Jacopo Lanzone1, Lorenzo Ricci2, Giovanni Assenza1, Martina Ulivi1, Vincenzo Di Lazzaro1, Mario Tombini3. 1. Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, University Campus Bio-Medico of Rome, via Álvaro del Portillo, 21, 00128 Rome, Italy. 2. Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, University Campus Bio-Medico of Rome, via Álvaro del Portillo, 21, 00128 Rome, Italy. Electronic address: ricci.lorenzo90@gmail.com. 3. Unit of Neurology, Neurophysiology, Neurobiology, Department of Medicine, University Campus Bio-Medico of Rome, via Álvaro del Portillo, 21, 00128 Rome, Italy. Electronic address: m.tombini@unicampus.it.
Abstract
OBJECTIVE: Transient epileptic amnesia (TEA) is an underestimated condition in emergency clinical setting, where most of transient amnesic episodes tend to be classified as transient global amnesia (TGA). We designed this study to evaluate the actual frequency of TEA in a real-life scenario and to highlight the features that can help clinicians distinguishing it from TGA. METHODS: We retrospectively collected clinical data of 83 patients who accessed our emergency ward for an abrupt onset of amnesic disorder, initially interpreted as TGA. All patients underwent neurological evaluation, magnetic resonance imaging (MRI) scan, and standard 21-channel scalp electroencephalography (EEG) recording (standard EEG [st-EEG]). Moreover, patients with borderline epileptiform abnormalities on st-EEG or with normal st-EEG but high clinical suspicion for TEA underwent a 16-channel 24-hour ambulatory EEG (24-h EEG). Clinical features, neurophysiological, and neuroimaging data were analyzed and compared in the two groups (TEA and TGA). RESULTS: Diagnosis of TEA, according to Zeman's criteria, was made in 15 patients (18%). From a clinical point of view recurrence (p < .001) and atypical symptoms such as confusion or language disorder (TGA plus manifestations), appear to be key elements in order to discriminate between TEA and TGA (80% of patients with TEA vs 7.8% of patients with TGA; p < .001). In our sample, duration of the episodes did not significantly differ between TGA and TEA, even though it is usually described as shorter for TEA. This result could be related with a prolonged postictal state in these patients. The analysis of st-EEG results evidenced low sensitivity for interictal epileptiform abnormalities (IEAs) detection (52.3%), with not conclusive data in distinguishing TEA from TGA. On the contrary, 24-h EEG showed IEAs in all patients with epilepsy, mostly during sleep, suggesting an essential diagnostic role of long-lasting EEG recording for TEA. Finally, structural abnormalities were more frequent in patients with TEA (26.6%). In the group with TGA, the only imaging alteration found was diffusion weighted imaging (DWI) hippocampal hyperintensity. CONCLUSION: Our findings show that in a real-life clinical scenario, TEA is frequent but often overlooked. However, simple clinical data and widely available neurophysiological examinations can truly help to effectively distinguish TEA from TGA.
OBJECTIVE: Transient epilepticamnesia (TEA) is an underestimated condition in emergency clinical setting, where most of transient amnesic episodes tend to be classified as transient global amnesia (TGA). We designed this study to evaluate the actual frequency of TEA in a real-life scenario and to highlight the features that can help clinicians distinguishing it from TGA. METHODS: We retrospectively collected clinical data of 83 patients who accessed our emergency ward for an abrupt onset of amnesic disorder, initially interpreted as TGA. All patients underwent neurological evaluation, magnetic resonance imaging (MRI) scan, and standard 21-channel scalp electroencephalography (EEG) recording (standard EEG [st-EEG]). Moreover, patients with borderline epileptiform abnormalities on st-EEG or with normal st-EEG but high clinical suspicion for TEA underwent a 16-channel 24-hour ambulatory EEG (24-h EEG). Clinical features, neurophysiological, and neuroimaging data were analyzed and compared in the two groups (TEA and TGA). RESULTS: Diagnosis of TEA, according to Zeman's criteria, was made in 15 patients (18%). From a clinical point of view recurrence (p < .001) and atypical symptoms such as confusion or language disorder (TGA plus manifestations), appear to be key elements in order to discriminate between TEA and TGA (80% of patients with TEA vs 7.8% of patients with TGA; p < .001). In our sample, duration of the episodes did not significantly differ between TGA and TEA, even though it is usually described as shorter for TEA. This result could be related with a prolonged postictal state in these patients. The analysis of st-EEG results evidenced low sensitivity for interictal epileptiform abnormalities (IEAs) detection (52.3%), with not conclusive data in distinguishing TEA from TGA. On the contrary, 24-h EEG showed IEAs in all patients with epilepsy, mostly during sleep, suggesting an essential diagnostic role of long-lasting EEG recording for TEA. Finally, structural abnormalities were more frequent in patients with TEA (26.6%). In the group with TGA, the only imaging alteration found was diffusion weighted imaging (DWI) hippocampal hyperintensity. CONCLUSION: Our findings show that in a real-life clinical scenario, TEA is frequent but often overlooked. However, simple clinical data and widely available neurophysiological examinations can truly help to effectively distinguish TEA from TGA.
Authors: Benjamin H Brinkmann; Philippa J Karoly; Ewan S Nurse; Sonya B Dumanis; Mona Nasseri; Pedro F Viana; Andreas Schulze-Bonhage; Dean R Freestone; Greg Worrell; Mark P Richardson; Mark J Cook Journal: Front Neurol Date: 2021-07-13 Impact factor: 4.003