Investigating silent pauses in connected speech: integrating linguistic, neuropsychological, and neuroanatomical perspectives across narrative tasks in post-stroke aphasia.

Introduction: Silent pauses are regarded as integral components of the temporal organization of speech. However, it has also been hypothesized that they serve as markers for internal cognitive processes, including word access, monitoring, planning, and memory functions. Although existing evidence across various pathological populations underscores the importance of investigating silent pauses' characteristics, particularly in terms of frequency and duration, there is a scarcity of data within the domain of post-stroke aphasia. Methods: The primary objective of the present study is to scrutinize the frequency and duration of silent pauses in two distinct narrative tasks within a cohort of 32 patients with chronic post-stroke aphasia, in comparison with a control group of healthy speakers. Subsequently, we investigate potential correlation patterns between silent pause measures, i.e., frequency and duration, across the two narrative tasks within the patient group, their performance in neuropsychological assessments, and lesion data. Results: Our findings showed that patients exhibited a higher frequency of longer-duration pauses in both narrative tasks compared to healthy speakers. Furthermore, within-group comparisons revealed that patients tended to pause more frequently and for longer durations in the picture description task, while healthy participants exhibited the opposite trend. With regard to our second research question, a marginally significant interaction emerged between performance in semantic verbal fluency and the narrative task, in relation to the location of silent pauses-whether between or within clauses-predicting the duration of silent pauses in the patient group. However, no significant results were observed for the frequency of silent pauses. Lastly, our study identified that the duration of silent pauses could be predicted by distinct Regions of Interest (ROIs) in spared tissue within the left hemisphere, as a function of the narrative task. Discussion: Overall, this study follows an integrative approach of linguistic, neuropsychological and neuroanatomical data to define silent pauses in connected speech, and illustrates interrelations between cognitive components, temporal aspects of speech, and anatomical indices, while it further highlights the importance of studying connected speech indices using different narrative tasks.

Persistent neuropsychiatric impairment in HCV patients despite clearance of the virus?!

One of the most disabling symptoms of hepatitis C virus (HCV) infection is chronic fatigue. While this is accepted for HCV polymerase chain reaction (PCR)-positive patients, a relationship between HCV infection and chronic fatigue is questioned after successful virus eradication. As fatigue is a subjective criterion, we aimed to evaluate in addition mood alterations and cognitive function in HCV-exposed patients with only mild liver disease and to assess a) possible interrelationships between these factors and health-related quality of life and b) the impact of viremia and former interferon treatment. One hundred and fifty-nine anti-HCV-positive individuals without advanced liver disease answered health-related quality of life (HRQoL), fatigue and depression questionnaires and underwent a battery of attention and memory tests. Accompanying diseases which could distort the results of the study such as HIV co-infection or drug addiction were exclusion criteria. The patients were subdivided into four groups according to their viremia status and interferon treatment history. Patients' data were evaluated with respect to norms given in the respective test manuals and in addition compared to those of 33 age-matched healthy controls. Eighty-five per cent of the patients had chronic fatigue, 50-60% mild depression or anxiety, 45% memory deficits and 30% attention deficits, irrespective of their HCV viremia status or treatment history. HRQoL correlated negatively with chronic fatigue (P<.001), while cognitive deficits-especially memory function-were independent from fatigue and depression. HCV infection may cause long-standing cerebral dysfunction that significantly impairs HRQoL and may even persist after clearance of the virus.

Linking infection and inflammation in acute ischemic stroke.

Infections after ischemic stroke are known to complicate the clinical course and worsen the outcome. Neuroinflammation is one of the predominant mechanisms of secondary progression of brain injury and infection and is far from being well understood. Experimental data demonstrate that ischemic stroke patients are at a higher risk for systemic infections if they show a pronounced anti-inflammatory response after the event, which is considered an indication of a stress-mediated reduction of immune competence. Only a small number of studies describe the time course of inflammation mediators after ischemic stroke in patients with early poststroke infections. Levels of inflammation mediators after the event of stroke differ, depending on clinical severity and concomitant infectious diseases. Thus, sequential dynamics of early inflammation must be considered in the development of both mechanism-targeting anti-inflammatory and anti-infectious treatment strategies in ischemic brain damage.

The temporal profile of inflammatory markers and mediators in blood after acute ischemic stroke differs depending on stroke outcome.

BACKGROUND: Early inflammation has been suggested as an important factor contributing to unfavorable prognosis after acute ischemic stroke. The present study aimed to clarify the temporal dynamics of discrete inflammatory markers/mediators for future mechanism-targeting anti-inflammatory strategies in ischemic brain damage. METHODS: Blood samples of 69 patients with transient ischemic attack or ischemic stroke were taken upon admission and at time points 6, 12 and 24 h, as well as 3 and 7 days after symptom onset for analysis of monocyte chemotactic protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), interleukin-6 (IL-6), C-reactive protein (CRP) and the brain damage marker S100B. Clinical scores (modified Rankin Scale, National Institute of Health Stroke Scale) were assessed on day 90. RESULTS: MCP-1, MMP-9, TIMP-1, IL-6, CRP and S100B showed significantly different time courses depending on stroke outcome. While the levels of IL-6, MCP-1 and MMP-9 increased already a few hours after symptom onset, CRP and S100B gradually rose commencing at 12-24 h. TIMP-1 demonstrated an extended plateau. By multiple linear regression analysis IL-6, MCP-1, TIMP-1 and S100B were determined to be independently related to clinical outcome scores at specific time points. CONCLUSIONS: Our data show important differences in the early time course of several potential markers for the complex network of inflammation and brain damage after ischemic stroke depending on stroke outcome. This must be considered for any therapeutical approach using anti-inflammatory treatment.