Transient autobiographic amnesia
EEG and single-photon emission CT evidence
of an organic etiology
Annalena Venneri, PhD; and Paolo Caffarra, MD

Article abstract-We describe a 44-year-old patient who had a transient attack of autobiographic amnesia. When
assessed during the attack, her learning abilities were normal, with no sign of anterograde amnesia. In the remote
memory domain, she showed a striking dissociation between a detailed knowledge of public events and famous people and
a complete loss of autobiographic information. During the attack, EEG recorded bilateral frontotemporal slow waves and
single-photon emission CT (SPECT) showed hypoperfusion in the right temporal and parietal lobes; no abnormalities were
detected when both EEG and SPECT were repeated 1week later. This case provides evidence for an organic etiology for
the episode and supports the hypothesis that autobiographic memory is independent of other forms of retrograde memory.
NEUROLOGY 1998;50: 186-191

Amnesia may be observed as a transient or permanent phenomenon. Transient global amnesia (TGA)
is common (see refs. 1 and 2 for a review). More
recently, a few cases of transient partial deficits of
memory, affecting verbal memory
or topographic memory4have been reported.
Cases of transient memory deficit with loss of personal identity can also be found in the literature (see
ref. 5 for a review). These have been classified as
cases of hysterical or psychogenic amnesia (psychogenic fugue), where the critical features for differentiating them from organic amnesia were loss of
personal identity (preserved in genuine cases of organic TGA) and preserved anterograde memory (normally greatly impaired in organic TGA).
We report a patient who suffered from a transient
autobiographic memory loss, from which she recovered spontaneously after 17 hours. Her neuropsychological and neuroimaging findings are discussed,
focusing on the differential diagnosis between an organic and a psychogenic etiology.
Case report. TB is a 44-year-old right-handed woman
with 13 years of formal education who works as a secretary
with no history of psychiatric disturbance or drug or alcohol abuse.
On June 12, 1993, during her morning coffee break, she
left her office and went into a nearby shop. At the checkout, she became confused and repeatedly asked the people
standing near to her what was happening. She could not
recall anything about herself and was so distressed that
the shop manager called an ambulance. She was admitted
after a few minutes t o the emergency room of Parma Hospital. Her neurologic examination disclosed no sign of sensory or motor deficits, and deep tendon reflexes were
symmetric. She was alert, spatially oriented, but unable to

recall any personal information about herself, her work,
and family contexts. She appeared worried and could not
understand why she could remember everything but information about herself.
TB’s profile appeared different from cases of TGA, because she could easily remember things that had happened
since the onset of the episode. An interview with a psychiatrist discovered no pathologic profile. Nor did we find by
interviewing her husband anything relevant or any possible motive that could justify desire to simulate amnesia
nor any stressful event that could have precipitated it. TB
was under no pharmacologic treatment of any kind. Her
routine blood and chemical investigations were within normal limits.
To ascertain the nature and the extent of TB’s memory
disorder, a neuropsychological examination was carried
out during her stay in the emergency room.
Neuropsychologic examination. TB was cooperative
and willing to perform the neuropsychologic tasks. She
performed normally on digit span (seven digits forward
and five backwardP and visuospatial span (five block^).^
She scored well within the range of performance of the
normal reference population on long-term memory tasks
such as prose memory (10.5), paired associate learning
(11.5),*and supra-span spatial learning (15.32).’ Her score
on an abstract reasoning taskg was close to the median
score achieved by the normal reference sample as well as
her performance on attention7J0 and language11J2 tests.
TB’s semantic knowledge was intact; she could name and
provide detailed physical descriptions of living and nonliving objects both after visual presentation and verbal description and name abstract things after verbal
description. She knew the meaning of some symbols (e.g.,
wedding ring) and meaningful gestures.
Retrograde memory. TB’s autobiographic memory was
tested on a formal standardized q~estionnairel~
intended

From the Department of Psychology (Dr. Venneri), University of Aberdeen, UK; and the Istituto di Neurologia (Dr. Caffarra), University of Parma, Italy.
Supported by M.U.R.S.T. grant 60%, 96 to P.C.
Received February 15, 1997. Accepted in final form July 21, 1997.
Address correspondence and reprint requests to Dr. Annalena Venneri, Department of Psychology, University of Aberdeen, King’s College, Aberdeen, AB24
2UB, UK.
186

Copyright 0 1998 by the American Academy of Neurology

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Figure 1. EEG performed during (a) and after (b) the episode of transient amnesia. Bilateral fi.ontotempora1 slow waves
were recorded during the attack. N o abnormalities were detected 1 week later.
to assess three periods of her life: childhoodadolescence,
early adulthood, and late adulthood, up to 2 years before
testing. She showed no recollection of any important event
in her life. TB could tell the examiner her name (she had
been told that by the hospital staff) but could not recollect
any personal information. When she first saw them, TB
failed t o recognize her husband and daughter, toward
whom she showed no emotional reaction. She was unable
to give details of her own education and occupation. Asked
if she could say something about the duties of a secretary,
she was able to list possible duties as well as those of other
professions (e.g., doctor, nurse, teacher). It was clear from
the examination that she had lost both episodic and semantic autobiographic memory.
On the Famous Face Recognition Test,14 TBs performance was a t ceiling; she could precisely indicate the face
corresponding t o the famous name stated by the examiner
among four alternatives. She could also promptly identify-and provide the corresponding name, although not requested-the familiar face among four choices (one famous
target and three unknown distracters) on the Familiarity
Check Test.14 Her knowledge of events that had been in
the news in the preceding 18 months was excellent. TB
recalled all the major events that had taken place in Italian politics (at that time many representatives of the leading party had been prosecuted for corruption) for which
she could recall time and place.
Seventeen hours after onset, after having had some
sleep, TB spontaneously recovered and was discharged.

Neurophysiologic and neuroimaging findings. During
the attack, the EEG recorded bilateral frontotemporal slow
waves (figure la).
High-resolution single-photon emission CT (SPECT)
was also carried out. Images were obtained with an annular SPECT (Vertex ADAC) with a spatial resolution of 7.2
mm full-width at half maximum (FWHM) in the center of
the axial plane. The injected dose of 99mTchexamethyl
propyleneamine oxime (HM-PAO) was 740 Mbq (20 mCi)
and imaging was performed 15 to 30 minutes after injection. Sixty-four axial slices, each 2 mm thick, were reconstructed. A SPECT image analysis was carried out on a
SUN (SPARC) work station. Circular regions of interest
(ROIs) were manually positioned on the cortical and subcortical structures and on the cerebellar hemispheres.
Mean counts were calculated for each ROI. Average values
were obtained from the multiple ROIs included in nine
anatomofunctional areas according to the Damasio and
Damasio15 atlas. The data were then analyzed as ratios
between counts for the SPECT study in each anatomofunctional region and the cerebellum count.
The SPECT investigation showed a considerable reduction in blood flow in the right temporal and parietal regions (figure 2a). No abnormalities were detected by the
EEG recorded 1week later (June 19, 1993) (see figure lb).
A second SPECT study was carried out on that occasion,
but no relevant abnormalities were detected (figure 2b).
No difference in blood flow was detected in the cerebellar regions, the two values being virtually identical; in
January 1998 NEUROLOGY 50 187

ric interview (MMPI questionnaire) was also administered;
her profile disclosed no personality abnormalities. Two
more years have elapsed since the follow-up, and t o the
best of our knowledge, no further episodes have occurred.

Figure 2. SPECT scans performed during (A) and after
(B) the episode of transient memory loss. Transverse images are shown on the left side of each figure and sagittal
images are shown on the right side of each figure. Hypoperfusion of the right temporal and parietal regions was
detected during the attack. Cerebral perfusion appeared
normal 1 week later.

contrast, a considerable blood flow increment (between
32% and 53%) was observed in the temporal and parietal
regions (table). The increment in other cortical areas was
not greater than 6%.
A CT was performed a few days later. No morphologic
abnormalities were detected.
Follow-up. TB was re-examined 1 year later. No further episodes were reported; TB manifested no psychiatric
disturbance since the foregoing episode of transient memory loss. During the re-examination, a structured psychiatTable Comparison between blood flow values expressed as ratios
of the values normalized to the cerebellum (raw counts shown in

parentheses) measured with SPECT during the attack (June 12)
and 1 week later (June 19)
Cerebral area

June 12, 1993

June 19, 1993

Increment (%)

Parietal

0.428 (30,557)

0.656 (46,808)

53.182

Temporal

0.588 (41,948)

0.782 (55,759)

32.924

Cerebellum

1(71,238)

1(71,257)

0.027

.

The increase in blood flow is represented by the absolute value of
the difference between the SPECT values obtained in the same
cerebral areas during the attack and 1 week later and computing
the percentage of increment with respect t o the values acquired
by the SPECT performed during the attack. The cerebral perfusion was virtually unmodified in the cerebellar regions; a marked
difference between the two SPECTs was detected in the parietal
and temporal areas.
188 NEUROLOGY 50 January 1998

Discussion. TB suffered an episode of transient
autobiographic amnesia, her transient memory loss
being confined to the autobiographic domain; her retrograde memory for famous people and events, her
semantic memory, and her anterograde memory
were all spared.
Etiology. Several etiologic hypotheses could justify TB’s cognitive profile. Malingering was ruled
out, because this patient had nothing to gain by simulating amnesia neither at the time of this episode
nor afterward as ascertained by the follow-up. A
more difficult problem is differentiating between
psychogenic and organic causes of amnesia, especially when no obvious damage to the gross structures of the brain is found. Without a clear “link
between brain and behavior,’’ this argues for a psychogenic label. However, on some occasions, abnormal brain functioning-in
absence of structural
damage-is accepted as evidence of an organic etiology for a phenomenon. For example, abnormalities of
the electrical activity of the brain (as detected with
EEG) without detectable structural damage is a
well-known cause of epilepsy; nobody, however, questions the organic origin of epilepsy. In this patient, in
addition to the neurophysiologic and neuroimaging
findings, the clinical presentation also supports an
organic etiology. Some authors16J7claim that loss of
personal identity is a critical feature of psychogenic
fugues, and it is rarely observed in organic amnesia.
But there is evidence that repetitive questioning is
characteristic of organic amnesia and is not observed
in psychogenic fugues.lS Indeed, TB’s great concern
about her condition is at odds with a sense of general
indifference toward the situation observed in fugue
states.lg Moreover, several people witnessed the onset of TB’s attack, whereas in cases of psychogenic
fugues, no clear testimony of the onset is available,
and often the patient is found wandering around,
sometimes even for several days.
Neurophysiology and neuroimaging. EEG abnormalities (both slow waves and sharp waves) in cases
of TGA have been reported many times (see ref. 5 for
review), but no clear agreement on the meaning of
these abnormalities is available. Some authors20
claim that in many cases these abnormalities are
rather nonspecific. TB’s EEG record during the attack showed bilateral frontotemporal slow waves
that were not detected by the record 1 week later.
However, EEG data alone would not support a
strong conclusion. TB underwent a cerebral SPECT
twice, during the attack and 1 week later. Yet, data
on the test-retest reliability of blood flow measurement with SPECT are scanty, and one should establish that the right temporoparietal hypoperfusion
detected during the attack cannot be accounted for
by low reliability of the SPECT technique or physio-

which may have a different location in the brain.
logic changes in perfusion of those areas. A study of
Some aspects (i.e., the generative retrieval cycle)
the reproducibility of SPECT resultsz1 has shown a
high positive correlation (with level of significance
may well be localized in the frontal areas; others
(i.e., the complex thematic knowledge base) might be
ranging from p < 0.001 to p < 0.01) between two
located in other neocortical areas and others (i.e., the
different measurements with SPECT. In this study,
phenomenologic record) in the posterior sensory arthe intraindividual variability between the measureeas. Either dysfunction of the neurologic pathways
ments ranged from 0.3%to 15% (mean 6.2%). Therethat connect these various areas o r damage to spefore, the proportion of the changes (ranging from
32% to 53%) in the temporal and parietal areas obcific areas-or indeed a combination of both-may
served in our patient’s results is extremely large,
result in autobiographic memory disturbances. This
indicating that the SPECT detected genuine pathoview justifies the heterogeneity of anatomic lesions
logic changes that caused TB’s amnesic episode. This
that resulted in loss of autobiographic information
rules out the hypothesis that the difference we dereported in the literature.
A recent study with PET35that aimed to establish
tected might be the result of a technical artefact. It
may be suggested that the changes might have been
the functional anatomy involved in the retrieval of afcaused by anxiety. However, TB’s SPECT profile
fect-laden autobiographic information has shown that
the neural substrate for autobiographic memory indoes not resemble those of cases of psychiatric disvolves “a network of primarily right hemispheric reease, including anxiety disturbances, which show abgions including temporomedial and temporolateral
normalities mainly in the frontal
cortex, amygdala and hippocampus-parahippocampus,
Mew studies have reported neuroimaging findings
insula, posterior cingulate cortex, temporoparietal corin TGA. Reduced brain perfusion and metabolism
(unilateral or bilateral, more frequently of the frontex, and prefkontal cortex” (p. 4277). Evidence from this
tal andfor temporal regions) detected with SPECT or
study seems to point to a widespread substrate for
autobiographic memory, probably because such memPET during TGA episodes has been repeatedly rep~rted.~
Several
~ - ~ ~physiopathologic explanations
ory involves affect-based information. The findings of
have been provided in those cases: ischemia, seithis activation study are strongly in agreement with
zures, and migraine. Our patient had no history of
the SPECT findings of our patient, who shows loss of
migraine, seizures, or vascular problems; however,
autobiographic information and decrease in blood flow
the possibility that the first SPECT might have
in the right temporoparietal areas. In this view, the
possibility that the simultaneous presence in our padetected postischemic hypoperfusion cannot be
tient of autobiographic memory loss and a decrease in
excluded.
Neuroanatomic considerations. Some ~ t u d i e s ~ ” ,blood
~ ~ flow in the right temporoparietal regions may be
emphasize the role of the frontal lobes in autobiomere coincidence seems rather unlikely.
graphic memory. A disparate finding is that of HokCognitive aspects. Permanent selective loss of
kanen et al.,32 who described a patient showing
memory for autobiographic information has been alisolated retrograde amnesia for autobiographic memready observed in a few cases.32,36-40
Therefore, it
ory after dysfunction of the left temporal lobe (deseems reasonable that the same phenomenon may be
tected by SPECT and EEG). TB’s temporary
observed as a transient loss. The transient nature of
abnormalities were localized bilaterally in the frontothe loss should not be surprising; episodes of partial
temporal regions (as recorded by EEG) and in the
memory loss have been already reported (e.g., verbal
right temporal and parietal lobes (as detected by
m e r n ~ r ytopographic
,~
memory”).As for other aspects
SPECT). The cerebral areas involved in the electrical
of memory, it is possible that memory for autobioand blood flow abnormalities in our patient partially
graphic information might be temporarily disrupted
overlap with those identified in other cases of autoand give rise to transient deficits, from which abrupt
biographic memory loss, thus supporting the hypothrecovery is possible.
esis of an organic etiology for TB’s amnesia.
The case we described provides further support for
The neuroanatomic evidence on the question of
the hypothesis of a fractionation of retrograde memwhich cerebral areas are concerned with autobioory into sub component^,^^ confirming the indepengraphic information is conflicting and inconclusive. A
dent status of autobiographic memory. TB showed a
descriptive
has been suggested to explain the
striking dissociation between her intact knowledge
cognitive organization of autobiographic memory.
of remote public events and famous people and
This model provides an integration of structures and
her complete loss of both episodic and semantic
processes involved in this type of memory, positing a
autobiographic information, components of autobiothematic organization for the cognitive architecture
graphic memory that have often been reported as
of autobiographic memory, according t o major life
dis~ociable.~~-~~~~~.~~
that although
events. However, C ~ n w a ysuggested
~~
Conclusion. This case provides evidence of a seautobiographic memory seems to have a very comlective transient deficit of memory affecting the autoplex cognitive architecture, some aspects of the
biographic domain whose onset, limited duration,
mode1 may be localized. A detailed discussion of the
and clinical presentation parallels cases of TGA. We
provided evidence of neurophysiologic and blood flow
model is beyond the aim of this article; we will only
abnormalities during the attack, with subsequent remention that it incorporates several steps, each of
January 1998 NEUROLOGY 50 189

turn to normality. On consideration of several etiologic hypotheses, we believe that the evidence is
strong enough to support an organic origin for the
episode.
The distinction between organic and psychogenic
amnesia, however, remains very subtle. Markowitsch19 stressed the similarities between the two
forms of amnesia from a cognitive point of view, suggesting that the actual mechanism responsible for
loss of memories for retrograde information is the
consequence of an inability of access to information
both in organic and psychogenic amnesia, because
both represent a temporary (and partial or selective)
memory loss. Despite these similarities, we argue
that a combination of clinical, neuropsychological,
neurophysiologic, and neuroimaging examinations
may provide some help for differentiating the etiology. As with TGA, however, the neurologic factor
triggering the episode remains unexplained.

Acknowledgment
We are grateful to Bruno Calbiani, Nuclear Medicine Unit, Parma
General Hospital, who performed the two SPECT studies.

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Correlations of flow velocity changes
during mental activity and recovery from
aphasia in ischemic stroke
M. Silvestrini, MD; E. Troisi, MD; M. Matteis, MD; C. Razzano, ST; and Carlo Caltagirone, MD

Article abstract-Mean flow velocity in the middle cerebral arteries (MCAs) during a rest period and during execution of
a word-fluency task were measured by means of bilateral transcranial Doppler ultrasonography in 26 stroke patients with
Broca’s aphasia and in 25 healthy controls. Changes in flow velocity were calculated as percentage of increase from rest to
mental activity. In patients, the evaluation was made within 21 days from onset of symptoms and after 2 months of speech
therapy, when they were classified into two groups on the basis of extent of recovery from aphasia: absent or slight
recovery (group 1, 10 patients) and good recovery (group 2 , 16 patients). During the word-fluency task in the first
evaluation, the increase in flow velocity in the left MCA was similar in controls and in group 2 patients. In both groups the
increase was higher than in group 1patients ( p < 0.0001). Changes in mean flow velocity on the right side were slight and
comparable in the three groups of study subjects. After speech therapy, group 1 patients showed a hemodynamic pattern
on both sides similar to that observed in the first examination. In group 2 patients, comparison between values of the first
and second evaluations showed that the increase of flow velocity in the left MCA was similar. On the right side, the
increase was higher in the second than in the first examination ( p < 0.01). These data further support the involvement of
cerebral areas contralateral to the lesion in functional recovery after stroke. Moreover, the presence of an activation of
areas in the lesioned hemisphere, soon after stroke onset, seems to be a predictor of recovery from aphasia.
NEUROLOGY 1998;50:191-195

Aphasia is a common and disabling symptom in
stroke. Early prediction of improvement is essential
for planning the reintegration of patients into social
life and their need for care and, more specifically, for
selecting subjects who might benefit most from rehab i l i t a t i ~ n .Prognostic
~.~
indicators have been widely
investigated. There is considerable uncertainty
about the role of patients’ clinical characteristic^,^
even if initial severity of the language disorder
Some studies have provided
seems to be re1e~ant.l.~
indications about the importance of location and size
of lesions evaluated with brain CT or MRI.‘j However, morphologic examinations are not able to detect structural lesions at the cellular or synaptic
level or functional changes in areas located in both
the affected and contralateral hemispheres. In this
respect, studies of cerebral metabolism and flow using PET have provided very interesting data about

the importance of residual functionality of structures
in the dominant h e m i ~ p h e r eand
~ , ~of early activation
of areas in the unaffected hemispheregJOin the recovery from aphasia and other neurologic deficits. These
functional data seem to be more reliable as early
predictors of the outcome of stroke patients than the
morphologic ones. Investigation techniques able to
provide data on cerebral regional flow and metabolism are, however, too expensive and not widely
available enough for routine use. With transcranial
Doppler ultrasonography (TCD) it is possible to obtain information about changes in cerebral activity
in both norma111J2and pathologic conditions.13 Our
aim in this study was to investigate the correlations
between cerebral hemodynamics detected with TCD
during mental activity requiring activation of the
damaged area and clinical course of aphasia in patients after stroke.

From the Clinic of Neurology (Drs. Silvestrini and Caltagirone), “Tor Vergata” University of Rome; and IRCCS “S. Lucia” (Drs. Troisi, Matteis, Razzano, and
Caltagirone), Rome, Italy.
Received December 24, 1996. Accepted in final form July 31, 1997.
Address correspondence and reprint requests to Dr. Mauro Silvestrini, Clinica Neurologica, Universita di Roma “Tor Vergata,” Ospedale S. Eugenio, P.le
dell’Umanesimo 10, 00144 Roma, Italy.
Copyright 0 1998 by the American Academy of Neurology

191

Transient autobiographic amnesia: EEG and single-photon emission CT evidence of an
organic etiology
Annalena Venneri and Paolo Caffarra
Neurology 1998;50;186-191
DOI 10.1212/WNL.50.1.186
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