Cerebrovascular risk factors and triggers in transient global amnesia patients with and without jugular valve incompetence: results from a sample of 243 patients.

BACKGROUND/AIMS: Different etiologies for transient global amnesia (TGA) have been proposed, such as venous flow abnormalities, spreading depression and migraine-related mechanisms like focal ischemia. Jugular vein valve incompetence (JVI) is commonly described in TGA patients, but its contributing role in TGA pathogenesis is still unknown. We investigated the possible relationship between JVI and pathogenetic mechanisms in TGA. METHODS: 243 TGA patients underwent clinical and neurological assessment. Demographic characteristics, TGA-precipitating factors and vascular comorbidities were carefully recorded. In each patient, JVI was assessed by Doppler ultrasonography. RESULTS: TGA patients were grouped according to the presence (n = 171, 70.4%) or absence (n = 72, 29.6%) of JVI. TGA patients with JVI showed a higher presence of precipitating factors, namely a Valsalva-like maneuver (JVI-positive vs. JVI-negative, 35.8 vs. 17.1%, p = 0.004) and emotional stress (36.6 vs. 21.4%, p = 0.023), but had fewer vascular comorbidities, namely hypertension (37.2 vs. 51.4%, p = 0.047) and carotid arteriosclerosis (20.5 vs. 31.9%, p = 0.050). CONCLUSIONS: These findings support the argument for the existence of at least 2 different TGA-associated mechanisms defined by JVI. On the one hand, JVI associated with a Valsalva-like maneuver and emotional stress supported the venous blood congestion hypothesis, and on the other, the JVI-negative group may have another vascular basis, unrelated to venous congestion.

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.

Transient global amnesia and brain lesions: new hints into clinical criteria.

BACKGROUND AND PURPOSE: Transient global amnesia (TGA) is the abrupt onset of anterograde amnesia with repetitive queries. Different hypotheses have been considered for its aetiology, but it still remains obscure. In 1990, Hodges and Warlow proposed clinical criteria for TGA. Applying these criteria, clinical studies looked for an unifying theory, considering TGA almost a primary and benign disorder. However, spare descriptions of TGA in patients with brain structural lesions have been reported. The aim of this study was to evaluate the prevalence of brain structural lesions among TGA patients. METHODS: One hundred and thirty clinically defined TGA were consecutively recruited. Among them, 13 patients (10%) showed brain structural lesions (TGA-b). RESULTS: No significant difference in clinical features, duration of TGA episode, age of onset, gender between primary TGA (TGA-p) and TGA-b were found. Triggering factors were comparable, suggesting that TGA-b should be considered in the spectrum of TGA, being clinically indistinguishable. CONCLUSIONS: Transient global amnesia deserves a careful neuroimaging study and clinical follow-up considering the high prevalence of brain lesions among these patients and the impossibility to exclude TGA-b by clinical features. The follow-up of these patients and the evaluation of involved brain areas might help to further elucidate the pathogenetic mechanisms of the disease.

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.

Temporal lobe asymmetry in patients with Alzheimer's disease with delusions.

OBJECTIVE: To test the hypothesis that delusions are associated with asymmetric involvement of the temporal lobe regions in Alzheimer's disease. METHODS: Temporal lobe atrophy was assessed with a linear measure of width of the temporal horn (WTH) taken from CT films. Temporal asymmetry was computed as the right/left (R/L) ratio of the WTH in 22 non-delusional and 19 delusional patients with Alzheimer's disease. Delusional patients had paranoid delusions (of theft, jealousy, persecution). None of the patients had misidentifications or other delusions of non-paranoid content. RESULTS: The R/L ratio indicated symmetric temporal horn size in the non-delusional (mean 1. 05 (SD 0.20), and right greater than left temporal horn in the delusional patients (mean 1.30, (SD 0.46); t=2.27, df=39, p=0.03). When patients were stratified into three groups according to the R/L ratio, 47% of the delusional (9/19) and 14% of the non-delusional patients (3/21; chi(2)=5.6, df=1, p=0.02) showed right markedly greater than left WTH. CONCLUSIONS: Predominantly right involvement of the medial temporal lobe might be a determinant of paranoid delusions in the mild stages of Alzheimer's disease.