Processing emotional tone from speech in Parkinson’s disease: A role for the basal ganglia

In this study, individuals with Parkinson's disease were tested as a model for basal ganglia dysfunction to infer how these structures contribute to the processing of emotional speech tone (emotional prosody). Nondemented individuals with and without Parkinson's disease (n = 21/group) completed neuropsychological tests and tasks that required them to process the meaning of emotional prosody in various ways (discrimination, identification, emotional feature rating). Individuals with basal ganglia disease exhibited abnormally reduced sensitivity to the emotional significance of prosody in a range of contexts, a deficit that could not be attributed to changes in mood, emotional-symbolic processing, or estimated frontal lobe cognitive resource limitations in most conditions. On the basis of these and broader findings in the literature, it is argued that the basal ganglia provide a critical mechanism for reinforcing the behavioral significance of prosodic patterns and other temporal representations derived from cue sequences (Lieberman, 2000), facilitating cortical elaboration of these events.     

Object alternation and orbitofrontal system dysfunction in Alzheimer's and Parkinson's disease

Previous performance on measures of frontal system function have suggested prominent orbitofrontal system damage in Alzheimer's disease, but not in Parkinson's dementia. Object alternation (OA), a task sensitive to orbitofrontal system dysfunction in non-human animals, was therefore administered to determine whether this measure would distinguish Alzheimer's from Parkinson's dementia. OA was significantly impaired in Alzheimer's disease compared to Parkinson's dementia, even though both groups were equated for severity of dementia. Although the patients with Parkinson's dementia also showed impairment on OA compared to normals, an error analysis revealed that the performance of the Alzheimer's patients, but not the Parkinson's patients, was characterized by abnormal response perseveration. The marked perseverative deficit in Alzheimer's disease may reflect orbitofrontal system dysfunction whereas the milder, and qualitatively different, deficits in Parkinson's disease may reflect dorsolateral frontal system involvement.     

Emotional processing following cortical and subcortical brain damage: contribution of the fronto-striatal circuitry

The present study examined the differential contribution of cortical and subcortical brain structures in emotional processing by comparing patients with focal cortical lesions (n = 32) to those with primarily subcortical dysregulation of the basal ganglia (Parkinson's disease n = 14). A standardized measure of emotional perception (Tübingen Affect Battery) was used. Only patients in the more advanced stages of Parkinson's disease and patients with focal damage to the (right) frontal lobe differed significantly from controls in both facial expression and affective prosody recognition. The findings imply involvement of the fronto-striatal circuitry in emotional processing.     

Impulse-control disorders in Parkinson's disease

Parkinson's disease is a neurodegenerative disorder characterized by bradykinesia, rigidity, postural instability, and resting tremor. Increasingly, Parkinson's disease has been associated with a broad spectrum of non-motor symptoms, such as olfactory loss, sleep disorders, autonomic dysfunction, cognitive impairment, psychosis, depression, anxiety, and apathy. In addition, a minority of Parkinson's disease patients develop compulsive behaviors while receiving dopamine-replacement therapy, including medication hoarding, pathological gambling, binge eating, hyperlibidinous behavior, compulsive shopping, and punding. These behaviors may result in psychosocial impairment for patients and therapeutic challenges for clinicians. This article reviews the anatomic substrates, behavioral spectrum, associated factors, and potential treatments for dopamine-replacement therapy-related compulsions in Parkinson's disease.     

What catatonia can tell us about "top-down modulation": a neuropsychiatric hypothesis

Differential diagnosis of motor symptoms, for example, akinesia, may be difficult in clinical neuropsychiatry. Symptoms may be either of neurologic origin, for example, Parkinson's disease, or of psychiatric origin, for example, catatonia, leading to a so-called "conflict of paradigms." Despite their different origins, symptoms may appear more or less clinically similar. Possibility of dissociation between origin and clinical appearance may reflect functional brain organisation in general, and cortical-cortical/subcortical relations in particular. It is therefore hypothesized that similarities and differences between Parkinson's disease and catatonia may be accounted for by distinct kinds of modulation between cortico-cortical and cortico-subcortical relations. Catatonia can be characterized by concurrent motor, emotional, and behavioural symptoms. The different symptoms may be accounted for by dysfunction in orbitofrontal-prefrontal/parietal cortical connectivity reflecting "horizontal modulation" of cortico-cortical relation. Furthermore, alteration in "top-down modulation" reflecting "vertical modulation" of caudate and other basal ganglia by GABA-ergic mediated orbitofrontal cortical deficits may account for motor symptoms in catatonia. Parkinson's disease, in contrast, can be characterized by predominant motor symptoms. Motor symptoms may be accounted for by altered "bottom-up modulation" between dopaminergic mediated deficits in striatum and premotor/motor cortex. Clinical similarities between Parkinson's disease and catatonia with respect to akinesia may be related with involvement of the basal ganglia in both disorders. Clinical differences with respect to emotional and behavioural symptoms may be related with involvement of different cortical areas, that is, orbitofrontal/parietal and premotor/motor cortex implying distinct kinds of modulation--"vertical" and "horizontal" modulation, respectively.     

Source memory in Parkinson's disease

Three experiments (ns = 14 per group) are reported which investigated the ability of Parkinson patients to remember the characteristics of conditions under which a memory was acquired. In Exp. 1, subjects were required to indicate for each item in a recognition memory test whether it was spoken by Experimenter 1 or by Experimenter 2 (external-external source memory). In Exp. 2, subjects had to indicate for each item whether it was generated by themselves or by the experimenter (internal-external source memory). In Exp. 3, subjects had to judge whether an item was generated by themselves in saying or in thinking (internal-internal source memory). We found that patients with Parkinson's disease were not impaired in the previous two kinds of source memory (Exp. 1 and 2) but were impaired in internal-internal source memory (Exp. 3) relative to the age-matched control groups. In addition, both groups' performance could be improved when given distinctive cues, i.e., perceptual cues in Exp. 1 and different-domain cues in Exp. 2. These results suggest that the availability of cues was critical for Parkinson's disease in source memory. Finally, the result of Exp. 2 also showed generation effects for patients with Parkinson's disease. The generation effect refers to better memory of information by people when they had to produce it, e.g., producing associates to a word, compared with memory of information given to them.     

Neurocognitive sequelae of pediatric sickle cell disease: a review of the literature.

This literature review summarizes all studies relating neuropsychological performance to neuroimaging findings in pediatric sickle cell disease (N=28; published 1991-2005). Although inconsistencies exist within and across domains, deficits in intelligence (IQ), attention and executive functions, memory, language, visuomotor abilities, and academic achievement have been identified. Overall neurocognitive compromise was revealed to be related to the level of neurological injury and the location of silent infarct. Attentional and executive dysfunction is prevalent and related to frontal lobe abnormalities.     

Alcohol: Effects on Neurobehavioral Functions and the Brain

Alcoholism results from an interplay between genetic and environmental factors, and is linked to brain defects and associated cognitive, emotional, and behavioral impairments. A confluence of findings from neuroimaging, physiological, neuropathological, and neuropsychological studies of alcoholics indicate that the frontal lobes, limbic system, and cerebellum are particularly vulnerable to damage and dysfunction. An integrative approach employing a variety of neuroscientific technologies is essential for recognizing the interconnectivity of the different functional systems affected by alcoholism. In that way, relevant experimental techniques can be applied to assist in determining the degree to which abstinence and treatment contribute to the reversal of atrophy and dysfunction.     

Neurocognitive Sequelae of Pediatric Sickle Cell Disease: A Review of the Literature

This literature review summarizes all studies relating neuropsychological performance to neuroimaging findings in pediatric sickle cell disease (N=28; published 1991–2005). Although inconsistencies exist within and across domains, deficits in intelligence (IQ), attention and executive functions, memory, language, visuomotor abilities, and academic achievement have been identified. Overall neurocognitive compromise was revealed to be related to the level of neurological injury and the location of silent infarct. Attentional and executive dysfunction is prevalent and related to frontal lobe abnormalities.     

Pragmatic communication skills in patients with Parkinson's disease

BACKGROUND: Pragmatic communication abilities may depend on intact frontal lobe systems. Independent evidence suggests that some persons with Parkinson's disease (PD) are impaired on measures of frontal lobe function. HYPOTHESIS: We therefore hypothesized in Study 1 that pragmatic communication skills would be impaired in some persons with PD and would be linked to frontal dysfunction in these patients. In Study 2 we hypothesized that PD patients would be unaware of their pragmatic communication deficits. METHODS: In Study 1 we administered tests of pragmatic abilities and frontal lobe functioning to twenty-two persons with Parkinson's disease (PD) and 10 healthy controls. In Study 2 we obtained self-ratings of pragmatic abilities from 11 PD patients and then checked these self-ratings against ratings of these same abilities by the patient's spouses. RESULTS: We found in Study 1 that patients with PD were: (a) significantly impaired on measures of pragmatic communication abilities, especially in the areas of conversational appropriateness, turn-taking, prosodics and proxemics, and that this impairment was significantly related to measures of frontal lobe function. In study 2 we found that PD patients overestimated their own abilities relative to spousal ratings of those abilities and thus were unaware of the extent of their problems with pragmatic social communication skills. CONCLUSION: We conclude that pragmatic social communication skills are impaired in PD and that this impairment may be related to frontal lobe dysfunction.     

Attention-deficit/hyperactivity disorder: perspectives from neuroimaging

Attention-deficit/hyperactivity disorder (ADHD) is a common childhood behavioral disorder most often characterized by inattentiveness, impulsivity, and hyperactivity. Current etiologic theories suggest that ADHD stems from abnormalities in dopaminergic and possibly noradrenergic brainstem nuclei that act to regulate a cortico-striato-thalamo-cortical network, believed to be critical for executive functions and the regulation of behavioral responses such as arousal, attention, and inhibition. Noninvasive structural and functional neuroimaging techniques provide a new avenue for exploring the validity of these theories. Despite their limitations, neuroimaging studies have provided a unique and otherwise inaccessible, biological perspective of ADHD. Collectively, the studies reviewed here reveal that dysfunction in arousal, behavioral inhibition, and attention associated with ADHD may result from structural abnormalities in frontostriatal regions that in turn result in diminished activity essential for normal function.     

Analysis of probabilistic classification learning in patients with Parkinson's disease before and after pallidotomy surgery

This study examined the characteristics of probabilistic classification learning, a form of implicit learning previously shown to be impaired in patients with basal ganglia dysfunction (e.g., Parkinson's disease). In this task, subjects learn to predict the weather using associations that are formed gradually across many trials, because of the probabilistic nature of the cue-outcome relationships. Patients with Parkinson's disease, both before and after pallidotomy, and age-matched control subjects, exhibited evidence of probabilistic classification learning across 100 training trials. However, pallidotomy appears to hinder the learning of associations most implicit in nature (i.e., weakly associated cues). Although subjects were most sensitive to single-cue associations when learning the task, there is evidence that cue combinations contribute significantly to probability learning. The utility of multiple dependent measures is discussed.     

Patterns of adaptation to Parkinson's disease

Forty-four 50- to 80-year-old Parkinson patients were interviewed about the effects of the disease on their lives. The Q-sort technique was used to analyze the interview data. In addition, the Symptom Checklist 90, the Mini-Mental State, and physician ratings of disease severity were obtained. Four clusters of patients were identified. Cluster I patients were sanguine and engaged; Cluster III patients were depressed and apprehensive about the future; Cluster III patients felt depressed, ashamed, and misunderstood; and Cluster IV patients were passive and resigned. Disease severity, but not demographic or other health variables, discriminated the groups. Patients with a mild to moderate impairment who adjusted effectively to their illness (Cluster I) were distinguished by an ability to put negative thoughts out of mind, by their belief that there are worse fates than having Parkinson's disease, and by efforts to influence certain aspects of their illness. The particular patterns of adaptation of the patients who were depressed and misunderstood (Cluster III) and passive and resigned (Cluster IV) seemed primarily a function of physical condition. This suggest that the degree to which personal attitudes can influence adaptation to somatic disease is limited by specific realities of the disease.     

Depersonalization disorder: a functional neuroanatomical perspective

Clinical reports of depersonalization suggest that attenuated emotional experience is a central feature of the condition. Patients typically complain of emotional numbness and some patients ascribe their feelings of unreality to a lack of affective "colouring" in things perceived. Recent neuroimaging and psychophysiological studies support these assumptions as they show both attenuated autonomic responses in depersonalization, and decreased activity within neural regions important for the generation of affective responses to emotive stimuli. Furthermore, findings from neuroimaging studies indicate increased prefrontal cortical activity in depersonalised patients, particularly within regions associated with contextualization and appraisal of emotionally-salient information rather than mood induction per se. Taken together, these finding suggest that symptoms of depersonalization, and in particular emotional numbing, may be related to a reversal of normal patterns of autonomic and neural response to emotive stimuli.     

Probing emotion in the developing brain: functional neuroimaging in the assessment of the neural substrates of emotion in normal and disordered children and adolescents

Virtually all developmental neuropsychiatric disorders involve some dysfunction or dysregulation of emotion. Moreover, many psychiatric disorders with adult onset have early subclinical manifestations in children. This essay selectively reviews the literature on the neuroimaging of affect and disorders of affect in children. Some critical definitional and conceptual issues are first addressed, including the distinctions between the perception and production of emotion and between emotional states and traits. Developmental changes in morphometric measures of brain structure are then discussed and the implications of such findings for studies of functional brain activity are considered. Data on functional neuroimaging and childhood depression are then reviewed. While the extant data in this area are meager, they are consistent with studies in adults that have observed decreased left-sided anterolateral prefrontal cortex activation in depression. Studies in children on the recognition of emotion and affective intent in faces using functional magnetic resonance imaging are then reviewed. These findings indicate that the amygdala plays an important role in such affective face processing in children, similar to the patterns of activation observed in adults. Moreover, one study has reported abnormalities in amygdala activation during a task requiring the judgment of affective intent from the eye region of the face in subjects with autism. Some of the methodological complexities of developmental research in this area are discussed, and directions for future research are suggested.     

Impaired perception of vocal emotions in Parkinson's disease: influence of speech time processing and executive functioning

Little is known about the underlying dimensions of impaired recognition of emotional prosody that is frequently observed in patients with Parkinson's disease (PD). Because patients with PD also suffer from working memory deficits and impaired time perception, the present study examined the contribution of (a) working memory (frontal executive functioning) and (b) processing of the acoustic parameter speech rate to the perception of emotional prosody in PD. Two acoustic parameters known to be important for emotional classifications (speech duration and pitch variability) were systematically varied in prosodic utterances. Twenty patients with PD and 16 healthy controls (matched for age, sex, and IQ) participated in the study. The findings imply that (1) working memory dysfunctions and perception of emotional prosody are not independent in PD, (2) PD and healthy control subjects perceived vocal emotions categorically along two acoustic manipulation continua, and (3) patients with PD show impairments in processing of speech rate information.     

O rem 自护理论消除帕金森退化反应的应用前景

由于帕金森的发病率逐年上升,并对患者生理、心理、社会等方面造成影响,本文对国内外O rem自护理论消除退化反应的相关文献以及在帕金森疾病中的应用前景进行报道。使用检索电子数据库以及查阅期刊文献。结果发现随着疾病的进展,帕金森会诱发机体一系列的退化反应,这严重影响了患者的生理、心理以及生活质量。大量文献报道了O rem自护理论在消除高血压、糖尿病等慢性疾病退化反应中的应用,但很少文献提及O rem自护理论在消除帕金森退化反应中的应用。笔者认为O rem自护理论有望在消除帕金森退化反应中应用。     

Brain network dysfunction in bipolar disorder

Bipolar disorder is a common psychiatric condition with significant associated morbidity and mortality. Despite its significance, the neurophysiology and neuropathology of this illness is incompletely understood. Recent advances in neuroimaging techniques have helped to begin clarifying these areas. Specifically, bipolar disorder appears to arise from abnormalities within discrete brain networks (eg, the anterior limbic network). The expression of the symptoms of bipolar disorder does not appear to result from single, localized brain lesions, but rather are emergent properties of dysfunction of these brain networks. As neuroimaging techniques continue to improve, the underlying neural basis of bipolar disorder will be clarified.     

过度担忧和广泛性焦虑障碍与rCBF关系的SPECT脑显像研究

目的：探查过度担忧者和GAD病人的r CBF变化,更好地了解导致病理性焦虑和GAD的神经病理生理学基础。方法：回顾性分析18例过度担忧者和61例GAD病人SPECT脑显像的结果。GAD患者再按病程分为3个亚组。计算各组患者特定脑区r CBF损伤的百分比及损伤的脑区数。结果：12例（66.7%）过度担忧者可见前额叶、基底节、扣带回、颞叶和枕叶r CBF增加（11例）和/或减少（9例）。58例（95.1%）GAD患者可见r CBF减少,主要累及中和下前额叶、中和下颞叶、前扣带、海马旁回、基底节和丘脑。大多数GAD患者累及的主要脑区等于或大于3个。GAD病人的r CBF损伤和病程之间存在一定的相关性。结论：结果支持GAD患者r CBF的变化是一个与担忧和焦虑等心理和情绪改变密切相关的慢性和渐进的过程。GAD的局部脑功能障碍是病理性焦虑产生的先决条件,并出现在局部脑结构异常之前。