Gene/Protein Disease Symptom Drug Enzyme Compound
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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant preparations of the cytokine interferon (IFN)-alpha are increasingly used to treat a number of medical conditions, including chronic viral hepatitis and several malignancies. Although frequently effective, IFN alpha induces a variety of neuropsychiatric adverse effects, including an acute confusional state that develops rapidly after initiation of high-dose IFN alpha, a depressive syndrome that develops more slowly over weeks to months of treatment, and manic conditions most often characterised by extreme irritability and agitation, but also occasionally by euphoria. Acute IFN alpha-induced confusional states are typically characterised by disorientation, lethargy, somnolence, psychomotor retardation, difficulties with speaking and writing, parkinsonism and psychotic symptoms. Strategies for managing delirium should be employed, including treatment of contributing medical conditions, use of either typical or atypical antipsychotic agents and avoidance of medications likely to worsen mental status. Significant depressive symptoms occur in 21-58% of patients receiving IFN alpha, with symptoms typically manifesting over the first several months of treatment. The most replicated risk factor for developing depression is the presence of mood and anxiety symptoms prior to treatment. Other potential, but less frequently replicated, risk factors include a past history of major depression, being female and increasing IFN alpha dosage and treatment duration. The available data support two approaches to the pharmacological management of IFN alpha-induced depression: antidepressant pretreatment or symptomatic treatment once IFN alpha has been initiated. Pretreatment might be best reserved for patients already receiving antidepressants or for patients who endorse depression or anxiety symptoms of mild or greater severity prior to therapy. Several recent studies demonstrate that antidepressants effectively treat IFN alpha-induced depression once it has developed, allowing the vast majority of subjects to complete treatment successfully. Recent data suggest that IFN alpha-induced depression may be composed of two overlapping syndromes: a depression-specific syndrome characterised by mood, anxiety and cognitive complaints, and a neurovegetative syndrome characterised by fatigue, anorexia, pain and psychomotor slowing. Depression-specific symptoms are highly responsive to serotonergic antidepressants, whereas neurovegetative symptoms are significantly less responsive to these agents. These symptoms may be more effectively treated by agents that modulate catecholaminergic functioning, such as combined serotonin-noradrenaline (norepinephrine) antidepressants, bupropion, psychostimulants or modafinil. Additional factors to consider in selecting an antidepressant include potential drug-drug interactions and adverse effect profile. Finally, IFN alpha appears capable of inducing manic symptoms. Mania, especially when severe, is a clinical emergency. When this occurs, IFN alpha and antidepressants should be stopped, an emergency psychiatric consultation should be obtained, and treatment with a mood stabilizer should be initiated.
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PMID:Neuropsychiatric adverse effects of interferon-alpha: recognition and management. 1569 25

A retrospective chart review characterizing changes in 17 male and 10 female Parkinson's disease (PD) patients undergoing deep brain stimulation (DBS) surgery indicated that 6 mo before surgery, patients lost a mean of 5.1 lbs, whereas in the 6 mo after surgery, subjects gained a mean of 10.1 lbs; 22% gained more than 14 lbs. In 10 patients followed an additional 6 mo, weight gain continued. This weight gain may be associated with decreased energy expenditure due to subsidence of chronic tremor. The magnitude of gain underscores the need for proactive management of body weight in PD patients undergoing DBS.
Parkinsonism Relat Disord 2005 Jun
PMID:Weight and body mass index in Parkinson's disease patients after deep brain stimulation surgery. 1587 86

Fatigue is a common problem in Parkinson's disease (PD). The Parkinson's Fatigue Scale (PFS) designed for measurement of fatigue in PD has not been validated in the US. The objective of this study was to validate the PFS by comparing it to the Fatigue Severity Scale (FSS). Fifty PD patients and 16 controls completed PFS, FSS and semi-structured interview. FSS and PFS were strongly correlated with one another and had high internal consistency, indicating that both are reliable scales. PD patients and healthy controls differed significantly on both measures. PD patients endorsed significantly more fatigue. The PFS is a reliable, valid fatigue measure.
Parkinsonism Relat Disord 2007 Oct
PMID:A comparison of fatigue measures in Parkinson's disease. 1705 31

Neuropsychiatric problems are common in Parkinson's disease (PD) but there is little information regarding how they impact on quality of life. PD patients without dementia (49) were assessed for low mood/depression, fatigue, apathy, sleep problems and hallucinations. Measures of quality of life and motor function were also obtained. Over 77% of the patients reported symptoms consistent with one or more neuropsychiatric problems. Low mood/depression, anxiety and the presence of hallucinations predicted poorer quality of life after controlling for motor symptoms. Additional to the motor symptoms, we found that specific neuropsychiatric problems may impact on quality of life for PD patients.
Parkinsonism Relat Disord 2008
PMID:A profile of neuropsychiatric problems and their relationship to quality of life for Parkinson's disease patients without dementia. 1762 63

Parkinsonism is a clinical syndrome characterized by bradykinesia, hypo-/akinesia, muscular rigidity, and resting tremor, mainly caused by Parkinson's disease (PD). Symptoms of PD are due to a progressive loss of nigral neurons causing striatal dopaminergic denervation. However, nigral degeneration is only a part of the underlying synucleinopathy, and clinical symptoms go far beyond motor parkinsonism. Olfactory disturbances, fatigue, pain, autonomic dysfunction, sleep fragmentation, depression, and dementia with or without psychosis are frequently seen. The variability in the expression of these signs and symptoms, as discussed in this paper, might be explained by the specific topographical sequence of the pathology, depending on the extent and progression of the degenerative process at defined sites. Better insight in the clinicopathological correlations of this disease may help to further develop early diagnosis and adequate therapeutic strategies.
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PMID:Variability in the clinical expression of Parkinson's disease. 1785 36

Fatigue is an important contributor to poor quality of life. The aim of our research was to identify factors associated with fatigue among patients with Parkinson's disease (PD). The sample consisted of 150 patients. The Multidimensional Fatigue Inventory (MFI), Unified Parkinson's Disease Rating Scale (UPDRS), Hospital Anxiety and Depression Scale (HADS) and Charlson co-morbidity index were used for analysis. Demographic data were obtained in a structured interview. T-test, chi(2)-test and general linear regression were used. Fatigue was reported in 81% of the patients, with the worst scores in physical fatigue. Mood disorders and worse UPDRS scores were associated with fatigue.
Parkinsonism Relat Disord 2008
PMID:Clinical and psychosocial factors associated with fatigue in patients with Parkinson's disease. 1789 Jan 36

Gaucher disease is a recessively inherited lysosomal storage disorder, caused by deficiency of glucocerebrosidase activity. Affected individuals usually present with hepatosplenomegaly, anaemia, thrombocytopenia, and skeletal diseases. A wide range of neurological manifestations have also been recognized in Gaucher patients including acute neurological deterioration in infancy, mental retardation, ocular motor apraxia, seizure, and parkinsonism. Although muscle weakness is not an uncommon finding in patients with Gaucher disease, the aetiology of weakness is not well understood. We prospectively investigated seven Gaucher patients and found that four of them (patients 1-4) had mild to moderate degree of proximal-predominant symmetrical muscle weakness in four limbs. By history, three patients (patients 1-3) developed insidious onset of nonprogressive muscle weakness in four limbs with easy muscle fatigue from adolescence. A needle electromyographic study detected some small, brief polyphasic waves in these four patients. Muscle biopsy in one patient (patient 1) showed a few atrophic type II muscle fibres without infiltration of Gaucher cells. Three patients (patients 1-3) continuously received enzyme replacement therapy with imiglucerase and their muscle strength seemed improved after two years. We concluded that Gaucher disease may be associated with myopathy.
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PMID:Myopathy in Gaucher disease. 1819 73

Recent years have brought increased awareness of and attention to the non-motor aspects of Parkinson's disease. Non-motor features encompass a surprisingly broad clinical spectrum that includes sensory dysfunction, behavioral abnormalities, autonomic impairment, sleep disturbances, and fatigue. Some of these features, such as impaired olfaction, REM sleep behavior disorder, and constipation, may develop long before the classic motor features of Parkinson's disease make their appearance, while others emerge in concert with disease progression. The early emergence of some non-motor features presents diagnostic opportunities, while the dopa-unresponsiveness of others poses treatment challenges, especially in the advanced stages of the disease.
Parkinsonism Relat Disord 2007
PMID:Non-motor parkinsonism. 1826 38

We evaluated whether the self-reported reduction of physical activity associated with fatigue in Parkinson's disease (PD) could be quantified with a wrist-worn activity monitor in 69 non-depressed PD patients. A questionnaire was used to assess the presence of fatigue. Outcome measures reflected activity, immobility and sustained activity above preset thresholds. Thirty PD patients suffering from fatigue did not differ from 39 PD patients (with similar disease severity) who were not suffering from fatigue. These results emphasize the need to explore the role of the mental aspects of fatigue in PD.
Parkinsonism Relat Disord 1997 Jan
PMID:Fatigue in Parkinson's disease is not associated with reduced physical activity. 1859 Oct 55

Machado-Joseph disease or spinocerebellar ataxia 3 (MJD/SCA3) is a clinically heterogeneous, neurodegenerative disorder characterized by varying degrees of ataxia, ophthalmoplegia, peripheral neuropathy, pyramidal dysfunction and movement disorder. MJD/SCA3 is caused by a CAG repeat expansion mutation in the protein coding region of the ATXN3 gene located at chromosome 14q32.1. Current hypotheses regarding pathogenesis favor the view that mutated ataxin-3, with its polyglutamine expansion, is prone to adopt an abnormal conformation, engage in altered protein-protein interactions and aggregate. Expanded CAG repeat length correlates with the range and severity of the clinical manifestations and inversely correlates with age of disease onset. Though MJD/SCA3 is classically described as affecting the cerebellum, brainstem and basal ganglia, recent neuropathology and neuroimaging series demonstrate involvement of other areas such as the thalamus and cerebral cortex. Clinically, much emphasis has been placed in the description and recognition of the non-motor symptoms observed in these patients, such as pain, cramps, fatigue and depression. Currently, no disease modifying treatment exists for MJD/SCA3. Standard of care includes genetic counseling, exercise/physical therapy programs, and speech and swallow evaluation. Symptomatic treatment for clinical findings such as depression, sleep disorders, parkinsonism, dystonia, cramps, and pain is important to improve the quality of life for those with MJD/SCA3.
Parkinsonism Relat Disord 2010 Jan
PMID:Caring for Machado-Joseph disease: current understanding and how to help patients. 1981 45


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