deficits, the
other cognitive profiles, which included attention, praxis, language and frontal function, were normal. The patient’s amnesia
and repetitive questioning gradually resolved after 6 h. The next morning, the patient was oriented and had recovered anterograde and recent retrograde memory,
but not memory during the attack.
Laboratory studies including complete
blood cell and platelet count, erythrocyte
sedimentation rate, blood electrolytes, creatinine, liver enzymes, cholesterol, triglycerides, prothrombin and partial thromboplastin time, antithrombin III-protein C
and protein S activity were all normal. In
addition, autoantibody screens were also
normal. Neither the electrocardiogram
from a 24-hour Holter monitor nor transthoracic echocardiography revealed any
cardiac abnormalities. The waking surface
EEG during the episode was normal. Brain

© 2006 S. Karger AG, Basel
0014–3022/06/0561–0054$23.50/0
Fax +41 61 306 12 34
E-Mail karger@karger.ch
www.karger.com

Accessible online at:
www.karger.com/ene

MRI studies 3 days after the attack, including gradient echo images, demonstrated a
focal intracerebral hemorrhage at the left
cingulate gyrus. The hippocampus, thalamus and basal ganglia appeared normal.
Magnetic resonance angiograms of the
brain were also normal (fig. 1).
A neuropsychological test for memory
function performed 7 days after the episode
was within normal limits. The Korean
Mini-Mental State Examination score was
29. On the 12-word list test from the Hopkins Verbal Learning Test for verbal memory the scores for immediate recall were
5 in the first trial, 7 in the second trial and
8 in the third trial; the result after a 20-min
delayed recall was 6, and the recognition
score was 9 (true positive 10 and false positive 1). The results of the Digit Span Test
for attention and immediate memory were
Forward 7 and Backward 5. The score for
the Korean version of the Boston Naming
Test for language was 51, and the scores for
the Word Fluency Test (animal, grocery
item and 3 Korean letters) were 15, 17, 6, 7,
7, respectively. The Go/No Go tasks and
the Luria Loop Test for frontal lobe function were normal. Positron emission topography scans using 18F-dexoyglucose
performed on the same day did not reveal
any abnormalities.
Discussion
Explanation of the mechanisms involved in a TGA have included the hypoxic-ischemic theory, which might best explain the findings of high prevalence of
emotional distress, personality traits, and

Joong-Seok Kim, MD
Department of Neurology, Kangnam St. Mary Hospital
505, Banpo-dong, Seocho-gu
Seoul, 137-070 (Korea)
Tel. +82 2 590 2091, Fax +82 2 599 9686, E-Mail neuronet@catholic.ac.kr

Downloaded from http://karger.com/ene/article-pdf/56/1/54/2717857/000095145.pdf by guest on 12 April 2024

Dear Sir,
Transient global amnesia (TGA) is a benign neurological syndrome characterized
by temporary loss of anterograde and recent retrograde memory with preserved
consciousness and self-awareness; it is usually accompanied by repetitive questioning
and temporal disorientation for a limited
period of time [1]. In the majority of TGA
cases, no cause can be identified; structural imaging is invariably normal and CSF
studies are generally not performed. EEGs
that have been performed during an episode have been reported to demonstrate no
epileptiform abnormalities [2]. Several different causes for this syndrome have been
proposed, including ischemia, migraine,
epileptic seizure, venous congestion and
psychological disturbances; however, there
remains no consensus on the etiology [3].
Moreover, TGA associated with intracerebral hemorrhage has rarely been reported.
The patient described here presented
with transient amnesia resulting from a left
cingulate lesion. This is of particular interest because these findings suggest that activity in the cingulate gyrus and its outflow pathways may lead to TGA.

Downloaded from http://karger.com/ene/article-pdf/56/1/54/2717857/000095145.pdf by guest on 12 April 2024

Fig. 1. Hemorrhage was found at the left cingulated gyrus on the T2-weighted axial image (a),
T1-weighted axial image (b), T1-enhanced axial
image (c), and gradient echo image (d). e, f The

hippocampus, thalamus and basal ganglia appeared normal on diffusion-weighted images. g,
h Magnetic resonance angiograms of the brain
were also normal.

Transient Global Amnesia

Eur Neurol 2006;56:54–56

55

56

It is of course possible that TGA may be
a coincidental finding in a patient with a
cingulate hemorrhage. However, the relationship between clinical TGA and the
subacute-stage hemorrhage of cingulate
gyrus, as well as the absence of other observed etiologies, favors a cause-and-effect
relationship, rather than a coincidental occurrence.
In our patient, the involvement of the
cingulate gyrus was thought to be due to a
wide range of possible causes, because the
etiology remains unclear and the lesion location was uncommon. The differential diagnosis may include superior sagittal sinus
thrombosis, subarachnoid hemorrhage,
vasculitides and hypertensive encephalopathy. However, these diseases can be excluded in our case due to the clinical presentation, normal laboratory findings and
absence of typical radiological signs such
as an empty delta.
In conclusion, although there remains
no consensus on the etiology of TGA, any
focal involvement of a memory-related
structure may cause TGA. This case may
aid in our understanding of the relationship between a lesion and the etiology of
TGA, despite the fact that a cause-and-effect relationship cannot be proven.

Eur Neurol 2006;56:54–56

References
1 Fisher CM, Adams RD: Transient global amnesia. Acta Neurol Scand 1964;40:S1–S83.
2 Jacome DE: EEG features in transient global
amnesia. Clin Electroenceph 1989; 20: 183–
192.
3 Pantoni L, Lamassa M, Inzitari D: Transient
global amnesia: a review emphasizing pathogenic aspects. Acta Neurol Scand 2000; 102:
275–83.
4 Ay H, Fruie KL, Yamada K, Korroshetz WJ:
Diffusion-weighted MRI characterize the
ischemic lesion in transient global amnesia.
Neurology 1998; 51:901–903.
5 Santos S, Lopez del Val J, Tejero C, Inguez C,
Lalana JM, Morales F: Transient global amnesia: a review of 58 cases. Rev Neurol 2000;
30:1113–1117.
6 Gass A, Gaa J, Hirsch J, Schwartz A, Hennerici MG: Lack of evidence of ischemic tissue
change in transient global amnesia on single-shot echo-planar diffusion-weighted
MRI. Stroke 1999; 30:2070–2072.
7 Strupp M, Bruning 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.

8 Strong AJ, Fabricius M, Boutelle MG, et al:
Spreading and synchronous depression of
cortical activity in acutely injured human
brain. Stroke 2002; 33:2738–2743.
9 Ravindran V, Jain S, Ming A, Bartlett RJ:
Transient global amnesia in a patient with
acute unilateral caudate nucleus ischemia. J
Clin Neurosci 2004;11:669–672.
10 Saito K, Kimura K, Minematsu K, Shiraishi
A, Nakajima M: Transient global amnesia associated with an acute infarction in the retrosplenium of the corpus callosum. J Neurol
Sci 2003;210:95–97.
11 Bogousslavsky J, Regli F: Transient global
amnesia and stroke. Eur Neurol 1988; 28:
106–110.
12 Jacome DE, Yanez GF: Transient global amnesia and left frontal hemorrhage. Postgrad
Med J 1988;64:137–139.
13 Warren JD, Chatterton B, Thompson PD: A
SPECT study of the anatomy of transient
global amnesia. J Clin Neurosci 2000;10:57–
59.
14 Schmidtke K, Reinhardt M, Krause T: Cereral perfusion during transient global amnesia: findings with HMPAO SPECT. J Nucl
Med 1998;39:155–159.
15 Laloux P, Brichant C, Cauwe F, Decoster P:
Technetium-99m HMPAO single photon
emission computed tomography imaging in
transient global amnesia. Arch Neurol 1992;
49:543–546.
16 Fujii K, Sadoshima S, Ishitsuka T, Kusuda K,
Kuwabara Y, Ichiya Y, Fujishima M: Regional cerebral blood flow and metabolism in patients with transient global amnesia: a positron emission tomography study. J Neurol
Neurosurg Psychiatry 1989;52:622–630.
17 Eustache F, Desgranges B, Aupee AM, Guillery B, Baron JC: Functional neuroanatomy
of amnesia: positron emission tomography
studies. Microsc Res Tech 2000;51:94–100.
18 Baron JC, Petit-Taboue MC, Le Doze F, Desgranges B, Ravenel N, Marchal G: Right
frontal cortex hypometabolism in transient
global amnesia. A PET study. Brain 1994;117:
545–552.
19 Fazio F, Perani D, Gilardi MC, Colombo F,
Cappa SF, Vallar G, et al: Metabolic impairment in human amnesia: a PET study of
memory networks. J Cereb Blood Flow
Metab 1992 ;12:353–358.
20 Yoshiura T, Mihara F, Ogomori K, Tanaka A,
Kaneko K, Masuda K: Diffusion tensor in
posterior cingulate gyrus: correlation with
cognitive decline in Alzheimer’s disease.
Neuroreport 2002;13:2299–2302.
21 Cammalleri R, Gangitano M, D’Amelio M,
Raieli V, Raimondo D, Camarda R: Transient
topographical amnesia and cingulate cortex
damage: a case report. Neuropsychologia
1996;34:321–326.

Yoon/Yoo/Shim/Lee/Kim

Downloaded from http://karger.com/ene/article-pdf/56/1/54/2717857/000095145.pdf by guest on 12 April 2024

Valsalva-like activities before onset of
symptoms as well as a high frequency of
cerebral infarction and ischemic changes
found on brain imaging [4, 5]. However,
there are some reports that argue against
an ischemic etiology for TGA that have
shown a lack of association between vascular risk factors and TGA, and signal changes on DWI from nonischemic causes [6].
Patients with intracerebral hemorrhage
presenting with TGA have also been reported, but rarely. Some investigators have
proposed a cortical spreading depression
as the cause of TGA. In a report by Strupp
et al. [7], description of widespread transient hyperintensities in the left or bilateral
mesial temporal lobes was observed in patients with acute TGA. The researchers believed that these findings were consistent
with a spreading depression. Additionally,
Strong et al. [8] reported cortical spreading
and synchronous depression on electrocorticography in patients after head injury
or intracranial hemorrhage.
Despite the unresolved etiology of
TGA, there is general agreement that pathological changes affect the mediobasal
temporal region, the hippocampus and the
parahippocampus. It has been reported
that TGA occurred in patients with acute
infarction of the hippocampus, thalamus,
caudate nucleus [9] and retrosplenium of
the corpus callosum [10], or with hemorrhage at the thalamus, lenticular nucleus
[11], and frontal lobe [12]. Studies utilizing
functional neuroimaging observations
suggest a dysfunction in memory-relevant
structures such as the prefrontal cortex,
hippocampus, temporal lobe or thalamus
during the acute stage of TGA [13–19].
These findings suggest that all loci identified have been within the areas of memory-relevant structures including the Papez
circuit, and most have been on the left side
of the brain.
Our patient presented with a TGA
which was related to a small hemorrhage
neighboring the left cingulate gyrus. The
findings from this case support that the
cingulate cortex, including the cingulum
which connects to the entorhinal, prefrontal cortex and other neocortical areas, may
be important to the memory circuit (Papez
circuit) and critical to the maintenance
and processing of cognitive function [20,
21].