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PubMedDate not supplied

[Does brain blood flow HMPAO SPECT withhold the vascular etiopathogenic theory of transient global amnesia?].

INTRODUCTION: Transient global amnesia (TGA) is a neurological disorder that consists in a sudden loss of anterograd memory and temporospatial disorientation during less than 24 hours. Several precipitating factors have been reported. Conventional neuroimaging scans usually are negative. Different etiopathogenic theories have been postulated but the vascular etiology is the most commonly accepted. CASE REPORTS: Three patients with a typical presentation of TGA are studied. In all of them two brain blood flow HMPAO SPECT were performed, within the first 48 hours from the onset and three months after as an evolutive control. The first patient showed a left temporal perfusion defect and temporoparietal hypoperfusion. The second showed frontotemporal hypoperfusion, temporal mesial defect and hypoperfusion in basal ganglia, all in the left side. The third patient showed thalamic hyperperfusion and cerebellum hypoperfusion, both in the left. In all of them, control SPECT normalized. CONCLUSION: Three etiopatogenic theories about TGA have been reported: epilepsy, migraine and blood flow impairment. In TGA neuroanatomic image and neurophysiologic studies usually do not show significative alterations. Conversely, functional studies as brain blood flow HMPAO SPECT, do show changes being the most common bilateral temporobasal hypoperfusion, although this is not the only pattern described. Causes of this variable behaviour remain unclear but can be related to different clinic expressions and, over all, to time of evolution from onset. The three cases in this study show three different perfusion patterns reported in TGA and all of them withhold the vascular etiopathogenic theory.

Adult↗
PubMedDate not supplied

[Transcranial Doppler during transient global amnesia].

INTRODUCTION: Transient global amnesia is a syndrome mainly characterised by an anterograde memory deficit, which disappears in less than 24 hours without leaving any kind of sequelae. Its aetiopathogenesis is still unclear. The ischemic theory became important after hypoperfusion was observed in the mesial region of the temporal lobe using different imaging techniques, although recently the use of diffusion-weighted magnetic resonance imaging by other authors has not revealed these alterations in the cerebral blood flow. CASE REPORT: We report on a transcranial Doppler study carried out in a female patient during the acute phase of the amnesia, with no evidence of hemodynamic alterations or significant asymmetries. Repeating the test after clinical recovery offered values that were similar to those of the previous study. CONCLUSIONS: It is posited that the basis of this process would not be related to ischemia but instead to a mechanism enabling spreading neurogenic depression that is similar to that which takes place during a migraine attack. Treatment with antiplatelet drugs would not, therefore, be recommended but calcium antagonists or beta blockers would be useful in preventing the clinical picture from being repeated.

Aged↗
PubMedDate not supplied

[Transient global amnesia (a study of 30 cases)].

The authors have studied 30 patients with transient global amnesia aged between 49 and 76 years (median age of 63 years), without focal neurologic signs that have been followed for periods varying between 6 months and 10 years. Three of the patients had recurrent attacks of transient global amnesia, and another three had a stroke, although at some distance from the amnesia attack. Association was noted with certain risk factors including high blood pressure, and angiopathic changes of the eye fundus (in 50% of the patients), dyslipidemia (in 30%), diabetes (in 10%), and essential polyglobulia (in 7%). Coagulation studies including thrombelastograms were carried out in 22 patients, and demonstrated hypercoagulability in 50% of them. Changes in the arterial wall were noted in 85% of the 14 patients in whom carotid sphygmograms were recorded. The presence of these risk factors could explain the occurrence of cerebrovascular accidents in patients with transient global amnesia. Electroencephalograms performed immediately or a short time after the amnesia attack have evidenced in 18 patients rapid-type dysrhythmia, or diffuse theta waves, predominantly located in the deep layers of the left and right temporal areas. The EEG tracings were either flat or normal in the remaining 12 patients. Of the 30 patients presenting with global transient amnesia only two had migraine in antecedents, and another six had headache during the evolution of amnesia. The neurologic examination did not reveal any abnormality in 27 of the patients. Sequelar signs of neurological deficits were noted in the remaining three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1998

Transient global amnesia and transient ischemic attack: a community-based case-control study.

OBJECTIVES: Few case-control studies of first-ever transient global amnesia (TGA), transient ischemic attack (TIA) and normal controls have been performed to date. We aimed to assess the prevalence of cerebrovascular risk factors in a well defined population of TGA patients. MATERIAL AND METHODS: We undertook a retrospective and prospective community-based case-control study of 170 first-ever TGA, 170 first-ever TIA and 170 normal controls. RESULTS: Age-matched analysis revealed that TGA cases had a significantly lower prevalence of atrial fibrillation and diabetes mellitus than TIA controls. The prevalence of cigarette smoking and diabetes mellitus was significantly higher in normal controls than in TGA cases. CONCLUSION: Our community-based case-control study showed that atrial fibrillation and diabetes mellitus, two important risk factors for cerebrovascular disease, were significantly more common in the TIA group than in the TGA one. These results make the thromboembolic pathogenesis of TGA unlikely.

Amnesia↗
PubMed1995

Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions.

BACKGROUND AND PURPOSE: The purpose of the present study was to make an attempt to ascertain the etiology of transient global amnesia (TGA), which is still disputed more than 30 years after the first description of this clinical entity. METHODS: In a case-control study, we compared the prevalence of vascular risk factors in 64 TGA patients with 64 first-ever transient ischemic attack (TIA) control subjects and 108 normal community-based control subjects matched for age and sex. We prospectively studied the vascular events and mortality rates of the TGA cases and of the TIA control subjects. Then we compared the outcome of the two groups using actuarial analysis based on survival curves. RESULTS: We did not find evidence of an increased risk of TGA associated with any vascular risk factor. In contrast to TIA control subjects, no TGA patient suffered stroke, myocardial infarction, or TIA during the follow-up period. Migraine was more common in TGA patients than in both normal and TIA control subjects. In three patients (4.5%), the TGA was eventually considered to be of epileptic origin. CONCLUSIONS: The results of our case-control and longitudinal studies point to the conclusion that TGA and TIA do not share the same etiology. Since half of our patients had a precipitating event in their history, it is reasonable to hypothesize that spreading depression may play a role in TGA. The significant positive association between migraine and TGA may support this hypothesis. Epilepsy may mimic TGA in a minority of cases.

Actuarial Analysis↗
PubMed1980

Transient global amnesia in childhood.

Transient global amnesia, a brief disorder of recent memory affecting middle-aged and elderly patients, is probably caused by transient ischaemia of the hippocampal regions and other parts of the limbic system related to memory functions. A 13-year-old boy with a single episode of transient global amnesia and a three-year history of recurrent headache is described. It is suggested that some acute confusional states encountered in children with migraine may represent obscured instances of transient global amnesia, and that a brief vasoconstriction of the arteries supplying hippocampal structures is probably responsible for both conditions.

Adolescent↗
PubMed2005

Increased incidence of jugular valve insufficiency in patients with transient global amnesia.

OBJECTIVE: While transient global amnesia (TGA) is a clinically well defined disorder, its etiology is poorly understood. Cerebral venous hypertension and subsequent damage to hippocampal and diencephalic structures are among the discussed hypothetical causes. Using a direct method for the study of retrograde flow during a Valsalva maneuver, we determined whether jugular valve insufficiency contributes to cerebral venous hypertension in patients with TGA. METHODS: Jugular valve closure was assessed by duplex sonography in 20 patients with TGA and 20 age and gender matched controls. The diagnosis of valvular insufficiency was made on the basis of recently established criteria. RESULTS: Valvular insufficiency (either left or right-sided, or bilateral) was identified in 85% of patients with TGA,and in 45% of controls (p = 0.008). All patients with involuntary Valsalva episodes immediately prior to TGA developed valvular insufficiency (n = 8; p = 0.13 compared with patients who did not recall such an event). The mean duration of the insufficiency jet did not differ significantly between patients with TGA (3.26 s) and controls (2.78 s; p = 0.315). However, patients with TGA who experienced a trigger event were characterized by significantly longer insufficiency reflux times (3.84 s) than those without (2.55 s; p = 0.03). CONCLUSIONS: TGA is associated with an increase in the prevalence of jugular insufficiency. Valvular insufficiency may lead to increased venous pressure transmission during a Valsalva maneuver and thus contribute to venous ischemia in TGA. The association of valvular insufficiency and longer reflux times with the occurrence of a trigger event further suggests that cerebral venous congestion is an important etiological factor in transient global amnesia.

Aged↗
PubMed1986

Leao's spreading depression in the hippocampus explains transient global amnesia. A hypothesis.

Transient global amnesia has been explained by epileptic mechanisms or transient ischemic attacks affecting the hippocampus. None of these two mechanisms appear likely. The animal experimental phenomenon entitled spreading depression of cortical electrical activity (SD) or spreading depression of Leao has been implicated in migraine pathogenesis and may be relevant to transient global amnesia. In experimental animals, SD in the hippocampus causes a temporary functional ablation lasting minutes to hours with full functional recovery. Glutamate, which is present in large amounts in the hippocampus, may experimentally elicit spreading depression, and strong emotional events may possibly liberate glutamate and bring about this reaction in human patients.

Amnesia↗
PubMedDate not supplied

[A study of the risk factors in transient global amnesia and its differentiation from a transient ischemic attack].

INTRODUCTION: 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. PATIENTS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Aged↗
PubMed1987

Transient global amnesia. When memory temporarily disappears.

Transient global amnesia is a benign condition of sudden onset that resolves spontaneously. Retrograde amnesia prevents recall of events antedating the episode by hours to years, and anterograde amnesia produces the characteristic features of inability to learn new material and repetitious questioning. Laboratory investigation of these patients is generally unrewarding. Transient global amnesia is easily distinguished from amnesia caused by head trauma or transient ischemic attack, confusional state, and functional amnesia. Although transient global amnesia is most likely caused by transient ischemia of brain structures important for memory, thromboembolic cerebrovascular disease is not the cause. The patient with transient global amnesia should be treated conservatively.

Amnesia↗
PubMed1987

Two cases of transient partial amnesia in the course of transient global amnesia.

In the course of transient global amnesia, two patients showed symptoms of transient partial amnesia. Close observation showed that at some time during the episode the patients had some degree of nonverbal memory, which recovered earlier than verbal memory. Careful observation of the progression of symptoms during an episode of transient global amnesia may often reveal symptoms of transient partial amnesia.

Amnesia↗
PubMed2000

[Transient global amnesia].

UNLABELLED: A DISTINCTIVE SYNDROME: Transient global amnesia is a very distinctive amnesic syndrome. The attack begins abruptly with massive anterograde verbal and non-verbal amnesia. Retrograde amnesia, variable in extent, is also present. A repetitive questioning behavior is usual. The memory impairment gradually resolves after almost always less than 12 hours. WELL-DEFINED CRITERIA: Specific criteria make it possible to distinguish transient global amnesia from psychogenic amnesia, acute confusional state and transient epileptic amnesia. "Pure" transient global amnesia is usually idiopathic and has a good prognosis. It is also distinguishable from symptomatic transient global amnesia. PATHOGENESIS: Functional imaging studies detect hippocampic or thalamic hypoperfusion. This oligemia may be secondary to neuronal dysfunction compatible with spreading depression. The pathogenic mechanisms remain unclear.

Amnesia, Transient Global↗