The black box of global aphasia: Neuroanatomical underpinnings of remission from acute global aphasia with preserved inner language function

Objective We studied an unusual case of global aphasia (GA) occurring after brain tumor removal and remitting one-month after surgery. After recovering, the patient reported on her experience during the episode, which suggested a partial preservation of language abilities (such as semantic processing) and the presence of inner speech (IS) despite a failure in overt speech production. Thus, we explored the role of IS and preserved language functions in the acute phase and investigated the neuroanatomical underpinnings of this severe breakdown in language processing. Method A neuropsychological and language assessment tapping into language production, comprehension, attention and working memory was carried out both before and three months after surgery. In the acute stage a simplified protocol was tailored to assess the limited language abilities and further explore patient's performance on different semantic tasks. The neuroanatomical dimension of these abrupt changes was provided by perioperative structural neuroimaging. Results Language and neuropsychological performance were normal/close to normal both before and three months after surgery. In the acute stage, the patient presented severe difficulties with comprehension, production and repetition, whereas she was able to correctly perform tasks that requested conceptual analysis and non-verbal operations. After recovering, the patient reported that she had been able to internally formulate her thoughts despite her overt phonological errors during the episode. Structural neuroimaging revealed that an extra-axial blood collection affected the middle frontal areas during the acute stage and that the white matter circuitry was left-lateralized before surgery. Conclusions We deemed that the global aphasia episode was produced by a combination of the post-operative extra-axial blood collection directly impacting left middle frontal areas and a left-lateralization of the arcuate and/or uncinated fasciculi before surgery. Additionally, we advocate for a comprehensive evaluation of linguistic function that includes the assessment of IS and non-expressive language functions in similar cases

Neurologic Involvement in COVID-19: Cause or Coincidence? A Neuroimaging Perspective

Despite a large cohort of 103 patients with COVID-19, the authors found a large number of symptomatic patients with negative neuroimaging findings, and no conclusions can be drawn concerning concrete associations between neuroimaging and COVID-19. The rapid spread of the coronavirus disease 2019 (COVID-19) pandemic has shaken hospitals worldwide. Some authors suggest that neurologic involvement could further complicate the disease. This descriptive study is a cross-sectional review of 103 patients diagnosed with COVID-19 who underwent neuroimaging (of a total of 2249 patients with COVID-19 in our center). Analyzed variables were neurologic symptoms and acute imaging findings. The most frequent symptoms that motivated neuroimaging examinations were mild nonfocal neurologic symptoms, code stroke (refers to patients presenting with signs and symptoms of stroke whose hyperacute assessment and care is prioritized), focal neurologic symptoms, postsedation encephalopathy, and seizures. No cases of encephalitis or direct central nervous system involvement were detected. Thirteen patients presented with acute ischemic events, and 7, with hemorrhagic events; however, most reported multiple vascular risk factors. Despite the large cohort of patients with COVID-19, we found a large number of symptomatic patients with negative neuroimaging findings, and no conclusions can be drawn concerning concrete associations between neuroimaging and COVID-19

Risk of Developing Epilepsy after Autoimmune Encephalitis

Background: Acute symptomatic seizures (ASS) are a common manifestation of autoimmune encephalitis (AE), but the risk of developing epilepsy as a sequela of AE remains unknown, and factors predisposing the development of epilepsy have not been fully identified. Objective: To assess the risk of developing epilepsy in AE and study related risk factors. Materials and methods: This was a retrospective single centre study including patients diagnosed with AE according to criteria described by Graus et al., with a minimum follow-up of 12 months after AE resolution. The sample was divided according to whether patients developed epilepsy or not. Results: A total of 19 patients were included; 3 (15.8%) had AE with intracellular antibodies, 9 (47.4%) with extracellular antibodies, and 7 (36.8%) were seronegative. During follow-up, 3 patients (15.8%) died, 4 (21.1%) presented relapses of AE, and 11 (57.89%) developed epilepsy. There was a significant association between the development of epilepsy and the presence of hippocampal atrophy in control brain magnetic resonance imaging (MRI) (p = 0.037), interictal epileptiform discharges (IED) on control electroencephalogram (EEG) (p = 0.045), and immunotherapy delay (p = 0.016). Conclusions: Hippocampal atrophy in neuroimaging, IED on EEG during follow-up, and immunotherapy delay could be predictors of the development of epilepsy in patients with AE

Lower Locus Coeruleus MRI intensity in patients with late-life major depression

Background: The locus coeruleus (LC) is the major noradrenergic source in the central nervous system. Structural alterations in the LC contribute to the pathophysiology of different neuropsychiatric disorders, which may increase to a variable extent the likelihood of developing neurodegenerative conditions. The characterization of such alterations may therefore help to predict progression to neurodegenerative disorders. Despite the LC cannot be visualized with conventional magnetic resonance imaging (MRI), specific MRI sequences have been developed to infer its structural integrity. Methods: We quantified LC signal Contrast Ratios (LCCRs) in late-life major depressive disorder (MDD) (n = 37, 9 with comorbid aMCI), amnestic Mild Cognitive Impairment (aMCI) (n = 21, without comorbid MDD), and healthy controls (HCs) (n = 31), and also assessed the putative modulatory effects of comorbidities and other clinical variables. Results: LCCRs were lower in MDD compared to aMCI and HCs. While no effects of aMCI comorbidity were observed, lower LCCRs were specifically observed in patients taking serotonin/norepinephrine reuptake inhibitors (SNRIs). Conclusion: Our results do not support the hypothesis that lower LCCRs characterize the different clinical groups that may eventually develop a neurodegenerative disorder. Conversely, our results were specifically observed in patients with late-life MDD taking SNRIs. Further research with larger samples is warranted to ascertain whether medication or particular clinical features of patients taking SNRIs are associated with changes in LC neurons