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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seasonal affective disorder (SAD) is characterized by annual major depressive episodes. It occurs most commonly in young women during autumn and winter with full remission during the following spring. The patient's mood is a combination of depression and anxiety accompanied by fatigue, loss of libido, and a reduction of socialization. Most of these patients complain of atypical vegetative symptoms (e.g. hypersomnia, carbohydrate craving, and weight gain). Hypotheses on the underlying mechanisms of these behavioural disorders indicate that environmental variables, e.g. climate, latitude, light, and changes in neurotransmitter function that occur naturally with the seasons, may be important. Phototherapy is being used increasingly for the treatment of SAD. The antidepressant response is contingent on the exposure of the patients' eyes to light. The biological basis of the diverse psychological and biological changes in SAD and the underlying mechanism of action of phototherapy are still unclear and require further study.
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PMID:[Seasonal depression]. 992 Oct 42

Antiepileptic drugs (AEDs) have various mechanisms of actions and therefore have diverse anticonvulsant, psychiatric, and adverse effect profiles. Two global categories of AEDs are identified on the basis of their predominant psychotropic profiles. One group has "sedating" effects in association with fatigue, cognitive slowing, and weight gain, as well as possible anxiolytic and antimanic effects. These actions may be related to a predominance of potentiation of gamma-aminobutyric acid (GABA) inhibitory neurotransmission induced by drugs such as barbiturates, benzodiazepines, valproate, gabapentin, tiagabine, and vigabatrin. The other group is associated with predominant attenuation of glutamate excitatory neurotransmission and has "activating" effects, with activation, weight loss, and possibly anxiogenic and antidepressant effects. This group includes agents such as felbamate and lamotrigine. Agents such as topiramate, with both GABAergic and antiglutamatergic actions, may have "mixed" profiles. Mechanisms of actions, activity in animal models of anxiety and depression, and clinical psychotropic effects of AEDs in psychiatric and epilepsy patients are reviewed in relationship to this proposed categorization. These considerations suggest the testable hypothesis that better psychiatric outcomes in seizure disorder patients could be achieved by treating patients with baseline "activated" profiles (insomnia, agitation, anxiety, racing thoughts, weight loss) with "sedating" predominantly GABAergic drugs, and conversely those with baseline "sedated" or anergic profiles (hypersomnia, fatigue, apathy, depression, sluggish cognition, weight gain) with "activating" predominantly antiglutamatergic agents. Systematic clinical investigation of more precise relationships of discrete mechanisms of actions to psychotropic profiles of AEDs is needed to assess the utility of this general proposition and define exceptions to this broad principle.
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PMID:Positive and negative psychiatric effects of antiepileptic drugs in patients with seizure disorders. 1049 35

The authors present the case of a patient treated in the Department of Infectious Diseases at CMUJ in Cracow. The patient's full clinical picture suggested the possibility of the development of neuroborreliosis and disguised the symptoms of a developing intracranial tumor. Neuroborreliosis was suspected due to epidemiologic history (a tick bite, erythema migrans), general symptoms (fatigue, hypersomnia, apathy, dysmnesia, concentration disorders) and neurological symptoms, seropositive tests for Borrelia burgdorferi in serum and cerebrospinal fluid (IgG), increased protein concentration in cerebrospinal fluid. Owing to the fact that the serologic criteria of neuroborreliosis were not fulfilled, and other symptoms (loss of consciousness) appeared, CT was done. The CT showed the presence of a tumor in the longitudinal fissure of the brain, which, after intraoperative and histopathological examination, was defined as meningioma.
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PMID:[The coexistence of an intracranial tumor and a positive epidemiologic history of Lyme borreliosis as the reason for diagnostic problems--case report]. 1069 87

Wilson's disease (WD) shows a wide heterogeneity in symptoms. In this case report we present hypersomnia as a symptom of WD. The male patient's complaints as fatigue, decreased level of concentration, and highly increased demand of sleeping started at his age of 21 years. No abnormality was found at physical examination. A moderate elevation in liver function tests was found, but all the other laboratory findings were within the normal range. The marked hypersomnia was verified by 24-h cassette EEG polisomnographic monitoring. No abnormality was found at physical examination. EEG, brain CT and MRI were normal. Neither toxic nor infectious disease was detectable. The diagnosis of WD was based on decreased coeruloplasmin level, increased baseline and forced urinary excretion of copper, and decreased level of serum copper. Kayser-Fleischer ring was not detectable. D-penicillamine (DPA) was introduced. At 8-10 months after the initiation of the therapy the patient's complaints gradually resolved. The control sleep record 14 months after the initiation of the DPA therapy was normal. Five years later the patient is currently on penicillamine treatment and he is free of any symptom.
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PMID:Hypersomnia in Wilson's disease: an unusual symptom in an unusual case. 1077 May 29

Hypersomnia (excessive sleepiness) refers to an increased sleep propensity with a subjective craving for sleep, involuntary naps and "sleep attacks" during the day and/or prolonged nighttime sleep with sleep drunkeness. Excessive sleepiness should be separated from fatigue and lack of energy associated with a variety of medical and psychiatric diseases. Hypersomnia is reported by 2-5% of the adult population and can lead to poor work, accidents and neuropsychiatric disturbances. Sleep apnea syndrome (SAS), narcolepsy, chronic sleep deprivation (insufficiency), and restless legs/periodic limb movements in sleep syndrome (RLS/PLMS) represent the most common causes of hypersomnia. The diagnosis of these conditions can often be suspected on clinical grounds. However, an overnight polysomnography and a multiple sleep latency test are often additionally required for definite diagnosis. Treatment options include nasal CPAP for SAS, stimulants for narcolepsy, sleep prolongation for sleep insufficiency, and dopaminergic agents for RLS/PLMS.
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PMID:[Hypersomnia--etiology, clinic, diagnosis and therapy of excessive sleepiness]. 1095 47

The obstructive sleep apnea syndrome is a highly prevalent and underdiagnosed disease. Repetitive arousals due to upper airway obstruction lead to hypersomnia. Due to the insidious onset, patients often underestimate the severity of their symptoms. Relatives can give helpful additional informations and should be involved in history taking and motivation for treatment. In general, GP's are confronted with the problem of fatigue and hypersomnia in the first line. They play the most important role in selecting patients for further investigations. The patient history helps to separate hypersomnia from fatigue. Hypersomnia indicates falling asleep at daytime in unappropriate situations, especially when the subject is passive. Often, a multidisciplinary approach including respiratory physicians, ENT specialists, orthopedic dentists and neurologists is warranted. Anatomic narrowing of the upper airway must be ruled out by clinical investigation. Overnight sleep studies detect apneas/hypopneas and repetitive arousals. Continuous positive airway pressure, applied by a nose mask and a flow generator remains the mainstay of therapy. Motivation, counseling and troubleshooting especially in the beginning of this therapy are of outmost importance. Ongoing research aims to improve comfort of nose masks and optimize function of flow generators.
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PMID:[Diagnosis of sleep apnea syndrome--role of family practitioner]. 1095 50

Mood and behavior changes that have a seasonal pattern were first called seasonal affective disorder (SAD) in 1984. SAD, which affects about 5% of Americans, is most common among reproductive-age women. Afflicted patients typically experience debilitating somatic complaints of fatigue, discomfort, lethargy and atypical depressive complaints of hypersomnia, increased appetite, carbohydrate craving, and weight gain. This article presents current issues in the clinical assessment and management of SAD.
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PMID:Diagnosing and managing seasonal affective disorder. 1097 35

Up to 40% of cases of Parkinson's disease are associated with the occurrence of depression. The symptoms of the patients' depressive state may be factors such as significant weight change, insomnia or hypersomnia, psychomotor retardation, fatigue or loss of energy, feelings of worthlessness or inappropriate guilt, decreased concentration and indecisiveness, and recurrent thoughts of death or suicidal ideation. Given these conditions, drugs prove ineffective in many cases. Electroconvulsive therapy (ECT) has been reported to be beneficial in cases of drug-resistant depression. ECT has also been applied to Parkinsonian patients with depression and found to be effective with both depression and the Parkinsonian symptom. Transcranial magnetic stimulation(TMS) has recently been investigated for application in cases of depression and has become known as a valuable tool for depression therapy. TMS is easily implemented even in outpatient therapy. TMS will make a great contribution to the therapy of depression with Parkinson's disease.
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PMID:[Parkinson's disease and depression]. 1106 58

Daytime tiredness and daytime sleepiness are frequent complaints occurring in 29% and 14% of the Austrian population. Epidemiological studies demonstrate a high comorbidity between nonorganic hypersomnia and mental disorders. Especially comorbidity with affective disorders increases steadily from the general population over primary to tertiary care settings. Diagnostic criteria of nonorganic hypersomnia have been described in the International Classification of Diseases (ICD-10). Nonorganic hypersomnia can be primary or associated with a number of psychiatric disorders such as reaction to severe stress or adjustment disorders, affective disorders, other functional disorders, tolerance to or withdrawal of CNS-stimulating substances and chronic use of CNS-sedating substances. Diagnostic procedures comprise case history and symptom evaluation, sleep-specific and supplementary investigations. Concerning the latter, this article will focus on sleep questionnaires, vigilance and psychological tests as well as CNS investigations. Therapy of nonorganic hypersomnia rests on 3 pillars: psychological, somatic and pharmacological treatment. In view of the wide variety of psychiatric causes, resulting in a number of therapeutic options, it seems desirable that apart from subjective clinical assessment also objective methods be used in diagnosis and treatment. On the neurophysiological level objective measures can be obtained by means of EEG mapping during the day and polysomnography at night. Different mental disorder patients show different brain activity patterns as compared with normal controls and different classes of psychotropic substances cause different changes in neurophysiological variables. The fact that the changes in electrophysiological brain activity caused by mental disorders are exactly opposite to those induced by the psychotropic drugs used for their treatment suggests a key-lock principle in the diagnosis and treatment of nonorganic hypersomnia.
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PMID:[Nonorganic hypersomnia: epidemiology, diagnosis, and therapy]. 1138 88

Comparisons of sleep patterns of various inbred strains of mice have revealed differences in daily amounts of slow-wave sleep and rapid-eye movement sleep, in circadian patterns of sleep, and in some parameters of the electroencephalograms both in healthy mice and in mice undergoing microbial infections. Technical considerations will probably be an important variable in achieving consensus between different independent studies that use a genetic approach to identify sleep-regulatory genes or mechanisms. However, despite such differences, current data suggest that both normal sleep and various sleep disorders either have a genetic basis or are influenced by genetically determined physiologic or environmental predispositions. Excessive sleepiness, abnormal sleep patterns, nonrestorative sleep, and fatigue are becoming increasingly pervasive in modern society. Identifying genes that influence vigilance may ultimately contribute to a better understanding of the processes that control normal sleep and contribute to sleep disorders and may eventually promote the development of interventions to prevent or alleviate these disabling medical conditions.
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PMID:Identifying genetic influences on sleep: an approach to discovering the mechanisms of sleep regulation. 1152 73


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