REVIEW

Transient Global Amnesia

Julieta E. Arena, MD, and Alejandro A. Rabinstein, MD

Abstract

Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of anterograde
amnesia (the inability to encode new memories), accompanied by repetitive questioning, sometimes with a
retrograde component, lasting up to 24 hours, without compromise of other neurologic functions. Herein,
we review current knowledge on the epidemiology, pathophysiology, clinical diagnosis, and prognosis of
TGA. For this review, we conducted a literature search of PubMed, with no date limitations, using the
following search terms (or combinations of them): transient global amnesia, etiology, pathophysiology, venous
hypertension, migraine, magnetic resonance imaging, computed tomography, electroencephalography, prognosis,
and outcome. We also reviewed the bibliography cited in the retrieved articles. Transient global amnesia is a
clinical diagnosis, and recognition of its characteristic features can avoid unnecessary testing. Several
pathophysiologic mechanisms have been proposed (venous insufficiency, arterial ischemia, and
migrainous or epileptic phenomena), but none of them has been proved to consistently explain cases of
TGA. Brain imaging may be considered and electroencephalography is recommended when episodes are
brief and recurrent, but otherwise no investigations are necessary in most cases. Data on long-term
prognosis are limited, but available information suggests that the relapse rate is low, the risk of stroke
and seizures is not considerably increased, and cognitive outcome is generally good.
ª 2015 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2015;90(2):264-272

T
ransient global amnesia (TGA) was
initially described in 1956 by Bender,1
From the Department of and at the same time but independently
Neurology, Mayo Clinic,
Rochester, MN.
by Courjon and Guyotat,2 as a syndrome char-
acterized by sudden and temporary memory
loss. Yet, it was not until 1964 that it gained
recognition as we know it today, when Fisher
and Adams3 described the syndrome as TGA.
Initially referred to as a heterogeneous clinical
syndrome, the approach to the condition was
refined by the diagnostic criteria proposed by
Caplan4 and consolidated by Hodges and
Warlow5,6 in 1990. Since the first description
of the disorder, a lot has been published about
its clinical characteristics, and several hypotheses
regarding its pathogenesis have been proposed.
Yet, the cause and mechanisms of TGA remain
unclear.
Several reviews on TGA have been pub-
lished,7-12 but they have all been addressed to
neurologists. However, TGA can be encountered
by internists, emergency department physicians,
and family medicine practitioners. We aim to
synthetize current knowledge and to propose a
practical approach to this condition that can be
useful for daily practice. Herein, we also review
the epidemiology, pathophysiology, diagnostic
criteria, differential diagnosis, and expected
long-term outcome of TGA.
The content of this review is based on a
literature search of PubMed, with no date lim-
itations, using the following search terms (or
combinations of them): transient global amnesia,
etiology, pathophysiology, venous hypertension,
migraine, magnetic resonance imaging, computed
tomography, electroencephalography, prognosis,
and outcome. We also reviewed the bibliogra-
phies cited in the retrieved articles. The studies
referenced in this article were selected based on
study quality and clinical relevance.
BASIC CONCEPTS ON MEMORY
Memory is the brain function that allows us to
encode, store, and retrieve information. It can
be divided into 3 different types: immediate or
working memory, short-term memory, and
long-term memory.13 Immediate memory refers
to the information that can be retained for a short
period of time without active involvement of the
memory pathways. It can be simply tested by
asking the patient to repeat a 7-digit number.
This type of memory can be affected by attention
or language impairment or by a lesion to the su-
perior frontal neocortex. Short-term memory
(also called episodic memory) implies the ability
to encode, store, and retrieve information after
minutes or hours; this is the type of memory
that requires normal functioning of the hippo-

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TRANSIENT GLOBAL AMNESIA

campus and parahippocampal areas located in

the medial temporal lobe. It can be tested at the
bedside by asking the patient about his or her ac-
tivities earlier in the day. Long-term or remote
memory relates to long-known information
(where we were born, which school we
attended); it includes semantic memory, which
enables us to have a general knowledge of con-
cepts, facts, and meanings (eg, definitions of
words), and it is supposed to rest in multiple
cortical regions, including the visual association
cortex, temporal cortex, and other cortical struc-
tures according to the type of memory involved.
A simplified memory circuit includes the
hippocampus on each side projecting to the
septal areas via the fornix, then to the mammil-
lary bodies, and subsequently to the anterior nu-
cleus of the thalamus; from there it projects
to the cingulate gyrus of the frontal lobe and
back to the hippocampus, thus completing
the Papez circuit, crucial for short-term memory
(Figure 1). Amnesia is caused by the disruption
of these pathways. Specific memory impair-
ments are determined by the site of involvement.
Affection of the hippocampus will produce
anterograde amnesia, characterized by the
inability to lay down new information.
EPIDEMIOLOGIC PROFILE
Transient global amnesia affects predominantly
middle-aged or elderly patients. Its annual inci-
dence has been reported to be 3.4 to 10.4 per
100,000 people.6,14-16 If we narrow it to the
population older than 50 years, the incidence in-
creases to 23.5 per 100,000 per year.17 It is more
common in individuals with migraine.18,19
ARTICLE HIGHLIGHTS
n Transient global amnesia is a condition that can be encountered
by internists, emergency department physicians, family medicine
practitioners, and, ultimately, neurologists. Its correct diagnosis
relies on recognition of the disease, which can prevent unnec-
essary testing.
n We propose a diagnostic algorithm for patients with sudden-
onset anterograde amnesia and present the diagnostic criteria
for transient global amnesia.
n Episodes are self-limited, and spontaneous improvement is
noted within 24 hours of onset.
n Available data to date indicate that long-term outcome is
generally good in terms of relapse rate and risk of stroke and
seizures. Information regarding long-term cognitive outcome is
scarce but suggests that these patients are not at higher risk for
cognitive impairment.
information. Other neurologic functions are pre-
served, including procedural memory. Thus,
these patients can perform previously learned ac-
tivities (eg, driving) without impairment. These
episodes are sometimes preceded by a precipi-
tating event, such as an activity associated with
a Valsalva maneuver, emotional stress, immer-
sion in cold or hot water, sexual intercourse, or
pain.
Patients having an episode of TGA are char-
acteristically not well aware of their problem,

CLINICAL PRESENTATION AND

DIAGNOSTIC CRITERIA
Transient global amnesia is a clinical syndrome
characterized by the sudden onset of anterograde
amnesia, accompanied by repetitive questioning,
sometimes with a retrograde component, lasting
up to 24 hours, and without compromise of other
neurologic functions. Typically, TGA is encoun-
tered in patients aged 50 to 70 years who are
brought to medical attention because they are
noticed to have acutely lost the ability to under-
stand their situation and grasp their surround-
FIGURE 1. The Papez circuit of short-term memory. The hippocampus on
ings. Patients repeatedly ask questions, such as each side projects to the septal areas via the fornix, then to the mammillary
“Why are we here?” “What time is it?” or “How bodies, the anterior nucleus of the thalamus, the cingulate gyrus of the
did I get here?” The answers are immediately frontal lobe, and back to the hippocampus.
forgotten owing to their inability to encode new

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 MAYO CLINIC PROCEEDINGS

and that is why they are often brought to
consultation by an observer of the episode.
They may appear restless or nervous and
confused, but alertness, self-orientation, recog-
nition of family members, speech, and motor,
sensory, and coordination functions are pre-
served. Mild vegetative symptoms may occur,
such as nausea, dizziness, and headache. If
other neurologic signs are present or con-
sciousness is impaired, other diagnoses should
be excluded. The memory deficit typically lasts
a few hours, often 4 to 6 hours, and always less
than 24 hours.9,20 Then the patient progres-
sively recovers the ability to register and store
new memories. A residual amnestic gap for
the duration of the episode is common.
No laboratory investigations can presently
confirm the diagnosis of TGA. Thus, the diag-
nosis relies on a detailed clinical history, cognitive
evaluation, and physical examination. The physi-
cian should bear in mind the differential diagno-
ses to run the tests necessary to discard them
when pertinent. Diagnostic criteria have been
proposed (Table 1).4-6 These criteria remain
valid, with a few modifications. The possibility
of associated retrograde amnesia is not included
in the criteria, but it is well recognized that pa-
tients with TGA can have some degree of retro-
grade amnesia during the episode, especially for
memories of events that occurred in recent
years.21,22 There are also some studies indicating
that other cognitive functions could also be
mildly affected, such as visuoperceptual ability.23
ADDITIONAL INVESTIGATIONS
When making a diagnosis of TGA, the ques-
tion is whether to pursue additional testing.
The main value of additional testing in TGA
is to exclude alternative diagnoses.
Brain imaging is often considered by clini-
cians who suspect TGA, but findings from head
computed tomography are typically normal,
and evidence on the utility of brain magnetic
resonance imaging (MRI) is conflicting. Case se-
ries and studies comparing patients with TGA
and those with transient ischemic attack (TIA)
or control cohorts have reported that patients
with TGA may frequently, but not always, show
hyperintense signal on diffusion-weighted imag-
ing (DWI) and sometimes on T2-weighted and
fluid-attenuated inversion recovery (FLAIR) se-
quences on either or even both hippocampi, pro-
vided that the MRI is performed within 48 hours
of symptom onset.24-28 Conversely, other studies
reported no MRI changes even in patients
scanned early.29,30
Even when there is evidence of hippocam-
pal restricted diffusion on DWI, these changes
are often reversible, as manifested by the lack
of persistent signal change on T2-weighted
or FLAIR sequences. Signal changes on T2-
weighted or FLAIR sequences can also be
reversible.31,32 This would indicate that the
changes are not due to ischemia or that ischemia
is not critical enough to cause an infarction. In
addition, the abnormal DWI signal is character-
istically confined to one or both hippocampi,
which is a very unusual pattern for ischemic
stroke. In typical cases of TGA, it is not neces-
sary to pursue a comprehensive stroke work-
up (ie, vascular imaging, cardiac evaluation,
and coagulation studies) as long as brain MRI
abnormalities are restricted to hippocampal
regions.
Internal jugular venous flow reversal (IJVFR)
and internal jugular vein valve incompetency
(IJVVI) have been proposed as potential patho-
physiologic mechanisms, and these phenomena
can be documented by Doppler studies of the in-
ternal jugular veins or by air-contrast ultrasound.
However, not all patients with TGA show IJVVI
or IJVFR, and not all individuals with IJVVI
will have an episode of TGA. In addition, jugular
venous flow studies are not commonly per-
formed, and, consequently, their reliability may
vary across centers. Hence, these studies cannot

TABLE 1. Diagnostic Criteria for Transient Global Amnesia

Attack must be witnessed and information available from a capable observer who was present for most of the attack
Clear-cut anterograde amnesia during the attack
Cognitive impairment limited to amnesia, without clouding of consciousness or loss of personal identity
No accompanying focal neurologic symptoms during the attack and no significant neurologic signs afterward
Absence of epileptic features
Resolution of the attack within 24 h
Patients with recent head injury or active epilepsy are excluded

n n
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TRANSIENT GLOBAL AMNESIA

be recommended as routine investigations to

DWI ¼ diffusion-weighted imaging; EEG ¼ electroencephalography; FLAIR ¼ fluid-attenuated inversion recovery; MRI ¼ magnetic resonance imaging; TEA ¼ transient epileptic amnesia; TGA ¼ transient global amnesia; TIA ¼
anticonvulsant
Response to
confirm or discard the diagnosis of TGA.

medications
The value of electroencephalography (EEG)
is also limited. During and after typical TGA ep-

Yes
No

No
isodes, EEG findings have been reported to be
normal.17,33,34 However, transient episodes of

Recurrence
of attacks
amnesia can be caused by seizures. These epi-
sodes, known as transient epileptic amnesia

High
Low

Low
(TEA), tend to be shorter and recurrent, and
they may be accompanied by other manifesta-

frontotemporal regions)
tions, such as oral automatisms and olfactory

Abnormal (temporal or
or gustatory hallucinations. Hence, EEG
should be performed when TEA is considered

EEG
likely and not to support or disprove the diag-
nosis of TGA.

Normal

Normal
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of TGA includes TIA
Hippocampal DWI hyperintensity,
or stroke in the posterior cerebral circulation,

DWI with T2-FLAIR permanent

Normal/hippocampal sclerosis
focal seizures (including TEA), postictal state, without permanent lesion
dissociative disorders or psychogenic amnesia,
posttraumatic amnesia, and metabolic disor-
MRI

ders such as hypoglycemia. The differentiating

features of some of these alternative diagnoses
or atrophy

are reviewed on Table 2. It is particularly lesion

important to remember that isolated memory
loss is a very infrequent presentation of acute
ischemic stroke. Meanwhile, seizures are char-
No/yes (oral automatisms,

acteristically shorter in duration than TGA and

Associated neurologic

olfactory or gustatory

more frequently recurrent.

Valsalva maneuver, emotional stress, immersion in cold or hot water, sexual intercourse, or pain.
symptoms

A diagnostic algorithm for a patient pre-

hallucinations)

senting with acute-onset anterograde amnesia

No/yes (any)

is proposed in Figure 2.
No

PATHOPHYSIOLOGIC MECHANISMS
The debate regarding the pathogenesis of TGA
impairment
permanent

has focused mainly on 3 distinct mechanisms:

Duration

Minutes to
<60 mind

vascular (due to venous flow disturbances or

4-6 h

focal arterial ischemia), epileptic, and migraine

related. It has also been reported that the CA1
subfield of the hippocampal cornu ammonis
Precipitating
TABLE 2. Differential Diagnosis of TGAa

(which is the part of the hippocampus most

factors

No/yesc

affected by TGA) would have a particular

Yesb

No

vulnerability to metabolic stress caused by

hypoxemia, B-amyloideinduced neurotoxicity,
risk factors
Risk factors

and ischemia; the degree of this local suscepti-

bility could be genetically determined.11,35,36
Migraine

Vascular

transient ischemic attack.

Often a few minutes.

Perhaps the leading hypothesis is that TGA

No

is caused by abnormal cerebral venous drainage

from the temporal lobes.37 It argues that precip-
TIA/stroke
Condition

Waking.

itating events associated with a Valsalva maneu-

TGA

TEA

ver and increased intrathoracic pressure would

b

d
a

prevent venous return to the superior vena

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Sudden onset of anterograde
memory impairment
Additional neurologic or
other symptoms
No Yes
Duration of a few minutes Consider other
Duration of hours
frequent relapses possible diagnoses
Exclude TEA Probable TGA • MRI brain
• Vascular evaluation
• Echocardiogram
• ECG
EEG
• +/– MRI brain • Laboratory test
• +/– EEG
• Clinical follow-up
FIGURE 2. Diagnostic algorithm for a patient presenting with sudden onset
anterograde amnesia. ECG ¼ electrocardiography; EEG ¼ electro-
encephalography; MRI ¼ magnetic resonance imaging; TEA ¼ transient
epileptic amnesia; TGA ¼ transient global amnesia.
cava and, consequently, would lead to retro-
grade jugular venous flow in the presence of ju-
gular valve incompetence. The resulting venous
hypertension in the medial temporal lobes
could explain memory impairment (Figure 3).
Several studies have shown that patients with
TGA have IJVFR or IJVVI more frequently
than control subjects, and this finding is even
more prevalent in patients with TGA starting
after a Valsalva maneuver.38-43 Patients with
TGA also have retrograde venous flow more
commonly than patients with TIA.39
Yet, there are some unresolved questions
regarding this hypothesis. It is not entirely clear
how IJVVI causes symptoms referable only to
the medial temporal lobes. The persistence of
memory impairment long after resolution of
the typically short-lasting intrathoracic hyper-
tension also remains unexplained. One pro-
posed possibility is that intracranial venous
hypertension could cause reactive arterial vaso-
constriction to compensate for the increased ce-
rebral blood volume, and the resulting relative
hypoperfusion would be responsible for the
amnesia in susceptible individuals.44 This could
be supported by evidence of temporal
n n
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MAYO CLINIC PROCEEDINGS
hypoperfusion during TGA episodes, as occa-
sionally disclosed by single-photon emission
computed tomography.45 But other questions
still demand answers. Why do TGA episodes
not happen more often in people with IJVVI
(ie, each time they have a Valsalva-like episode)?
Why do some individuals with proven IJVVI
never develop TGA? Why do some episodes
of TGA seem to occur in the absence of a trig-
gering factor conceivably associated with
increased intrathoracic venous pressure?
The arterial ischemia hypothesis is mostly
supported by the DWI changes on MRI. How-
ever, as previously mentioned, these changes
are inconsistently present, reversible with
time, and do not respect a clear arterial terri-
tory. Hypoperfusion has been shown to occur
in patients with TGA,45 but the frequency and
severity of this phenomenon is not well exam-
ined. Ischemic symptoms lasting as long as
most TGA episodes are commonly associated
with permanent lesions on MRI, which is not
the case in most patients with TGA.31,32,46
Several studies on vascular risk factors identi-
fied only migraine as being more prevalent in
patients with TGA compared with those with
TIA and healthy age- and sex-matched control
subjects,6,18 whereas hypertension, diabetes
mellitus, previous ischemic stroke, and atrial
fibrillation were found to have a lower preva-
lence in patients with TGA.47
Transient global amnesia was also proposed
to share pathophysiologic mechanisms with
migraine. A large population-based study indi-
cated that patients with migraine, particularly
middle-aged women, are more prone to experi-
ence TGA.19 It has been proposed that cortical
spreading depression could explain both condi-
tions, in the case of TGA by altering CA1 neuron
excitability.11,48 Cortical spreading depression
would act like a glutamate-mediated transient
depolarization, followed by long-lasting sup-
pression of neuronal activity, and may lead to
damage to CA1 neurons.11,49 However, it seems
that the threshold for triggering a cortical
spreading depression response in the hippo-
campus is much higher than that needed in
other cortical regions, and patients do not usu-
ally experience symptoms of migraine during
TGA,11 which makes the hypothesis of a shared
pathogenesis less likely.
Although focal seizures arising from the
mesial temporal lobe can mimic episodes of
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TRANSIENT GLOBAL AMNESIA

TGA,8 the absence of epileptiform abnormalities

during and after episodes of TGA and the rela-
tively prolonged duration of the amnesia without
propagation of the cerebral dysfunction to other
brain regions argue against the notion that most
TGA episodes could be epileptic in nature.17,33,34

TREATMENT
There is no specific treatment for TGA. Epi-
sodes are self-limited, and improvement is
noted within 24 hours without any interven-
tion. It seems prudent to avoid any activity
that could raise intrathoracic venous pressure
until the amnesia is resolved. When alternative
diagnoses are suspected (eg, seizures or
ischemic stroke/TIA), focused investigations
FIGURE 3. Venous hypothesis for the pathogenesis of transient global
should be pursued to determine whether acute
amnesia (TGA). It is proposed that retrograde venous flow and the ensuing
treatment or secondary prevention for these
venous hypertension could explain the occurrence of TGA. Increased
disorders might be indicated. intrathoracic pressure, as caused by a Valsalva maneuver, could trigger
retrograde venous flow in patients with valve incompetence in the internal
LONG-TERM OUTCOME IN PATIENTS WITH jugular veins. The resulting venous congestion would preferentially affect the
TGA function of the medial temporal lobes, thus inciting the anterograde amnesia.
Transient global amnesia is generally considered The graphic on the right illustrates the venous blood drainage from the medial
a benign condition. However, there are few temporal lobes. Blood from the temporal lobes is drained by the basal veins
studies on the long-term outcome of patients of Rosenthal and the internal cerebral veins, which, in turn, drain into the vein
who have experienced TGA regarding the risk of Galen, and from there to the straight sinus, confluens, transverse sinuses,
of recurrence and the incidence of cognitive and sigmoid sinuses, and, finally, into the internal jugular veins.
decline, stroke, and seizures over time.
Reported recurrence rates for TGA have
varied considerably (between 2.9% and clinically normal or have no awareness of any
impairment.58-62 Some of them may even fulfill
23.8%) among different studies (Table 3).
the criteria for mild cognitive impairment.63
The reason for such a spread in the rate of re-
Moreover, patients with repeated episodes of
currences found in different studies is unclear.
TGA have been reported to have greater impair-
There is no correlation with the length of
follow-up, and it does not seem to be explained ment in memory and visuoperceptual func-
by the size of the cohort. The sensitivity of the tions than those who experienced a single
definition used to identify cases of TGA may be attack when they were examined at least 1
important, as suggested by the fact that the month after the episode.23 The long-term risk
of cognitive decline has not been sufficiently
study reporting the highest recurrence rate
evaluated, but 1 study with an average follow-
included definite and probable episodes of
up of 82.2 months showed that the incidence
TGA within the recurrences.14 Use of less sen-
sitive but more specific definitions could result
in lower rates of recurrence. Rates of 8% to 18% TABLE 3. Reported Recurrence Rates for Transient Global Amnesia
over 6 to 7 years may be reasonable to cite to Recurrence Size of Mean length of
patients, but more precise estimates and infor- Reference, year rate (%) cohort (No.) follow-up (mo)
mation on risk factors for TGA recurrence still Melo et al,50 1992 2.9 51 39
need to be acquired through further research. Pantoni et al,51 2005 8 51 81.6
Several studies have reported complete re- Zorzon et al,18 1995 9.4 64 45.6
covery of cognitive function 5 days to 6 months Gandolfo et al,52 1992 18.6 102 82.2
after the TGA episode.54-57 However, other in- Koltzsch et al,53 1996 23 53 NR
vestigators have noted that memory dysfunc- Miller et al,14 1987 23.8 277 80
tion may persist after the acute phase of the NR ¼ not reported.
TGA episode, even when patients seem

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of dementia in patients with TGA was 2.9%,
and this was similar to the rate in their general
population.52
Transient global amnesia does not seem to
confer an increased risk of ischemic stroke.
Available information suggests that patients
with TGA have a similar risk of stroke, myocar-
dial infarction, and peripheral artery disease as
the general population, and this risk is signifi-
cantly lower than that of patients with TIA or
lacunar syndrome.18,51,52 Also, in a subset of
12 individuals from the Framingham Heart
Study who had an episode of TGA, the investi-
gators noted that these patients had a similar
vascular risk factor profile and risk of future ce-
rebrovascular events as stroke-free and seizure-
free controls matched for Framingham Heart
Study cohort, sex, and year of birth.64 Recently,
a study using a state registry including 4299 pa-
tients with TGA demonstrated that the stroke
risk after the diagnosis of TGA (0.54%) was
similar to that after the diagnosis of migraine
(0.22%), was lower than the risk after the diag-
nosis of seizure (0.90%), and was much lower
than that after the diagnosis of TIA (4.72%).65
Risk of seizures in patients with TGA has not
been demonstrated to be increased compared
with other populations. Studies that showed a
slightly higher risk of seizures on long-term
follow-up concluded that at least some of the
patients with later seizures could have had a
seizure mimicking TGA on diagnosis. This
was suggested by either abnormal interictal
EEG findings or reinterpretation of the initial
clinical manifestations.6,14,51
CONCLUSION
Transient global amnesia is not a rare condi-
tion. It typically presents in patients aged 50
to 70 years, and it is frequently preceded by a
Valsalva maneuver. Diagnosis is clinical, and
its semiological hallmark is the inability to
form new memories, although some retrograde
amnesia can occasionally be present. Non-
cognitive functions are always preserved, and
the presence of aphasia, hemiparesis, sensory
loss, or incoordination indicates a different
diagnosis and demands additional evaluation.
When patients undergo brain MRI within 2
days of the episode, the scan may show some de-
gree of restricted diffusion on the DWI sequence
on one or both hippocampi. However, these
changes are most often transient, and they are
n n
270 Mayo Clin Proc. February 2015;90(2):264-272
MAYO CLINIC PROCEEDINGS
generally not followed up by radiologic evidence
of infarction in the affected area. Therefore,
vascular work-up is not necessary in typical
cases of TGA. An EEG is recommended when
the episodes are brief, recurrent, or associated
with adventitious movements or sensory distur-
bances. Regional impairment of venous drainage
seems to be the most solid hypothesis to explain
the pathogenesis of TGA; although jugular valve
incompetence is prevalent in patients with TGA,
investigation for this condition with Doppler
and air-contrast ultrasound is neither confirma-
tive of the diagnosis of TGA nor necessary for its
management. The clinical course is self-limited,
and the short-term prognosis is favorable. Mem-
ory usually recovers fully within days, but mild
residual impairment can occasionally persist
for weeks. Less is known about long-term prog-
nosis. Recurrent episodes of TGA are relatively
uncommon but can certainly occur over the
years. Available data suggest that TGA does not
affect the future risk of cerebrovascular events,
but more information is needed regarding the
long-term risk of epilepsy and, particularly,
cognitive decline.
Abbreviations and Acronyms: DWI = diffusion weighted
imaging; ECG = electrocardiography; EEG = electroen-
cephalography; FLAIR = fluid-attenuated inversion recovery;
IJVFR = internal jugular venous flow reversal; IJVVI =
internal jugular vein valve incompetency; MRI = magnetic
resonance imaging; TEA = transient epileptic amnesia; TGA =
transient global amnesia; TIA = transient ischemic attack
Correspondence: Address to Alejandro A. Rabinstein, MD,
Department of Neurology, Mayo Clinic, 200 First St SW,
Mayo W8B, Rochester, MN 55905 (rabinstein.alejandro@
mayo.edu).
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