Materiały źródłowe

• #1 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #2 Transient Global Amnesia (TGA): Causes & Symptoms

  https://my.clevelandclinic.org/health/diseases/21028-transient-global-amnesia

  Even though researchers have been studying transient global amnesia for over 50 years, theyre still not sure what causes it or why it happens. […] Researchers dont know the exact cause of transient global amnesia (TGA). But they believe its due to a temporary issue in your hippocampus the part of your brain that plays a significant role in learning and memory. […] Some research suggests that TGA results from a lack of sufficient blood flow (ischemia) or oxygen flow (hypoxia) to your brain. Other research suggests that TGA may be related to seizure activity in your brain.

• #3 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology – PubMed

  https://pubmed.ncbi.nlm.nih.gov/35743444/

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] Furthermore, the demonstration by diffusion-weighted MRI of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of TGA. […] In this review, we summarize current knowledge on the anatomy, vascularization and function of the hippocampus. Furthermore, we discuss the emerging theories on the etiology and the pathophysiological cascade leading to an impairment of hippocampal function during the attacks.

• #4 Acute-onset amnesia: transient global amnesia and other causes | Practical Neurology

  https://pn.bmj.com/content/22/3/201

  Acute-onset amnesia is a dramatic neurological presentation that can cause considerable concern to both patient and clinician. […] Transient global amnesia (TGA) is the most common cause of acute-onset amnesia, and is characterised by a profound anterograde and retrograde amnesia that typically lasts for up to 24 hours. […] Although TGA has a strikingly stereotypical presentation, it can be challenging to distinguish from other causes of acute-onset amnesia, including posterior circulation strokes, transient epileptic amnesia, psychogenic amnesia, post-traumatic amnesia, and toxic/drug-related amnesia. […] Regardless of cause and the dramatic presentation, non-ischaemic acute-onset amnesia generally has a favourable prognosis.

• #5 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Despite all the theories and studies, there is no definitive evidence supporting any of these mechanisms, so the etiology of TGA remains elusive. […] On the other hand, based on the nature of cognitive impairment during the episodes, there is the consensus that the symptoms are due to the transient dysfunction of the medial temporal lobe, particularly of the hippocampus. […] The selective location of DWI-MRI lesions in the CA-1 sector of the hippocampal cornu ammonis has suggested that the cellular stress of CA-1 neurons has a pivotal role in the pathophysiology of hippocampal dysfunction during TGA. […] Future advances in the knowledge of the mechanisms that regulate physiological mnemonic processes will allow us to clarify the pathophysiological correlates of the acute phase of TGA and, in particular, to decipher which trigger induces the pathophysiological cascade that affects the involved brain structures.

• #6 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #7 Transient Global Amnesia (TGA): Causes & Symptoms

  https://my.clevelandclinic.org/health/diseases/21028-transient-global-amnesia

  Even though researchers have been studying transient global amnesia for over 50 years, theyre still not sure what causes it or why it happens. […] Researchers dont know the exact cause of transient global amnesia (TGA). But they believe its due to a temporary issue in your hippocampus the part of your brain that plays a significant role in learning and memory. […] Some research suggests that TGA results from a lack of sufficient blood flow (ischemia) or oxygen flow (hypoxia) to your brain. Other research suggests that TGA may be related to seizure activity in your brain.

• #8 Transient Global Amnesia

  https://mobile.fpnotebook.com/Neuro/Cognitive/TrnsntGlblAmns.htm

  Hippocampus is key in the creation of short-term memory. […] Increased intrathoracic pressure and Jugular Venous Pressure may decrease Hippocampus perfusion. […] Dysfunction of bilateral medial Temporal Lobes, and Hippocampus. […] MRI Brain DWI has shown bright punctate foci in Hippocampus of TGA patients. […] Associations with Migraine Headache, Temporal Lobe ischemia or partial complex Seizures have been postulated. […] Venous congestion and venous reflux is also postulated as cause. […] May explain why some TGA episodes are preceded by straining or Valsalva Maneuver.

• #9 Transient Global Amnesia Is an Experience You’ll Never Forget

  https://www.webmd.com/brain/features/transient-global-amnesia

  Neurologists dont yet know exactly how TGA happens, but research points to brief venous hypertension in the brain. This temporarily deprives the brains two memory-forming hippocampi of oxygen. What we dont understand is exactly what is happening on a physiological level, says Sicotte. Theres a decrease in blood flow, but why? […] In an episode of TGA, the machinery our brain uses to make new memories and also access old memories is offline, Sicotte explains. Its like a switch goes off. Maybe its a protective mechanism. […] TGA is a source of fascination for neurologists, a syndrome that reminds both medical trainees and laypeople how much we still have to learn about the way memories form, encode, vanish, and come back.

• #10 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #11 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] The identification by diffusion-weighted (DWI) Magnetic Resonance Imaging (MRI) of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of the disease. […] However, the observation that emotional and psychological distress are frequent precipitating events among TGA cases also leads us to hypothesize that there is a psychogenic cause behind this disease.

• #12 Transient global amnesia: current perspectives | NDT

  https://www.dovepress.com/transient-global-amnesia-current-perspectives-peer-reviewed-fulltext-article-NDT

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of an extraordinarily large reduction of anterograde and a somewhat milder reduction of retrograde episodic long-term memory. […] Recent data suggest that the vulnerability of CA1 neurons to metabolic stress plays a pivotal part in the pathophysiological cascade, leading to an impairment of hippocampal function during TGA. […] The clinical picture of TGA has led researchers to investigate focal injury to the neurological circuits involved in memory as a potential etiology of the syndrome. […] Current evidence points to the formation of early memory within the hippocampal/entorhinal cortex network and its eventual transference to remote memories stored in the neocortex network. […] Particular attention has been given to the cornu ammonis (CA1) field of the hippocampus, which has been hypothesized to play a central role in the pathophysiology of TGA given its extraordinary sensitivity to cell stress.

• #13 SciELO Brazil – Transient global amnesia: clinical features and prognostic factors suggesting recurrence Transient global amnesia: clinical features and prognostic factors suggesting recurrence

  https://www.scielo.br/j/anp/a/VvjGnSkjFx9mN9rFbHgxzLJ/

  Transient global amnesia (TGA) is a syndrome characterized by sudden anterograde amnesia of less than 24 hours in duration, in the absence of other neurological symptoms. […] The pathophysiological mechanisms of TGA remain uncertain. The main hypothesis involves passive hypoxia due to abnormal jugular drainage of the temporal lobes. For this reason, when there is an increase in intrathoracic pressure, as in the Valsalva maneuver, retrograde jugular flow occurs, which is responsible for the appearance of TGA. […] It has been previously suggested that internal jugular valve insufficiency contributes to TGA pathogenesis. […] However, no Doppler finding predicted TGA recurrence. […] Ischemic restrictive diffusion along the lateral hippocampus (mainly CA1) can be observed in up to 85% of patients using high-resolution MRI techniques.

• #14 :: JCN :: Journal of Clinical Neurology

  https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2008.4.2.59

  One of the hypotheses for the etiology of TGA is transient cerebral ischemia. […] The increased vulnerability of the hippocampus and the venous drainage might help to explain why memory structures are the first to be involved. […] Clinical and experimental data show that hippocampal CA1 neurons are critically involved in the process of memory consolidation by exhibiting a relay function in direct and polysynaptic intrahippocampal circuits, and lesions in this area are sufficient to produce clinically significant memory impairment. […] Pathophysiologically, neurons of the CA1 sector (Sommer sector) of the cornu ammonis are of particular interest since they show a selective vulnerability to cellular metabolic stress (e.g., during hypoxemia and ischemia) that leads to the glutamate- and calcium-induced and apoptosis mediated 'delayed neuronal death’ of affected neurons 1-3 days after hypoxia.

• #15 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #16 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #17 Guideline “Transient Global Amnesia (TGA)” of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline | Neurological Research and Practice | Full Text

  https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-023-00240-0

  The cause of TGA is still unknown, but numerous findings in recent years point to a multifactorial genesis. […] Since the pathomechanism of TGA has not yet been definitively clarified, a multifactorial or multi-causal process seems likely. […] Because the pathomechanism of TGA is not yet clearly known, no evidence-based recommendations can be made regarding prophylaxis. […] This notion is supported by imaging findings using diffusion-weighted magnetic resonance imaging, which shows hippocampal lesions in more than half of patients in the acute stage. […] TGA patients with and without DWI lesions do not differ in terms of clinical symptoms and cognitive functions over the long term. […] Functional and morphometric MRI studies and quantitative EEG analyses were able to show changes in functional connectivity in the limbic system and hippocampus.

• #18 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology – PubMed

  https://pubmed.ncbi.nlm.nih.gov/35743444/

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] Furthermore, the demonstration by diffusion-weighted MRI of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of TGA. […] In this review, we summarize current knowledge on the anatomy, vascularization and function of the hippocampus. Furthermore, we discuss the emerging theories on the etiology and the pathophysiological cascade leading to an impairment of hippocampal function during the attacks.

• #19 Transient global amnesia – UpToDate

  https://www.uptodate.com/contents/transient-global-amnesia/print

  Transient global amnesia (TGA) is a clinical syndrome characterized by the acute onset of anterograde amnesia (the inability to form new memories). […] A single, definite etiology has not been determined, although epidemiologic and imaging data support several putative pathophysiologic processes, including vascular, migraine, epileptic, and psychogenic mechanisms.

• #20 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] The identification by diffusion-weighted (DWI) Magnetic Resonance Imaging (MRI) of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of the disease. […] However, the observation that emotional and psychological distress are frequent precipitating events among TGA cases also leads us to hypothesize that there is a psychogenic cause behind this disease.

• #21 Transient Global Amnesia | AAFP

  https://www.aafp.org/pubs/afp/issues/2022/0100/p50.html

  Transient global amnesia (TGA) is a clinical syndrome characterized by anterograde amnesia, mild retrograde amnesia, and confusion up to 24 hours. […] The pathophysiology of TGA is not well understood but may be related to impaired venous drainage of the hippocampus. […] Events that increase intrathoracic pressure are associated with TGA and may cause jugular venous hypertension, suggesting that impedance of venous drainage from the hippocampus is involved. Impedance of venous drainage is hypothesized to cause transient ischemia from secondary poor perfusion and sludging. […] The association between migraine headache and TGA has not been clarified, but hippocampal migraine vascular changes have been hypothesized. The increased prevalence in older patients suggests that age-associated intracerebral changes, especially vascular changes, may increase the risk of TGA.

• #22 Factors determining recurrence in transient global amnesia | BMC Neurology | Full Text

  https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-020-01658-8

  Aetiology of transient global amnesia (TGA) remains uncertain, though many have been proposed, including ischaemic, migrainous or epileptic pathologies. […] Multiple mechanisms have been proposed for the aetiology of TGA. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. […] Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. […] One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. […] Family history of dementia was found to be associated with recurrence of TGA. […] We believe TGA is a distinctive clinical syndrome arising from different mechanisms. It may recur in 16% of those who have a background of head injury, depression or a family history of dementia.

• #23 Transient Global Amnesia Clinical Presentation: History, Physical, Causes

  https://emedicine.medscape.com/article/1160964-clinical

  Transient global amnesia (TGA) is a well-described syndrome, but one whose exact etiology is not yet completely understood. […] Many mechanisms have been proposed, but no single cause can explain fully all the features of TGA. These include migraine variant, temporal lobe seizure, and TIA. […] There is a demonstrated association between TGA and migraine. […] Precipitants of TGA frequently include physical exertion, overwhelming emotional stress, pain, cold-water exposure, sexual intercourse, and Valsalva maneuver. […] The exact mechanism that produces transient global amnesia is unclear. […] One theory proposed by Lewis is that venous congestion causes disrupted blood flow to the thalamic or mesial temporal structures. […] The frequently cited triggers for TGA can increase either sympathetic activity and/or intrathoracic pressure. […] Conditions predisposing to this scenario might include venous anatomy anomalies, integrity of jugular vein valves, timing of the trigger, and severity of the inciting event.

• #24 Transient Global Amnesia Causes and Symptoms

  https://www.verywellhealth.com/transient-global-amnesia-2488851

  Transient global amnesia (TGA) is a mysterious syndrome causing a relatively brief inability to form new memories. […] The cause of TGA is still unknown, but the symptoms suggest dysfunction in the medial temporal lobe, the area of the brain that contains the hippocampus and is critical for the formation of new memories. […] Theories include a transient change in blood flow to these regions, or perhaps a migrainous phenomenon involving slow changes in electrical activity. […] While transient decrease in blood flow (a transient ischemic attack or „TIA”) to the hippocampus can mimic TGA, TGA usually lasts longer than a typical transient ischemic attack. […] Some studies suggest that migraines are associated with TGA.

• #25 Transient global amnesia – Wikipedia

  https://en.wikipedia.org/wiki/Transient_global_amnesia

  Transient global amnesia (TGA) is a neurological disorder whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. […] The underlying cause of TGA remains enigmatic. The leading hypotheses are some form of epileptic event, a problem with blood circulation around, to or from the brain, or some kind of migraine-like phenomenon. […] Cerebral ischemia is a frequently disputed possible cause, at least for some segment of the TGA population, and until the 1990s it was generally thought that TGA was a variant of transient ischemic attack (TIA) secondary to some form of cerebrovascular disease. […] Other vascular origins remain a possibility, however, according to research of jugular vein valve insufficiency in patients with TGA.

• #26 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The etiology is unknown. Suggested causes have included a transient ischemic attack, migraine, epilepsy, vein thrombosis, central nervous system tumors, saline-contrast transthoracic echocardiography, transoesophageal echocardiography, drug intoxication or other toxic and metabolic disturbances, circadian rhythmicity, possible stress induced with impact on the hippocampus, cold water immersion, post-traumatic stress disorder, and hysteria. A transient ischemic attack that affects the hippocampi and associated mesial structures was thought to be a leading cause of transient global amnesia, although many contest this view. Supporting evidence includes PET and SPECT studies that show hypoperfusion and hypometabolism in the hippocampi and associated mesial structures during an attack with resolution following the attack. Wang and colleagues detected hyperintensities in the head, body, and caudate of CA1 and in the hippocampal tail on diffusion-weighted imaging during the acute phase after onset of transient global amnesia symptoms. The authors suggested that, due to the presence of microstructural sequelae, ischemic lesions in the hippocampus may be associated with transient global amnesia. Lesions can typically be detected 12 to 48 hours after the onset of symptoms, though they often resolve. However, patients with transient global amnesia do not present with an increased risk of subsequent stroke compared to individuals with transient ischemic attacks. Ogawa and colleagues suggested increased cytotoxicity in lesions found in the CA1 region of the hippocampus in patients with transient global amnesia, which led to cytotoxic edema in the lesion areas. Using ultra-high field 7 T MRI, hippocampal lesions, initially detected during the acute phase of transient global amnesia, did not show focal sequelae; this highlights the importance of diffusion-weighted imaging during the acute phase.

• #27 Longitudinal Cerebral Perfusion Change in Transient Global Amnesia Related to Left Posterior Medial Network Disruption | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145658

  The pathophysiology of transient global amnesia (TGA) is not fully understood. […] Several etiological factors, such as migraine, epilepsy, cerebral ischemia, venous flow abnormalities, have been proposed as possible explanations. […] Instead of arterial ischemia, recent studies have reported venous congestion or venous reflux with subsequent ischemia combined with jugular valve insufficiency. […] Therefore, the question remains as to how cerebral ischemia or hypoperfusion is related to the occurrence of TGA. […] We identified left hemispheric lateralized hypoperfusion that may be related to posterior medial network disruption. These findings may be a contributing factor to the pathophysiology of TGA. […] One possible explanations is abnormal cerebral venous drainage, which is the leading hypothesis of the underlying pathophysiologic mechanisms of TGA.

• #28 Longitudinal Cerebral Perfusion Change in Transient Global Amnesia Related to Left Posterior Medial Network Disruption | PLOS One

  https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145658

  Therefore, hypoperfusion at the precuneus, which is the primary component of the posterior medial system, may have implications in the interactions regarding hippocampal formation. […] In conclusion, we identified left hemispheric lateralized hypoperfusion at the initial stage of TGA using longitudinal SPECT scans, which may be related to posterior medial network disruption with left dominancy, in connection with recent studies.

• #29 Transient global amnesia – Wikipedia

  https://en.wikipedia.org/wiki/Transient_global_amnesia

  A history of migraine is a statistically significant risk factor for the development of TGA. […] Amnesia is often a symptom in epilepsy, and for that reason people with known epilepsy are disqualified from most studies of TGA. […] The prognosis of „pure” TGA is very good, as by definition, symptoms resolve within 24 hours. […] TGA may have multiple etiologies and prognoses.

• #30 Transient global amnesia: Risk factors, features, prognosis | NDT

  https://www.dovepress.com/transient-global-amnesia-risk-factors-imaging-features-and-prognosis-peer-reviewed-fulltext-article-NDT

  Transient global amnesia (TGA) was first described by Bender in 1956 and is characterized by sudden, temporary, and anterograde memory loss. This study aimed to explore the possible mechanisms of and lesions responsible for TGA. […] The exact pathogenesis of TGA is unknown. Nevertheless, various etiological hypotheses, including arterial ischemia, migraine, venous reflux disorder, and seizure, have been presented. The arterial ischemia theory is dominant, so TGA is classified as a transient ischemic attack. […] Migraine may be a risk factor of TGA, and cerebral infarction may be one of the pathogeneses. The brain area responsible for TGA may involve a memory loop comprising the hippocampal CA1 region and the fornix column among other parts. […] In summary, our study indicated that several of the patients with TGA had hippocampal ischemic injury and that the possible mechanisms involved microembolization and arterial spasm among other processes.

• #31 Transient global amnesia | Handouts | MedLink Neurology

  https://www.medlink.com/handouts/transient-global-amnesia

  The cause of transient global amnesia is unknown. The part of the brain vital for memory is the hippocampus. Each side of the brain has one and each is shaped like a banana or a seahorse (the word hippocampus is derived from the Greek for seahorse). The hippocampi lie on the inner, underside of the brain. […] The difficulty in trying to explain transient global amnesia is how a process or mechanism would selectively depress or inhibit the action of the hippocampus and not affect any other parts of the brain. It can’t be a simple reduction in the blood supply to the organ. Something seems to depress the metabolism of that part of the brain in a way similar to the depression of the brain that causes the 'aura’ of a severe migraine. At present this is the best theory: that there is a sudden inhibition of the nerve cells in the hippocampus and that this inhibition seems to spread throughout the hippocampus on both sides of the brain, almost like the ripples that spread out after a stone is thrown into a pool of calm water. The most plausible theory to date is that transient global amnesia is an unusual form of prolonged, migraine-like aura.

• #32 Factors determining recurrence in transient global amnesia | BMC Neurology | Full Text

  https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-020-01658-8

  Aetiology of transient global amnesia (TGA) remains uncertain, though many have been proposed, including ischaemic, migrainous or epileptic pathologies. […] Multiple mechanisms have been proposed for the aetiology of TGA. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. […] Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. […] One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. […] Family history of dementia was found to be associated with recurrence of TGA. […] We believe TGA is a distinctive clinical syndrome arising from different mechanisms. It may recur in 16% of those who have a background of head injury, depression or a family history of dementia.

• #33 Transient global amnesia: Risk factors, features, prognosis | NDT

  https://www.dovepress.com/transient-global-amnesia-risk-factors-imaging-features-and-prognosis-peer-reviewed-fulltext-article-NDT

  Our study found a significant difference in the history of migraine between the groups. Similar to the findings of previous studies, our results supported that migraine is a risk factor of TGA. […] Valsalva movement might induce TGA. The possible pathogenesis may involve venous hypertension in the medial temporal lobe or abnormal embolism.

• #34 Transient global amnesia – Wikipedia

  https://en.wikipedia.org/wiki/Transient_global_amnesia

  A history of migraine is a statistically significant risk factor for the development of TGA. […] Amnesia is often a symptom in epilepsy, and for that reason people with known epilepsy are disqualified from most studies of TGA. […] The prognosis of „pure” TGA is very good, as by definition, symptoms resolve within 24 hours. […] TGA may have multiple etiologies and prognoses.

• #35 Recurrent transient amnesia: a case of transient epileptic amnesia misdiagnosed as transient global amnesia

  https://www.e-acn.org/journal/view.php?number=647

  Transient epileptic amnesia (TEA) is a rare form of temporal lobe epilepsy that is characterized by recurrent observable episodes of transient amnesia that spare cognitive functions other than memory and are corroborated by epileptiform abnormalities in electroencephalography (EEG), clinical manifestations of epilepsy, or a good response to antiseizure therapy. […] When clinical features of epileptic events and EEG abnormalities are absent, TEA may be misdiagnosed as transient global amnesia (TGA) due to this condition exhibiting similar clinical features. […] Although the pathophysiology of TEA is unclear, acute transient anterograde amnesia is thought to result from a combination of abnormal epileptic discharges in the temporal lobe and dysfunction in the hippocampus and other legions involved in memory formation and storage.

• #36 Recurrent transient amnesia: a case of transient epileptic amnesia misdiagnosed as transient global amnesia

  https://www.e-acn.org/journal/view.php?number=647

  Although epileptiform discharges are not present in TGA, slow waves can often be observed in the left or both temporal lobes. […] This case indicates that TEA should be included in the differential diagnosis of memory loss in adults. The possibility of TEA should be considered in cases with pure memory loss, and detailed history-taking targeting epileptic origins along with repeated EEG tests should be conducted when symptoms appear repeatedly. The role of EEG as a critical diagnostic tool in TEA and its clear response to antiseizure medications should be emphasized.

• #37 Is transient global amnesia a form of non-convulsive status epilepticus?

  https://acnr.co.uk/articles/is-transient-global-amnesia-a-form-of-non-convulsive-status-epilepticus/

  Transient global amnesia (TGA) is a clinically defined syndrome of acute hippocampal dysfunction lasting several hours. Its pathophysiology remains elusive, and current hypotheses favour a non-epileptic cause. But hypothetically TGA might share a common mechanism with its closest mimic, namely transient epileptic amnesia. […] Numerous hypotheses regarding pathophysiology have been put forward, but controversy remains and there is no clear winner yet. […] The currently employed diagnostic criteria are an empirical construct that does not reflect a particular pathophysiology (but implies a particularly good prognosis). […] So, could transient global amnesia be an epileptic phenomenon? If the answer is ‘yes’, then it might actually be a benign form of NCSE. […] In conclusion, the pathophysiology of TGA remains unknown. A benign ictal (NCSE) or a post-ictal phenomenon should be considered as possible causes.

• #38 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] The identification by diffusion-weighted (DWI) Magnetic Resonance Imaging (MRI) of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of the disease. […] However, the observation that emotional and psychological distress are frequent precipitating events among TGA cases also leads us to hypothesize that there is a psychogenic cause behind this disease.

• #39

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Some authors believe that stress-induced catecholamine release may lead to hypoxia or ischemia, whereas others believe that the neurotransmitters involved may affect the formation of memory. […] Severe emotional reactions may contribute to the destabilization of the CA1 sector of the hippocampus via massive glutamate release. […] It is worthy to note that physical or psychological precipitating factors seem to be responsible for up to 90% of TGA episodes. […] The occurrence of a distinct precipitating event and repetitive questioning (in the absence of head trauma) seem to be key features in making the diagnosis of TGA. […] However, considering such pathophysiological variability, when facing TGA, if the clinical picture remains unclear, neuropsychological testing and/or other neurological tests, that is, electroencephalogram and brain MRI, a prompt follow-up monitoring clinical condition, together with cardiovascular, neurophysiological (electroencephalography) and neuroradiological (brain MRI) assessments can be helpful to establish a right treatment (pharmacological or psychological support). […] Fortunately, the natural course of TGA is usually benign, self-limited, and without long-term residual sequelae, but a prompt diagnosis is mandatory to properly approach such clinical entity.

• #40

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Some authors believe that stress-induced catecholamine release may lead to hypoxia or ischemia, whereas others believe that the neurotransmitters involved may affect the formation of memory. […] Severe emotional reactions may contribute to the destabilization of the CA1 sector of the hippocampus via massive glutamate release. […] It is worthy to note that physical or psychological precipitating factors seem to be responsible for up to 90% of TGA episodes. […] The occurrence of a distinct precipitating event and repetitive questioning (in the absence of head trauma) seem to be key features in making the diagnosis of TGA. […] However, considering such pathophysiological variability, when facing TGA, if the clinical picture remains unclear, neuropsychological testing and/or other neurological tests, that is, electroencephalogram and brain MRI, a prompt follow-up monitoring clinical condition, together with cardiovascular, neurophysiological (electroencephalography) and neuroradiological (brain MRI) assessments can be helpful to establish a right treatment (pharmacological or psychological support). […] Fortunately, the natural course of TGA is usually benign, self-limited, and without long-term residual sequelae, but a prompt diagnosis is mandatory to properly approach such clinical entity.

• #41

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Some authors believe that stress-induced catecholamine release may lead to hypoxia or ischemia, whereas others believe that the neurotransmitters involved may affect the formation of memory. […] Severe emotional reactions may contribute to the destabilization of the CA1 sector of the hippocampus via massive glutamate release. […] It is worthy to note that physical or psychological precipitating factors seem to be responsible for up to 90% of TGA episodes. […] The occurrence of a distinct precipitating event and repetitive questioning (in the absence of head trauma) seem to be key features in making the diagnosis of TGA. […] However, considering such pathophysiological variability, when facing TGA, if the clinical picture remains unclear, neuropsychological testing and/or other neurological tests, that is, electroencephalogram and brain MRI, a prompt follow-up monitoring clinical condition, together with cardiovascular, neurophysiological (electroencephalography) and neuroradiological (brain MRI) assessments can be helpful to establish a right treatment (pharmacological or psychological support). […] Fortunately, the natural course of TGA is usually benign, self-limited, and without long-term residual sequelae, but a prompt diagnosis is mandatory to properly approach such clinical entity.

• #42

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Transient global amnesia (TGA) is characterized by a sudden onset of anterograde and retrograde amnesia, sometimes associated with mild subclinical neuropsychological deficits and vegetative symptoms, lasting for days after the episode. […] The main risk factors for TGA are considered migraine history, cardiovascular risk factors, that is, ischemic heart disease, carotid atheromasia, and psychophysical stress. […] Close precipitating events for TGA are considered emotional stress (i.e., triggered by gastric endoscopy, birth/death announcement, and difficult/exhausting workday), physical effort (i.e., gardening, house work, and sawing wood), physical exertion (including sexual activity), and water contact/temperature change (i.e., hot bath/shower and cold swim). […] Patients with TGA are more likely to exhibit irritability or anxiety.

• #43 Transient global amnesia: Psychiatric precipitants, features, and comorbidities | MDedge

  https://blogs.the-hospitalist.org/content/transient-global-amnesia-psychiatric-precipitants-features-and-comorbidities

  Several studies have demonstrated psychiatric precipitants, features, and comorbidities associated with TGA. Of the TGA cases associated with precipitating events, 29% to 50% are associated with an emotional stressor. Examples of emotional stressors include a quarrel, the announcement of a birth or suicide, and a nightmare. During its acute phase, TGA has been shown to present with mood and anxiety symptoms. Moreover, during episodes, patients often demonstrate features of panic attacks, such as dizziness, fainting, choking, palpitations, and paresthesia. Finally, patients with TGA are more likely to have psychiatric comorbidities than those without the condition. In a study of 25 patients who experienced TGA triggered by a precipitant, Inzitari et al found a strong association of TGA with phobic personality traits, including agoraphobia and simple phobic attitudes (ie, fear of traveling far from home or the sight of blood). Pantoni et al replicated these results in 2005 and found that in comparison to patients with TIA, patients with TGA are more likely to have personal and family histories of psychiatric disease. A 2014 study by Dohring et al found that compared to healthy controls, patients with TGA are more likely to have maladaptive coping strategies and stress responses. Patients with TGA tended to exhibit increased feelings of guilt, take more medication, and exhibit more anxiety compared to healthy controls.

• #44 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Transient global amnesia (TGA) is a clinical syndrome characterized by the sudden onset of a temporary memory disorder with a profound anterograde amnesia and a variable impairment of the past memory. […] The debate regarding the etiology of this disease has focused mainly on three different mechanisms: vascular (due to venous flow changes or focal arterial ischemia), epileptic, and migraine related. However, to date there is no scientific proof of any of these mechanisms. […] The identification by diffusion-weighted (DWI) Magnetic Resonance Imaging (MRI) of lesions in the CA1 field of the hippocampus cornu ammonis led us to hypothesize that the selective vulnerability of CA1 neurons to metabolic stress could play a role in the pathophysiology of the disease. […] However, the observation that emotional and psychological distress are frequent precipitating events among TGA cases also leads us to hypothesize that there is a psychogenic cause behind this disease.

• #45 Transient Global Amnesia – Neurologic Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/neurologic-disorders/function-and-dysfunction-of-the-cerebral-lobes/transient-global-amnesia

  The etiology of transient global amnesia is not clear. Suggested mechanisms include those related to migraine, hypoxia and/or ischemia, venous flow abnormalities, or seizures, as well as psychologic factors. […] Recent data suggest that vulnerability of neurons in the CA1 area of the hippocampus to metabolic stress is pivotal; the resulting damage triggers a cascade of changes that lead to impaired hippocampal function.

• #46 :: JCN :: Journal of Clinical Neurology

  https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2008.4.2.59

  One of the hypotheses for the etiology of TGA is transient cerebral ischemia. […] The increased vulnerability of the hippocampus and the venous drainage might help to explain why memory structures are the first to be involved. […] Clinical and experimental data show that hippocampal CA1 neurons are critically involved in the process of memory consolidation by exhibiting a relay function in direct and polysynaptic intrahippocampal circuits, and lesions in this area are sufficient to produce clinically significant memory impairment. […] Pathophysiologically, neurons of the CA1 sector (Sommer sector) of the cornu ammonis are of particular interest since they show a selective vulnerability to cellular metabolic stress (e.g., during hypoxemia and ischemia) that leads to the glutamate- and calcium-induced and apoptosis mediated 'delayed neuronal death’ of affected neurons 1-3 days after hypoxia.

• #47 Transient Global Amnesia – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK442001/

  Transient global amnesia is a sudden onset of anterograde amnesia accompanied by a temporary period of retrograde amnesia, primarily affecting middle-aged and older individuals. […] The etiology of transient global amnesia remains largely unknown, with multiple theories proposed but none conclusively proven. […] The origin of transient global amnesia is believed to involve the mediobasal temporal lobe, including the hippocampus, particularly the CA1 or Sommer sector. […] The hippocampus is especially vulnerable to various metabolic stresses, potentially due to its sensitivity to cytotoxic glutamatergic uptake or release. […] Affected areas can be unilateral or bilateral, although they are more commonly found on the left side. […] Functional magnetic resonance imaging (MRI) has shown bilaterally reversible defects; both functional MRI and quantitative electroencephalography (EEG) studies have demonstrated changes in functional connectivity in the hippocampus and limbic system.

• #48 Transient global amnesia: Psychiatric precipitants, features, and comorbidities | MDedge

  https://blogs.the-hospitalist.org/content/transient-global-amnesia-psychiatric-precipitants-features-and-comorbidities

  The etiology and pathogenesis of transient global amnesia (TGA) are poorly understood, and TGA remains one of the most enigmatic syndromes in clinical neurology. Theories regarding the pathogenesis of TGA are diverse and include vascular, epileptic, migraine, and stress-related etiologies. Early theories suggested arterial ischemia and epileptic phenomena as etiologies of TGA. The venous theory posits that TGA stems from jugular venous incompetency, causing venous flow and subsequent venous congestion in the medial temporal lobe, wherein lies the hippocampus. This theory is supported by several studies showing venous valve insufficiency as detected by ultrasonographic evaluation during the Valsalva maneuver in patients with TGA. This pathophysiologic mechanism may explain the occurrence of TGA in a specific cluster of cases, including men whose TGA episodes are precipitated by physical stress or the Valsalva maneuver. The migraine theory and stress theory share a similar proposed neurophysiologic mechanism. The migraine theory stems from migraines being a known risk factor for TGA, particularly in middle-aged women. The stress theory is based on the known emotional precipitants and psychiatric comorbidities associated with TGA. Notably, both the migraine theory and stress theory implicate the role of excessive glutamate release as well as CNS depression. Glutamate targets the CA1 region of the hippocampus, which is involved in TGA and is known to have the highest density of N-methyl-D-aspartate receptors among hippocampal regions. Given the heterogeneity of the demographics and stressors associated with TGA, multiple mechanisms for the disease process may coexist, leading to a similar clinical picture. In 2006, Quinette et al performed a multivariate analysis of variables associated with TGA, including age, sex, medical history, and presentation. They demonstrated 3 clusters of TGA pictures: women with anxiety or a personality disorder; men with physical precipitating events; and younger patients (age 56) with a history of migraine. These findings suggest TGA may have unique precipitants corresponding to multiple neurophysiologic mechanisms.

• #49 :: JCN :: Journal of Clinical Neurology

  https://www.thejcn.com/DOIx.php?id=10.3988/jcn.2008.4.2.59

  CA1 is known to be the sector most vulnerable to hypoxia, and is supplied by only one large ventral artery, whereas the other regions (i.e., CA2-CA4) are supplied by one large dorsal artery and several small arteries. […] These anatomical differences could make CA1 more vulnerable to ischemia than the other sectors.

• #50 Transient Global Amnesia Clinical Presentation: History, Physical, Causes

  https://emedicine.medscape.com/article/1160964-clinical

  Transient global amnesia (TGA) is a well-described syndrome, but one whose exact etiology is not yet completely understood. […] Many mechanisms have been proposed, but no single cause can explain fully all the features of TGA. These include migraine variant, temporal lobe seizure, and TIA. […] There is a demonstrated association between TGA and migraine. […] Precipitants of TGA frequently include physical exertion, overwhelming emotional stress, pain, cold-water exposure, sexual intercourse, and Valsalva maneuver. […] The exact mechanism that produces transient global amnesia is unclear. […] One theory proposed by Lewis is that venous congestion causes disrupted blood flow to the thalamic or mesial temporal structures. […] The frequently cited triggers for TGA can increase either sympathetic activity and/or intrathoracic pressure. […] Conditions predisposing to this scenario might include venous anatomy anomalies, integrity of jugular vein valves, timing of the trigger, and severity of the inciting event.

• #51

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Transient global amnesia (TGA) is characterized by a sudden onset of anterograde and retrograde amnesia, sometimes associated with mild subclinical neuropsychological deficits and vegetative symptoms, lasting for days after the episode. […] The main risk factors for TGA are considered migraine history, cardiovascular risk factors, that is, ischemic heart disease, carotid atheromasia, and psychophysical stress. […] Close precipitating events for TGA are considered emotional stress (i.e., triggered by gastric endoscopy, birth/death announcement, and difficult/exhausting workday), physical effort (i.e., gardening, house work, and sawing wood), physical exertion (including sexual activity), and water contact/temperature change (i.e., hot bath/shower and cold swim). […] Patients with TGA are more likely to exhibit irritability or anxiety.

• #52 Transient global amnesia – GPnotebook

  https://gpnotebook.com/pages/general-information/transient-global-amnesia

  Transient global amnesia (TGA) is a temporary and isolated disorder of memory. […] possible that it may result from different mechanisms such as venous congestion with valsalva-like activities before symptom onset, arterial thromboembolic ischaemia and vasoconstriction due to hyperventilation. […] close precipitating events for TGA are considered emotional stress (i.e., triggered by gastric endoscopy, birth/death announcement, and difficult/exhausting workday), physical effort (i.e., gardening, house work, and sawing wood), physical exertion (including sexual activity), and water contact/temperature change (i.e., hot bath/shower and cold swim). […] remote precipitating events, with onset reported weeks prior to TGA, are considered anxiety triggered by conflict at home or work, health problems, and financial stressors. […] There is a correlation between TGA and migraine. […] a population-based study concluded that an episode of TGA does not increase the risk of subsequent cerebrovascular events, seizures, or cognitive impairment.

• #53 Transient global amnesia – GPnotebook

  https://gpnotebook.com/pages/general-information/transient-global-amnesia

  Transient global amnesia (TGA) is a temporary and isolated disorder of memory. […] possible that it may result from different mechanisms such as venous congestion with valsalva-like activities before symptom onset, arterial thromboembolic ischaemia and vasoconstriction due to hyperventilation. […] close precipitating events for TGA are considered emotional stress (i.e., triggered by gastric endoscopy, birth/death announcement, and difficult/exhausting workday), physical effort (i.e., gardening, house work, and sawing wood), physical exertion (including sexual activity), and water contact/temperature change (i.e., hot bath/shower and cold swim). […] remote precipitating events, with onset reported weeks prior to TGA, are considered anxiety triggered by conflict at home or work, health problems, and financial stressors. […] There is a correlation between TGA and migraine. […] a population-based study concluded that an episode of TGA does not increase the risk of subsequent cerebrovascular events, seizures, or cognitive impairment.

• #54 Transient global amnesia: Psychiatric precipitants, features, and comorbidities | MDedge

  https://blogs.the-hospitalist.org/content/transient-global-amnesia-psychiatric-precipitants-features-and-comorbidities

  The etiology and pathogenesis of transient global amnesia (TGA) are poorly understood, and TGA remains one of the most enigmatic syndromes in clinical neurology. Theories regarding the pathogenesis of TGA are diverse and include vascular, epileptic, migraine, and stress-related etiologies. Early theories suggested arterial ischemia and epileptic phenomena as etiologies of TGA. The venous theory posits that TGA stems from jugular venous incompetency, causing venous flow and subsequent venous congestion in the medial temporal lobe, wherein lies the hippocampus. This theory is supported by several studies showing venous valve insufficiency as detected by ultrasonographic evaluation during the Valsalva maneuver in patients with TGA. This pathophysiologic mechanism may explain the occurrence of TGA in a specific cluster of cases, including men whose TGA episodes are precipitated by physical stress or the Valsalva maneuver. The migraine theory and stress theory share a similar proposed neurophysiologic mechanism. The migraine theory stems from migraines being a known risk factor for TGA, particularly in middle-aged women. The stress theory is based on the known emotional precipitants and psychiatric comorbidities associated with TGA. Notably, both the migraine theory and stress theory implicate the role of excessive glutamate release as well as CNS depression. Glutamate targets the CA1 region of the hippocampus, which is involved in TGA and is known to have the highest density of N-methyl-D-aspartate receptors among hippocampal regions. Given the heterogeneity of the demographics and stressors associated with TGA, multiple mechanisms for the disease process may coexist, leading to a similar clinical picture. In 2006, Quinette et al performed a multivariate analysis of variables associated with TGA, including age, sex, medical history, and presentation. They demonstrated 3 clusters of TGA pictures: women with anxiety or a personality disorder; men with physical precipitating events; and younger patients (age 56) with a history of migraine. These findings suggest TGA may have unique precipitants corresponding to multiple neurophysiologic mechanisms.

• #55 Transient Global Amnesia: Background, Pathophysiology, Epidemiology

  https://emedicine.medscape.com/article/1160964-overview

  The precise pathophysiology of transient global amnesia is not clear. The findings reported with positron emission tomography (PET), diffusion-weighted MRI (DWI), single photon emission computed tomography (SPECT) and MR spectroscopy (MRS) have indicated various brain regions that are affected in TGA. […] On PET and DWI, blood flow to specific brain areas that involve memory appears to be disrupted transiently during TGA. This includes the thalamus and/or mesial temporal structures (in particular the amygdala and hippocampus). […] Overall, the variety of findings on functional imaging studies may support the notion that TGA is a syndrome with not only a variety of precipitating causes but also of differing mechanisms.

• #56 Forget About It: Diagnosis and Management of Transient Global Amnesia in the Emergency Department — BROWN EMERGENCY MEDICINE BLOG

  http://brownemblog.com/blogposts/2024/3/25/forget-about-it-diagnosis-and-management-of-transient-global-amnesia-in-the-emergency-department

  Transient global amnesia (TGA) is a period of sudden amnesia that involves the inability to recall recent memories as well as the inability to form new memories. […] While the specific cause of TGA is unknown, up to 90% of cases include a precipitating event before symptom onset; these can include rapid temperature fluctuations, sexual intercourse, severe emotional/physical stress, pain, and medical procedures. […] Pathogenesis of TGA involves the disruption of the neural connections that form memories, known as the Papez circuit. […] Temporary interruption of these normal processes prevents access to and storage of short-term memories. […] Several studies have identified a correlation between TGA and the presence of abnormal, non-ischemic lesions in the left hippocampus or left medial temporal lobe seen on MRI diffuse-weighted imaging. […] Ischemia, however, does represent a rare cause of isolated amnesia and some experts advocate for MRI evaluation for all patients with suspected TGA.

• #57 Transient Global Amnesia Is an Experience You’ll Never Forget

  https://www.webmd.com/brain/features/transient-global-amnesia

  Neurologists dont yet know exactly how TGA happens, but research points to brief venous hypertension in the brain. This temporarily deprives the brains two memory-forming hippocampi of oxygen. What we dont understand is exactly what is happening on a physiological level, says Sicotte. Theres a decrease in blood flow, but why? […] In an episode of TGA, the machinery our brain uses to make new memories and also access old memories is offline, Sicotte explains. Its like a switch goes off. Maybe its a protective mechanism. […] TGA is a source of fascination for neurologists, a syndrome that reminds both medical trainees and laypeople how much we still have to learn about the way memories form, encode, vanish, and come back.

• #58 Guideline “Transient Global Amnesia (TGA)” of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline | Neurological Research and Practice | Full Text

  https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-023-00240-0

  Larner developed a neural network model of memory function and suggested, among other things, that loss of fault tolerance of hippocampal neural networks leads to a failure of synaptic transmission in these networks and thus to memory impairment. […] Cerebral ischemia as a cause of TGA is considered unlikely. […] Although atrial septal defects seem to be much more frequent in TGA patients (55%) as compared to the general population (25%), it remains unexplained for the time being how paradoxical emboli could trigger such a monomorphic and always transient neurological deficit. […] In summary, these findings most likely suggest that TGA is based on a transient dysfunction, particularly of the hippocampus, based on a multifactorial etiology, such that several of the factors described above must interact for TGA to occur.

• #59 Transient Global Amnesia | American Journal of Neuroradiology

  https://www.ajnr.org/ajnr-case-collections-diagnosis/transient-global-amnesia

  Defined as a sudden onset of antegrade amnesia that lasts up to 24 hours. […] Pathophysiology: not clearly known. Vasospasm (migraine-like), focal ischemia, venous flow abnormality and epileptic phenomena proposed. Related to vulnerability of CA1 neurons subfield of the hippocampal’s cornu ammonis to metabolic stress.

• #60 Guideline “Transient Global Amnesia (TGA)” of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline | Neurological Research and Practice | Full Text

  https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-023-00240-0

  The cause of TGA is still unknown, but numerous findings in recent years point to a multifactorial genesis. […] Since the pathomechanism of TGA has not yet been definitively clarified, a multifactorial or multi-causal process seems likely. […] Because the pathomechanism of TGA is not yet clearly known, no evidence-based recommendations can be made regarding prophylaxis. […] This notion is supported by imaging findings using diffusion-weighted magnetic resonance imaging, which shows hippocampal lesions in more than half of patients in the acute stage. […] TGA patients with and without DWI lesions do not differ in terms of clinical symptoms and cognitive functions over the long term. […] Functional and morphometric MRI studies and quantitative EEG analyses were able to show changes in functional connectivity in the limbic system and hippocampus.

• #61 Transient Global Amnesia

  https://fpnotebook.com/Neuro/Cognitive/TrnsntGlblAmns.htm

  Hippocampus is key in the creation of short-term memory. […] Increased intrathoracic pressure and Jugular Venous Pressure may decrease Hippocampus perfusion. […] Dysfunction of bilateral medial Temporal Lobes, and Hippocampus. […] MRI Brain DWI has shown bright punctate foci in Hippocampus of TGA patients. […] Associations with Migraine Headache, Temporal Lobe ischemia or partial complex Seizures have been postulated. […] Venous congestion and venous reflux is also postulated as cause. […] May explain why some TGA episodes are preceded by straining or Valsalva Maneuver.

• #62 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The etiology is unknown. Suggested causes have included a transient ischemic attack, migraine, epilepsy, vein thrombosis, central nervous system tumors, saline-contrast transthoracic echocardiography, transoesophageal echocardiography, drug intoxication or other toxic and metabolic disturbances, circadian rhythmicity, possible stress induced with impact on the hippocampus, cold water immersion, post-traumatic stress disorder, and hysteria. A transient ischemic attack that affects the hippocampi and associated mesial structures was thought to be a leading cause of transient global amnesia, although many contest this view. Supporting evidence includes PET and SPECT studies that show hypoperfusion and hypometabolism in the hippocampi and associated mesial structures during an attack with resolution following the attack. Wang and colleagues detected hyperintensities in the head, body, and caudate of CA1 and in the hippocampal tail on diffusion-weighted imaging during the acute phase after onset of transient global amnesia symptoms. The authors suggested that, due to the presence of microstructural sequelae, ischemic lesions in the hippocampus may be associated with transient global amnesia. Lesions can typically be detected 12 to 48 hours after the onset of symptoms, though they often resolve. However, patients with transient global amnesia do not present with an increased risk of subsequent stroke compared to individuals with transient ischemic attacks. Ogawa and colleagues suggested increased cytotoxicity in lesions found in the CA1 region of the hippocampus in patients with transient global amnesia, which led to cytotoxic edema in the lesion areas. Using ultra-high field 7 T MRI, hippocampal lesions, initially detected during the acute phase of transient global amnesia, did not show focal sequelae; this highlights the importance of diffusion-weighted imaging during the acute phase.

• #63 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The etiology is unknown. Suggested causes have included a transient ischemic attack, migraine, epilepsy, vein thrombosis, central nervous system tumors, saline-contrast transthoracic echocardiography, transoesophageal echocardiography, drug intoxication or other toxic and metabolic disturbances, circadian rhythmicity, possible stress induced with impact on the hippocampus, cold water immersion, post-traumatic stress disorder, and hysteria. A transient ischemic attack that affects the hippocampi and associated mesial structures was thought to be a leading cause of transient global amnesia, although many contest this view. Supporting evidence includes PET and SPECT studies that show hypoperfusion and hypometabolism in the hippocampi and associated mesial structures during an attack with resolution following the attack. Wang and colleagues detected hyperintensities in the head, body, and caudate of CA1 and in the hippocampal tail on diffusion-weighted imaging during the acute phase after onset of transient global amnesia symptoms. The authors suggested that, due to the presence of microstructural sequelae, ischemic lesions in the hippocampus may be associated with transient global amnesia. Lesions can typically be detected 12 to 48 hours after the onset of symptoms, though they often resolve. However, patients with transient global amnesia do not present with an increased risk of subsequent stroke compared to individuals with transient ischemic attacks. Ogawa and colleagues suggested increased cytotoxicity in lesions found in the CA1 region of the hippocampus in patients with transient global amnesia, which led to cytotoxic edema in the lesion areas. Using ultra-high field 7 T MRI, hippocampal lesions, initially detected during the acute phase of transient global amnesia, did not show focal sequelae; this highlights the importance of diffusion-weighted imaging during the acute phase.

• #64 Guideline “Transient Global Amnesia (TGA)” of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline | Neurological Research and Practice | Full Text

  https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-023-00240-0

  The cause of TGA is still unknown, but numerous findings in recent years point to a multifactorial genesis. […] Since the pathomechanism of TGA has not yet been definitively clarified, a multifactorial or multi-causal process seems likely. […] Because the pathomechanism of TGA is not yet clearly known, no evidence-based recommendations can be made regarding prophylaxis. […] This notion is supported by imaging findings using diffusion-weighted magnetic resonance imaging, which shows hippocampal lesions in more than half of patients in the acute stage. […] TGA patients with and without DWI lesions do not differ in terms of clinical symptoms and cognitive functions over the long term. […] Functional and morphometric MRI studies and quantitative EEG analyses were able to show changes in functional connectivity in the limbic system and hippocampus.

• #65 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The pathogenesis of transient global amnesia is unclear. Anterograde and retrograde memory defects in transient global amnesia may be due to an interruption in the transfer of data into and out of long-term storage. It has also been suggested that transient global amnesia is related to a functional disturbance in the brain episodic-memory network. Amnestic states are well known to correlate with damage to components of the limbic system, such as the hippocampi and other mesial temporal structures. Hodel and colleagues examined differences in cortical thickness and brain neural pathways or networks in patients with transient global amnesia and 18 age- and gender-matched controls. Findings suggest that patients with transient global amnesia had lower structural connectivity and cortical thickness in regions of the limbic system compared to neurologically healthy controls. SPECT and PET studies conducted during episodes of transient global amnesia show bilateral mesial temporal hypoperfusion, and PET studies indicate hypometabolism in the left temporal and bilateral parieto-occipital lobes as well as hypermetabolism in bilateral inferior frontal regions. In some patients, transient hyperperfusion of the medial temporal or occipito-cerebellar area has been found and is suggested to be related to changes in regional cerebral blood flow associated with different pathophysiological bases for transient global amnesia. Kim and colleagues reported the presence of significant hypoperfusion in six patients in the left hippocampus, left thalamus, and bilateral cerebellum, which was congruous with previous findings of hypoperfusion of the left hemisphere hippocampal and thalamic structures. Follow-up SPECT scans noted resolution of regional cerebral blood flow within the hippocampus and thalamus. The range of findings in SPECT studies is likely due to variable timings of scans following a transient global amnesia event and other patient-specific characteristics, such as whether the individual experiences recurrent episodes versus a single episode of transient global amnesia.

• #66 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The pathogenesis of transient global amnesia is unclear. Anterograde and retrograde memory defects in transient global amnesia may be due to an interruption in the transfer of data into and out of long-term storage. It has also been suggested that transient global amnesia is related to a functional disturbance in the brain episodic-memory network. Amnestic states are well known to correlate with damage to components of the limbic system, such as the hippocampi and other mesial temporal structures. Hodel and colleagues examined differences in cortical thickness and brain neural pathways or networks in patients with transient global amnesia and 18 age- and gender-matched controls. Findings suggest that patients with transient global amnesia had lower structural connectivity and cortical thickness in regions of the limbic system compared to neurologically healthy controls. SPECT and PET studies conducted during episodes of transient global amnesia show bilateral mesial temporal hypoperfusion, and PET studies indicate hypometabolism in the left temporal and bilateral parieto-occipital lobes as well as hypermetabolism in bilateral inferior frontal regions. In some patients, transient hyperperfusion of the medial temporal or occipito-cerebellar area has been found and is suggested to be related to changes in regional cerebral blood flow associated with different pathophysiological bases for transient global amnesia. Kim and colleagues reported the presence of significant hypoperfusion in six patients in the left hippocampus, left thalamus, and bilateral cerebellum, which was congruous with previous findings of hypoperfusion of the left hemisphere hippocampal and thalamic structures. Follow-up SPECT scans noted resolution of regional cerebral blood flow within the hippocampus and thalamus. The range of findings in SPECT studies is likely due to variable timings of scans following a transient global amnesia event and other patient-specific characteristics, such as whether the individual experiences recurrent episodes versus a single episode of transient global amnesia.

• #67 Transient global amnesia | MedLink Neurology

  https://www.medlink.com/articles/transient-global-amnesia

  The pathogenesis of transient global amnesia is unclear. Anterograde and retrograde memory defects in transient global amnesia may be due to an interruption in the transfer of data into and out of long-term storage. It has also been suggested that transient global amnesia is related to a functional disturbance in the brain episodic-memory network. Amnestic states are well known to correlate with damage to components of the limbic system, such as the hippocampi and other mesial temporal structures. Hodel and colleagues examined differences in cortical thickness and brain neural pathways or networks in patients with transient global amnesia and 18 age- and gender-matched controls. Findings suggest that patients with transient global amnesia had lower structural connectivity and cortical thickness in regions of the limbic system compared to neurologically healthy controls. SPECT and PET studies conducted during episodes of transient global amnesia show bilateral mesial temporal hypoperfusion, and PET studies indicate hypometabolism in the left temporal and bilateral parieto-occipital lobes as well as hypermetabolism in bilateral inferior frontal regions. In some patients, transient hyperperfusion of the medial temporal or occipito-cerebellar area has been found and is suggested to be related to changes in regional cerebral blood flow associated with different pathophysiological bases for transient global amnesia. Kim and colleagues reported the presence of significant hypoperfusion in six patients in the left hippocampus, left thalamus, and bilateral cerebellum, which was congruous with previous findings of hypoperfusion of the left hemisphere hippocampal and thalamic structures. Follow-up SPECT scans noted resolution of regional cerebral blood flow within the hippocampus and thalamus. The range of findings in SPECT studies is likely due to variable timings of scans following a transient global amnesia event and other patient-specific characteristics, such as whether the individual experiences recurrent episodes versus a single episode of transient global amnesia.

• #68 Guideline “Transient Global Amnesia (TGA)” of the German Society of Neurology (Deutsche Gesellschaft für Neurologie): S1-guideline | Neurological Research and Practice | Full Text

  https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-023-00240-0

  The cause of TGA is still unknown, but numerous findings in recent years point to a multifactorial genesis. […] Since the pathomechanism of TGA has not yet been definitively clarified, a multifactorial or multi-causal process seems likely. […] Because the pathomechanism of TGA is not yet clearly known, no evidence-based recommendations can be made regarding prophylaxis. […] This notion is supported by imaging findings using diffusion-weighted magnetic resonance imaging, which shows hippocampal lesions in more than half of patients in the acute stage. […] TGA patients with and without DWI lesions do not differ in terms of clinical symptoms and cognitive functions over the long term. […] Functional and morphometric MRI studies and quantitative EEG analyses were able to show changes in functional connectivity in the limbic system and hippocampus.

• #69 Transient global amnesia – Wikipedia

  https://en.wikipedia.org/wiki/Transient_global_amnesia

  A history of migraine is a statistically significant risk factor for the development of TGA. […] Amnesia is often a symptom in epilepsy, and for that reason people with known epilepsy are disqualified from most studies of TGA. […] The prognosis of „pure” TGA is very good, as by definition, symptoms resolve within 24 hours. […] TGA may have multiple etiologies and prognoses.

• #70

  https://journals.lww.com/md-journal/fulltext/2018/10120/risk_factors_of_transient_global_amnesia__three.53.aspx

  Some authors believe that stress-induced catecholamine release may lead to hypoxia or ischemia, whereas others believe that the neurotransmitters involved may affect the formation of memory. […] Severe emotional reactions may contribute to the destabilization of the CA1 sector of the hippocampus via massive glutamate release. […] It is worthy to note that physical or psychological precipitating factors seem to be responsible for up to 90% of TGA episodes. […] The occurrence of a distinct precipitating event and repetitive questioning (in the absence of head trauma) seem to be key features in making the diagnosis of TGA. […] However, considering such pathophysiological variability, when facing TGA, if the clinical picture remains unclear, neuropsychological testing and/or other neurological tests, that is, electroencephalogram and brain MRI, a prompt follow-up monitoring clinical condition, together with cardiovascular, neurophysiological (electroencephalography) and neuroradiological (brain MRI) assessments can be helpful to establish a right treatment (pharmacological or psychological support). […] Fortunately, the natural course of TGA is usually benign, self-limited, and without long-term residual sequelae, but a prompt diagnosis is mandatory to properly approach such clinical entity.

• #71 The long-term prognosis of Transient Global Amnesia: a systematic review

  https://www.degruyterbrill.com/document/doi/10.1515/revneuro-2020-0110/html?lang=en&srsltid=AfmBOooeXVkMCPgqjZsct7Pj1CxvxEpCtu4v3xfbhG6AGGqyHhoMXr2A

  Transient Global Amnesia (TGA) constitutes an enigmatic amnestic condition. […] In view of the admittedly limited knowledge regarding the nature of TGA, we decided to systematically review existing evidence for the generally regarded benign course of the disease. […] The long-term risks of dementia, epilepsy, psychological-emotional disturbances, as well as long-term vascular and (vascular or nonvascular) mortality risks, were evaluated. […] Overall, retrieved evidence was suggestive of similar vascular and mortality risks in TGA patients and HC, while TIA individuals exhibited elevated risks. […] On the other hand, studies for dementia and epilepsy obtained contradictory results, indicating both a similar and an increased risk in the TGA group compared to the HC group. […] Therefore, additional high-quality studies are warranted for the acquisition of more determining conclusions regarding the long-term risk of dementia and epilepsy in TGA.

• #72 The long-term prognosis of Transient Global Amnesia: a systematic review

  https://www.degruyterbrill.com/document/doi/10.1515/revneuro-2020-0110/html?lang=en&srsltid=AfmBOooeXVkMCPgqjZsct7Pj1CxvxEpCtu4v3xfbhG6AGGqyHhoMXr2A

  Transient Global Amnesia (TGA) constitutes an enigmatic amnestic condition. […] In view of the admittedly limited knowledge regarding the nature of TGA, we decided to systematically review existing evidence for the generally regarded benign course of the disease. […] The long-term risks of dementia, epilepsy, psychological-emotional disturbances, as well as long-term vascular and (vascular or nonvascular) mortality risks, were evaluated. […] Overall, retrieved evidence was suggestive of similar vascular and mortality risks in TGA patients and HC, while TIA individuals exhibited elevated risks. […] On the other hand, studies for dementia and epilepsy obtained contradictory results, indicating both a similar and an increased risk in the TGA group compared to the HC group. […] Therefore, additional high-quality studies are warranted for the acquisition of more determining conclusions regarding the long-term risk of dementia and epilepsy in TGA.

• #73 Transient global amnesia – GPnotebook

  https://gpnotebook.com/pages/general-information/transient-global-amnesia

  Transient global amnesia (TGA) is a temporary and isolated disorder of memory. […] possible that it may result from different mechanisms such as venous congestion with valsalva-like activities before symptom onset, arterial thromboembolic ischaemia and vasoconstriction due to hyperventilation. […] close precipitating events for TGA are considered emotional stress (i.e., triggered by gastric endoscopy, birth/death announcement, and difficult/exhausting workday), physical effort (i.e., gardening, house work, and sawing wood), physical exertion (including sexual activity), and water contact/temperature change (i.e., hot bath/shower and cold swim). […] remote precipitating events, with onset reported weeks prior to TGA, are considered anxiety triggered by conflict at home or work, health problems, and financial stressors. […] There is a correlation between TGA and migraine. […] a population-based study concluded that an episode of TGA does not increase the risk of subsequent cerebrovascular events, seizures, or cognitive impairment.

• #74 Transient Global Amnesia (TGA): Care Instructions | Kaiser Permanente

  https://healthy.kaiserpermanente.org/health-wellness/health-encyclopedia/he.transient-global-amnesia-tga-care-instructions.bo1030

  What causes TGA is not fully known. But, in some cases, an intense workout, sex, or stress may cause an episode. […] TGA does not increase the chance that you will have a stroke or seizures in the future.

• #75 Factors determining recurrence in transient global amnesia | BMC Neurology | Full Text

  https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-020-01658-8

  Aetiology of transient global amnesia (TGA) remains uncertain, though many have been proposed, including ischaemic, migrainous or epileptic pathologies. […] Multiple mechanisms have been proposed for the aetiology of TGA. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. […] Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. […] One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. […] Family history of dementia was found to be associated with recurrence of TGA. […] We believe TGA is a distinctive clinical syndrome arising from different mechanisms. It may recur in 16% of those who have a background of head injury, depression or a family history of dementia.

• #76 Factors determining recurrence in transient global amnesia | BMC Neurology | Full Text

  https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-020-01658-8

  Aetiology of transient global amnesia (TGA) remains uncertain, though many have been proposed, including ischaemic, migrainous or epileptic pathologies. […] Multiple mechanisms have been proposed for the aetiology of TGA. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. […] Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. […] One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. […] Family history of dementia was found to be associated with recurrence of TGA. […] We believe TGA is a distinctive clinical syndrome arising from different mechanisms. It may recur in 16% of those who have a background of head injury, depression or a family history of dementia.

• #77 Factors determining recurrence in transient global amnesia | BMC Neurology | Full Text

  https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-020-01658-8

  Aetiology of transient global amnesia (TGA) remains uncertain, though many have been proposed, including ischaemic, migrainous or epileptic pathologies. […] Multiple mechanisms have been proposed for the aetiology of TGA. One hypothesis is that retrograde venous flow leads to venous congestion, possibly due to increased thoracic pressure or jugular valve incompetence, which in turn causes a transient ischemia due to hypoperfusion. […] Ischaemia from thromboembolism constitutes a contrasting hypothesis on pathogenesis. […] One final hypothesis is that TGA is a type of migrainous aura, occurring due to cortical spreading depression, leading to cellular metabolic stress in vulnerable CA-1 sector neurons. […] Family history of dementia was found to be associated with recurrence of TGA. […] We believe TGA is a distinctive clinical syndrome arising from different mechanisms. It may recur in 16% of those who have a background of head injury, depression or a family history of dementia.

• #78 Clinical manifestation and imaging characteristics of transient global amnesia: patent foramen ovale as an underlying factor

  https://www.imrpress.com/journal/JIN/20/3/10.31083/j.jin2003077/htm

  This study showed that patients with PFO had fewer or no underlying vascular risk factors (e.g., hypertension and diabetes) as compared to those without PFO. They also had fewer cases of typical chronic ischemia on brain MRI than those without PFO. These results suggest an ischemic event caused by a different mechanism rather than a typical vascular risk factor. The embolus formed in the venous system can travel through the shunt flow via the PFO, causing infarction mainly in the posterior circulation. […] The effect of preceding extreme stress on TGA is not fully known. Among the patients with PFO and HSI on DWI, 82.8% reported experiencing extreme stress before the occurrence of TGA. This was mainly accompanied by excessive crying or anger. […] The reports of previous studies regarding the cause of TGA have not been consistent, and this could be because the differences in patient characteristics were not considered. The results of this study do not suggest that all cases of TGA are associated with PFO. However, there is the possibility of a paradoxical thromboembolic event due to shunting through the PFO, regardless of the known vascular risk factors. […] This study showed that 5% (n = 7) of the patients had recurrent TGA during the follow-up period (lasting for at least 4 years), and they all had PFO. None of the patients experienced any other vascular events during the follow-up period, regardless of the presence of PFO.

• #79 Transient global amnesia: current perspectives | NDT

  https://www.dovepress.com/transient-global-amnesia-current-perspectives-peer-reviewed-fulltext-article-NDT

  The underlying etiology of TGA remains obscure with multiple proposed mechanisms, such as arterial ischemia, venous congestion, migraine, and psychogenic disorders. […] Venous congestion with retrograde cerebral flow is another prominent hypothesis for the pathophysiology behind TGA. […] There are several potential etiologies that may be responsible for TGA, including arterial ischemia, venous congestion, migraine, and psychogenic disorders. […] Selective vulnerability of hippocampal CA1 neurons to metabolic stress seems to play a crucial part in the pathophysiological cascade that leads to a transient perturbation of memory pathways in TGA.

• #80 Forgetting the Unforgettable: Transient Global Amnesia Part I: Pathophysiology and Etiology

  https://www.mdpi.com/2077-0383/11/12/3373

  Despite all the theories and studies, there is no definitive evidence supporting any of these mechanisms, so the etiology of TGA remains elusive. […] On the other hand, based on the nature of cognitive impairment during the episodes, there is the consensus that the symptoms are due to the transient dysfunction of the medial temporal lobe, particularly of the hippocampus. […] The selective location of DWI-MRI lesions in the CA-1 sector of the hippocampal cornu ammonis has suggested that the cellular stress of CA-1 neurons has a pivotal role in the pathophysiology of hippocampal dysfunction during TGA. […] Future advances in the knowledge of the mechanisms that regulate physiological mnemonic processes will allow us to clarify the pathophysiological correlates of the acute phase of TGA and, in particular, to decipher which trigger induces the pathophysiological cascade that affects the involved brain structures.

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