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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.

Neurological involvement following coronavirus disease 19 (COVID-19) is thought to have a neuroinflammatory etiology. Co-ultraPEALut (an anti-inflammatory molecule) and luteolin (an anti-oxidant) have shown promising results as neuroinflammation antagonists. The aim of this study was to describe cognitive impairment in patients with post-COVID-19 treated with co-ultraPEALut. The Montreal Cognitive Assessment (MoCA), the Prospective–Retrospective Memory Questionnaire (PRMQ), the Fatigue Severity Scale (FSS), and a subjective assessment were administered at baseline and after 10 months. Patients treated with co-ultraPEALut were retrospectively compared with controls. Twenty-six patients treated with co-ultraPEALut showed a significant improvement in PRMQ (T0: 51.94 ± 10.55, T1: 39.67 ± 13.02, p < 0.00001) and MoCA raw score (T0: 25.76 ± 2.3, T1: 27.2 ± 2, p 0.0260); the MoCA-adjusted score and the FSS questionnaires also showed an improvement, even though it was not statistically significant; and 80.77% of patients reported a subjective improvement. In the control subjects (n = 15), the improvement was not as pronounced (PRMQ T0: 45.77 ± 13.47, T1: 42.33 ± 16.86, p 0.2051; FSS T0: 4.95 ± 1.57, T1: 4.06 ± 1.47, p 0.1352). Patients treated with co-ultraPEALut and corticosteroids were not statistically different from those treated with co-ultraPEALut alone. Neuro-post-COVID-19 patients treated with co-ultraPEALut scored better than controls in MoCA and PRMQ questionnaires after 10 months: this may support the importance of neuroinflammation modulation for neuro-long-COVID-19. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Closing-in behavior (CIB) is observed in copying tasks (graphic or gestural) when the copy is performed near or on the top of the model. This symptom has been classically considered to be a manifestation of constructional apraxia and is often associated with a visuospatial impairment. More recent work emphasizes the attentional and/or executive nature of the behavior and its association with frontal lobe dysfunction. We describe three patients in whom CIB was associated with posterior parietal deficits of different etiologies (stroke in Patient 1 and dementia in Patients 2 and 3). In copying figures, Patient 1 produced the shape with high accuracy but the rendering overlapped the model, while for Patients 2 and 3 the copies were distorted but overlapping or in close proximity to the target. In gesture imitation, Patient 2 performed the gestures toward the examiner’s space, while Patient 1 showed a peculiar form of CIB: when he was asked to place the ipsilesional arm in a position that mirrored the contralesional hand, Patient 1 moved his hand toward his contralesional hand. Patient 3 did not present gestural CIB. While CIB in Patient 1 was associated with selective deficits in executive functions and attention, additional visuospatial deficits were observed in Patients 2 and 3. The latter two patients showed a general visuoconstructional deficit. These case studies support a primary attentional account of CIB but also suggest that visuoconstructional impairments may contribute to the emergence of CIB, in some subjects. This evidence argues for different types of CIB with different cognitive and neural underpinnings. Furthermore, the data support the hypothesis of a differential involvement of fronto-parietal network in CIB. [ABSTRACT FROM AUTHOR]

Falk's paper provides a nice cross-species perspective and an interesting background to formulate a theory of the evolution of human language. However, the author does not provide a complete overview and analysis of the origins of language and takes for granted the 'continuity hypothesis.' Also her 'infant parking theory' is questionable, as it is not well supported by observations.

Recent research in comparative psychology suggests that similarities between the behaviour of two individuals may not be the consequence of imitation only, but also of nonimitative social-learning processes. In the present study we aimed to investigate whether these alternative learning processes can take place in human adults, specifically in patients whose ability to imitate has been reduced by brain damage. Left (LBD) and right (RBD) brain-damaged patients were asked to perform four tool use tasks in three experimental conditions: exposure to the apparatus (N); demonstration of the correct solution (C); and demonstration of a failed attempt followed by the correct solution to the problem (I + C). Results suggest that the left hemisphere is indeed critical for action and that selective neuropsychological deficits can affect action imitation and selection of goal-directed movements, independently from each other. Findings also indicate that when the ability to imitate actions is lowered emulation may become available. [ABSTRACT FROM AUTHOR]

We report the case of OTM who presented with dynamic aphasia following a stroke that occurred in the left basal ganglia. He showed drastically reduced spontaneous speech in the context of well preserved naming, repetition and comprehension skills. OTM was particularly impaired in generating words, sentences and phrases when cued by a stimulus allowing many response options. By contrast, when a single response was strongly suggested by a stimulus, he could generate verbal responses adequately. OTM's non-verbal response generation abilities varied across tasks. He performed in the normal range in a motor movement generation test and he produced as many figures as controls when tested on a figural fluency task. He showed, however, many perseverations on this test. Moreover in a random number generation task he produced more responses that were part of ascending and descending series of numbers. The patient's impairments are interpreted as a consequence of two deficits. The first of these consists of an inability to generate verbal responses particularly in situations of high competition and involves the function of left frontal regions. The second deficit is one of impaired novel thought generation as evidenced by perseverations. This second deficit has been proposed to be a function of basal ganglia damage. [ABSTRACT FROM AUTHOR]