脑卒中后疲劳的研究进展

本文就脑卒中后疲劳的概念、发病率、诊断、危险因素、发生机制及治疗等方面的研究进展进行综述。脑卒中后疲劳是卒中恢复期独立于抑郁的常见症状,影响患者的康复与生存质量。脑卒中后疲劳的发生机制尚未明确,可能与社会心理及生物学因素均有关。生物学机制包括了梗塞部位或脑部基础病变累及特定的皮层-皮层下环路,以及免疫、神经内分泌及神经递质异常等。目前尚无肯定的有效治疗方法。     

Pathological correlates of poststroke depression in elderly patients.

OBJECTIVE: The authors examined the relationship between poststroke depression and location of stroke. METHODS: They performed a clinicopathological analysis of 95 consecutively autopsied elderly initial-stroke survivors. RESULTS: The severity of brain vessel arteriosclerosis and frequency of brain vascular lesions were not significantly different between 21 cases with poststroke depression and 74 cases without. Earlier death was the only variable significantly associated with poststroke depression. No lesion pattern characterized the depression group. CONCLUSIONS: Neuropathological data confirm that depression is associated with worse prognosis in elderly stroke patients and lend support to the hypothesis that psychological rather than neurological factors are the main determinants of poststroke depression.     

卒中后疲劳的药物治疗与康复研究进展

卒中后疲劳是卒中恢复期的常见症状,显著影响患者的康复及远期预后.本文就卒中后疲劳的药物治疗与康复研究进展进行综述.在进行药物与康复治疗之前,应全面识别引起疲劳的可能原因,包括精神心理、躯体疾患及药物的潜在因素.迄今尚未有药物被证实对卒中后疲劳确切有效.认知及分级活动训练是目前唯一经过随机对照试验证实有效的治疗手段.     

The psychological correlates of fatigue in Parkinson's disease: Contribution of maladaptive metacognitive beliefs

IntroductionPsychological factors can underlie fatigue in neurological disorders, but its relationship to fatigue in Parkinson's disease (PD) has not been explored. We assessed the association between maladaptive metacognitive beliefs and presence of fatigue in PD.MethodsNinety-eight consecutive outpatients with PD (61% male; median age: 66.50 years) were assessed in terms of demographic, clinical, medication treatment, cognitive, or behavioural characteristics including metacognitive beliefs (Metacognitions Questionnaire-30 or MCQ). Fatigue was ascertained by PD-related diagnostic criteria. Univariate statistical approach (Mann-Whitney and Pearson chi-square tests) was used to compare PD patients with (f-PD) or without (nf-PD) fatigue in terms of demographic, clinical, medication treatment, cognitive, behavioural, and metacognitive measures.ResultsTwenty-one PD patients (21%) displayed fatigue. The f-PD group scored higher on the MCQ-total score, MCQ-Cognitive Confidence subscale, and all behavioral measures (p_s < 0.01) relative to nf-PD. They also had a more advanced Hoehn and Yahr stage and Unified Parkinson's Disease Rating Scale-III score.ConclusionMaladaptive metacognitive beliefs such as the lack of cognitive confidence may play a key role to trigger and maintain fatigue in PD. Future studies, using a multivariate statistical approach, are needed to confirm these preliminary findings in a larger sample of patients with fatigue and to assess if modification of such metacognitive beliefs has the potential to ameliorate fatigue in PD.     

Risk factors for and correlates of poststroke depression following discontinuation of antidepressants

The authors randomly assigned nondepressed patients at least 3 months poststroke to receive nortriptyline, fluoxetine, or placebo for 3 months using double-blind methodology. Patients were followed at 3, 6, 9, and 21 months for new onset of depression. In patients treated with antidepressants, lesion volume and degree of social impairment were associated with subsequent late-onset of poststroke depression at 6 and 9 months. In the placebo group, severity of impairment in activities of daily living, at 3 and 9 months, was associated with late onset poststroke depression. Differences in the clinical/pathological correlates may reflect subtle differences in the pathophysiology of poststroke depression following prophylactic antidepressants.     

Self-mutilation in personality disorders: psychological and biological correlates.

OBJECTIVE: The goal of this study was to determine whether self-mutilators with personality disorders differ from nonmutilators with personality disorders in impulsivity, aggression, and other psychopathology and whether serotonergic dysfunction contributes to self-mutilation. METHOD: Twenty-six self-mutilators with personality disorders were matched to 26 control subjects with personality disorders for gender, age, education, axis I diagnosis of affective disorder, and axis II diagnosis of personality disorder. Numerous indexes of psychopathology as well as CSF 5-hydroxyindoleacetic acid (5-HIAA) levels and platelet imipramine binding sites (Bmax) and affinity (Kd) were determined. RESULTS: Self-mutilators had significantly more severe character pathology, had greater lifetime aggression, and were more antisocial than the control subjects. The self-mutilators scored higher on the Hamilton Rating Scale for Depression but not on the Beck Depression Inventory or the Beck Hopelessness Scale. The two groups did not differ on the Buss-Durkee Hostility and Guilt Inventory or on the Sensation Seeking Scale. The degree of self-mutilation was significantly correlated with impulsivity, chronic anger, and somatic anxiety. Both self-mutilation and impulsivity showed significant negative correlations with Bmax, although the two groups did not differ in CSF 5-HIAA levels or in platelet imipramine binding. CONCLUSIONS: The results demonstrate the contribution of severe character pathology, aggression, impulsivity, anxiety, and anger to self-mutilation and provide preliminary support for the hypothesis of underlying serotonergic dysfunction facilitating self-mutilation.     

Endocrine response patterns and psychological correlates

A group of young men volunteering for military service in the United States Navy were studied during an acute stress situation. The subjects (S's) (N = 62) were non-swimmers, and they all had to jump from a 5-foot platform into the deep end of a swimming pool. Before and after the exposure, blood and urine samples were taken for endocrine analysis. The Defense Mechanism Test (DMT), the Coping Operations Preference Enquiry (COPE), Joffe and Nanitch Scales for Defenses (J&N), and a Mood Questionnaire (MQ) were administered. For the endocrine reactions, postsamples, 3 factors emerged: a Cortisol factor, a Testosterone factor, and a Catecholamine factor. There was a significant correlation between the Cortisol factor and defense mechanisms, evaluated both by the DMT and the paper-and- pencil tests. Furthermore, there was a significant relationship between high anxiety, and defense mechanisms on the one hand, and physiological responses on the other.     

Clinical neurophysiology of fatigue.

Fatigue is a multidimensional concept covering both physiological and psychological aspects. Chronic fatigue is a typical symptom of diseases such as cancer, multiple sclerosis (MS), Parkinson's disease (PD) and cerebrovascular disorders but is also presented by people in whom no defined somatic disease has been established. If certain criteria are met, chronic fatigue syndrome can be diagnosed. The 4-item Abbreviated Fatigue Questionnaire allows the extent of the experienced fatigue to be assessed with a high degree of reliability and validity. Physiological fatigue has been well defined and originates in both the peripheral and central nervous system. The condition can be assessed by combining force and surface-EMG measurements (including frequency analyses and muscle-fibre conduction estimations), twitch interpolation, magnetic stimulation of the motor cortex and analysis of changes in the readiness potential. Fatigue is a well-known phenomenon in both central and peripheral neurological disorders. Examples of the former conditions are multiple sclerosis, Parkinson's disease and stroke. Although it seems to be a universal symptom of many brain disorders, the unique characteristics of the concomitant fatigue also point to a specific relationship with several of these syndromes. As regards neuromuscular disorders, fatigue has been reported in patients with post-polio syndrome, myasthenia gravis, Guillain-Barré syndrome, facioscapulohumeral dystrophy, myotonic dystrophy and hereditary motor and sensory neuropathy type-I. More than 60% of all neuromuscular patients suffer from severe fatigue, a prevalence resembling that of patients with MS. Except for several rare myopathies with specific metabolic derangements leading to exercise-induced muscle fatigue, most studies have not identified a prominent peripheral cause for the fatigue in this population. In contrast, the central activation of the diseased neuromuscular system is generally found to be suboptimal. The reliability of the psychological and clinical neurophysiological assessment techniques available today allows a multidisciplinary approach to fatigue in neurological patients, which may contribute to the elucidation of the pathophysiological mechanisms of chronic fatigue, with the ultimate goal to develop tailored treatments for fatigue in neurological patients. The present report discusses the different manifestations of fatigue and the available tools to assess peripheral and central fatigue.     

Clinicopathological correlates of behavioral and psychological symptoms of dementia

Behavioral and psychological symptoms are commonly observed in a majority of demented patients at some time during the course of their illness. Many of these psychiatric manifestations, especially those related to mood, may be early expressions of dementia and/or mild cognitive impairment. The literature suggests that behavioral and psychological symptoms of dementia (BPSD) are an integral part of the disease process. The dissociation, in many cases, between BPSD and the rather linear decline in cognitive functions suggests that independent pathophysiological mechanisms give rise to these symptoms. A review of the neuroimaging and neuropathology literature indicates that BPSD are the expression of regional rather than diffuse brain pathology. Psychotic symptoms in demented patients usually demonstrate preferential involvement of the frontal lobe and/or limbic regions. Visual hallucinations differentiate themselves from other psychotic symptoms by their tendency to involve the occipital lobes. There is a significant association between apathy and structural changes of the anterior cingulate gyrus. White matter hyperintensities occur in a significant number of depressed patients; otherwise, there is lack of association between depression and either specific brain changes or affected regions. Strictly neuropathological explanations are likely to be insufficient to explain BPSD. Environmental changes, neurochemical abnormalities, past psychiatric history (including premorbid personality), social history (e.g., intellectual achievement and life-long learning), family history, and genetic susceptibility are factors, among others, that influence BPSD.     

Serum cytokine and glucose levels as predictors of poststroke fatigue in acute ischemic stroke patients

Fatigue is a common but often overlooked symptom after stroke. This study investigated whether stroke type, infarct volume, and laterality, as well as the levels of various cytokines and other blood components in the acute phase of acute ischemic stroke (AIS), can predict the level of fatigue at 6, 12, and 18 months after its onset. In 45 patients with acute stroke, serum levels of C-reactive protein, hemoglobin, glucose, and 13 cytokines were measured within 72 h of stroke onset. The cytokine measurements were performed using BioPlex XMap technology (Luminex). The acute serum levels of interleukin (IL)-1β and glucose were positively correlated with the score on the Fatigue Severity Scale (FSS) at 6 months after the stroke (r = 0.37, p = 0.015, and r = 0.37, p = 0.017, respectively). The acute serum levels of IL-ra and IL-9 were negatively correlated with FSS score at 12 months after the stroke (r = −0.38, p = 0.013, and r = −0.36, p = 0.019, respectively). The FSS score at 12 months after stroke was significantly lower in patients with radiologically confirmed infarction than in those without such confirmation (p = 0.048). The FSS score at 18 months was not correlated with any of the measured variables. High acute serum levels of glucose and IL-1β, and low IL1-ra and IL-9 may predict fatigue after AIS, indicating that the development of poststroke fatigue can be accounted for by the proinflammatory response associated with AIS. These novel findings support a new cytokine theory of fatigue after stroke. However, more research is needed to validate the results of this study.     

Biological and psychological correlates of self-reported and objective sleep measures

ObjectiveObjective and self-reported sleep are only moderately correlated and it is uncertain if these two types of sleep measures are associated with distinct biological and psychological outcomes.MethodsParticipants were 119 healthy women aged 26 years on average. Cortisol and blood pressure assessed over one day were the measures of biological function. Psychological variables included optimism, life satisfaction, positive and negative affect as well as emotional distress. Sleep was assessed with the Pittsburgh Quality Index (PSQI), wrist actigraphy and sleep diaries.ResultsGlobal sleep ratings on the PSQI were unrelated to objective sleep efficiency, duration or latency. Sleep duration derived from sleep diaries was highly correlated with objective duration but was unrelated to the PSQI measure. More disturbed sleep on the PSQI was associated with lower psychological wellbeing, as indicated by reduced levels of optimism, life satisfaction and positive affect as well as greater negative affect and emotional distress. Objective sleep efficiency was reduced among participants with lower positive and higher negative affect but there were no other associations between objective sleep indicators and psychological variables tested in our study. Participants with poorer self-reported sleep had lower cortisol awakening response while those with longer objective sleep latency had higher diastolic blood pressure, independently of covariates.ConclusionOur study reveals that self-reported and objective sleep measures, in particular those regarding sleep quality, are weakly associated but have different psychological and biological correlates. This suggests that findings relating self-reported sleep may not necessarily be corroborated by objective sleep indicators.     

Immunological and psychological dysfunction in patients receiving immunotherapy for chronic fatigue syndrome.

Associations between immunological and psychological dysfunction in 33 patients with Chronic Fatigue Syndrome (CFS) were examined before and in response to treatment in a double blind, placebo-controlled trial of high dose intravenous immunoglobulin. Only those patients who received active immunotherapy demonstrated a consistent pattern of correlations between improvement in depressive symptoms and markers of cell-mediated immunity (CMI). This finding lends some support to the hypothesis that depressive symptoms in patients with CFS occur secondary to, or share a common pathophysiology with, immunological dysfunction. This pattern and the lack of strong associations between depression and immunological disturbance prior to treatment are less supportive of the view that CFS is primarily a form of depressive disorder or that immunological dysfunction in patients with CFS is secondary to concurrent depression.