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Transient global amnesia

Transient global amnesia (TGA) is a rare neurological syndrome characterized by the sudden onset of anterograde amnesia, in which individuals cannot form new memories, accompanied by mild retrograde amnesia affecting recall of recent events and a state of temporary confusion or disorientation, typically lasting between 1 and 10 hours but not exceeding 24 hours, with full spontaneous recovery and no persistent neurological deficits.^[1]^[2]^[3] The condition most commonly affects adults aged 50 to 80, with an annual incidence of approximately 5 to 10 cases per 100,000 people in the general population, rising to 23 to 32 per 100,000 among those over 50, and showing no significant gender predominance.^[1]^[2] Symptoms include repetitive questioning about one's whereabouts or recent activities due to impaired short-term memory, while personal identity, language skills, and immediate attention remain intact, distinguishing TGA from more severe conditions like stroke or epilepsy.^[1]^[3] During an episode, affected individuals appear alert but bewildered, often preserving awareness of their amnesia itself.^[2] The exact cause of TGA remains unknown, though it is considered benign and self-limited, with proposed mechanisms involving transient dysfunction in the hippocampus—a brain region critical for memory formation—possibly due to metabolic stress, reduced blood flow, venous congestion, or excitatory toxicity.^[1] Potential triggers include physical exertion, emotional stress, immersion in cold or hot water, sexual activity, mild head trauma, or exposure to pain, and it may occur more frequently in those with a history of migraines, affecting 12% to 30% of cases.^[1]^[3] Diagnosis is primarily clinical, relying on a detailed history to exclude mimics such as transient ischemic attack or seizure, often supported by neuroimaging like MRI, which may reveal punctate lesions in the hippocampus 24 to 72 hours post-episode in about two-thirds of patients.^[1]^[2] Management involves supportive care in a hospital setting for monitoring, with no specific pharmacological treatment required, as episodes resolve completely without intervention.^[1]^[2] Prognosis is excellent, with full memory restoration and no increased risk of dementia or cerebrovascular events, though recurrence occurs in fewer than 10% of cases, and a slight association with later epilepsy development has been noted in some studies.^[1]^[2] Despite its alarming presentation, TGA does not indicate underlying serious pathology in most instances and carries a low mortality rate directly attributable to the condition.^[1]

Clinical features

Amnestic symptoms

Transient global amnesia (TGA) is characterized by the sudden onset of anterograde amnesia, in which affected individuals are unable to form new memories following the initiation of the episode.^[3] This impairment manifests as a profound disruption in encoding recent experiences, leading to a temporary void in the continuity of autobiographical memory.^[4] Despite this deficit, patients typically retain the capacity for immediate recall of events occurring within seconds to minutes prior, allowing brief interactions but preventing retention beyond that span.^[4] In addition to anterograde amnesia, TGA often involves variable retrograde amnesia, where recall of events from hours to days preceding the onset is impaired, though this loss rarely extends to more remote periods such as years earlier.^[2] The retrograde component is generally milder and less consistent than the anterograde deficit, affecting personal episodic memories while sparing foundational aspects of long-term memory.^[5] This selective memory gap underscores the focal nature of the amnestic syndrome in TGA. Critically, TGA spares semantic memory, which encompasses general knowledge and facts about the world, as well as procedural memory, enabling the performance of learned skills such as driving or using utensils without disruption.^[4] Patients remain fully alert and attentive throughout the episode, with no evidence of aphasia, apraxia, or other cognitive impairments beyond the amnestic features.^[3] For instance, an individual may recognize family members and engage in conversation but repeatedly fail to remember the details of that interaction moments later.^[2]

Behavioral manifestations

During episodes of transient global amnesia (TGA), individuals commonly display repetitive questioning regarding their current situation, time, and location, often asking the same queries multiple times without retaining the answers provided. This behavior arises from the underlying anterograde amnesia and is observed in approximately 92% of TGA cases.^[6] Patients typically exhibit mild confusion or perplexity, appearing disoriented to their temporal and spatial context but without progressing to delirium or full disorientation to self. They remain alert and attentive, with intact immediate recall for information presented moments earlier, distinguishing this state from more severe cognitive impairments.^[6]^[7] Personal identity and remote autobiographical memory are fully preserved, allowing affected individuals to recognize themselves, recall lifelong events, and know their name and basic personal details without disruption. This preservation underscores the selective nature of the episode, affecting only recent and ongoing memory formation.^[6]^[8] Anxiety or agitation may occur in some cases, stemming from the patient's partial awareness of their memory failure, leading to emotional distress or mild restlessness. However, these reactions are not universal and tend to be transient.^[9] Notably absent are any focal neurological signs, such as motor weakness, sensory deficits, ataxia, or impairments in speech or vision, which helps differentiate TGA from stroke or other acute neurological events.^[6]

Typical progression

Transient global amnesia (TGA) episodes characteristically exhibit an abrupt onset without prodromal symptoms, frequently occurring during everyday activities such as walking or conversing.^[1] The anterograde amnesia develops rapidly, often reaching maximal severity within minutes of initiation, rendering patients incapable of forming new memories while preserving other cognitive functions.^[10] The overall duration of a TGA episode ranges from 1 to 24 hours, with a mean length of 4 to 6 hours in most cases.^[11] Throughout the acute phase, the amnesia remains profound, though patients may exhibit repetitive questioning as a hallmark of their disorientation to time and events.^[1] Toward the latter part of the episode, there is a gradual improvement in the ability to encode new information, marking the transition to resolution. Anterograde amnesia typically resolves first, followed by a brief persistence of partial retrograde amnesia, which recovers in a telescopic manner—remote memories returning before more recent ones outside the amnestic period.^[1] Full cognitive recovery ensues spontaneously, restoring patients to their baseline without any lasting neurological impairments.^[12] Recurrence within the same day is exceedingly rare.^[1]

Diagnosis

Clinical criteria

The diagnosis of transient global amnesia (TGA) relies on standardized clinical criteria to ensure accurate identification based on the patient's history and observed presentation. The seminal criteria were established by Hodges and Warlow in 1990 following a prospective study of 153 cases of acute transient amnesia, where 114 met the strict diagnostic thresholds for TGA.^[13] These criteria require the following features to be present:

The episode must be witnessed by an observer and reported as such.
There is acute onset of anterograde amnesia, often accompanied by repetitive questioning due to impaired immediate recall.
No clouding of consciousness or loss of personal identity occurs.
Absence of focal neurological symptoms or deficits during or after the episode.
No clinical features suggestive of epilepsy, such as auras, automatisms, or convulsions.
No recent head trauma or active epilepsy history.
The amnesia resolves completely within 24 hours, with no residual cognitive impairment beyond possible mild retrograde amnesia gaps.

An additional common feature is temporal disorientation, where patients repeatedly inquire about the current time or date, while retaining insight into their personal identity.^[13] Exclusion of alternative causes, such as metabolic, toxic, or psychiatric conditions, is essential through clinical history to confirm TGA. The primary presenting feature is the sudden anterograde amnesia, which forms the core of these diagnostic thresholds.^[13] Updated guidelines from the German Society of Neurology (2023), building on the Hodges and Warlow framework, reinforce these criteria while emphasizing the need to rule out transient epileptic amnesia, particularly in cases with recurrent episodes, through exclusion of epileptiform activity or seizure-like features.^[14]

Neuroimaging findings

Neuroimaging plays a supportive role in the diagnosis of transient global amnesia (TGA), primarily to exclude alternative conditions, with imaging typically ordered following established clinical criteria. Routine computed tomography (CT) scans or immediate magnetic resonance imaging (MRI) performed during the acute phase are often normal and do not contribute to the acute diagnosis of TGA.^[1] Diffusion-weighted imaging (DWI) on MRI, conducted 24-96 hours after symptom onset, reveals punctate hyperintensities in the CA1 region of the hippocampus in approximately 30-50% of TGA cases, with rates varying from 25% to 85% depending on MRI timing, slice thickness, and protocol; appearing as small, unilateral or bilateral lesions.^[15]^[16] These lesions are thought to reflect transient ischemia or excitotoxicity in the vulnerable hippocampal tissue, and they typically resolve within 10-14 days, with any associated T2 hyperintensities fading without permanent sequelae.^[16] Recent studies from 2023 to 2025 affirm that these DWI findings are supportive of TGA but not diagnostic on their own, as their absence does not rule out the condition, and clinical correlation remains essential; early MRI within 24 hours should be avoided to minimize false negatives due to the delayed appearance of lesions.^[15] Electroencephalography (EEG) has no routine role in TGA evaluation unless epileptic seizures are suspected, such as in recurrent cases exceeding three episodes per year, where it may show nonspecific theta or delta waves but is otherwise unremarkable.

Differential diagnosis

Transient global amnesia (TGA) requires careful differentiation from other acute amnestic syndromes to exclude life-threatening conditions like cerebrovascular events. The primary goal in the differential diagnosis is to identify features that distinguish TGA's benign, self-limited anterograde and retrograde amnesia from pathologies involving focal neurological deficits, recurrent episodes, or underlying psychiatric factors.^[1] Stroke or transient ischemic attack (TIA) is a critical mimic, particularly involving the posterior cerebral artery territory affecting the hippocampus, and is characterized by abrupt onset of focal deficits such as language impairment, motor weakness, or sensory loss, often in patients with vascular risk factors like hypertension or atrial fibrillation. In contrast to TGA, these events may show diffusion-weighted imaging (DWI) abnormalities indicating infarction, and recurrence risk is influenced by modifiable cardiovascular factors rather than being rare and benign. A high proportion of TGA cases are initially misdiagnosed as stroke, with one study reporting the diagnosis missed in 90% of initial presentations, highlighting the need for prompt neuroimaging to confirm the absence of vascular lesions in pure TGA.^[4]^[17] Transient epileptic amnesia (TEA) presents with shorter-duration episodes, typically lasting minutes to under one hour, often multiple times per year, and may include subtle seizure semiology like oral automatisms or hallucinations alongside predominantly retrograde amnesia. Unlike TGA's isolated, non-recurrent event, TEA is associated with interictal electroencephalogram (EEG) abnormalities in temporal or frontotemporal regions and responds to anticonvulsant therapy, distinguishing it as a form of limbic epilepsy.^[1]^[4] Migraine aura can mimic TGA through transient confusional states or amnestic episodes, but is typically accompanied by headache, visual or sensory auras, and occurs in younger patients with a personal or family history of migraine; the amnesia is less profound and resolves within 4-72 hours without the repetitive questioning hallmark of TGA. Approximately 12-30% of TGA patients have a migraine history, suggesting possible overlap via mechanisms like cortical spreading depression, but the absence of vascular risk factors and normal neuroimaging support TGA over migrainous infarction.^[1]^[17] Psychogenic amnesia, often linked to dissociative or conversion disorders, features inconsistent memory loss influenced by psychological stress or trauma, persisting for days or longer without organic neurological findings on examination or imaging. This contrasts with TGA's acute, time-limited episode in otherwise neurologically intact individuals, and diagnosis relies on psychiatric evaluation rather than exclusion of structural pathology.^[4]^[18]

Etiology and pathophysiology

Precipitating events

Precipitating events precede approximately 50% of transient global amnesia (TGA) episodes, representing a temporal association first noted in clinical descriptions from the 1960s, without established causality.^[19]^[20] Physical exertion is among the most common triggers, often involving strenuous activities such as heavy lifting, cycling, or swimming that incorporate Valsalva maneuvers.^[20]^[21] Emotional stress frequently precipitates TGA, encompassing psychologically charged situations like arguments, receipt of shocking news, or anxiety-inducing events such as a family member's surgery or the birth of a grandchild.^[20]^[21] Sexual activity serves as a precipitating factor in about 8-10% of documented cases, typically occurring post-coitally.^[19] Environmental exposures, including immersion in cold water or abrupt temperature changes like hot baths, have also been associated with onset in roughly 20% of episodes in some cohorts.^[19]^[21]

Vascular mechanisms

One proposed mechanism for transient global amnesia (TGA) involves transient hypoperfusion in the medial temporal lobe, particularly affecting the CA1 region of the hippocampus, which is highly susceptible to ischemic injury.^[22] This hypoperfusion may lead to temporary dysfunction in memory processing without permanent damage, aligning with the self-limited nature of TGA episodes.^[23] Possible causes of this hypoperfusion include venous congestion, often triggered by Valsalva maneuvers during exertion; arterial hypotension; or microvascular spasm in hippocampal blood vessels.^[23] These vascular disturbances could transiently reduce blood flow to the hippocampus, precipitating the amnestic syndrome.^[24] Diffusion-weighted imaging (DWI) frequently reveals punctate hyperintense lesions in the hippocampus during or shortly after TGA episodes, interpreted as evidence of brief cytotoxic edema and excitotoxic injury from ischemia.^[25] These lesions typically resolve within days, supporting a reversible ischemic process rather than infarction.^[26] A 2025 Medscape review emphasizes that while vascular ischemia is a leading hypothesis, there is no consensus on it as the sole cause of TGA.^[27] Animal models, such as gerbils subjected to transient forebrain ischemia, demonstrate that CA1 hippocampal neurons exhibit vulnerability to oxygen deprivation lasting 5-10 minutes, resulting in delayed cell death if prolonged but potentially reversible if brief.^[28] This temporal window mirrors the duration of TGA symptoms and underscores the region's selective sensitivity.^[29]

Alternative hypotheses

One prominent alternative hypothesis posits that transient global amnesia (TGA) arises from a migrainous mechanism involving cortical spreading depression (CSD) in the hippocampus, a wave of neuronal depolarization that temporarily disrupts memory encoding and retrieval. This process, analogous to the aura phase in migraine attacks, is thought to selectively impair hippocampal function without causing permanent damage, leading to the characteristic anterograde amnesia. Studies have shown that TGA occurs more frequently in individuals with a personal history of migraine, with an odds ratio of approximately 2.5, and up to 30% of TGA patients report prior migraines. Furthermore, the migraine hypothesis gains support from reports of familial TGA cases, where episodes often co-occur with migraine in affected relatives, suggesting a potential genetic predisposition shared between the conditions.^[1]^[30]^[31]^[32]^[33]^[34] Another proposed model frames TGA as an epileptic phenomenon, specifically subtle temporal lobe seizures originating in the limbic system without overt convulsions or loss of consciousness. In this view, brief ictal activity disrupts hippocampal circuits, mimicking the amnestic features of TGA while resolving spontaneously. Although rare, interictal electroencephalogram (EEG) findings in some TGA patients may reveal temporal lobe epileptiform discharges or nonspecific slowing, supporting this hypothesis in select cases. However, the 2023 German Society of Neurology guidelines emphasize that epilepsy is unlikely the primary cause of most TGA episodes, citing the consistent absence of ictal EEG abnormalities during attacks and the lack of progression to epilepsy in follow-up studies.^[35]^[36]^[32] Emerging theories explore other non-vascular pathways, including disruption of memory engrams—distributed neuronal ensembles responsible for encoding and recalling experiences. Recent research proposes that TGA results from a transient failure in engram activation within the hippocampal CA3 region, possibly triggered by spreading depolarization, which prevents new memory formation (engraphy) and impairs retrieval (ecphory), creating a self-limited amnestic gap without latent memories forming during the episode. Additional models invoke psychogenic overload, where acute emotional stress overwhelms cognitive processing, leading to reversible hippocampal dysfunction in individuals with underlying psychiatric vulnerabilities such as phobic traits or depression history. Neurotransmitter imbalances, particularly involving glutamatergic or GABAergic systems, have also been suggested as contributors to this overload, though evidence remains preliminary and tied to stress-induced excitotoxicity. These hypotheses often overlap with precipitating emotional stress, highlighting TGA's potential responsiveness to psychological factors.^[37]^[32]^[38]^[26]

Management and prognosis

Acute management

The acute management of transient global amnesia (TGA) primarily involves supportive care and the exclusion of life-threatening mimics, as the condition is self-limited and resolves spontaneously without specific intervention.^[1]^[4] Patients and their families should receive reassurance regarding the benign nature of TGA, with placement in a quiet environment to minimize anxiety and repetitive questioning during the amnestic episode.^[1]^[39] Intravenous thiamine may be administered empirically to rule out Wernicke encephalopathy, particularly in cases with potential nutritional deficiencies.^[1] To exclude differentials such as stroke, seizure, or metabolic derangements, urgent neuroimaging with non-contrast computed tomography (CT) or magnetic resonance imaging (MRI) is recommended if clinical features suggest vascular involvement, such as focal neurological deficits.^[40]^[4] Basic laboratory evaluations, including glucose, electrolytes, complete blood count, and toxicology screening, are performed to identify potential causes like hypoglycemia or intoxication.^[1]^[41] Electroencephalography (EEG) may be considered if epileptic amnesia is suspected, though it is not routine.^[40] No targeted pharmacotherapy exists for TGA, and unnecessary agents such as sedatives or anticonvulsants should be avoided to prevent confounding the clinical picture or causing adverse effects.^[1]^[4] Hospital observation is typically warranted for the first 24 hours to monitor resolution and confirm the absence of complications, with discharge appropriate once anterograde amnesia has fully abated and mimics are excluded.^[1]^[41] This approach aligns with the prognosis of spontaneous recovery, usually within 6 to 24 hours.^[39]

Long-term outcomes

Patients with transient global amnesia (TGA) experience complete recovery in all cases, with no permanent memory loss or cognitive decline following the episode.^[42] The amnesia resolves fully within 24 hours, and long-term follow-up studies confirm the absence of lasting neurological deficits. The recurrence rate of TGA is estimated at 5-10% over 5-10 years of follow-up, though rates vary across studies from 2.9% to 23.8% in cohorts with at least three years of observation.^[30] Recurrence is more likely in individuals with multiple prior episodes, with some reports indicating an elevated risk associated with factors such as migraine history or depression.^[43] A 2024 Israeli single-center study of 104 patients reported a recurrence rate of 11.5%, with an average interval of 5.1 years between episodes.^[44] TGA does not confer an increased risk of stroke, dementia, or epilepsy in the long term.^[42] Large cohort analyses have shown no elevated incidence of cerebrovascular events or seizures compared to age- and sex-matched controls, even after adjusting for cardiovascular risk factors.^[45] Similarly, prospective studies indicate no heightened risk for subsequent dementia development.^[30] A 2024 Israeli study underscores the excellent prognosis of TGA, with rare progression to other neurological conditions and no evidence of long-term sequelae in the cohort followed for up to six years.^[44] Emphasizing the benign nature of TGA through patient education is crucial for alleviating anxiety and promoting reassurance post-episode.^[44]

Epidemiology

Incidence and demographics

Transient global amnesia (TGA) is a rare neurological disorder, with an annual incidence ranging from 3 to 10 cases per 100,000 person-years in the general population.^[1] This rate increases substantially with age, reaching approximately 24 to 32 cases per 100,000 person-years among individuals over 50 years.^[1] Reported rates may vary due to differences in study methodologies and potential underdiagnosis, particularly in elderly populations where episodes might be attributed to age-related cognitive decline.^[4] TGA predominantly affects middle-aged and older adults, with peak incidence between 50 and 70 years and a mean age of onset around 60 years.^[46] There is no significant gender predominance.^[1] There is no strong geographic variation in incidence, with reported rates ranging from 2.9 to 10 per 100,000 across regions such as the United States, Spain, and Italy, likely reflecting differences in study methodologies rather than true disparities.^[47] Higher reporting tends to occur in developed countries equipped with advanced diagnostic tools like neuroimaging.^[47] Underdiagnosis may be more prevalent among the elderly, where TGA episodes could be mistaken for other age-related cognitive issues.^[4]

Risk factors

A history of migraine is associated with an increased risk of transient global amnesia (TGA), with a nationwide cohort study reporting an incidence rate ratio of 2.48 for TGA among migraine patients compared to controls.^[48] This elevated risk is particularly pronounced in female patients aged 40-60 years, where the ratio reaches 3.18.^[48] Vascular risk factors such as hypertension are commonly observed in TGA patients, present in up to 37.5% of cases in some cohorts, though their direct causal role remains uncertain.^[49] The strongest predictor of TGA recurrence is a prior episode, with overall recurrence rates ranging from 3% to 27% across studies, though typically reported around 10%.^[1]^[50] Younger age at the initial episode heightens this recurrence risk, as patients experiencing TGA under 70 years old without cerebral microangiopathy face a 24.5% chance of recurrence within five years.^[50] Conversely, the absence of hypertension and related microangiopathy appears linked to higher recurrence susceptibility, suggesting a protective effect from established vascular changes.^[50] Emotional or physical stressors represent situational risks that may precipitate TGA in susceptible individuals, often overlapping with acute triggers like exertion or psychological strain.^[49] No clear genetic factors have been identified for TGA, though rare familial cases hint at possible hereditary components without established inheritance patterns.^[1]

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