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1.
This study investigates phonetic categorisation and cue weighting in adolescents and young adults with Specific Language Impairment (SLI). We manipulated two acoustic cues, vowel duration and F1 offset frequency, that signal word-final stop consonant voicing ([t] and [d]) in English. Ten individuals with SLI (14.0–21.4 years), 10 age-matched controls (CA; 14.6–21.9 years) and 10 non-matched adult controls (23.3–36.0 years) labelled synthetic CVC non-words in an identification task. The results showed that the adolescents and young adults with SLI were less consistent than controls in the identification of the good category representatives. The group with SLI also assigned less weight to vowel duration than the adult controls. However, no direct relationship between phonetic categorisation, cue weighting and language skills was found. These findings indicate that some individuals with SLI have speech perception deficits but they are not necessarily associated with oral language skills.  相似文献   

2.
IntroductionLevodopa-induced dyskinesia in patients with Parkinson's disease (PD) has been shown to be associated with an abnormal plasticity in the motor cortex. We investigated whether changes in the excitability of inhibitory and excitatory motor circuits could underlie maladaptive mechanisms associated with dyskinesia.MethodsUsing single and paired transcranial magnetic stimulation (TMS), we studied motor threshold, silent period (SP) duration, intracortical facilitation (ICF), short intracortical inhibition (SICI) and low- and high-intensity long intracortical inhibition (LICI) in 10 dyskinetic and 10 non-dyskinetic patients, matched for disease and treatment duration, before (OFF state) and after (ON state) levodopa, and in 10 healthy controls.ResultsIn the OFF state, the two groups of patients showed similar motor cortex excitability with a reduced SICI compared to controls. LICI was weaker and increasing stimulation intensity had a lower effect on SP duration in dyskinetic patients than in controls. In dyskinetic patients, in contrast to non-dyskinetic patients, levodopa failed to increase SICI and SP duration, and potentiated to a lesser extent the effect of increasing the stimulation intensity on LICI. Although levodopa improved motor symptoms to a similar extent in both dyskinetic and non-dyskinetic patients, it failed to activate effectively the excitability of the inhibitory systems in dyskinetic patients.DiscussionThese findings suggest that dyskinesia is associated with an abnormal effect of levodopa on cortical motor inhibitory circuits.  相似文献   

3.
Recently, a growing number of studies have been published involving phonetic and acoustic analyses on the rare motor-speech disorder known as Foreign Accent Syndrome (FAS). These studies have relied on pre- and post-trauma speech samples to investigate the acoustic and phonetic properties of individual cases of FAS speech. This study presents detailed acoustic analyses of the speech characteristics of two new cases of FAS using identical pre- and post-recovery speech samples, thus affording a new level of control in the study of Foreign Accent Syndrome. Participants include a 48-year-old female who began speaking with an “Eastern European” accent following a traumatic brain injury, and a 45-year-old male who presented with a “British” accent following a subcortical cerebral vascular accident (CVA). The acoustic analysis was based on 18 real words comprised of the stop consonants /p/, /t/, /k/; /b/, /d/, /g/ combined with the peripheral vowels /i/, /a/ and /u/ and ending in a voiceless stop. Computer-based acoustic measures included: (1) voice onset time (VOT), (2) vowel durations, (3) whole word durations, (4) first, second and third formant frequencies, and (5) fundamental frequency. Formant frequencies were measured at three points in the vowel duration: (a) 20%, (b) 50%, and (c) 80% to assess differences in vowel ‘onglides’ and ‘offglides’. The acoustic analysis allowed precise quantification of the major phonetic features associated with the foreign quality of participants' FAS speech. Results indicated post-recovery changes in both duration and frequency measures, including a tendency toward more normal VOT production of voiced stops, changes in average vowel durations, as well as evidence from formant frequency values of vowel backing for both participants. The implications of this study for future research and clinical applications are also considered.  相似文献   

4.
Background‘Dropped head’ and ‘bent spine’ phenomena are recognized clinical presentations of neuromuscular disorders. Similar symptoms are known in patients with parkinsonian syndromes, but their pathophysiology remains unclear. One hypothesis is a relation between the movement disorder and the skeletal muscle pathology.MethodsWe describe detailed histopathological data from 19 consecutive skeletal muscle biopsies in patients with idiopathic Parkinson's disease (PD) and concomitant ‘dropped head’ or ‘bent spine’ syndrome. A biochemical analysis of the respiratory chain complexes was also performed, and clinical, electrophysiological, and imaging data were analyzed.ResultsThe subjects developed neuromuscular symptoms 2.7 ± 2.4 years after onset of PD. We found no correlation with the age at onset of the disease, disease duration, or severity. We found no evidence for dystonia nor did we find any relationship between their anti-parkinsonian medication, and possible drug side effects. Muscle biopsies were abnormal in all patients. Based on histopathological criteria we divided the muscle pathology into three different groups, i.e. necrotizing myopathy, inflammatory myopathy, and myopathy with mitochondrial abnormalities. Biochemical analysis of respiratory chain complexes revealed abnormalities in nine patients.Conclusions‘Dropped head’ and ‘bent spine’ symptoms in association with PD appear to be accompanied by a wide spectrum of histopathological abnormalities in skeletal muscle. A muscle biopsy should be performed to identify potentially treatable conditions (i.e. inflammatory myopathies).  相似文献   

5.
《L'Encéphale》2016,42(4):367-373
BackgroundPsychiatric disorders are consistent with the gene x environment model, and non-specific environmental factors such as childhood trauma, urbanity, and migration have been implicated. All of these factors have in common to dysregulate the biological pathways involved in response to stress. Stress is a well-known precipitating factor implicated in psychiatric disorders such as depression, bipolar disorder, anxiety, and possibly schizophrenia. More precisely, psychosocial stress induces dysregulation of the hypothalamic-pituitary-adrenal axis (HPA) and could modify neurotransmission, which raises the question of the involvement of stress-related biological changes in psychotic disorders. Indeed, the literature reveals dysregulation of the HPA axis in schizophrenia. This dysregulation seems to be present in the prodromal phases (UHR subjects for ultra-high risk) and early schizophrenia (FEP for first episode psychosis). Thus, and following the stress–vulnerability model, stress could act directly on psychotic onset and precipitate the transition of vulnerable subjects to a full-blown psychosis.ObjectiveThe present paper reviews the literature on stress and onset of schizophrenia, with consideration for the causal role vs. associated role of HPA axis dysregulation in schizophrenia and the factors that influence it, in particular during prodromal and earlier phases. We also discuss different methods developed to measure stress in humans.MethodologyWe performed a bibliographic search using the keywords ‘cortisol’, ‘glucocorticoid’, ‘HPA’ with ‘UHR’, ‘CHR’, ‘at-risk mental state’, ‘first episode psychosis’, ‘schizotypal’, ‘prodromal schizophrenia’ in Medline, Web of Knowledge (WOS), and EBSCO completed by a screening of the references of the selected articles.ResultsStress has been studied for many years in schizophrenia, either by subjective methods (questionnaires), or objective methods (standardized experimental protocols) with biological sampling and/or brain imaging methods. These methods have suggested a link between dysregulation of the HPA axis and psychotic symptoms both through abnormal basal levels of cortisol and flattened reactivity to social stress. Imaging results suggest indirect modifications, including abnormal pituitary or hippocampal volume. Several factors dysregulating the HPA axis have also been highlighted, such as consumption of drugs (i.e. cannabis), childhood trauma or genetic factors (such as COMT, or MTHFR variants). Psychological stress induces subcortical dopaminergic activation attributable to hypothalamic-pituitary-adrenal (HPA) axis dysregulation. This dysregulation is present in the prodromal phase (UHR) in patients who have experienced a first psychotic episode (FEP) and in siblings of schizophrenic patients. Stress dysregulation is a plausible hypothesis to understand the psychosis onset.DiscussionThe effect of stress on brain pathways could participate to the mechanisms underlying the onset of psychotic symptoms, both as a precipitating factor and as a marker of a predisposing vulnerability. This dysregulation fits into the gene x environment model: in subjects with genetic predispositions, stressful environmental factors can modify biological pathways implicated in psychiatric disorders, promoting the emergence of symptoms. However, many confounding factors obscure the literature, and further studies are needed in schizophrenic patients, UHR and FEP patients to clarify the precise role of stress in psychotic transition. Identification of stress biomarkers could help diagnosis and prognosis, and pave the way for specific care strategies based on stress-targeted therapies.  相似文献   

6.
Background and Objectives: Serotonin transporter (5-HTT) gene allelic variants were shown to be associated with Neuroticism and Harm Avoidance but the results were not replicated in other studies. The current investigation was undertaken in a further attempt to study the relationship between 5-HTT polymorphism and personality traits.

Subjects and Methods: To evaluate a spectrum of personality traits, MMPI was administered to a sample including patients with affective disorders (n=114), patients with schizophrenia spectrum illnesses (n=110) and psychiatrically well controls (n=124). All groups were genotyped for VNTR-17 and functional insertion-deletion (5-HTTLPR) polymorphisms.

Results: An association was found between 5-HTTLPR polymorphism and scores on three MMPI scales: Psychopathic deviance, Paranoia and Schizophrenia in patients with affective disorders and Schizophrenia in normal subjects. Both affected and control individuals with ‘ss’ genotype exhibited lower scores on these scales.

Conclusion: We demonstrated that functional deletion/insertion allelic variation associated with decreased expression of serotonin transporter (‘s’ allele or ‘ss’ genotype) may restrict expression of schizoid traits in normal subjects and patients with affective disorders.  相似文献   

7.
ObjectiveStudies have provided evidence of heterogeneity within chronic fatigue syndrome (CFS), but few have used data from large cohorts of CFS patients or replication samples.Methods29 UK secondary-care CFS services recorded the presence/absence of 12 CFS-related symptoms; 8 of these symptoms were recorded by a Dutch tertiary service. Latent Class Analysis (LCA) was used to assign symptom profiles (phenotypes). Regression models were fitted with phenotype as outcome (in relation to age, sex, BMI, duration of illness) and exposure (in relation to comorbidities and patient-reported measures).ResultsData were available for 7041 UK and 1392 Dutch patients. Almost all patients in both cohorts presented with post-exertional malaise, cognitive dysfunction and disturbed/unrefreshing sleep, and these 3 symptoms were excluded from LCA. In UK patients, six phenotypes emerged: ‘full’ polysymptomatic (median 8, IQR 7-9 symptoms) 32.8%; ‘pain-only’ (muscle/joint) 20.3%; ‘sore throat/painful lymph node’ 4.5%; and ‘oligosymptomatic’ (median 1, IQR 0-2 symptoms) 4.7%. Two ‘partial’ polysymptomatic phenotypes were similar to the ‘full’ phenotype, bar absence of dizziness/nausea/palpitations (21.4%) or sore throat/painful lymph nodes (16.3%). Women and patients with longer duration of illness were more likely to be polysymptomatic. Polysymptomatic patients had more severe illness and more comorbidities. LCA restricted to 5 symptoms recorded in both cohorts indicated 3 classes (polysymptomatic, oligosymptomatic, pain-only), which were replicated in Dutch data.ConclusionsAdults with CFS may have one of 6 symptom-based phenotypes associated with sex, duration and severity of illness, and comorbidity. Future research needs to determine whether phenotypes predict treatment outcomes, and require different treatments.  相似文献   

8.
《Clinical neurophysiology》2017,128(7):1354-1363
ObjectiveTo evaluate EEG functional connectivity in the sensory-motor network, during wake and sleep, in patients with Huntington Disease (HD).Methods23 patients with HD and 23 age- and sex-matched healthy controls were enrolled. EEG connectivity analysis was performed by means of exact Low Resolution Electric Tomography (eLORETA).ResultsIn wake, HD patients showed an increase of delta lagged phase synchronization (T = 3.60; p < 0.05) among Broadman’s Areas (BA) 6-8 bilaterally; right BA 6-8 and right BA 1-2-3; left BA 1-2-3 and left BA 4. In NREM, HD patients showed an increase of delta lagged phase synchronization (T = 3.56; p < 0.05) among left BA 1-2-3 and right BA 6-8. In REM, HD patients showed an increase of lagged phase synchronization (T = 3.60; p < 0.05) among the BA 6-8 bilaterally (delta band); left BA 1-2-3 and right BA 1-2-3 (theta); left BA 1-2-3 and right BA 4 (theta); left BA 1-2-3 and right BA 1-2-3 (alpha).ConclusionsOur results may reflect an abnormal function of the motor areas or an effort to counterbalance the pathological motor output.SignificanceOur results may help to understand the pathophysiology of sleep-related movement disorders in Huntington’s Disease, and to define therapeutically strategies.  相似文献   

9.
PurposeThis study aimed to investigate parenting stress expressed by parents before and two years after their children's epilepsy surgery.MethodsSubjects: Parents of 31 consecutively included surgery patients with epilepsy and parents of 31 healthy sex- and age-matched control children were the subjects of this study. Materials and procedure: The questionnaire ‘Parenting Stress Index’, which distinguishes a Parent domain (stress leading parents to feel themselves inadequate) from a Child domain (child features felt by parent to cause stress) was completed before surgery of the patients and two years thereafter. At both time points, intelligence examination of the child was part of a comprehensive neuropsychological assessment, as were evaluations of recent stress-enhancing life events and epilepsy severity.ResultsPrior to surgery, total parenting stress was significantly higher in parents of patients than in parents of controls. Two years after surgery, total parenting stress had decreased significantly in parents of patients. The scores on parent-related subscales Role Restriction and Spouse and on the child-related subscale Distractibility/Hyperactivity, all relatively high before surgery, decreased significantly. Still, parents of patients experienced significantly more stress compared with parents of controls mainly because of persistently higher stress scores in parents of patients on the subscale Role Restriction (Parent domain) and on five of six subscales in the Child domain. Intelligence of the child was associated with parenting stress: the lower the child's intelligence, the higher the stress score on the subscale Distractibility/Hyperactivity and the lower the stress score on the subscale Mood. Stress decreased more in parents of patients who became seizure-free after surgery than in parents of patients with recurrent seizures.ConclusionsParenting stress decreases but does not normalize in the first two years after epilepsy surgery. Parents should be offered counseling on epilepsy-related intricacies contributing to parenting stress, immediately after diagnosis as well as after epilepsy surgery, notwithstanding the resulting seizure status of the child.  相似文献   

10.
《Clinical neurophysiology》2020,131(5):1011-1018
ObjectiveRecent findings suggested that subclinical epileptiform activity is prevalent during sleep in a significant proportion of Alzheimer’s Disease (AD) patients. The aims of our study were: (A) comparing the frequency of subclinical epileptiform activity during the sleep in a sample diagnosed with ‘probable’ AD and Mild Cognitive Impairment (MCI) due to AD, and in healthy subjects; (B) evaluating epileptiform EEG activity as a function of different sleep stages within a well-controlled polysomnographic setting.MethodsWe prospectively enrolled 50 ‘probable’ AD patients (73 ± 7.0 years) and 50 subjects with MCI due to AD (72 ± 6.7 years) without history of seizures, comparing them with 50 controls (69 ± 6.7 years). Patients underwent to a full-night video-PSG.ResultsSubclinical epileptiform activity was detected in 6.38% of ‘probable’ AD patients, 11.63% of MCI due to AD subjects and 4.54% of controls (p = 0.43). The comparisons between the three groups for the frequency of epileptiform activity did not reach statistically significant differences neither for total sleep nor for any sleep period considered.ConclusionsOur study shows that, when controlling for sleep stages and the influence of psychoactive drugs, AD patients and MCI due to AD subjects do not exhibit a higher frequency of epileptiform discharges during sleep compared to healthy subjects.SignificanceSubclinical epileptiform activity during sleep does not discriminate ‘probable’ AD from MCI due to AD and healthy controls.  相似文献   

11.
BackgroundA primary brain tumor (PBT) is often a fatal disease of the nervous system and has a serious impact on health-related quality of life (HRQOL). Presence of epilepsy and adverse reactions from tumor and epilepsy treatments may cause additional decline in HRQOL.ObjectivesWe aimed to study the impact of epileptic seizures on cognition, mood, and HRQOL in patients with brain tumor-related epilepsy.Materials and methodPatients were grouped on an ordinal scale according to epilepsy burden from none to severe based on the presence of epileptic seizures and seizure frequency: L1, no epilepsy; L2, with epilepsy, seizure-free in the last 6 months with antiepileptic drugs; and L3, with epilepsy, at least one seizure in the last 6 months with AEDs. Health-related quality of life was measured by Functional Assessment of Cancer Therapy—Brain (FACT-Br) and Quality of Life in Epilepsy—31 (QOLIE-31) tools, cognition by the Montreal Cognitive Assessment (MoCA) tool and Frontal Assessment Battery (FAB), mood by the Hospital Anxiety and Depression Scale (HADS), activities of daily living (ADLs) by the Barthel Index (BI), and performance status by the Karnofsky Performance Status (KPS) scale in patients with primary brain tumors at least one month following neurosurgery with or without radiotherapy and chemotherapy.ResultsEighty-one patients with a diagnosis of primary brain tumors were recruited. Sixty-eight percent of patients were diagnosed with primary brain tumor-related epilepsy, 50.61% patients had cognitive impairment, 33% had abnormal scores in the anxiety scale, and 34% had abnormal scores in the depression scale. There were no statistically significant differences in these scores among L1, L2, and L3 groups.There were statistically significant differences in duration of disease and KPS and BI scores between L1 and L3 groups. The L3 group has significantly longer duration of disease and scored low in both the BI and KPS scale when compared to the L1 group.All patients with primary brain tumors scored significantly low in FACT-Br ‘physical well-being’ (PWB) and ‘emotional well-being’ (EWB) and high in ‘social well-being’ (SWB) when compared to healthy controls. When scores of each group were individually compared to healthy controls, the L3 group showed the lowest scores in PWB, EWB, and ‘functional well-being’. In SWB, L1 and L2 groups showed statistically significantly high scores when compared to normative data.The QOLIE-31 applied to groups with epilepsy showed statistically significantly lower scores in the L3 group when compared to the L2 group in ‘cognitive’ and ‘social functioning’ domains.On multivariate analysis, both poor performance status and frequency of seizures were found to be independent risk factors for poor HRQOL when FACT-Br mean scores were compared. Level of seizures was found to be an independent risk factor for poor HRQOL when QOLIE-31 scores were compared between L2 and L3 groups.DiscussionPresence of brain tumors could be attributed to cognitive impairment irrespective of the presence of epilepsy in our cohort. High seizure burden is an independent risk factor for poor HRQOL in patients with primary brain tumors. The QOLIE-31 is a more sensitive tool than the FACT-Br because of the presence of a seizure-related questionnaire.  相似文献   

12.
Abstract

Objectives: The objective of this study was to determine whether a breakdown in proteins regulating cortical iron homeostasis could be involved in the pathophysiology of mood disorders.

Methods: Levels of select proteins responsible for cortical iron transport were quantitated by Western blotting of Brodmann’s (BA) areas 6 and 10 from patients with major depressive disorder (n?=?13), bipolar disorder (n?=?12) and age/sex matched controls (n?=?13).

Results: We found the inactive form of ceruloplasmin was lower in BA 6 from males compared to females. Levels of copper containing ceruloplasmin was lower in BA 6 from suicide completers whilst levels of amyloid precursor protein, TAU and transferrin were higher in BA 10 from those individuals. The level of prion protein was lower in BA 6 from subjects with major depressive disorder.

Conclusions: Our data suggests that perturbation in cortical iron transport proteins is not prevalent in mood disorders. By contrast, our data suggests changes in iron transport proteins in BA 6 and BA 10 are present after suicide completion. If these changes were present before death, they could have had a role in the genesis of the contemplation and completion of suicide.  相似文献   

13.
ABSTRACT

Background: Alzheimer’s disease (AD) can involve changes in communication and can lead to mutism in severe cases. Oral communication may be impaired by phonetic-motor disorders, such as apraxia of speech (AOS), or by language disorders, such as aphasia. Therefore, the identification of manifestations of AOS and phonemic paraphasias in patients with AD is critical to understanding the communication changes and determining the therapeutic planning.

Aims: To identify the distribution of phonetic–phonological manifestations in older patients with AD and healthy older subjects and assess whether these manifestations indicate the origin of the changes, including a predominantly phonetic-motor origin, a predominantly phonological–linguistic origin, or both.

Methods & Procedures: This cross-sectional study evaluated 90 patients with AD and 30 healthy older volunteers. All of the participants underwent the same repetition task for phonetic and phonological assessments using the current classification of phonetic–phonological manifestations; this classification distinguishes characteristics that are mostly related to AOS from other signs that are mostly related to aphasia. Negative binomial regression analysis was conducted to compare the amount of each manifestation presented by the two groups.

Outcomes & Results: The patients with AD showed significantly more signs of aphasia (self-correction, and vowel and consonant substitutions), AOS (prolonged intervals and extended vowel duration), and AOS or aphasia (distortion, omission, attempts at the syllable level, distorted substitutions, and additions) than the healthy older volunteers.

Conclusions: Older adults with AD presented phonetic and phonological changes of aphasia and AOS and, consequently, limitations in symbolic–linguistic planning and motor planning.  相似文献   

14.
目的利用基于体素的形态学分析(VBM)研究原发性帕金森病患者嗅觉相关脑区结构改变及其与嗅觉障碍之间的关系,探讨其作为早期诊断的可能性。方法应用"五味嗅觉测试液"对26例诊断明确的早期原发性帕金森病患者进行嗅觉功能检测,并与年龄、病程和病情严重程度[帕金森病统一评价量表(UPDRS)]进行相关分析。磁化准备快速梯度回波序列获取三维结构图像,SPM5软件后处理,通过配准、分割获得白质密度图像,经调试获得白质体积图像。结果帕金森病组患者嗅觉察觉阈值和嗅觉识别阈值分别为0.66±0.84和2.41±0.74,显著高于对照组的-0.64±0.83和1.08±0.54(Z=4.455,P=0.000;t=4.898,P=0.000)。帕金森病组患者嗅觉功能与年龄(察觉阈值:r_s=0.199,P=0.330;识别阈值:r_s=0.256,P=0.207)、病程(察觉阈值:r_s=0.123,P=0.550;识别阈值:r_s=0.055,P=0.789)及UPDRSⅢ评分(察觉阈值:r_s=0.229,P=0.260;识别阈值:r_s=0.379,P=0.056)无明显相关性;UPDRS总评分与嗅觉察觉阈值无相关性(r_s=0.314,P=0.118),但与嗅觉识别阈值呈正相关(r_s=0.397,P=0.045)。与对照组相比,原发性帕金森病组患者右侧枕叶(BA17~19区)、左侧扣带回后部(BA23,30,31区)、左侧枕叶(BA18,19区)和左侧中央旁小叶(BA3~5区)白质密度,以及双侧枕叶(BA17~19区)、左侧扣带回后部(BA23,30,31区)和左侧中央旁小叶(BA3~5区)白质体积均增加,且左侧扣带回后部白质密度增加与嗅觉识别阈值呈负相关(r_s=0.496,P=0.010)。结论原发性帕金森病患者嗅觉功能明显减退,但与年龄及病程均无相关性。有嗅觉减退的早期帕金森病患者其嗅觉相关脑区,尤其是神经纤维通过的白质脑区存在明显的病理变化,可能提示帕金森病患者嗅觉障碍是中枢神经变性的结果。与此同时,VBM法作为一种客观分析方法,弥补了兴趣区分析法的缺点,可以广泛用于帕金森病或神经变性疾病的诊断分析。  相似文献   

15.
16.
《Clinical neurophysiology》2010,121(9):1410-1419
ObjectiveAsperger syndrome, belonging to the autistic spectrum of disorders, involves deficits in social interaction and prosodic use of language but normal development of formal language abilities. Auditory processing involves both hyper- and hypoactive reactivity to acoustic changes.MethodsResponses composed of mismatch negativity (MMN) and obligatory components were recorded for five types of deviations in syllables (vowel, vowel duration, consonant, syllable frequency, syllable intensity) with the multi-feature paradigm from 8–12-year old children with Asperger syndrome.ResultsChildren with Asperger syndrome had larger MMNs for intensity and smaller MMNs for frequency changes than typically developing children, whereas no MMN group differences were found for the other deviant stimuli. Furthermore, children with Asperger syndrome performed more poorly than controls in Comprehension of Instructions subtest of a language test battery.ConclusionsCortical speech-sound discrimination is aberrant in children with Asperger syndrome. This is evident both as hypersensitive and depressed neural reactions to speech-sound changes, and is associated with features (frequency, intensity) which are relevant for prosodic processing.SignificanceThe multi-feature MMN paradigm, which includes variation and thereby resembles natural speech hearing circumstances, suggests abnormal pattern of speech discrimination in Asperger syndrome, including both hypo- and hypersensitive responses for speech features.  相似文献   

17.
ABSTRACT

The goal of this study was to investigate the phonetic realisation of the voicing feature in two tumour resection-related Spanish speakers with apraxia of speech. Temporal parameters related to the phonological contrast of voicing in Spanish have been analysed for intervocalic voiced and voiceless obstruents embedded in isolated words and nonwords, and compared with data collected from healthy speakers. Results indicate that in devoiced productions, where VOT values fitted the ‘voiceless stops’ category, vowel duration values matched those of voiced stops and suggested the preservation of contextual voicing cues. An attempt at preserving a consonant/vowel duration ratio consistent with aerodynamic predictions for voicing contrast has been observed in apraxic correct production as well as in devoicing errors, but not in the control group, which could be interpreted as a compensatory mechanism.  相似文献   

18.
ObjectiveTo examine pre-attentive acoustic change detection in schizophrenia patients with and without auditory hallucinations via mismatch negativity (MMN) extracted from a multi-feature paradigm.MethodsThis study examined the electroencephalograph (EEG)-derived MMN, recorded across 32 sites, in 12 hallucinating patients (HPs) with schizophrenia, 12 non-hallucinating patients (NPs) with schizophrenia and 12 healthy controls (HCs). MMN was recorded in response to a multi-feature MMN paradigm [Näätänen, R., et al., 2004. The mismatch negativity (MMN): towards the optimal paradigm. Clin. Neurophys. 115, 140–144] which employs frequency, duration, intensity, location and gap deviants. Differences in source localization were probed using standardized low resolution brain electromagnetic tomography (sLORETA).ResultsHPs showed significantly smaller MMNs to duration deviants compared to HCs and NPs, as well as smaller MMNs to intensity deviants compared to HCs. Regionalized differences between HCs and each of the patient groups were observed in response to frequency deviants. There were no significant group effects for location or gap deviants, or for MMN latency. Source localization using sLORETA showed no significant differences in MMN generator location across groups for any of the deviant stimuli.ConclusionsThe often-reported robust MMN deficit to duration deviants may be specific to schizophrenia patients afflicted with auditory hallucinations. Furthermore, by using symptom-specific groups, novel deficits of pre-attentive auditory processing, such as that observed to intensity deviants in HPs, may be revealed.SignificanceThe differential responding observed between both groups of patients with schizophrenia has implications for automatic processing within the auditory cortex of hallucinating patients and suggests that care must be taken when recruiting participants in studies involving schizophrenia to ensure consistent, replicable results.  相似文献   

19.
《Clinical neurophysiology》2020,131(9):2140-2147
ObjectiveSpeech deficits are common in Parkinson’s disease, and behavioural findings suggest that the deficits may be due to impaired monitoring of self-produced speech. The neural mechanisms of speech deficits are not well understood. We examined a well-documented electrophysiological correlate of speech self-monitoring in patients with Parkinson’s disease and control participants.MethodsWe measured evoked electroencephalographic responses to self-produced and passively heard sounds (/a/ phonemes) in age-matched controls (N = 18), and Parkinson’s disease patients who had minor speech impairment, but reported subjectively experiencing no speech deficits (N = 17).ResultsDuring speaking, auditory evoked activity 100 ms after phonation (N1 wave) was less suppressed in Parkinson’s disease than controls when compared to the activity evoked by passively heard phonemes. This difference between the groups was driven by increased amplitudes to self-produced phonemes, and reduced amplitudes passively heard phonemes in Parkinson’s disease.ConclusionsThe finding indicates that auditory evoked activity is abnormally modulated during speech in Parkinson’s patients who do not subjectively notice speech impairment. This mechanism could play a role in producing speech deficits in as the disease progresses.SignificanceOur study is the first to show abnormal early auditory electrophysiological correlates of monitoring speech in Parkinson’s disease patients.  相似文献   

20.
IntroductionPatients with Parkinson's disease (PD) are often confronted with difficult medical decisions, which might be hampered by cognitive impairment or chronic stress. Little is known, however, about the capacity to make medical decisions and the influence of cognition and stress on this ability. This study determined whether non-demented Parkinson's disease patients are able to make medical decisions and whether this capacity is influenced by cognition and stress.MethodsForty-six Parkinson's disease patients and 94 healthy controls were assessed with the MacArthur Competence Assessment Tool for Treatment during which participants were presented with deep brain stimulation as a treatment option for a fictional Parkinson's disease patient. Furthermore, all participants were examined with a stress questionnaire and a neuropsychological test battery.ResultsParkinson's disease patients performed better on the total scale and ‘Understanding’ subscale of the MacArthur Competence Assessment Tool for Treatment than healthy controls. Lower performance on the Concept Shifting Test in the Parkinson's disease group and lower performance on Letter Digit Substitution Test in the healthy control group predicted lower medical decision-making capacity. No association was found between stress and medical decision-making.ConclusionNon-demented Parkinson's disease patients show no impairments in medical decision-making compared to healthy controls. In fact, Parkinson's disease patients have a better understanding of their disease and the benefits and risks of treatment options than healthy controls. Psychomotor speed and attention were negatively associated with medical decision-making in both groups. This implies that when these cognitive functions decline, the capacity to make medical decisions also declines.  相似文献   

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