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Transient global amnesia is a well known syndrome, characterised by sudden loss of short term memory with retrospective amnesia, that appears in otherwise good healthy subjects. Transient global amnesia is often unknown and misunderstood. Authors explain pathogenetic hypothesis and diagnostic criteria, showing some clinical cases.
Transient global amnesia (TGA) is generally believed to be a transient ischemic attack affecting short-term memory centers. A recent three-year follow-up found a high incidence of subsequent dementia and stroke in patients with TGA. We studied the course (average, 46 months) of 32 patients with TGA and found a low rate of recurrence (12.5%), dementia (6%), or transient ischemic attacks (3%). Transient global amnesia would appear to carry a more benign prognosis than classical transient ischemic attacks.
Transient global amnesia is an unusual syndrome involving a transient memory loss and inability to form new memories, without affecting other cognitive functions. Although the patient often lacks insight into the problem, the syndrome is very frightening for family members, who frequently present to the ED. The evaluation of the syndrome is the subject of some controversy. This review presents current understanding about the causes of transient global amnesia and an approach to the ED evaluation of the syndrome.
Transient global amnesia is a momentary neurological accident frequently encountered in subjects over 50 years of age. Its diagnosis is purely clinical and rests on the sudden occurrence of retention amnesia associated with retrograde amnesia without disturbances in speech or other neurological deficits. The amnesia totally regresses within less than 24 hours. Paraclinical examinations add nothing to the diagnosis. The cause of transient global amnesia is unknown, and the various hypotheses that have been put forward (e.g. epilepsy, transient ischaemia or migraine) have not been confirmed by clinical and epidemiological studies. Despite a low, but real risk of recurrence, the prognosis is perfectly benign, and there is no need for curative or preventive treatment.
Transient global amnesia is a benign, self-limiting disorder primarily involving a disturbance of memory. It occurs in late middle and older aged adults. Patients with this syndrome do not have a history of head trauma, drug or alcohol intoxication, hypoglycemia or psychologic dysfunction. Once the episode has cleared, there are no residual deficits except amnesia for the events which occurred during the episode. This article includes a case presentation in addition to discussion of the clinical features, etiology, treatment and nursing interventions for the patient with a transient global amnesia episode.
Transient global amnesia (TGA), characterised by a profound anterograde amnesia, is a model of interest to study the acquisition of novel meanings independent of episodic functioning. Three patients were tested during a TGA attack, two in the early recovery phase and the third during the acute phase of TGA, with a semantic priming task involving a restructuring process of conceptual knowledge. During TGA, all patients demonstrated priming effects. Results obtained the day after the episode with the same task showed that these effects persisted at least one day. Episodic memory seems not to be critical for the formation of novel connections among unrelated semantic representations, in accordance with Tulving's model of memory, i.e. episodic memory is not necessary for the acquisition of semantic information.
Transient global amnesia (TGA) is an inability to form new memories. The pathophysiology and cause of TGA have not been defined. We examined the changes of internal jugular venous flow patterns in 21 patients with TGA and 21 age-matched and sex-matched controls using duplex ultrasonography during two Valsalva manoeuvres (blocking venous return through the superior vena cava). During both manoeuvres a retrograde flow component was seen significantly more frequently in the TGA group than in the controls. Ten patients reported Valsalva-like activities preceding TGA. In these patients a retrograde flow component took place more frequently than in those who did not report preceding Valsalva-like activities. Our results lend support to the hypothesis that TGA may be attributable to venous congestion, and consequent venous ischaemia to bilateral diencephalic or hippocampal structures.
Transient global amnesia (TGA) is usually considered to produce a profound impairment of long-term episodic memory, while at the same time sparing working memory. However, this neuropsychological dissociation has rarely been examined in detail. While a few studies have assessed some components of working memory in TGA, the results that have been obtained are far from conclusive. To clarify this issue, we carried out a comprehensive investigation of working memory in 10 patients during a TGA attack. In the first study, we report the results from three patients examined with a battery of neuropsychological tests designed to assess each of the three subcomponents of Baddeley's model of working memory. In a second study, seven different patients underwent neuropsychological investigations that focused specifically on the central executive system, using a protocol derived from a study by Miyake and colleagues. Our findings showed that subcomponents of working memory, such as the phonological loop and visuo-spatial sketch pad, were spared in TGA patients. Specific executive functions that entailed inhibitory control, dual task performance, updating and shifting mechanisms were also found to be normal. However, we found significantly impaired performance for the Brown-Peterson test, and that TGA patients were significantly impaired in the recollection of their episodic memories. They also made reduced numbers of 'remember' compared with 'know' judgments in the episodic memory test several days after TGA. On the basis of our findings, it would appear that the episodic memory deficit during TGA is not related to elementary aspects of executive functioning. Our data also highlight the nature of the cognitive mechanisms involved in the Brown-Peterson task, which may well depend on long-term memory (such as the process of semantic encoding). Lastly, the selective deficit in recollective episodic memories observed in TGA may be principally related to medial temporal lobe abnormalities that have been reported in this syndrome.
Transient global amnesia (TGA) is a transient, benign neurological syndrome, characterized by global loss of memory, preserved consciousness and self-awareness, associated with some behavioral changes (in particular, repetitive questioning). It generally resolves within 24 h. Mild brain stem symptoms can often be demonstrated during the attack, but major neurological abnormalities never occur. The only sequel is a permanent amnesic gap for the duration of the episode. The episode is often preceded by typical precipitating events, such as physical activity, emotional stress, acute pain, comprising haemodynamic changes of the body. The diagnosis is easy provided one is acquainted with the syndrome. The prevalence of vascular risk factors is low and the risk for stroke is not increased. Although much evidence indicates the possibility of a causative ischaemia in the inferomedial parts of the temporal lobes, an atherothrombo-embolic TIA is not the cause of TGA, and TGA is unrelated to cerebrovascular disease in general. In the author's view, the cause of TGA is a transient ischemic attack (TIA) but a haemodynamic one of the vertebrobasilar system, producing a transient dysfunction of inferomedial parts of the temporal lobes, regions that are particularly sensitive to impaired blood supply. For a full pathogenetic explanation of TGA, clarification of the underlying mechanisms is a prerequisite. This touches on the genesis of migraine and Leao's spreading depression phenomenon. The term 'amnesic TIA' would reflect the pathogenesis more appropriately.
Transient global amnesia is a disease of nonuniform pathogenesis. Based on review of the literature, etiology, prevalence, clinical pictures and differentiation of this interesting but not always recognized syndrome have been discussed in the article.
Transient global amnesia(TGA) had been recognized as a disease without abnormal findings on neuroimaging before magnetic resonance(MRI) imaging was practicable. Recently, abnormal findings on MRI reported in cases of TGA. We here reported a case of TGA showing a transient abnormal intensity in left hippocampus on MRI diffusion-weighted image. A 52-year-old man suddenly became to unable to keep his recent memory without histories of trauma or epilepsy. He showed no abnormal neurologic findings excepting for the recent memory. MRI performed within an hour after onset demonstrated no abnormality on T1- and T2-weighted images. Diffusion-weighted image (b = 1,000) showed hyperintensity in the left medial temporal lobe, and the apparent diffusion coefficient(ADC) in this region was lower(72.8 cm2/s) than that in the contralateral region(94.4 cm2/s). TGA was completely resolved 17 hours after onset.
Transient global amnesia (TGA) is an unusual form of the amnestic syndrome, clinically characterized by profound disturbance of short-term memory with preservation of immediate recall and long-term memory. Spontaneous recovery is the rule and is usually complete within several hours. The etiology of TGA is not clear. It is considered to be caused by transient ischemia confined to the medial temporal lobe, an area supplied by branches of the vertebrobasilar system. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff. Besides pulsating headache, the dominant symptoms are vertigo, ataxic gait, tinnitus, dysarthria, paraeshesia in the hands, homonymous hemianopsia and sometimes drop-attacks. These symptoms are associated with vertebrobasilar system dysfunction. In this paper, three migraine patients, suffering from one episode of TGA, were reported. All patients were women. Case 1 was a 48-year-old woman with a history of common migraine. Case 2 was a 48-year-old woman with a history of classic migraine. Case 3 was a 59-year-old woman with a common migraine. Family history of migraine exists in case 1 and case 3. Their migrainous attacks began in their twenties and thirties. They suddenly suffered migraine with the symptoms of vertebrobasilar dysfunction. These symptoms are ataxic gait (Case 1, 2, 3), dysarthria (Case 1, 2), vertigo (Case 1, 3) and homonymous hemianopsia (Case 1, 3). Simultaneously three patients had TGA. Duration of retrograde amnesia were about twenty-four hours (Case 1), about thirty minutes (Case 2) and about three hours (Case 3).(ABSTRACT TRUNCATED AT 250 WORDS)
Transient global amnesia (TGA) was found in 41 of 76 patients admitted to the North Carolina Baptist Hospital with temporary disturbances of memory. Risk factors for stroke were present in 26 (63%) of these 41 patients, and additional risk factors developed in 9 (27%) of the 33 patients available for follow-up. Follow-up evaluation in 33 patients (80%) for periods ranging from 1 to 17 years (mean, 60.3 months) revealed a low rate of recurrence (18%) and a still lower rate of progression to stroke (6%). No transient ischemic attacks were reported during this period. In 2 patients, multiple recurrences of TGA ceased after treatment of the underlying condition (polycythemia in 1 case and myxomatous degeneration of the mitral valve in the other.
Transient global amnesia (TGA) is a syndrome of selective loss of recent memory without other neurological deficits. Auditory and visual P300s were recorded during and after TGA to investigate the contribution of the short-term memory system to P300 generation. The auditory P300 during TGA was comparable to that recorded 1 week and 9 months after TGA. In contrast to the auditory modality, the visual target P300 was reduced in amplitude during TGA and at 1 week after the attack. The P300 to novel visual stimuli was also reduced during TGA. Both target and novelty visual P300 recovered by 9 months after TGA. The results support the notion that the neuronal networks responsible for P300 generation are modality dependent and that brain structures perfused by the posterior circulation are involved in visual P300 generation.
Transient global amnesia is often attributed to a seizure, vascular cause, or migraine, but the outcome is usually benign. The presence of migraine and important risk factors for stroke necessitates close patient monitoring. Anti-platelet therapy should be considered.
Transient global amnesia is a clinical syndrome characterized by sudden onset of short-term memory loss followed by retrograde amnesia in an otherwise healthy subject. During the attack, the patient remains alert and retains much of his personal identity. The patient usually becomes upset and concerned about his memory loss. This condition may be diagnosed incorrectly as hysteria, psychosis, or temporal lobe seizure, despite its unique clinical features.
Transient global amnesia is an alarming but benign disorder of middle age, which prevents both the formation of new memories, and the retrieval of recently formed ones, for some hours. Research over the last 10 years has shed light on the epidemiology, neuropsychology, functional anatomy and differential diagnosis of this distinctive condition, and clarified its management.
Three neuroscientists traveled on different occasions from New York to Europe to attend scientific meetings. In an attempt to minimize "jet lag," they all took triazolam, 0.5 mg, during the flight. In addition to the medication, they also consumed ethyl alcohol to a variable degree, none to clinical intoxication. All three experienced an episode of anterograde amnesia that lasted several hours. In two of the individuals, neurologists associated with them did not detect any memory disturbance at the time. These episodes of transient global amnesia were evidently secondary to the triazolam or the combination of triazolam and ethyl alcohol. These episodes suggest caution if using this medication to avoid jet lag, especially if ethyl alcohol will be consumed.