Objective: To explore quantitative measurements of the visual attention and neuroelectrophysiological relevance of memory deficits in temporal lobe epilepsy (TLE) by eye tracking and electroencephalography (EEG).Methods: Thirty-four TLE patients and twenty-eight healthy controls were invited to complete neurobehavioral assessments, cognitive oculomotor tasks, and 24-h video EEG (VEEG) recordings using an automated computer-based memory assessment platform with an eye tracker. Visit counts, visit time, and time of first fixation on areas of interest (AOIs) were recorded and analyzed in combination with interictal epileptic discharge (IED) characteristics from the bilateral temporal lobes.Results: The TLE patients had significantly worse Wechsler Digit Span scores [F(1, 58) = 7.49, p = 0.008]. In the Short-Term Memory Game with eye tracking, TLE patients took a longer time to find the memorized items [F(1, 57) = 17.30, p < 0.001]. They had longer first fixation [F(1, 57) = 4.06, p = 0.049] and more visit counts [F(1, 57) = 7.58, p = 0.008] on the target during the recall. Furthermore, the performance of the patients in the Digit Span task was negatively correlated with the total number of IEDs [r(28) = −0.463, p = 0.013] and the number of spikes per sleep cycle [r(28) = −0.420, p = 0.026].Conclusion: Eye tracking appears to be a quantitative, objective measure of memory evaluation, demonstrating memory retrieval deficits but preserved visual attention in TLE patients. Nocturnal temporal lobe IEDs are closely associated with memory performance, which might be the electrophysiological mechanism for memory impairment in TLE.
Aims To compare different patterns of memory impairment in patients with two subtypes of mesial temporal lobe epilepsy (MTLE) and healthy controls. Methods Thirty‐five healthy controls and 41 patients with MTLE were recruited, of which 25 patients were diagnosed as hippocampal sclerosis (HS‐MTLE), and the rest 16 patients were lesion‐negative (MRI‐neg MTLE). Participants completed the Wechsler memory assessment and a short‐term memory game on an automated computer‐based memory assessment platform with an eye tracker. Results Both the MRI‐neg MTLE and HS‐MTLE groups took longer time to complete the short‐term memory game than healthy controls (p < 0.001, Cohen's d = 1.087; p = 0.047, Cohen's d = 0.787). During the memory encoding phase, the MRI‐neg MTLE group spent significantly shorter time than healthy controls on the difficult levels with three (p = 0.004, Cohen's d = 0.993) and four targets (p = 0.016, Cohen's d = 0.858). During the memory decoding phase, the HS‐MTLE group spent less time looking on the targets compared to controls when recalling and finding four targets (p = 0.004, Cohen's d = −0.793), while the MRI‐neg MTLE group spent significantly longer time on the distractors and shorter time on the region of interests (ROIs) for all difficulty levels (all p < 0.05) than controls. Furthermore, the eye tracking data were correlated with the scores of the Wechsler Memory Scale after Bonferroni correction (p < 0.05). Conclusion Patients with MRI‐neg MTLE demonstrate impaired memory mostly due to attention deficits, while those with HS‐MTLE show memory impairment with relative sparing of attention. Eye tracking technology has the potential of facilitating the investigation of the mechanism of memory defect in MTLE and can serve as a supplementary neuropsychological tool for clinical diagnosis and long‐term monitoring.
Myelin-oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is an autoimmune-mediated demyelinating disease of the central nervous system (CNS). Patients with MOGAD may develop any combination of optic neuritis (ON), myelitis, brainstem syndrome and encephalitis. Reports of MOGAD with cranial nerve involvement are rare. Herein, we report a MOGAD patient with cranial neuropathies. In addition, we summarized the clinical features of the previously reported six MOG-IgG-positive cases with cranial nerve involvement and discussed the underlying mechanisms of MOGAD involving cranial nerves. Cranial neuropathy is an emerging phenotype in MOGAD, which has characteristics of both central and peripheral nervous system (PNS) involvement, with the trigeminal nerve being the most commonly affected nerve. MOG antibody testing in patients with cranial neuropathies is warranted, and immunotherapy is advocated when the risk of relapse is high. Although higher antibody titers and persistently positive serological test results are predictive of disease recurrence, the long-term outcomes of MOG-IgG-positive patients with cranial neuropathies remain largely unknown.
ObjectiveThe features of cerebral metabolism associated with loss of consciousness in patients with temporal lobe epilepsy (TLE) have not been fully elucidated. We aim to investigate the alterations in cortical-subcortical metabolism in temporal lobe epilepsy with impaired awareness seizures (IAS).MethodsRegional cerebral metabolism was measured using fluorine-18-fluorodeoxyglucose positron emission tomography (18F-FDG PET) in patients with TLE-IAS and healthy controls. All patients had a comprehensive evaluation to confirm their seizure origin and lateralization. Videos of all seizures were viewed and rated by at least two epileptologists to identify the state of consciousness when a seizure occurred. By synthesizing the seizure history, semeiology, and video EEG of all patients, as long as the patients had one seizure with impaired awareness, she/he will be included. 76 patients with TLE-IAS and 60 age-matched healthy controls were enrolled in this study. Regional cerebral metabolic patterns were analyzed for TLE-IAS and healthy control groups using statistical parametric mapping. Besides, we compared the MRI-negative patients and MRI-positive patients with healthy controls, respectively.ResultsThere were no significant differences in the age and sex of TLE-IAS patients and healthy control. TLE-IAS patients showed extensive bilateral hypermetabolism in the frontoparietal regions, cingulate gyrus, corpus callosum, occipital lobes, basal ganglia, thalamus, brainstem, and cerebellum. The region of metabolic change was more extensive in right TLE-IAS than that of the left, including extensive hypometabolism in the ipsilateral temporal, frontal, parietal, and insular lobes. And contralateral temporal lobe, bilateral frontoparietal regions, occipital lobes, the anterior and posterior regions of the cingulate gyrus, bilateral thalamus, bilateral basal ganglia, brainstem, and bilateral cerebellum showed hypermetabolism. The TLE patients with impaired awareness seizure showed hypermetabolism in the cortical-subcortical network including the arousal system. Additionally, 48 MRI-positive and 28 MRI-negative TLE-IAS patients were included in our study. TLE-IAS patients with MRI-negative and MRI-positive were both showed hypermetabolism in the cingulate gyrus. Hypometabolism in the bilateral temporal lobe was showed in the TLE-IAS with MRI-positive.ConclusionThese findings suggested that the repetitive consciousness impairing ictal events may have an accumulative effect on brain metabolism, resulting in abnormal interictal cortical-subcortical metabolic disturbance in TLE patients with impaired awareness seizure. Understanding these metabolic mechanisms may guide future clinical treatments to prevent seizure-related awareness deficits and improve quality of life in people with TLE.
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