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PubMedDate not supplied

[Transient global amnesia--possible aetiopathogenetic mechanisms].

Transient global amnesia is a clinically well defined syndrome, characterized by transient isolated epizodes of confusion with inability to acquire new data, repetitive quieries, retrograde amnesia and absence of other neurologic symptoms or signs. Eighteen patients who presented at admission the clinical picture of transient global amnesia were, after the examination, classified in three groups: patients with symptoms or signs of transitory focal ischemia, migraine group, and miscellaneous group. The transitory global amnesia in patients suffering from atherosclerotic changes of the vascular system is usually the first manifestation of transitory ischaemic attack pointing to the vascular insufficiency of the posterior cerebral regions as the cause of attack. The typical transient global amnesia is not a rare phenomenon, but it supposes the existence of the precipitating factors. Although its "pure" form is usually benign, the appearance of other factors such as cerebral neoplasms, involved in the aetiology of transient global amnesia, requires the complete clinical examination of each individual with these symptoms.

Amnesia, Transient Global↗
PubMedDate not supplied

Brain stem dysfunction in transient global amnesia.

A patient with transient global amnesia also had transient bilateral gaze nystagmus which was detected both by conventional bedside examination and upon electronystagmographic recording. The nystagmus was absent one week later indicating recovery of the temporary brain stem deficit. The recording of objective evidence of brain stem dysfunction in the form of gaze nystagmus in a patient who had transient global amnesia, suggests that both were due to a transient ischemic attack involving the cerebral blood supply in the vertebrobasilar distribution.

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PubMed1975

[Amnestic episodes. (Isolated episodes of confusion with amnesia, amnesic ictus, transient global amnesia)].

The author, by giving an outline of one particular case as well as a survey of the relevant literature on transient global amnesia, describes the characteristic clinical picture that is characterized by a sudden loss of what is known as the short-time memory, which usually lasts for several hours, as well as by retrograde amnesia which sometimes dates back to many years. The condition gradually fades away within a few hours or during a night's sleep, and what remains is lack or loss of memory for the episodic period or sometimes retrograde amnesia. Relapses were not observed in the majority of patients. The disease usually develops in people in their sixth to eighth decades of life. The cause of the disease is not yet fully understood. Accordingly, it is justified to use such terms as autochthonous or cryptogenic amnestic episodes. The disease is also discussed from a differential diagnosis point of view.

Age Factors↗
PubMed1998

Recovery of function processes in human amnesia: evidence from transient global amnesia.

There are few clues as to the processes that underlie recovery of function from human amnesia. Evidence is offered from the perspective of a study of recovery of function during an episode of transient global amnesia (TGA) that occurred as a complication of a cerebral angiographic procedure being carried out in a neurosciences centre, and where there was therefore a unique opportunity to examine acute changes in memory function. This allowed us to conduct the first quantitative study where shrinkage of anterograde and retrograde memory loss was plotted at four separate intervals throughout the acute recovery process, and also 24 hr later. Recovery of retrograde amnesia preceded recovery from anterograde amnesia. Resolution of a naming deficit more closely paralleled recovery from retrograde amnesia rather than anterograde amnesia. Within retrograde amnesia for public events, there was a temporal gradient of memory loss, with more recent events affected to a greater degree than earlier events. Within anterograde amnesia, picture recognition memory preceded recovery of story recall memory. On the basis of these findings, and related observations in the published literature, it is proposed that recovery from some types of human amnesia, such as that associated with TGA, follows a 'lateral-to-medial' rule--lateral inferotemporal areas that play a major role in retrograde amnesia recover first from hypometabolism related to the TGA attack, followed by 'interface' areas such as the rhinal and parahippocampal cortices that are considered to have a role in both anterograde and retrograde memory functioning, with the last areas to recover physiological integrity being discrete limbic-diencephalic structures such as the hippocampus.

Adult↗
PubMed2005

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.

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PubMed2005

[Temporal changes of diffusion-weighted MR images in a patient with transient global amnesia].

The pathogenesis of transient global amnesia (TGA) remains uncertain, although it is featured by characteristic clinical symptoms. We present a patient with TGA, in which diffusion-weighted MR image showed a punctuate hyperintense lesion in the left CA1 subfield of the hippocampus adjoining the lateral ventricle 24 hours after the onset. This lesion was observed with FLAIR image after 9 days from the onset, and therefore was considered to be a delayed ischemic lesion. A SPECT and PET studies 7 days after the onset showed a decrease of the CBF, CMRO2 and CMRglu, and was compatible with a delayed ischemic lesion. However, there were no cardiovascular risk factors nor abnormalities of vascular supply, and therefore the reason for microcirculatory disturbances remained unclear.

Amnesia, Transient Global↗
PubMed2006

Recurrency in transient global amnesia: a retrospective study.

Transient global amnesia (TGA) is a well-defined clinical syndrome of unknown etiology, which often occurs once in life. Several mechanisms have been proposed but only trigger events have been clearly associated with the attack such as physical exertion, emotional stress, sexual intercourse or immersion in cold water. According to our knowledge, this is the first study, which associates trigger events and TGA recurrency. The aim of this retrospective study was to evaluate the risk factors which contribute to TGA recurrency. TGA patients consecutively admitted, performed clinical and neurological evaluation, electroencephalogram and structural brain imaging scan. TGA-trigger events were evaluated and comorbidities were carefully recorded. The risk factor sum was calculated as the sum of the considered triggers. Eighty-five TGA patients were grouped according to the presence of single TGA (n = 73) or two episodes of TGA (n = 12). The 14.11% of patients experienced two episodes. A logistic regression analysis showed that the more increased number of TGA the more number of trigger events (P < 0.11; chi2 = 6.38; beta = -3.29). These observations claim that TGA may be considered a complex epiphenomenon, and the sum of the trigger factors can be responsible for recurring of this almost unique-in-life event.

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PubMed1981

Transient global amnesia.

3 cases of transient global amnesia (TGA) are reported. Transient ischaemia is probably the cause of the condition in the majority of cases although other mechanisms, particularly epilepsy, may be responsible in some. TGA may not be reported by the patient and may be misdiagnosed as a psychiatric disturbance. An acute confusional or delirious state can also produce an episode of amnesia with inability to remember events which occurred during the period of cerebral dysfunction. In TGA, however, there is an acute and temporary failure to record events without the evidence of more generalised dysfunction which occurs in delirium. During the 3 episodes reported here the patients were able to carry on with their everyday activities and to complete structured tasks, such as the preparation of a meal. TGA appears, at least in some individuals, to carry the prognosis of transient cerebral ischaemia.

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PubMed2004

Marijuana-induced transient global amnesia.

A 6-year-old boy accidentally became intoxicated with marijuana secondary to ingesting cookies laced with marijuana. He presented with retentive memory deficit of sudden onset that was later diagnosed as transient global amnesia. Transient global amnesia as a result of marijuana intoxication is an extremely rare event.

Acute Disease↗
PubMedDate not supplied

Transient global amnesia after sexual intercourse.

BACKGROUND: Transient global amnesia presents as paroxysmal, transient loss of memory function and has been shown to have a number of inciting factors. AIMS: To report a case and its inciting factor in order to heighten awareness of the condition. METHODS: A 56-year-old woman who presented with TGA after sexual intercourse is reported. RESULTS: The episode of TGA resolved after 14 hours. Results of laboratory tests including MRI brain and MR angiogram and venogram were normal. CONCLUSION: An inciting event can often be identified for TGA and a targeted history should be used to help elicit such events.

Amnesia, Transient Global↗
PubMed2006

Detection of intracranial venous reflux in patients of transient global amnesia.

BACKGROUND: The mechanism of transient global amnesia (TGA) is not clear. Attempting to support the hypothesis that retrograde venous hypertension causing cerebral venous ischemia plays a role in the pathogenesis of TGA, the authors used cranial three-dimensional time-of-flight (TOF) MR angiography (MRA) to detect a possible intracranial retrograde venous flow in TGA patients. METHODS: The frequency of abnormal venous signals on cranial three-dimensional TOF MRA was compared in 10 TGA patients with the signals in 50 age- and gender-matched normal individuals. In TGA patients with abnormal venous signals, other examinations (cerebral digital subtraction angiography, upper extremity digital subtraction venography [DSV], and thoracic inlet MRI) were performed to elucidate the etiology of these abnormal intracranial venous flow patterns. RESULTS: Abnormal venous signals on three-dimensional TOF MRA were found in five (50%) of the TGA patients and none of the control subjects (p < 0.001). Compression leading to occlusion of the left brachiocephalic vein by the sternum and aorta during regular breathing, as depicted by upper extremity DSV and thoracic inlet MRI, occurred consistently among these five TGA patients with abnormal venous signals. CONCLUSIONS: Retrograde intracranial venous flow caused by left brachiocephalic vein occlusion was found only in patients with transient global amnesia (TGA). This result suggests that TGA patients may have an underlying impairment of cerebral venous outflow that increases their vulnerability to TGA attack.

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PubMed1983

Transient global amnesia.

The syndrome of transient global amnesia (TGA) is defined and described. Characteristic features, epidemical data, variables possibly provoking TGA, its possible etiology and anatomical basis are reviewed. A transient disturbance in the formation of lasting new memories (usually of less than one day) and a retrograde amnesia (which includes the period of the attack and possibly a short time before) are considered as the main features of TGA. A further trait of TGA is the high age of most of the patients subjected to it (58 years on the average). TGA most likely is based on a transient change in the blood supply of certain regions of the brain. The mechanism by which this change happens is still hypothetical. Regions of the limbic system, in particular the area of the temporal lobe and the hippocampal formation, appear to be affected most likely. Uncertain are: the existence of factors provoking the outbreak of an amnesic attack, the likeliness of multiple episodes of TGA and the neuropsychological alterations in patients who suffered a transient global amnesic attack. The outcome of this review suggests, however, that the incidence of recurrent attacks of TGA is higher than previously assumed and that a transient global amnesic attack may be followed by lasting behavioral deteriorations.

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PubMed1990

The complex episode of transient global amnesia.

In most reports, Transient Global Amnesia (TGA) consisted of a single episode of total amnesia. The detailed investigation on the process of recovery from amnesia in the present two cases of TGA indicated the existence of a complex episode of TGA which consisted of a sequence of episodes of total amnesia.

Amnesia↗
PubMed1998

Aetiology of transient global amnesia.

The pathophysiology of transient global amnesia (TGA) has been obscure since the definition of this syndrome more than 30 years ago. Current hypotheses include migraine, seizure, or transient cerebral arterial ischaemia. However, none of these potential mechanisms explain both the absence of other neurological signs or symptoms during TGA, and its frequent precipitating activities: many of which would be expected to result in marked increases in venous return from the arms to the superior vena cava. Patients with TGA also commonly have a Valsalva manoeuvre at the onset of attacks. I suggest that a Valsalva manoeuvre, blocking venous return through the superior vena cava, may allow brief retrograde transmission of high venous pressure from the arms to the cerebral venous system, resulting in venous ischaemia to the diencephalon or mesial temporal lobes and to TGA.

Amnesia↗
PubMedDate not supplied

Computer tomography in transient global amnesia.

16 patients with transient global amnesia (TGA) have been investigated by computer tomography. 3 had a completed stroke associated with the TGA. The findings of computer tomography were normal in 7 patients. Atrophy alone was seen in 2 patients. A single hypodense lesion was found in 6 patients; a bilateral lesion in 1 patient. All 3 patients with amnesic stroke showed a hypodense lesion in the CT.

Adult↗
PubMed1996

Transient global amnesia: disease or syndrome?

Transient global amnesia (TGA) has been defined as the presence of an impairment of short-term memory, retrograde amnesia and repetitive queries, without any other neurological signs or symptoms. The precise pathophysiology of TGA is unclear, although thromboembolic, epileptic, migrainous and metabolic mechanisms have been suggested. We have studied the clinical, biohumoral, electroencephalographic and neuro-imaging data relating to 25 patients with TGA, and found a prevalence of hypertension and hypercholesterolemia. We also found a higher incidence of electrical changes in the patients whose TGA was of shorter duration, whereas brain CT scans revealed ischemic lesions more frequently in the patients with TGA of longer duration. Our findings seem to confirm the hypothesis that TGA is a heterogeneous clinical syndrome consisting of pure and ischemic forms.

Adult↗