Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infectious diseases, especially hepatitis C, are prevalent among drug abusers. Interferon-alpha (IFN-alpha) is the pharmacological treatment of choice for this condition. Patients being treated with IFN-alpha can be expected to experience such psychiatric side-effects as development of depression, mania, irritability, changes in personality, hallucinations or delirium. In addition, certain patients are considered to be at greater risk of developing neuropsychiatric side-effects. Individuals meeting the following criteria are particularly vulnerable: over 40 years of age; having central nervous system abnormalities; a previous neurological or psychiatric history; a past familial psychiatric history; use of narcotics or having alcohol or substance use disorders; being HIV-positive; coadministration of other cytokines; receiving high doses of IFN-alpha (> 6 million units). We report the case of a 29-year-old patient with chronic non-active hepatitis C, a previous psychiatric history of polydrug abuse (cannabis, heroin and illegal use of the psychotropic drug biperiden) and anxiety disorder. Two weeks after the initiation of IFN-alpha treatment, he developed fatigue, sleeplessness and persecutory delusions. The patient responded partially to the discontinuation of the IFN-alpha treatment. Due to the presence of three risk factors in this patient, he was considered to belong to the group of patients being 'at high risk' of developing neuropsychiatric side-effects. This is the first case report of major depressive disorder with psychotic features in such a 'high-risk patient'. This case report may prompt other research by showing the importance of the close monitoring, and the prevention of the progression of IFN-alpha-related psychiatric disorders in 'a high-risk patient'.
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PMID:Major depressive disorder with psychotic features induced by interferon-alpha treatment for hepatitis C in a polydrug abuser. 1567 Nov 36

Several studies have reported high rates of depression in multiple sclerosis (MS) with a lifetime prevalence of approximately 50% and an annual prevalence of 20% not uncommon. Concern about the potential of new drug treatments to exacerbate or precipitate depression in MS has led to increased interest in the relation between MS and depression. This review on MS and depression identifies the following key issues: How common is depression in people with MS? Is depression in MS associated with lesions in specific regions of the central nervous system? Is there an increased risk of suicide in MS? Is there a higher than expected incidence of anxiety disorders in MS? Are fatigue and depressed mood related in MS? Is there a relation between depression and cognitive impairment in MS? Which psychosocial variables affect the development of depression in MS? Does treatment with interferon increase the risk of depression? How effective are treatments for MS patients with depression? Each of these issues is briefly reviewed with critical commentary, and some priorities for future research are suggested.
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PMID:Depression in multiple sclerosis: a review. 1577 30

This review discusses the clenching-grinding spectrum from the neuropsychiatric/neuroevolutionary perspective. In neuropsychiatry, signs of jaw clenching may be a useful objective marker for detecting or substantiating a self-report of current subjective emotional distress. Similarly, accelerated tooth wear may be an objective clinical sign for detecting, or substantiating, long-lasting anxiety. Clenching-grinding behaviors affect at least 8 percent of the population. We argue that during the early paleolithic environment of evolutionary adaptedness, jaw clenching was an adaptive trait because it rapidly strengthened the masseter and temporalis muscles, enabling a stronger, deeper and therefore more lethal bite in expectation of conflict (warfare) with conspecifics. Similarly, sharper incisors produced by teeth grinding may have served as weaponry during early human combat. We posit that alleles predisposing to fear-induced clenching-grinding were evolutionarily conserved in the human clade (lineage) since they remained adaptive for anatomically and mitochondrially modern humans (Homo sapiens) well into the mid-paleolithic. Clenching-grinding, sleep bruxism, myofacial pain, craniomaxillofacial musculoskeletal pain, temporomandibular disorders, oro-facial pain, and the fibromyalgia/chronic fatigue spectrum disorders are linked. A 2003 Cochrane meta-analysis concluded that dental procedures for the above spectrum disorders are not evidence based. There is a need for early detection of clenching-grinding in anxiety disorder clinics and for research into science-based interventions. Finally, research needs to examine the possible utility of incorporating physical signs into Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition posttraumatic stress disorder diagnostic criteria. One of the diagnostic criterion that may need to undergo a revision in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition is Criterion D (persistent fear-circuitry activation not present before the trauma). Grinding-induced incisor wear, and clenching-induced palpable masseter tenderness may be examples of such objective physical signs of persistent fear-circuitry activation (posttraumatic stress disorder Criterion D).
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PMID:The clenching-grinding spectrum and fear circuitry disorders: clinical insights from the neuroscience/paleoanthropology interface. 1578 58

Obsessive-compulsive disorder (OCD) is considered an anxiety disorder, but shows comorbidity with other disorders in the affective and impulsive-compulsive spectra, including anxiety disorders, major depression, and drug addictions. Subclinical OCD symptoms are relatively common in nonclinical populations and share common neurobiological substrates with clinical OCD. In this nonclinical community sample, the relationship between the severity of obsessions and compulsions, as measured by the Yale-Brown Obsessive Compulsive Scale, related to the intensity of negative emotions (anger, depression, tension, confusion, and fatigue) but not positive emotion (vigor), as measured by the Profile of Mood States. These relationships were independent of demographic influences and psychoactive drug use frequency (alcohol, cannabis, opioid, major stimulants, MDMA, and hallucinogens). These likely reflect common neurobiological substrates for emotional and behavioral regulation in prefrontal-subcortical/limbic circuits, which show normal variations in the general population.
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PMID:Mood in relation to subclinical obsessive-compulsive symptoms. 1580 13

Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested as a natural animal model of human depression and mood disorders.
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PMID:Metabolic depression in hibernation and major depression: an explanatory theory and an animal model of depression. 1606 29

The aim of this retrospective study was to evaluate the risk factors, clinical features and co-morbid disorders of depressive disorder in children below the age of 12 years. Children who attended the child guidance clinic between January 2000 and December 2003 formed the subjects for the study. The diagnosis of depressive disorder was based on DSMIV diagnostic criteria for Major Depressive Disorder, Single episode. There were 26 boys and 19 girls. Stress at school and in the family was significantly associated with depressive disorder. Children with depressive disorder had significantly more family members affected with mental illnesses. The clinical features included diminished interest in play and activities, excessive tiredness, low self- esteem, problems with concentration, multiple somatic complaints, behavior symptoms like anger and aggression, recent deterioration in school performance and suicidal behavior. Majority of children had other associated psychiatric disorders which included dysthymic disorder, anxiety disorders, conduct disorder and conversion disorder.
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PMID:Clinical profile of depressive disorder in children. 1682 Jun 61

Patients with neurologic disorders commonly experience sleep dysfunction and psychiatric disorders. The most common sleep dysfunction is insomnia, which is a primary symptom in 30% to 90% of psychiatric disorders. Insomnia and fatigue are prominent symptoms of anxiety disorders and major depression, including patients who are treated but have residual symptoms. Anxiety and depressive disorders account for 40% to 50% of all cases of chronic insomnia. It is also recognized that primary insomnia and other primary sleep disorders produce symptoms that are similar to those reported by patients with psychiatric disorders. A clinician must judge whether sleep deprivation causes mood disturbance or whether depressive or anxiety disorder represents the primary reason for sleep dysfunction. When insomnia is comorbid with mild to moderate depression, therapy should begin with bedtime dosing of sedating antidepressants such as mirtazapine, nefazodone, or tricyclic antidepressants, which are preferred because of their sedative effects, although side effects may limit their usefulness. Intervention for chronic insomnia is similar in nonpsychiatric and psychiatric patients. Behavioral therapies, particularly cognitive behavioral therapy, and lifestyle changes show significant long-term efficacy as treatments for chronic insomnia. Sedative hypnotic agents are the most studied agents to treat insomnia, particularly those that are active through the benzodiazepine receptor-GABA complex, such as benzodiazepines, eszopiclone, zaleplon, and zolpidem. The new melatonin-receptor agonist ramelteon has not yet been studied in psychiatric patients. Prescription of adjunctive trazodone 50 to 150 mg is a common clinical practice to treat comorbid insomnia during antidepressant therapy, but published data are surprisingly limited when considered against the frequent usage of trazodone. Although there has been insufficient research on the use of atypical antipsychotic agents in severe insomnia, psychiatrists use quetiapine, olanzapine, or other agents to lessen agitation that disrupts sleep onset or maintenance. When insomnia or hypersomnia continues even as mood, anxiety, or thought disorders improve with standard therapy, the physician should consider the potential presence of underlying sleep disorders.
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PMID:Treatment of sleep dysfunction and psychiatric disorders. 1690 76

Parkinson's disease is primarily considered a motor disease characterized by rest tremor, rigidity, bradykinesia and postural disturbances. However, neuropsychiatric complications, including mood and anxiety disorders, fatigue, apathy, psychosis, cognitive impairment, dementia, sleep disorders and addictions, frequently complicate the course of the illness. The pathophysiologic features of these complications are multifaceted and include neuropathophysiologic changes of a degenerative disease, exposure to antiparkinsonian treatments and emotional reactions to having a disabling chronic illness. Changes in mental status have profound implications for the well-being of patients with Parkinson's disease and of their caregivers. Treatment is often efficacious but becomes a challenge in advanced stages of Parkinson's disease. In this article, we review the key clinical features of neuropsychiatric complications in Parkinson's disease as well as what is known about their epidemiologic characteristics, risk factors, pathophysiologic features and management.
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PMID:Recognition and management of neuropsychiatric complications in Parkinson's disease. 1714 92

Our objectives were to investigate thyroid abnormalities and autoimmunity in 120 patients affected by fibromyalgia (FM) and to study their relationships with clinical data and symptoms. Thyroid assessment by means of antithyroglobulin antibodies, antithyroid peroxidase antibodies, free triiodo-thyronine, free thyroxine, and thyroid stimulating hormone analyses was carried out. The clinical parameters "Fibromyalgia Impact Questionnaire", pain, tender points, fatigue, and other symptoms, and the presence of depression or anxiety disorders were evaluated. The basal thyroid hormone levels of FM patients were in the normal range, while 41% of the patients had at least one thyroid antibody. Patients with thyroid autoimmunity showed a higher percentage of dry eyes, burning, or pain with urination, allodynia, blurred vision, and sore throat. Correlations found between thyroid autoimmunity and age or with the presence of depression or anxiety disorders were not significant. However, in the cohort of post-menopausal patients, the frequency of thyroid autoimmunity was higher with respect to pre-menopausal patients. In conclusion, autoimmune thyroiditis is present in an elevated percentage of FM patients, and it has been associated with the presence of typical symptoms of the disease.
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PMID:Association between thyroid autoimmunity and fibromyalgic disease severity. 1748 49

Myasthenia gravis (MG) is a chronic, autoimmune disease involving neuromuscular junctions. It is frequently associated with symptoms such as loss of muscle strength, difficulty in respiration and swallowing, diplopia and ptosis. All chronic diseases, including MG, may have psychiatric consequences in terms of coping and adaptation. Psychiatric morbidity usually appears as anxiety disorders, such as panic disorder and generalised anxiety disorder, and as depressive disorders. However, there are very few data on the prevalence and aetiology of such psychiatric symptoms in patients with MG, and those available in the literature are generally from old studies with poor methodology. The interaction between MG and psychiatric disorders needs to be appreciated, especially in the primary care setting, since the symptoms may overlap. MG may be under-recognised initially because the psychiatric symptoms may coincide with those of the actual disease, such as fatigue, lack of energy and shortness of breath. On the other hand, co-morbid psychiatric symptoms that appear during the course of the illness may be misdiagnosed as true myasthenic symptoms; thus, leading to unnecessary drug treatment. Differentiation of the aetiology of these symptoms might alter the treatment choice and, therefore, affect the treatment success rate and patients' well-being. Psychiatric treatments must be carefully planned because of the risk of aggravating the underlying neurological disease. Even though there appears to be an intricate relationship between MG and psychiatric symptoms, there is very limited information on this subject. As such, prospective, randomised, controlled pharmaco/psychotherapy studies are needed to better direct the management of patients and, thus, improve quality of life during the course of the illness.
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PMID:Mood and anxiety disorders in patients with myasthenia gravis: aetiology, diagnosis and treatment. 1752 Dec 27


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