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PubMed2005

Evidence of acute ischemic tissue change in transient global amnesia in magnetic resonance imaging: case report and literature review.

Transient global amnesia is a benign syndrome of sudden-onset alteration of behavior with temporary dysfunction of anterograde and recent retrograde memory. Its neural substrates remain uncertain. Possible causes include ischemia, migraine, and epilepsy. The authors report a case of a 62-year-old man with a transient attack of memory disturbance, suggestive of transient global amnesia, in which magnetic resonance imaging performed 48 hours after onset showed left mesial temporal lobe signal changes on diffusion-weighted imaging and fluid-attenuated inversion recovery images. The findings and a literature review lend further support to the ischemic pathogenesis of transient global amnesia as a possible etiology, and underscore the role of diffusion-weighted imaging in the diagnosis of this condition.

Amnesia, Transient Global↗

PubMed2003

Transient global amnesia in a young adult with cyanotic heart disease.

The etiology of transient global amnesia is poorly understood, particularly in children and young adults. Transient global amnesia may follow a wide range of precipitating events. Proposed causes have included vascular event, seizure, and migraine. A young man with cyanotic congenital heart disease experienced an episode of transient global amnesia in the setting of polycythemia. Differential diagnosis of acute confusional episodes in children should include transient global amnesia, as well as confusional migraine, and should include evaluation for underlying coagulation abnormalities and polycythemia.

Adult↗

PubMed1988

Transient global amnesia and stroke.

Four patients who experienced isolated transient global amnesia had computed tomographic evidence for a cerebral infarct (3 cases) or hemorrhage (1 case). The medial part of the temporal lobe was involved in 2 patients (left in 1, right in 1), the left lentiform nucleus in 1 patient, and the left thalamus in 1 left-handed patient. These findings suggest that transient global amnesia may be associated with stroke in some cases, but it has no localizing value within the temporodiencephalic structures. No cerebrovascular events occurred over a 1-to 5-year follow-up, suggesting that transient global amnesia with infarction or hemorrhage is not a strong predictor of further stroke.

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PubMed1977

Transient global amnesia due to a dominant hemisphere tumor.

Transient global amnesia is generally regarded as a benign syndrome of probable vascular etiology. We describe a man who experienced a single episode of transient global amnesia and subsequently developed a progressive dominant hemispheric syndrome. Neuroradiologic investigations and the patient's subsequent death strongly suggest that his disease was due to a left temporal-parietal mass lesion. Although the syndrome is most often benign, such patients should be examined for mass lesions.

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PubMed1980

Musical performance during transient global amnesia.

An organist had an episode of transient global amnesia during a recital. Despite a severe immediate-memory deficit, he performed complex organ music. This case suggests that the localization of the cerebral deficit in transient global amnesia is distinct from the cerebral centers necessary for performance of instrumental music.

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PubMedDate not supplied

Transient global amnesia and cerebral infarct: a case report.

Transient global amnesia refers to a sudden and isolated dysfunction of memory for recent events, lasting a few hours. The pathogenesis of this neurological disorder is still uncertain. The most accepted hypotheses concern ischaemic, epileptic and migraine causes. We now report a case of transient global amnesia associated with computed tomography evidence for a hypodense area in the left thalamus 10 days after the transient memory dysfunctions.

Amnesia↗

PubMedDate not supplied

[Transient global amnesia: a review of 58 cases].

INTRODUCTION: Transient global amnesia (TGA) is a clinical condition in which the etiopathogenesis is still not clear. The most generally accepted theory is of a vascular origin, although epilepsy or migraine have also been considered to possibly be the cause. OBJECTIVE: To make a retrospective review of the risk factors, etiopathogenesis and clinical characteristics of 58 patients with TGA. PATIENTS AND METHODS: The variables recorded were compared with those from two control groups: one of healthy individuals and one of patients with transient ischemic attacks (TIA). RESULTS: The average age of the patients with TGA was 66.01 years. The risk factors included: arterial hypertension (58.62%), dyslipemia (15.51%) and migraine (8.62%). In three patients the EEG showed weak bilateral frontotemporal interference. Cerebral CT scans were done in all cases and were found to be pathological in 23, with lacunar multinfarct the commonest abnormality. With regard to patients with TIA, these were older (66.01 vs 72.94), smoked more (1.72% vs 12.06%) and a previous stroke was more frequent (8.62% vs 31.03%). We did not find differences regarding dyslipemia, atrial fibrillation, arterial hypertension or cardiac ischemia. However, the prevalence of vascular risk factors was significantly higher in patients with TGA as compared to healthy controls. CONCLUSION: We suggest that the etiopathogenesis of TGA is probably a transient ischemic phenomenon triggered (or not) following an attack of migraine.

Adult↗

PubMed2004

Transient global amnesia -- not always a benign process.

OBJECTIVES: 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. MATERIAL AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Adult↗

PubMed1989

[Positron emission tomography in two cases of transient global amnesia].

We encountered two cases of typical transient global amnesia (a 53-year-old woman and a 50-year-old man). Both cases showed no evidence of abnormal findings which caused the attack on examinations of CSF, EEG, brain CT, brain MRI and cerebral angiography. Examinations of positron emission tomography, using 15O labeled CO2 and O2, were performed on 14 and 8 days after the attack in the female and male cases, respectively, and those disclosed decreased regional blood flow (CBF), increased oxygen extraction ratio (OER), and decreased oxygen metabolic ratio (CMRO2) in the bilateral medial temporal and occipital lobes, which were supplied by the bilateral posterior cerebral arteries. PET, performed on about one month after the attack, revealed normalized values of CBF, OER, CMRO2 in both cases. These findings strongly suggested that transient global amnesia in our cases may be related to ischemia of the bilateral posterior cerebral arteries.

Amnesia↗

PubMed1988

Transient global amnesia: characterization of anterograde and retrograde amnesia.

Five patients with transient global amnesia (TGA) were given neuropsychological tests during and after their episode. During TGA, all patients were impaired on tests of new learning ability for both verbal and nonverbal material. Retrograde amnesia was patchy and covered a variable period of time before the onset of the episode: from about 36 hours in one case to 4 years in two cases. Some cognitive impairment in addition to amnesia was present during the episode. For example, patients copied a complex figure more poorly during the episode than afterwards. All patients had normal memory at follow-up testing. These data are consistent with the idea that the amnesic symptoms of TGA are caused by transient bilateral dysfunction of medial temporal brain structures important for memory.

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PubMed1998

Proton magnetic resonance spectroscopy during transient global amnesia.

There is uncertainty about the etiology of transient global amnesia and none of the pathogenetic hypotheses proposed so far, i.e. transient ischemia, epileptic discharge and spreading depression of cortical electrical activity, is completely satisfactory. Using water suppressed proton magnetic resonance spectroscopy we studied one patient during a typical episode of transient global amnesia and 2 weeks thereafter in order to investigate the metabolic changes in the hippocampal region. In both hippocampi, spectra of N-acetyl-aspartate, creatine-phosphocreatine, compounds containing choline and lactate failed to show changes consistent with cerebral ischemia, both in the acute phase and in the follow-up. Spreading depression in response to emotional stress seems a likely explanation in this patient, who suffered from migraine in the past.

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PubMed2006

[Transient global amnesia: indications for a syndrome involving cerebral venous stasis].

In 3 patients, a woman aged 58 and 2 men aged 61 and 58, respectively, who presented to the Emergency Clinic with sudden antegrade and retrograde amnesia, the diagnosis 'transient global amnesia' (TGA) was made. In the first and the last patient the TGA was preceded by a Valsalva-like manoeuvre, i.e. vomiting and tying the shoelaces while bending over and holding his breath, respectively. Until recently, TGA was assumed to have three possible causes: arterial ischaemia (transient ischaemic attack; TIA), migraine and epilepsy. A fourth and more recent hypothesis is cerebral venous stasis. This is in accord with the haemodynamic changes that have been described as a provoking factor in TGA. A Valsalva-like manoeuvre increases the intrathoracic pressure, followed by venous reflux in the internal jugular vein. The resultant cerebral venous congestion can cause temporary ischaemia of mesiotemporal structures, such as the hippocampus, and lead to transient cerebral dysfunction. Recent studies support this haemodynamic pathogenesis. The aetiology of TGA is probably multifactorial, with cerebral venous stasis probably playing an important role. There is still no good explanation for the observation that a causative factor usually leads to a TGA in the same person only once.

Amnesia, Transient Global↗

PubMed1999

Episodic memory in transient global amnesia: encoding, storage, or retrieval deficit?

OBJECTIVES: To assess episodic memory (especially anterograde amnesia) during the acute phase of transient global amnesia to differentiate an encoding, a storage, or a retrieval deficit. METHODS: In three patients, whose amnestic episode fulfilled all current criteria for transient global amnesia, a neuropsychological protocol was administered which included a word learning task derived from the Grober and Buschke's procedure. RESULTS: In one patient, the results suggested an encoding deficit, and in two others, a storage deficit. CONCLUSIONS: The encoding/storage impairment concerning anterograde amnesia documented in our patients stands in clear contrast with the impairment in retrieval which must underly the retrograde amnesia that also characterises transient global amnesia. This dissociation in turn favours the idea of a functional independence among the cognitive mechanisms that subserve episodic memory.

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PubMed1997

Changes in cerebral blood flow and vasoreactivity in response to acetazolamide in patients with transient global amnesia.

OBJECTIVE: Previous reports about changes in cerebral blood flow (CBF) in transient global amnesia disclosed decreased flow in some parts of the brain. However, CBF analyses in most reports were qualitative but not quantitative. The purpose of this study was to determine changes in CBF in transient global amnesia. METHODS: The CBF was measured and the vasoreactive response to acetazolamide was evaluated in six patients with transient global amnesia using technetium-99m hexamethylpropylene amine oxime single-photon emission computed tomography (SPECT). The CBF was measured during an attack in two patients and soon after an attack in the other four. About one month later, CBF was re-evaluated in each patient. RESULTS: Two patients examined during an attack and one patient examined five hours after an attack had increased blood flow in the occipital cortex and cerebellum. Three patients examined at six to 10 hours after an attack had decreased blood flow in the thalamus, cerebellum, or putamen. These abnormalities of blood flow almost disappeared in all patients one month after onset. The vasodilatory response to acetazolamide, which was evaluated initially using SPECT, was poor in areas of increased blood flow. By the second evaluation of CBF with acetazolamide, the vasodilatory response had returned to normal. CONCLUSIONS: In a patient with transient global amnesia, CBF increased in the vertebrobasilar territory during the attack and decreased afterwards. The vasodilatory response to acetazolamide may be impaired in the parts of the brain with increased blood flow. It is suggested that transient global amnesia is distinct from migraine but may share the same underlying mechanism.

Acetazolamide↗

PubMed1985

"Psychometric" assessment during transient global amnesia.

A patient "psychometrically" assessed during an attack of transient global amnesia showed total inability to form new long term memories but normal immediate recall. There was nearly perfect preservation of other psychological functions with good recall of distant events and no dysphasia, dyslexia, dysgraphia, dyspraxia, right-left disorientation, constructional apraxia or visual agnosia. Calculation was probably also normal. Some of the 5 previously reported patients, who have been similarly studied during attacks of transient global amnesia, showed evidence of damage to the brain beyond the hippocampal forniceal system. The present patient demonstrates the market selectivity of memory disturbance in "pure transient global amnesia".

Amnesia↗

PubMed2004

Transient global amnesia heralding basilar artery thrombosis.

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.

Amnesia, Transient Global↗

PubMed2007

Transient global amnesia in the district general hospital.

Cases of transient global amnesia (TGA) seen by one consultant neurologist over a 4-year period (2002-2005 inclusive) were identified. Of 10 possible cases, eight fulfilled suggested diagnostic criteria. Five cases were seen as ward consultations, three in outpatient clinics; seven were seen in district general hospitals. Six of the eight cases had already been seen by hospital physicians, whose working diagnoses included stroke/TIA and epilepsy. In some cases, this had resulted in inappropriate investigation, treatment and advice. Although rare, TGA is a diagnosis both hospital physicians and general practitioners need to be aware of in order to avoid potential pitfalls. The critical importance of collateral history in reaching the diagnosis is emphasised.

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PubMed2005

Transient global amnesia may be caused by cerebral vein thrombosis.

Transient global amnesia (TGA) is a disorder of unknown aetiology, characterized by sudden loss of anterograde memory, in the absence other neurological signs or symptoms, followed by complete recovery in less than 24h. Precipitating actions such as strenuous physical activity or valsalva-like manoeuvres are frequently reported. Since first described in 1958, by Fisher and Adams, the possible pathophysiology has undergone much speculation. Nonconvulsive epileptic seizures, migraine, paradoxical embolism thorough a patent foramen ovale, and transient ischemic attacks have been proposed as potential mechanisms. One of the latest hypotheses is that venous congestion causes either ischemia or induces spreading depression in the medial temporal lobes. It has been demonstrated that retrograde flow in the internal jugular veins occurs more frequently during valsalva manoeuvres in TGA patients than in controls, supporting a dysfunctional venous circulation as part of the pathogenesis. However, earlier hypotheses typically fail to explain the relatively low recurrence rate of TGA, lack of comorbidity and the relation to precipitating events. If cerebral venous hypertension was the solely cause of TGA it would presumably be much more common with very high recurrence rates among those predisposed of the condition. Structural changes observed in MRI and SPECT studies along with reports of mild cognitive impairment lasting much longer than the amnestic episodes, indicate that TGA is less transient and perhaps somewhat less benign than earlier believed. Many cases of TGA seem to be associated with factors of increased risk of cerebral venous thrombosis, such as polycythemia, antiphospholipid antibodies, venous hypertension, female sex and more. We suggest that most cases of TGA may be due to small thrombi in the deep cerebral venous system. Small venous thrombi may difficult to visualize even when using modern imaging technology. Further studies of TGA patients with for example blood analysis of D-dimer together with MR venography or CT venography could be done to evaluate this new hypothesis.

Amnesia, Transient Global↗