11, 12 Formal neuropsychological testing was performed, depending on the treating physician's judgment.ĬTP was performed on a LightSpeed 16 Advantage (16 detectors GE Healthcare, Milwaukee, Wisconsin) until November 2005 and a LightSpeed VCT (64 detectors GE Healthcare) thereafter, by using their commercially available software. The duration of amnesia was determined by serial bedside testing of the capability to retain at least 4 words of a standardized 5-word list. We collected the following parameters: demographics (age, sex) cerebrovascular risk factors, including hypertension, hyperlipidemia, diabetes mellitus, smoking history, atrial fibrillation, previous cerebrovascular event (stroke or transient ischemic attack) or TGA high-risk alcohol consumption defined as exceeding 24 g/day and the presence of a triggering event (emotional or physical). Exclusion criteria were poor-quality CTP and a proved ischemic lesion on DWI after an initial TGA diagnosis. Additional examinations such as electroencephalography and DWI were performed as considered necessary by the treating physician. All patients underwent neurologic evaluation, and the diagnosis of TGA was made if the criteria of Hodges and Warlow 10 were met. CTP was part of the standard diagnostic protocol of the hospital to detect cerebral ischemia from June 2002 until April 2006 and has been performed at the discretion of the treating physician since April 2006. We included and retrospectively analyzed those patients admitted to the emergency department of the University Hospital of Lausanne from June 2002 to April 2014 who had a final diagnosis of TGA and underwent CTP within 24 hours of admission. We, therefore, aimed to determine the frequency and localization of perfusion abnormalities in patients with acute TGA by using CTP to investigate its potential diagnostic value and to better elucidate the pathogenesis of this disorder. 9 To our knowledge, results using CTP for acute TGA diagnosis have not been published. 8 However, the authors did not specify whether structures relevant for memory were involved.ĬTP is widely used for the early diagnosis of acute ischemic stroke and TIA, though its true value remains to be established by appropriate research. Images in a case series of patients with TGA who underwent PWI within 24 hours of symptom onset showed unilateral perfusion abnormalities in 4 of the 28 patients (1 in the anterior, 1 in the posterior, and 2 in the middle cerebral artery territory). 7 Although the specific sites of impairment have been identified, the underlying etiology of TGA remains elusive. 3 ⇓– 5 Punctate signal hyperintensities appearing in 1 or both hippocampi on DWI were first described by Matsui et al 6 in a classic TGA case in 2002 and then more systematically by Sedlaczek et al. 1, 2įunctional brain imaging with SPECT and PET shows local disturbances in regional blood flow (usually hypoperfusion, rarely hyperperfusion) and in oxygen/glucose metabolism, most frequently in 1 or both medial temporal lobes. Repetitive questioning and anxiety are often present, but other focal neurologic disturbances are usually absent. Transient global amnesia (TGA) is characterized by the sudden onset of antero- and retrograde amnesia that is often triggered by an acute emotional or physical event and spontaneously resolves within 24 hours. Cerebral venous hypertension due to incompetence of the internal jugular valve may play a role in the pathogenesis of TGA.ABBREVIATION: TGA transient global amnesia Paradoxical embolism due to PFO as a cause of TGA is not confirmed in our study. TGA patients have fewer vascular risk factors than TIA patients. ACUV detected jugular valve incompetence in 72.9% TGA, 35.7% TIA and 39.5% controls (TGA vs. No statistical difference was found between the 3 groups with regard to PFO. TGA patients and controls showed a lower prevalence for vascular risk factors than TIA patients. Retrograde jugular venous flow was tested with air contrast ultrasound venography (ACUV). PFO was studied by contrast transcranial duplex sonography. The aim of this study was to identify potential risk factors for TGA, vascular risk factors, the role of patent foramen ovale (PFO) and of retrograde jugular venous flow.ġ38 subjects entered the study, including 48 patients with TGA, 42 age-matched patients with transient ischaemic attack (TIA) and 48 controls. The aetiology of transient global amnesia (TGA) is still unknown.
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