The Stolen Memory: A Case of Transient Global
To the Editor:
new memories recovers gradually, in minutes to hours, with an
average of 4 to 6 hours (1), leaving only a dense amnesic gap for
the duration of the episode. Transient global amnesia is likely to
be due to an acute impairment of the hippocampus (2) but the
etiopathogenesis is debated. Ischemia, epileptiform activity, and
psychological factors may contribute to TGA.
The strongest argument in favor of the ischemic etiology is the
presence of a small area of restricted diffusion-weighted imaging
(DWI) signal in the hippocampus, which appears in the magnetic
resonance imaging (MRI) scan data of most patients with TGA (1,3).
Diffusion-weighted imaging hypersignal indicates cytotoxic edema;
therefore, it is considered the hallmark of brain ischemia (4).
Nevertheless, an analysis of risk factors leads to the conclusion that
the cerebrovascular etiology is unlikely, even in individuals with
DWI lesions (5). An epileptic origin has been considered (6) but it
appears unlikely, because of the long duration and the low recur-
rence rate of the episodes and the absence of convulsions, impair-
ment of consciousness, or other signs of cortical dysfunction (7).
Finally, psychogenic origin has been proposed: TGA commonly
occurs in periods of stress, overwork, and emotional arousal (7) or
after stressful events, pain, or sexual intercourse.
As follows, we describe a patient with TGA in whom the
clinical, neuroimaging, and electroencephalogram (EEG) find-
ings demonstrate a transient, reversible, dysfunction of the
ransient global amnesia (TGA) is a clinical syndrome
characterized by the abrupt onset of anterograde amnesia
without other neurological deficits. The ability to lay down
assault for robbery in which her handbag was stolen. She fell to
the ground, but she did not report physical injuries or head
trauma and she did not lose consciousness. In the following
minutes, she developed memory impairment. The relatives re-
ferred that she kept repeating the same questions. No abnormal
movements, automatisms, or impairment of consciousness were
observed. She presented to the Emergency Department 1 hour
after the assault; she was well oriented but presented a severe
anterograde amnesia. She was apyrexial, blood pressure was
130/80 mmHg, heart rate was 80 beats per minute (bpm)
rhythmic, and blood gas analysis and blood essays were normal.
The medical and neurologic histories were unremarkable. No
anxiety, mood disorder, or sleep complaints were reported. In
the anamnesis, she was born from eutocic delivery and she never
suffered from febrile convulsions, head traumas, loss of con-
sciousness, or migraine. She took no medications, and she
denied smoke and alcohol assumption. Neck ultrasonography
and transthoracic echocardiogram were negative; in particular,
no signs of patent foramen ovale were detected. Computed
tomography scan was negative. Brain MRI, performed 36 hours
after the onset, showed a punctuate area of restricted diffusion in
the left hippocampus (Figure 1A); no other abnormality was
present. Electroencephalogram showed a focus of slow waves
and spikes in the left frontotemporal leads (Figure 1B). Dipole
source analysis (Advanced Source Analysis software 3.1, ANT
Software BV Colosseum 2, Enschede, The Netherlands) demon-
strated that the generator of these EEG spikes closely overlapped
with the MRI lesion (Figure 1C). The patient fully recovered in 5
hours and only an amnesic lacuna persisted concerning the
events that occurred in the 60 minutes immediately following the
A 65-year-old woman was the victim of an
(3.5) of restricted diffusion is visible in the left hippocampus (white arrow). (B): EEG performed the day after the admission (36hours after the onset of TGA,
the lower right corner. (C): Results of the dipole source analysis performed by means of Advanced Source Analysis software version 3.1 ( software BVC
axial views. EEG, electroencephalogram; MRI, magnetic resonance imaging; TGA, transient global amnesia.
BIOL PSYCHIATRY 2010;67:e31–e32
© 2010 Society of Biological Psychiatry
assault. No treatment was started. Two months later, the MRI
lesion and the EEG focus were no longer detectable.
for definite TGA (8). The clinical, neuroimaging, and EEG data
do not permit drawing any definite conclusion concerning the
etiopathogenesis of TGA in our patient; nevertheless, we believe
that our observations are consistent with a transient dysfunction
of the hippocampus with morphological (MRI) and neurophys-
iological (EEG) correlates. In fact, the TGA in our patient was
associated with a reversible DWI abnormality in the left hip-
pocampus; the EEG showed a left temporal lobe focus; and the
EEG source modeling, within the limits of this technique (9),
confirmed the co-localization of MRI and EEG abnormalities
The hippocampus is a crucial structure for memory. It repre-
sents the site of storage of episodic memory (10) before it is
transformed into long-term memory in the neocortex (11). The
hippocampus is a particularly vulnerable region of the brain. In
particular, the CA1 region of the hippocampus, which seems to
be selectively involved in TGA (12), is one of the most vulnerable
areas to ischemia (13). This occurs because the hippocampal
artery supplies an internal anastomosis forming a link between
an upper and a lower artery: this creates a watershed area, called
“hypoxia-susceptible sector of Sommer.”
The hippocampus is also particularly vulnerable to excito-
toxic mechanisms: it is proven that high extracellular glutamate
concentrations have an epileptogenic role in seizures arising
from mesial temporal lobe (14,15). Moreover, a wide variety of
stressful events, including emotional experiences, may overex-
cite the hippocampus and induce glutamate release, which
triggers the spreading depression and the functional ablation of
the hippocampus (16,17). This excitotoxicity-induced damage
can produce both EEG discharges (14,15) and abnormal DWI
In conclusion, in our patient, the TGA was associated with a
transient structural and functional modification of the hippocam-
pus, with intracellular edema reflected by DWI and paroxysmal
activity resulting in EEG epileptiform discharges. This observa-
tion suggests that TGA may be a model of a reversible hippocam-
pal dysfunction associated with acute MRI and EEG abnormali-
ties that do not necessarily support an ischemic or epileptic
Our patient fulfilled all the diagnostic criteria
The authors report no biomedical financial interests or po-
tential conflicts of interest.
Giacomo Della Marca
Department of Neurosciences
Policlinico Universitario “A. Gemelli”
L.go A. Giamelli, 8
00168 Rome, Italy
Vincenzo Di Lazzaro
Department of Neurosciences
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