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Purpose: We present two patients who developed neurogenic stuttering after long COVID-19 related to SARS-CoV-2 infection. Methods and Results: Both patients experienced both physical (e.g., fatigue) and cognitive difficulties, which led to impaired function of attention, lexical retrieval, and memory consolidation. Both patients had new-onset stuttering-like speech dysfluencies: Blocks and repetitions were especially evident at the initial part of words and sentences, sometimes accompanied by effortful and associated movements (e.g., facial grimaces and oro-facial movements). Neuropsychological evaluations confirmed the presence of difficulties in cognitive tasks, while neurophysiological evaluations (i.e., electroencephalography) suggested the presence of “slowed” patterns of brain activity. Neurogenic stuttering and cognitive difficulties were evident for 4–5 months after negativization of SARS-CoV-2 nasopharyngeal swab, with gradual improvement and near-to-complete recovery. Conclusions: It is now evident that SARS-CoV-2 infection may significantly involve the central nervous system, also resulting in severe and long-term consequences, even if the precise mechanisms are still unknown. In the present report, long COVID-19 resulted in neurogenic stuttering, as the likely consequence of a “slowed” metabolism of (pre)frontal and sensorimotor brain regions (as suggested by the present and previous clinical evidence). As a consequence, the pathophysiological mechanisms related to the appearance of neurogenic stuttering have been hypothesized, which help to better understand the broader and possible neurological consequences of COVID-19.

This case series describes three patients affected by severe acute respiratory syndrome coronavirus 2, who developed polyradiculoneuritis as a probable neurological complication of coronavirus disease 2019 (COVID‐19). A diagnosis of Guillain Barré syndrome was made on the basis of clinical symptoms, cerebrospinal fluid analysis, and electroneurography. In all of them, the therapeutic approach included the administration of intravenous immunoglobulin (0.4 gr/kg for 5 days), which resulted in the improvement of neurological symptoms. Clinical neurophysiology revealed the presence of conduction block, absence of F waves, and in two cases, a significant decrease in amplitude of compound motor action potential cMAP. Due to the potential role of inflammation on symptoms development and prognosis, interleukin‐6 (IL‐6) and IL−8 levels were measured in serum and cerebrospinal fluid during the acute phase, while only serum was tested after recovery. Both IL‐6 and IL‐8 were found increased during the acute phase, both in the serum and cerebrospinal fluid, whereas 4 months after admission (at complete recovery), only IL‐8 remained elevated in the serum. These results confirm the inflammatory response that might be linked to peripheral nervous system complications and encourage the use of IL‐6 and IL‐8 as prognostic biomarkers in COVID‐19.

Background: Diagnosis of prodromal Alzheimer's disease (AD) still represents a hot topic and there is a growing interest for the detection of early and non-invasive biomarkers. Although progressive episodic memory impairment is the typical predominant feature of AD, communicative difficulties can be already present at the early stages of the disease. Objective: This study investigated the narrative discourse production deficit as a hallmark of CSFdefined prodromal AD and its correlation with cerebral hypoperfusion pattern. Method: Narrative assessment with a multilevel procedure for discourse analysis was conducted on 28 subjects with Mild Cognitive Impairment (15 MCI due to AD; 13 MCI non-AD) and 28 healthy controls. The diagnostic workup included CSF AD biomarkers. Cerebral hypoperfusion pattern was identified by SPECT image processing. Results: The results showed that the discourse analysis of global coherence and lexical informativeness indexes allowed to identify MCI due to AD from MCI non-AD and healthy subjects. These findings allow to hypothesize that the loss of narrative efficacy could be a possible early clinical hallmark of Alzheimer’s disease. Furthermore, a significant correlation of global coherence and lexical informativeness reduction with the SPECT hypoperfusion was found in the dorsal aspect of the anterior part of the left inferior frontal gyrus, supporting the hypothesis that this area has a significant role in communicative efficacy, and in particular, in semantic selection executive control. Conclusion: This study contributes to the understanding of the neural networks for language processing and their involvement in prodromal Alzheimer's disease. It also suggests an easy and sensitive tool for clinical practice that can help identifying individuals with prodromal Alzheimer’s disease.

Shame plays a fundamental role in the regulation of our social behavior. One intriguing question is whether amygdala might play a role in processing this emotion. In the present single-case study, we tested a patient with acquired damage of bilateral amygdalae and surrounding areas as well as healthy controls on shame processing and other social cognitive tasks. Results revealed that the patient's subjective experience of shame, but not of guilt, was more reduced than in controls, only when social standards were violated, while it was not different than controls in case of moral violations. The impairment in discriminating between normal social situations and violations also emerged. Taken together, these findings suggest that the role of the amygdala in processing shame might reflect its relevance in resolving ambiguity and uncertainty, in order to correctly detect social violations and to generate shame feelings.

Whether motor and linguistic representations of actions share common neural structures has recently been the focus of an animated debate in cognitive neuroscience. Group studies with brain-damaged patients reported association patterns of praxic and linguistic deficits whereas single case studies documented double dissociations between the correct execution of gestures and their comprehension in verbal contexts. When the relationship between language and imitation was investigated, each ability was analysed as a unique process without distinguishing between possible subprocesses. However, recent cognitive models can be successfully used to account for these inconsistencies in the extant literature. In the present study, in 57 patients with left brain damage, we tested whether a deficit at imitating either meaningful or meaningless gestures differentially impinges on three distinct linguistic abilities (comprehension, naming and repetition). Based on the dual-pathway models, we predicted that praxic and linguistic performance would be associated when meaningful gestures are processed, and would dissociate for meaningless gestures. We used partial correlations to assess the association between patients’ scores while accounting for potential confounding effects of aspecific factors such age, education and lesion size. We found that imitation of meaningful gestures significantly correlated with patients’ performance on naming and repetition (but not on comprehension). This was not the case for the imitation of meaningless gestures. Moreover, voxel-based lesion-symptom mapping analysis revealed that damage to the angular gyrus specifically affected imitation of meaningless gestures, independent of patients’ performance on linguistic tests. Instead, damage to the supramarginal gyrus affected not only imitation of meaningful gestures, but also patients’ performance on naming and repetition. Our findings clarify the apparent conflict between associations and dissociations patterns previously observed in neuropsychological studies, and suggest that motor experience and language can interact when the two domains conceptually overlap. * Abbreviations : AAT : Aachener Aphasie Test

Imitation is a sensorimotor process whereby the visual information present in the model's movement has to be coupled with the activation of the motor system in the observer. This also implies that greater the similarity between the seen and the produced movement, the easier it will be to execute the movement, a process also known as ideomotor compatibility. Two components can influence the degree of similarity between two movements: the anatomical and the spatial component. The anatomical component is present when the model and imitator move the same body part (e.g., the right hand) while the spatial component is present when the movement of the model and that of the imitator occur at the same spatial position. Imitation can be achieved by relying on both components, but typically the model's and imitator's movements are matched either anatomically or spatially. The aim of this study was to ascertain the contribution of the left and right hemisphere to the imitation accomplished either with anatomical or spatial matching (or with both). Patients with unilateral left and right brain damage performed an ideomotor task and a gesture imitation task. Lesions in the left and right hemispheres gave rise to different performance deficits. Patients with lesions in the left hemisphere showed impaired imitation when anatomical matching was required, and patients with lesions in the right hemisphere showed impaired imitation when spatial matching was required. Lesion analysis further revealed a differential involvement of left and right hemispheric regions, such as the parietal opercula, in supporting imitation in the ideomotor task. Similarly, gesture imitation seemed to rely on different regions in the left and right hemisphere, such as parietal regions in the left hemisphere and premotor, somatosensory and subcortical regions in the right hemisphere.

Normally we can perform a variety of goal-directed movements effortlessly. However, damage to the parietal cortex may dramatically reduce this ability, giving rise to optic ataxia and limb apraxia. Patients with optic ataxia show clear misreaches towards targets when presented in the peripheral visual field, whereas limb apraxia refers to the inability to use common tools or to imitate simple gestures. In the present paper we describe the case of a left-brain damaged patient, who presented both symptoms. We systematically investigated both spatial and temporal parameters of his movements, when asked to reach and grasp common objects to move (Experiment 1) or to use them (Experiment 2), presented either in the central or peripheral visual field. Different movement parameters changed in relation to the goal of the task (grasp to move vs. grasp to use), reflecting a normal modulation of the movement to accomplish tasks with different goals. On the other hand, grip aperture appeared to be more affected from both task goal and viewing condition, with a specific decrement observed when CF was asked to use objects presented peripherally. On the contrary, a neat effect of the viewing condition was observed in the spatial distribution of the end-points of the movements, and of the horizontal end point in particular, which were shifted towards the fixation point when reaching towards peripheral targets. We hypothesized that optic ataxia and limb apraxia have a differential effect on the patient’s performance. The specific presence of optic ataxia would have an effect on the movement trajectory, but both symptoms might interact and influence the grasping component of the movement. As a ‘cognitive side of motor control impairment’, the presence of limb apraxia may have increased the task demands in grasping to use the objects thus exacerbating optic ataxia.