Recurrent Transient Global Amnesia Research Articles

Recurrent Transient Global Amnesia in a Hot and Humid Machinery Room

Transient global amnesia (TGA) is characterized by abrupt onset temporary dysfunction of anterograde and retrograde amnesia without other neurologic deficits. We encountered a 53-year-old man who developed recurrent TGA while working in a hot and humid machinery room (33℃ and 64% relative humidity). Heat exposure and physical exertion may facilitate the leakage of cytokines into the systemic circulation so as to cause a cerebral endothelial insult. Functional insufficiency of the hippocampus and its connections caused by physical and environmental factors may be related to recurrent attacks. Key Words: Transient global amnesia, Diffusion-weighted MRI, Hot and humid condition

Association of diffusion weighted imaging abnormalities and recurrence in transient global amnesia

Since the first description of transient global amnesia (TGA) in 1964, its etiology has remained obscure. Reversible diffusion weighted imaging (DWI) hyperintensities in the hippocampus have been found on MRI of some patients with TGA during acute events. The implication of this is not well understood. We identified 47 patients with TGA between November 2004 and November 2009, and enrolled 27 patients with brain MRI within 72 hours of symptom onset for analysis and recorded subsequent relapse or stroke occurrence during follow-up. Nine of the 27 patients had reversible hippocampal punctuate hyperintensities, with complete resolution noted on a second MRI on average 4 months after the initial TGA. Patients with a first relapse (their second TGA attack) had a significantly higher association of DWI hippocampal abnormalities ( p = 0.03) compared to patients with their first TGA event. None of the 27 patients had a stroke or further relapse during the mean follow-up period of 32.6 months. Thus, patients with recurrent TGA have a significantly higher association of reversible DWI abnormality.

Falling (or Ascending) Into Oblivion: Transient Global Amnesia With Paragliding

Back to table of contents Previous article Next article LettersFull AccessFalling (or Ascending) Into Oblivion: Transient Global Amnesia With ParaglidingIsabel Milheiro, M.D., Sofia Rocha, M.D., and Álvaro Machado, M.D.Isabel MilheiroSearch for more papers by this author, M.D., Sofia RochaSearch for more papers by this author, M.D., and Álvaro MachadoSearch for more papers by this author, M.D.Published Online:1 Oct 2011https://doi.org/10.1176/jnp.23.4.jnpe40AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Transient global amnesia (TGA) is a syndrome characterized by an abrupt onset of severe anterograde, and variable retrograde, memory impairment, which is self-limited, leaves no cognitive sequelae, and usually does not recur.1 Although some precipitants are well established (e.g., exercise and sexual intercourse), its etiology remains largely unknown.1We present a patient in whom TGA occurred when paragliding. A 33-year-old healthy man was brought to our attention by two friends, with whom he had practiced paragliding for many years. On that afternoon, they were flying in a local valley, at an altitude of approximately 2,000 meters. After a 20-minute flight and a flawless descent and landing, he seemed rather anxious and started to repeatedly ask the same questions, like “What am I doing here?” and “How did I get here?”. At examination, he was fully alert and well-oriented, slightly impatient, and anxious to know what was happening to him. He could not remember anything from that day or retain any new piece of information. He continued to ask the same questions, incapable of evoking any word from a given list, could not point to purposely hidden objects in the examination room after a 2-minute interval, and was unable to recall any information related to his presence in the hospital. Neurological examination was otherwise normal. Laboratory work-up, brain CT, and EEG were unrevealing. The patient soon started to recover, and was completely back to normal in about 5 hours, retaining a memory gap for this period.In attempting to explain what happens in TGA, several mechanisms have been proposed: vascular hypoxic or ischemic damage, migraine-like cortical spreading depression, or transient epileptic phenomena, affecting brain regions known to be crucial for episodic memory, in particular, the hippocampal formation.1 The occurrence of TGA in a high-altitude setting was first noted by Litch in 1999.2 Since then, apart from his case series of four individuals, all developing symptoms at very high altitudes (above 3,500 meters),3 we have found only an additional case in a man who got sick while skiing at 2,000 meters.4 In all these instances, the same pathophysiological cascade was proposed: diminished inspiratory oxygen pressure leading to hyperventilation, which results in hypocapnia and subsequent vasoconstriction, compromising the perfusion of critical brain memory regions or, alternatively, acting as a trigger for cortical depression spreading. Also, as cerebral blood flow is controlled by a fine balance between hypoxic vasodilatation and hypocapnic vasoconstriction, autoregulation abnormalities, as previously postulated to occur in TGA,5 can further aggravate a net disequilibrium toward cerebral vasoconstriction. Although this can well be what happened to our patient, it should be acknowledged that in this, as well as in other reported cases, it is virtually impossible to discard completely other co-occurring factors, such as physical exertion or emotional stress.Psychiatry and Mental Health Dept.Neurology Dept. Hospital de Braga PortugalCorresponding author: Álvaro Machado; e-mail: [email protected]com1. Quinette P , Guillery-Girard B , Dayan J , et al.: What does transient global amnesia really mean? review of the literature and thorough study of 142 cases. Brain 2006; 129(Pt 7):1640–1658Crossref, Medline, Google Scholar2. Litch JA , Bishop RA : Transient global amnesia at high altitude. N Engl J Med 1999; 340:1444Crossref, Medline, Google Scholar3. Litch JA , Bishop RA : High-altitude global amnesia. Wilderness Environ Med 2000; 11:25–28Crossref, Medline, Google Scholar4. Bucuk M , Tomic Z , Tuskan-Mohar L , et al.: Recurrent transient global amnesia at high altitude. High Alt Med Biol 2008; 9:239–240Crossref, Medline, Google Scholar5. Roach ES : Transient global amnesia: look at mechanisms, not causes. Arch Neurol 2006; 63:1338–1339Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByEpidemiology of TGA (2): Possible Precipitating Factors11 June 2022 Volume 23Issue 4 Fall 2011Pages E40-E40 Metrics PDF download History Published online 1 October 2011 Published in print 1 October 2011

A study of right-left shunt in transient global amnesia

Introduction Transient global amnesia (TGA) is a disorder of unknown aetiology. In recent studies, TGA was associated with a right to left shunt (RLS). We studied the presence of the RLS in patients with TGA and we compared this series with patients who had suffered a transient ischaemic attack (TIA). Patients and methods We included 66 consecutive TGA patients. In these patients a transcranial Doppler was performed to determine the presence of a RLS. We collected data on the TGA episode, vascular risk factors, migraine history, recurrence of TGA and neuroimaging in patients with and without RLS. We compared the prevalence of the RLS in TGA series with 59 patients with TIA. Results The prevalence of RLS was 21.2% in patients with TGA. The RLS was associated with the migraine history (40% versus 13%; p=0.014) and a Valsalva manoeuvre as a triggering factor (50% versus 14.5%; p=0.022). A greater prevalence of RLS was detected in patients with TIA (55.9% versus 21.2%; p < 0.001). Conclusions The RLS prevalence in TGA patients is similar to the general population but significantly lower than the prevalence in TIA patients. The association with a Valsalva manoeuvre as a precipitating factor in the TGA patients with RLS could play a role in the aetiopathogenesis of the TGA.

発作の誘因として静脈還流圧上昇の関与がうたがわれた一過性全健忘の３症例：高磁場脳ＭＲＩをもちいた検討

We present 3 patients with transient global amnesia (TGA). Patient 1 was a 67-year-old man who had developed TGA 5 years ago. He showed sudden onset amnesia immediately after he quarreled with his wife loudly during driving. Three-Tesla (3T) diffusion-weighted magnetic resonance imaging (DWI) taken 18 hours after onset revealed a small hyperintense signal area in the right CA1 subfield of the hippocampus. Patient 2 was a 66-year-old woman who showed sudden onset amnesia immediately after she walked for about 20 minutes holding a heavy luggage with her arms. 3T DWI taken 64 hours after onset revealed a small hyperintense signal area in the left CA1 subfield of the hippocampus. Patient 3 was a 68-year-old woman who showed sudden onset amnesia immediately after she hurriedly cleaned up her house with a cleaner. 3T DWI taken 48 hours after onset revealed small hyperintense signal areas in the left CA1 subfield and the right subiculum proper of the hippocampus. She developed TGA recurrence 6 months after the first episode of TGA. All these 3 patients had no cardiovascular diseases. Their amnesia resolved within 5-6 hours. Magnetic resonance venography (MRV) revealed hypoplasia of the left transverse sinus in Patient 1 and Patient 3, and aplasia of the left transverse sinus in Patient 2. Ultrasound studies revealed a retrograde flow component of internal jugular vein during Valsalva maneuver in Patient 2. We speculate that an increased venous pressure might have precipitated cerebral venous ischemia in the hippocampus, which is most vulnerable to ischemic insults.

Transient global amnesia -- its clinical and pathophysiological basis and prognosis.

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.

Transient global amnesia.

30 patients aged between 45 and 78 years and who had suffered from transient global amnesia (TGA), were seen at the Department of Neurology, Pordenone Public Hospital, in the period 1978 to 1982. 25 patients had one or more risk factors for cerebrovascular disease, such as hypertension, cardiac abnormalities, diabetes and hyperlipidemia. EEG examination revealed abnormal activity only in 7 patients. Brain Computed Tomography showed cerebral atrophy in 10 and hypodense lesions in 3 patients. 16 patients had been followed up for a mean interval of 20 months. During the follow-up period, 4 patients had recurrent TGA and one had a transient ischemic attack in the vertebrobasilar arterial system. In the follow-up group, 15 patients showed permanent memory impairment. The high incidence of risk factors for cerebrovascular disease seems to confirm that TGA is probably due to transient cerebral ischemia. The high rate of permanent memory impairment, almost always connected with the coexistence of cerebrovascular risk factors, is not in agreement with the postulated good prognosis of TGA.

Recurrent Transient Global Amnesia at High Altitude

We report the case of a 57-year-old man who experienced recurrent episodes of memory loss that resemble transient global amnesia (TGA). The first episode lasted 20 minutes, and the second was 8 hours long.

The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism is not significantly correlated to Transient Global Amnesia: Preliminary results of an on-going study in Brescia Province, Italy

Transient Global Amnesia (TGA) is a well defined pure amnesic clinical syndrome characterized by acute loss of memory in middle aged people. The aetiology of TGA is still unknown but clinical and neuroimaging studies support a hippocampi involvement, and some reports suggested a possible common genetic background in cases of familial TGA. A single nucleotide polymorphism (SNP) in the Brain-derived neurotrophic factor (BDNF) gene that causes a valine to methionine substitution at codon 66 (Val66Met) has been demonstrated to affect human memory and hippocampal function in the development and maintenance of adult neurons. Aim of this study was to evaluate the role of BDNF Val66Met polymorphism on TGA risk and all TGA clinical features. Ninety-eight TGA patients and 93 age-matched controls were enrolled in the study. Each patient underwent clinical and neurological examination, routine blood examination, EEG, Jugular vein valve (JVI) competence assessment, and neuroimaging study. TGA characteristics were carefully recorded. The distribution of BDNF genotype did not differ in TGA patients compared to controls (BDNF GG: 58.2% vs 55.9%, GA: 33.7% vs 36.6%, AA: 8.1% vs 7.5%, P=.91) as well as allele frequency (BDNF G, TGA vs CON: 75.0% vs 74.2, P=.47). No significant differences in age at onset, disease duration and recurrence or the presence of predisposing factors between TGA patients carrying BDNF AA, BDNF GA and BDNF GG genotype were found. This study, that firstly looked at genetic background in TGA, did not show a significant correlation between the BDNF Val66Met polymorphism and age of onset, risk factors, duration or recurrence of TGA.

Recurrent Orthostatic Global Amnesia in a Patient with Postoperative Hyperfibrinogenemia

Transient global amnesia (TGA) is characterized by sudden, temporary dysfunction of antegrade and recent retrograde memory without other neurologic deficits. Although there is sometimes a precipitating event, the origin of TGA remains controversial. We encountered a patient who developed recurrent TGA when upright, in whom the symptom promptly and regularly resolved when supine. Symptoms began about a week after cardiac surgery concurrent with marked hyperfibrinogenemia and acceleration of the erythrocyte sedimentation rate, and abated without recurrence when these laboratory abnormalities were ameliorated by anticoagulant and corticosteroid therapy. Diagnostic studies, including temporal artery biopsy and cerebral angiography, disclosed no anatomic vascular pathology. This is the first report of TGA associated with postoperative inflammation in which amnesia was provoked by orthostatic positioning. In conclusion, these observations implicate ischemia caused by hemodynamic vascular insufficiency as a possible cause of TGA.

Recurrent Transient Global Amnesia with Intrathecal Baclofen

A middle-aged woman began experiencing spells of profound anterograde amnesia several months after beginning intrathecal baclofen treatment for generalized dystonia. Her spells met criteria for transient global amnesia, but were unusual because of their frequent recurrence and because their frequency was somewhat dose-dependent on baclofen. Fludrocortisone decreased the frequency of these episodes, and sublingual nitroglycerin both prevented and terminated them. Baclofen-induced amnesia in rodents is a reliable model of memory impairment. In contrast, baclofen-induced memory impairment in humans is uncommon. Baclofen- associated transient global amnesia has not previously been reported.

Transient Global Amnesia After General Anesthesia

Transient global amnesia (TGA) is an amnestic syndrome, clinically dramatic but benign in nature. The hallmark of TGA is brief inability to form new memories and recall past memories despite otherwise normal neurological function. In a significant number of patients with TGA a stressful precipitating factor can be identified. We report two cases of TGA after uneventful general anesthesia. Anesthesia per se does not appear to be a direct trigger of TGA, as our first patient had a second anesthetic the next day without recurrence of TGA. Because the presentation of TGA can be dramatic and may mimic an acute cerebral ischemic event, a thorough neurologic evaluation should be pursued.

La amnesia global transitoria recurrente, una manifestación de la enfermedad isquémica cerebrovascular

Transient Global Amnesia (TGA) is a self-limited anterograde memory loss related classically to transient ischemic attacks (TIA), migraine and epilepsy. This study intended to describe clinical characteristics, the vascular risk factors and the evolution of TGA and to define clinical factors associated with recurrence.Of 139 patients with TGA, 124 were followed up for a mean time of 71.9 (39) months; these patients were compared with other 124 patients with TIA. The TGA group was subdivided in 2 subgroups: Unique-TGA (98 cases): 1 episode, and recurrent-TGA (26 cases): 2 or more episodes. Recurrent-TGA were also compared with unique-TGA and the TIA groups.The mean age of patients of the TGA group was 63 (7.96) and 58% were women. 30% had a history of migraine and 30% had anxiety. The risk of annual recurrence was 4.4%. Recurrent-TGA patients had more electroencephalographic registers showing non-epileptogenic abnormalities. The TIA group had more vascular risk factors and displayed more ischemic events during the follow-up. Recurrent-TGA patients had the same vascular risk factors as TIA patients and they also had a significantly more frequent history of stroke and trend to suffer new ischemic events than patients in the unique-TGA group.There is no vascular pathology substrate in TGA patients, suggesting an ischemic etiology due to arteriosclerosis or cardioembolism. Patients with recurrent TGA constitute a subgroup with more vascular risk factors and an increased risk to suffer new strokes. For that reason we propose that these patients be studied as ischemic patients.

Estudio de los factores de riesgo en la amnesia global transitoria y su diferenciación del accidente isquémico transitorio

Transient global amnesia (TGA) is a clinical condition that has been described in many studies, but its pathophysiology is not fully understood. In recent years the theory of valvular insufficiency in the jugular vein has been added to the classical hypotheses that link it to migraine, to epilepsy and -the most widely accepted- to transient ischemic attacks (TIA), although the real origin of the condition has still not been determined. In a retrospective study we compared 131 patients diagnosed with TGA between 1993 and 2004 with 262 patients who were diagnosed as having TIA over the same period. Mean age was 65.94 years in TGA versus 71.11 years in the case of TIA. There was a higher rate of arterial hypertension among the patients with TGA and diabetes mellitus was more frequent among those with TIA (p<0.05 in both cases). Emboligenic heart disease was scarce among patients with TGA. The number of patients with a history of ischaemic heart disease and a history and the development of cerebrovascular diseases was greater among those with TIA than in cases of TGA (p<0.05). The TGA recurrence rate was 12%. The percentage of pathological findings in the CAT brain scan was higher in patients with TIA (p<0.05). There are no significant differences between patients with TGA and TIA as far as treatment on hospital discharge is concerned. TGA does not seem to be a symptom of an arteriosclerotic pathology nor does it appear to offer a higher risk of heart or cerebrovascular disease and, therefore, antiaggregating therapy would not be indicated in such cases.

Transient global amnesia -- not always a benign process.

Transient global amnesia (TGA) is an episodic dysfunction of declarative memory, which is assumed to be a benign disorder. Brain perfusion single photon emission computed tomography (SPECT) was shown to be abnormal during the acute stage and to become normal with normalization of memory function. No data are known about the brain perfusion pattern among these patients with recurrent TGA. Sixteen patients with TGA were studied with an initial brain imaging during the acute stages of their attack, and a second imaging was performed after 3 months. In the event of a patients having a second abnormal brain perfusion HMPAO SPECT, a third imaging was performed after 1 year. Hypofusion perfusion was demonstrated in all cases during the acute stage. In all patients who had a first TGA, a normal SPECT was demonstrated after 3 months. In three patients with recurrent TGA, the brain perfusion remained abnormal after 3 months and after 1 year. A normal perfusion in TGA after 3 months can be expected in a patient with a first attack. In patients with recurrent TGA attacks, a persistent focal hypoperfusion can be expected. This subgroup of patients may demonstrate a non-benign type of TGA, eventually due to a different etiology of event.

Clinical features, vascular risk factors, and prognosis for transient global amnesia in Chinese patients

Transient global amnesia (TGA) is an intriguing clinical syndrome that has not been studied in a series of Chinese patients. From 1989 to 1995, we observed 28 consecutive patients with TGA. Their clinical characteristics, risk factors, and outcome were retrospectively reviewed and analyzed. There were 13 men and 15 women with a mean age of 62 years (range, 39 to 76). The duration of amnesic attack ranged from 20 minutes to 24 hours (mean, 8 hours), with the majority (76%) of attacks lasting for 2 to 12 hours. In 9 (32%) of the 28 patients, the TGA was triggered by a potential precipitating factor including bathing, emotional stress, and headache. The most prominent symptom exhibited by patients during an attack was repetitive questioning, which occurred in 21 (75%) of the 28 patients. No focal neurological abnormality was noted during or after the attack. Electroencephalograms were obtained in 26 patients after experiencing TGA, which showed nonspecific findings in 6 patients and were normal in 20. In 21 patients who had cranial computed tomography scans, cortical atrophy was found in 5 (24%), focal infarction in 4 (19%), and the results were negative in 12 (57%). Hypertension was the predominant vascular risk factor (11 cases, 39%), then hyperlipidemia (7 cases, 25%), and smoking (3 cases, 11%). No vascular risk factor was found in 13 patients (46%). Recurrent TGA was found in 5 patients (18%), and stroke in 2 (7%). Our study largely confirms the demographic pattern, clinical characteristics, and prognosis of TGA patients reported from the western countries. Although the cause is uncertain, TGA is a relatively benign entity.

Transient global amnesia. A case control study.

A case control study of transient global amnesia (TGA), transient ischaemic attacks (TIA) and normal controls is described. Each of the 51 TGA patients, selected between January 1985 and March 1990, was compared with four controls (two TIAs and two normals) for the presence of vascular risk factors (hypertension, diabetes, smoking habits, cholesterol, triglycerides and haematocrit levels, heart disease, previous stroke), previous TGA, migraine, psychiatric illness and recent head trauma. Patients with TGA had less diabetes, hypercholesterolaemia and hypertriglyceridaemia than TIA. TGA subjects had significantly more hypertension (odds ratio = 3.31) and migraine (odds ratio = 8.67) than normal controls. During a mean of 17.4 mths of follow-up (range 1-96 mths), three subjects had recurrent TGA, one sustained a TIA and a minor stroke, but none had seizures. Thrombo-embolism and epilepsy are unlikely to be the cause of this benign disorder. The role is stressed of appropriate precipitants, including haemodynamic changes, and of individual susceptibility (of which migraine is probably a marker) in the genesis of TGA.

A case-control study of transient global amnesia.

To evaluate risk factors and prognosis of transient global amnesia (TGA), three groups of 30 subjects each affected respectively by: (1) first-ever TGA; (2) first-ever transient ischaemic attack (TIA); (3) depressive neurosis, were compared. Prevalence of cerebrovascular risk factors was similar in patients with TGA and TIA, but significantly lower in the third group. CT showed more hypodense lesions in TIA patients than in those with TGA. In a mean follow-up of 36 months, five TGA patients experienced a TIA and three others had recurrence of TGA, but none suffered stroke or myocardial infarction. In the TIA group, four had recurrence of TIA, two suffered a stroke and two others a myocardial infarction, whereas none had TGA attacks. None of the patients of the third group had any ischaemic event during follow-up. The similar prevalence of risk factors, but the different prognosis between TGA and TIA patients, suggest that TGA is an ischaemic event, probably not triggered by thromboembolism but by a different, possibly vasospastic, mechanism.

Pathogenesis and natural history of transient global amnesia.

Fourteen patients aged between 49 and 92 years who had suffered from one or more attacks of transient global amnesia (TGA) have been followed for a mean interval of 30 months. Thirteen patients had one or more risk factors for cerebrovascular disease, such as hypertension, cardiac abnormalities, diabetes and hyperlipidemia. Clinical evidence for vertebrobasilar arterial insufficiency was demonstrated in 11 cases. EEG examination revealed bitemporal or bioccipital slow wave activity. Four-vessel arteriography showed atherosclerotic, stenotic, or occlusive lesions predominantly in the vertebrobasilar and posterior cerebral arterial systems. Five patients without recurrence of TGA showed no permanent impairment of memory, whereas eight who had recurrent attacks of TGA showed permanent memory impairment as well as mild visual-spatial or visual-motor dyspraxia as judged by neuropsychological tests on follow-up visits. "Amnesic stroke" with permanent and gross memory defect and dyspraxia occurred in two patients. It is concluded that the majority of transient global amnesic episodes in the elderly or in those with the risk factors listed above result from cerebrovascular insufficiency particularly in the territory of vertebrobasilar and posterior cerebral arterial systems (which supply major portions of the ascending reticular activating system, parahippocampal-fornical-mamillary system, inferomedial aspects of the temporal lobe and occipital lobe). Repeated attacks of TGA are not rare and with each attack the likelihood increases of permanent memory deficits and progressive dementia. A rarer outcome is cerebral infarction in the territory of posterior cerebral arteries commonly referred to as "amnesic stroke."