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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epilepsy is a chronic disorder that adversely affects social, vocational, and psychological functioning. Despite the variety and complexity of the negative clinical associations with epilepsy, depression is remarkable in prevalence and related adverse effects on health status. An estimated 30-50% of persons with refractory epilepsy have major depression, and depression has a stronger correlation than seizure rate with quality of life. Suicide is one of the leading causes of death in epilepsy. Available data indicate that depression may result from underlying brain dysfunction rather than social and vocational disability. Most patients with depression are not screened systematically for the diagnosis, and are subsequently not treated. Although the density of serotonin receptors is greatest in limbic brain regions commonly involved in human epilepsy, such as the mesial temporal and prefrontal areas, no prior randomized controlled trials have evaluated the efficacy of serotonin reuptake inhibitors for depression in epilepsy.
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PMID:Depression in epilepsy: ignoring clinical expression of neuronal network dysfunction? 1518 42

The brain is an organ elaborated and functioning from substances present in the diet. Dietary regulation of blood glucose level (via ingestion of food with a low glycemic index ensuring a low insulin level) improves the quality and duration of intellectual performance, if only because at rest the adult brain consumes 50 p. 100 of dietary carbohydrates, 80 p. 100 of them for energy purposes. The nature of the amino acid composition of dietary proteins contributes to good cerebral function; tryptophan plays a special role. Many indispensable amino acids present in dietary proteins help to elaborate neurotransmitters and neuromodulators. Omega-3 fatty acids provided the first coherent experimental demonstration of the effect of dietary nutrients on the structure and function of the brain. First it was shown that the differentiation and functioning of cultured brain cells requires omega-3 fatty acids. It was then demonstrated that alpha-linolenic acid (ALA) deficiency alters the course of brain development, perturbs the composition and physicochemical properties of brain cell membranes, neurones, oligodendrocytes, and astrocytes (ALA). This leads to physicochemical modifications, induces biochemical and physiological perturbations, and results in neurosensory and behavioral upset. Consequently, the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for infants (premature and term) conditions the visual and cerebral abilities, including intellectual abilities. Moreover, dietary omega-3 fatty acids are certainly involved in the prevention of some aspects of cardiovascular disease (including at the level of cerebral vascularization), and in some neuropsychiatric disorders, particularly depression, as well as in dementia, notably Alzheimer's disease. Their deficiency can prevent the satisfactory renewal of membranes and thus accelerate cerebral aging. Iron is necessary to ensure oxygenation, to produce energy in the cerebral parenchyma, and for the synthesis of neurotransmitters. The iodine provided by the thyroid hormone ensures the energy metabolism of the cerebral cells. The absence of iodine during pregnancy induces severe cerebral dysfunction, leading to cretinism. Manganese, copper, and zinc participate in enzymatic mechanisms that protect against free radicals, toxic derivatives of oxygen. The use of glucose by nervous tissue implies the presence of vitamin B1. Vitamin B9 preserves memory during aging, and with vitamin B12 delays the onset of signs of dementia, provided it is administered in a precise clinical window, at the onset of the first symptoms. Vitamins B6 and B12, among others, are directly involved in the synthesis of neurotransmitters. Nerve endings contain the highest concentrations of vitamin C in the human body. Among various vitamin E components, only alpha-tocopherol is involved in nervous membranes. The objective of this update is to give an overview of the effects of dietary nutrients on the structure and certain functions of the brain.
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PMID:[The role of nutritional factors on the structure and function of the brain: an update on dietary requirements]. 1545 64

Hepatic encephalopathy is the most obvious neurological consequence of chronic hepatitis C virus (HCV) infection. There are also case reports of HCV-associated cerebral vasculitis. This review is concerned with the possibility of an effect of HCV on cerebral dysfunction, occurring at an early stage of chronic infection, prior to the development of cirrhosis and unrelated to vasculitis. There is emerging evidence of mild, but significant neurocognitive impairment in HCV infection, which cannot be attributed to substance abuse, coexistent depression, or hepatic encephalopathy. In vivo magnetic resonance spectroscopy and neurophysiological studies have suggested that a biological mechanism may underlie these cognitive findings. The recent detection of HCV genetic sequences in postmortem brain tissue raises the intriguing possibility that HCV infection of the central nervous system may be related to the reported neuropsychological symptoms and cognitive impairment.
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PMID:Central nervous system involvement in hepatitis C virus infection. 1555 29

Arguments exist as to the cause of chronic fatigue syndrome (CFS). Some think that it is an example of symptom amplification indicative of functional or psychogenic illness, while our group thinks that some CFS patients may have brain dysfunction. To further pursue our encephalopathy hypothesis, we did spinal taps on 31 women and 13 men fulfilling the 1994 case definition for CFS and on 8 women and 5 men serving as healthy controls. Our outcome measures were white blood cell count, protein concentration in spinal fluid, and cytokines detectable in spinal fluid. We found that significantly more CFS patients had elevations in either protein levels or number of cells than healthy controls (30 versus 0%), and 13 CFS patients had protein levels and cell numbers that were higher than laboratory norms; patients with abnormal fluid had a lower rate of having comorbid depression than those with normal fluid. In addition, of the 11 cytokines detectable in spinal fluid, (i) levels of granulocyte-macrophage colony-stimulating factor were lower in patients than controls, (ii) levels of interleukin-8 (IL-8) were higher in patients with sudden, influenza-like onset than in patients with gradual onset or in controls, and (iii) IL-10 levels were higher in the patients with abnormal spinal fluids than in those with normal fluid or controls. The results support two hypotheses: that some CFS patients have a neurological abnormality that may contribute to the clinical picture of the illness and that immune dysregulation within the central nervous system may be involved in this process.
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PMID:Spinal fluid abnormalities in patients with chronic fatigue syndrome. 1564 84

To determine whether neuropsychiatric manifestations in patients with systemic lupus erythematosus (SLE) are influenced by antibodies against the human N-methyl-D-aspartate (NMDA) receptor types NR2a or NR2b. A decapeptide was synthesized containing a sequence motif present in the extracellular ligand-binding domain of NMDA receptors NR2a and NR2b, bound by the monoclonal murine anti-DNA antibody R4A. In an ELISA with the murine monoclonal R4v as positive control, plasma samples of 57 patients with SLE were examined for the anti-peptide (anti-NR2) antibody after the patients had been subjected to comprehensive psychological and cognitive testing. Poor performance on the Visual Paired Associates test (immediate), the Grooved Pegboard test, as well as high scores on the Beck Depression Inventory, and scales D-2 (depression), Pd-4 (psychopathic deviate), Sc-8 (schizophrenia), and Ma-9 (hypomania) of the MMPI-2 were significantly associated with elevated levels of anti-NR2 antibodies. The findings in several domains indicate an association between anti-NR2 antibodies and depressed mood in addition to decreased short-time memory and learning. Antibodies to NMDA receptors thus may represent one of several mechanisms for cerebral dysfunction in patients with SLE.
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PMID:Neuropsychiatric disturbances in SLE are associated with antibodies against NMDA receptors. 1580 72

The evidence regarding the co-morbidity of chronic hepatitis C, psychiatric illness and intravenous drug abuse is reviewed from the literature. Also the occurrence and the treatment of psychiatric side effects during treatment with interferon in patients with a history of drug abuse are reviewed. There is insufficient evidence for a specific hepatitis C induced depression or fatigue, but a direct link between hepatitis C and cerebral dysfunction is not excluded. Immune system activation rather than drug use may explain cerebral symptoms. In HCV positive substance users anxiety and depression are more prevalent than in HCV negative substance users. During treatment with regular or pegylated (PEG) interferon depression is a frequent side effect (ca 30%) and occurs independently from pre-existing psychiatric disorders or drug abuse. A history of drug abuse per se does not increase the risk of depression as a side effect of interferon treatment. It is extremely important to monitor symptoms of depression in the early weeks of treatment and to start antidepressant treatment as early as possible. Antidepressants should be continued throughout the interferon treatment period. There are insufficient data to assess these situations in which preventive antidepressant treatment should be started before interferon treatment. Clinical judgement can, however, lead to preventive antidepressant treatment, even at subclinical levels of depression. A cut off score of > 10 on the Beck Depression Inventory before interferon treatment is associated with a higher risk of depression during treatment. Both selective serotonin reuptake inhibitors and other classes of antidepressants can be used.
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PMID:Hepatitis C, interferon alpha and psychiatric co-morbidity in intravenous drug users (IVDU) : guidelines for clinical practice. 1583 90

Migraine is an episodic headache disorder affecting more than 10% of the general population. Migraine arises from a primary brain dysfunction that leads to activation and sensitization of the trigeminovascular system. A major incompletely understood issue in the neurobiology of migraine concerns the molecular and cellular mechanisms that underlie the primary brain dysfunction and lead to activation and sensitization of the trigeminovascular system, thus generating and maintaining migraine pain. Here the author reviews recent discoveries that have advanced our understanding of these mechanisms toward a unifying pathophysiological hypothesis, in which cortical spreading depression (CSD), the phenomenon underlying migraine aura, assumes a key role. In particular, the author discusses the main recent findings in the genetics and neurobiology of familial hemiplegic migraine and the insights they provide into the molecular and cellular mechanisms that may lead to the increased susceptibility of CSD in migraineurs.
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PMID:Migraine: new molecular mechanisms. 1606 23

Epilepsy is a chronic disorder that has been associated with other specific health problems. Evidence from recent clinical and basic investigations indicates that aspects of cerebral dysfunction associated with a lowered seizure threshold may also predispose toward other disorders such as depression, cognitive impairment, sleep disorders, and migraine. Similarly, certain types of brain injury may also increase the risk of adverse antiepileptic drug (AED) effects. For example, a history of febrile seizures is associated with a three fold increase in the occurrence of negative psychiatric effects of two newer AEDs. Poor fitness and obesity are also reported at higher rates in epilepsy. Some comorbid conditions in epilepsy, such a depression and anxiety, may have a greater influence on subjective health status than does seizure rate. Management strategies employed in the outpatient clinic to maximize overall health outcomes should include screening and treatment for the commonly coexistent conditions in persons with epilepsy.
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PMID:Epilepsy and common comorbidities: improving the outpatient epilepsy encounter. 1612 Apr 91

In chronic hepatitis type C fatigue, depression and neuropsychiatric complications of interferon treatment are more frequently reported than in the other parenchymal liver diseases. It contributes to a significant reduction of health related quality of life (HRQL) in those patients. It is believed that psychiatric disorders are the result of brain dysfunction caused by the virus. The hypothesis of neurotropic character of HCV infection is supported by the detection of HCV-RNA in brain tissue, identification of brain-specific quasispecies variants of hepatitis C virus, specific detection of negative-strand viral RNA in the astroglia of patients with acquired-immunodeficiency syndrome and demonstration of metabolic changes resembling HIV-1 encephalopathy in the basal ganglia of patients with chronic hepatitis C. On the other hand there is good evidence that decreased HRQL is directly related to the consciousness of infection and hence, is not of the organic nature. Some authors suggest that patient's worry and anxiety, aggravated by some mass-media and the lack of knowledge, may be a strong determinant of psychological status. Given the complex nature of symptoms in chronic hepatitis C therapy should include education on the natural history of HCV infection and results of treatment, psychotherapy and medical treatment of depression and anxiety. Moreover, antiviral therapy should be considered in highly motivated patients despite lack of clear clinical indications for treatment.
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PMID:[Chronic HCV infection--disease of body or disease of soul?]. 1619 May 74

The psychopathology of stroke encompasses several psychiatric and behavioral disorders that have high prevalence in the geriatric population, reduce the patient autonomy and increase the caregiver's burden. These disorders are usually associated with other cognitive and neurological deficits, and are labelled as neuropsychiatric when the whole clinical picture is consistent with the specific dysfunction of a neural system or brain region. Thus the neuropsychiatry of stroke comprises disorders of the perception/identification of the self and the environment (anosognosia of hemiplegia, misidentification syndromes, confabulations, visual hallucinations, delirium and acute confusional state), amotivational syndromes (apathy and athymhormia), disorders of emotional reactivity (blunted affect, emotional incontinence, irritability, catastrophic reactions), poor impulse or ideation control (mania) and personality changes. The clinical profile of the subcortical vascular dementia also points to specific brain dysfunction (frontal-subcortical pathways) that manifests with behavioral (depression, emotionalism, irritability) and cognitive symptoms (psychomotor retardation, attention, executive and memory deficits). However, post-stroke depression and anxiety, which have a more variable clinical presentation and might be assimilated, for several aspects, to post-traumatic or adaptive disorders, are disorders less characterized in their neural correlates.
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PMID:[Psychopathology of stroke]. 1631 15


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