Depressive Disorders In Epilepsy Research Articles

Screening for anxiety and depressive disorders in epilepsy: current state of the art

Screening for anxiety and depressive disorders in epilepsy: current state of the art

The Progress in Diagnosis and Treatment of Exosomes and MicroRNAs on Epileptic Comorbidity Depression.

The occurrence of epilepsy can increase the incidence of depression, and the risk of epilepsy in the patients with depression is also high, both of which have an adverse effect on the life and the psychology of the patient, which is not conducive to the prognosis of the patients with epilepsy. With lucubrating the function of exosomes and microRNAs, some scholars found that the exosomes and its microRNAs have development prospect in the diagnosis and treatment of the disease. MicroRNAs are involved in the regulation of seizures and depression, as biomarkers, that can significantly improve the management of epileptic patients and play a preventive role in the occurrence of epilepsy and epilepsy depressive disorder. Moreover, due to its regulation to genes, appropriate application of microRNAs may have therapeutic effect on epilepsy and depression with the characteristics of long distance transmission and stability of exosomes, to a certain extent. This provides a great convenience for the diagnosis and treatment of epileptic comorbidity depression.

Systematic Review and Meta-Analysis of Anxiety and Depression in Youth With Epilepsy.

The aim of this systematic review and meta-analysis was to provide an estimate of the prevalence of anxiety and depressive disorders in youth with epilepsy (YWE). It also aimed to calculate the overall magnitude of observed differences in anxiety and depressive symptoms reported by YWE compared with healthy controls and investigate whether any factors moderated anxiety and depression outcomes in YWE. Following prospective registration, electronic databases were searched up until October 2018. Studies were included if they reported on the rate of anxiety or depression in samples of YWE, and/or if they used valid measures of anxious or depressive symptomatology in YWE compared with a healthy control sample. Twenty-three studies met inclusion criteria. The overall pooled prevalence of anxiety disorders in YWE was 18.9% (95% confidence interval [CI] 12.0%-28.5%), and for depression the pooled prevalence was 13.5% (95% CI 8.8%-20.2%). In samples of YWE compared with healthy controls, significantly higher anxiety (d = 0.57, 95% CI 0.32-0.83, p < .000) and depressive (d = 0.42, 95% CI 0.16-0.68, p < .000) symptomatology was reported. YWE report anxiety and depressive disorders and symptoms to a significantly higher degree than youth without epilepsy. There is also evidence that certain anxiety disorders (e.g. generalized anxiety disorder, separation anxiety disorder) are particularly elevated, perhaps reflecting the unique impact of epilepsy on youth psychopathology. Research is needed to understand the risk factors associated with anxiety and depressive disorders in epilepsy, and better understand how these symptoms change across development.

The contribution of brain dysfunction in the formation of depressive disorders in epilepsy

The contribution of brain dysfunction in the formation of depressive disorders in epilepsy

Systematics and principles of therapy for depressive disorders in epilepsy

Relying on a comprehensive investigation, the author proposes the typology of depressive disorders in epilepsy by identifying ictal, preictal, interictal, and postictal conditions. Risk factors for depressive symptoms are considered. Main approaches to therapy for depressions are offered. Particular emphasis is placed on the normothymic activity of a number of anticonvulsants. Valproates, and depakine in particular, as a normothymic agent are shown to be beneficial in treating affective disorders.

Reevaluating the prevalence and diagnostic subtypes of depressive disorders in epilepsy.

Depressive disorders are common among patients with epilepsy (PWE). The aim of this study was to estimate the prevalence of different forms of depressive disorders among PWE treated in the outpatient setting. A group of consecutive PWE that visited the epilepsy outpatient clinic was invited to participate in the study. Ninety-six patients met inclusion criteria and were examined by a trained psychiatrist using standardized measures. A diagnosis of a current major depression was established in 21 (22.3%) out of 96 participants. Furthermore, almost 20% of the study group fulfilled criteria for mood disorder categories other than MDD, adding up to over 40% of PWE suffering from any mood disorder category. Older age and later age at seizure onset, as well as unemployment, were associated with an increase in the odds of MDD diagnosis. A number of limitations are to be considered: the sample size is relatively small, and the findings may not be representative of PWE in general because our population represents a sample coming from a single outpatient clinic with a higher ratio of drug-resistant epilepsy. Major depression as well as other forms of depressive disorders are common among PWE. Unemployment, age, and age at seizure onset are important factors associated with major depression among PWE.

The treatment of depressive disorders in epilepsy: What all neurologists should know

One of every three patients with epilepsy (PWE) will experience a depressive disorder in the course of their life, often associated with anxiety symptoms or a full blown anxiety disorder. Clearly, the high prevalence of these psychiatric comorbidities calls for their early identification and management. This article provides practical strategies in the management of depressive episodes in PWE. Contrary to long-held beliefs, the use of antidepressant drugs are safe in PWE when used at therapeutic doses. Antidepressant drugs of the selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) families are the first line of therapy in depressive disorders, and failure to achieve complete symptom remission after a trial of an SSRI or SNRI at optimal doses should be followed by a second trial with a drug from the other antidepressant family. In developing countries, antidepressant drugs of these two antidepressant families are not always available, and tricyclic antidepressants (TCAs) are the drugs of choice. Although there are no differences in efficacy among the three families of antidepressants, TCAs have a lower tolerability and higher toxicity, with greater mortality risk associated with cardiotoxic effects in overdoses. Cognitive behavior therapy is another treatment modality that has been shown to be effective in the treatment of depressive disorders in patients with and without epilepsy. Its use should be considered together with pharmacotherapy or by itself.

DEPRESSIVE DISORDERS IN EPILEPSY

Depressive disorders are the most frequent psychiatric comorbidity in epilepsy but very often remain unrecognized and untreated. We examined 103 epileptic patients, aged 18-60 years, 40 males and 63 females, for the presence of interictal depressive disorder. All subjects underwent clinical psychiatric examination, including evaluation on Hamilton Depression Rating Scale (HAM-D17). A questionnaire for demographic and seizure-related variables was also completed. Concurrent depressive disorder (clinically presented according to ICD-10 diagnostic criteria) affected 28.3% of all evaluated patients. Based on HAM-D-17 scores depression was defined as mild 80% of all depressed patients, moderate 17% and severe 3%. Atypical presentation of interictal depressive disorder was frequent. Depression has a tremendous effect on one’s family, social and psychological functioning, even more than the actual seizure frequency and severity. Diagnostic difficulties come through the atypical mode of presentation of depressive disorders in epilepsy. Proper neuropsychiatric evaluation is essential for improving treatment and quality of life for patients with epilepsy.

Depression in epilepsy: a complex relation with unexpected consequences

The recent significant increase in research on depressive disorders in epilepsy has led to a greater recognition of its negative impact on multiple aspects of these patients' lives. Thus, a review of this topic could not be timelier. A population-based study suggests that a lifetime history of depressive disorders is relatively frequent in epilepsy patients. Contrary to long-held beliefs, the relation between these two disorders is bidirectional and a history of depression can often be identified before the first seizure has ever happened. Such a relation is the expression of common pathogenic mechanisms operant in both conditions, among which decreased binding of serotonin-1A receptors appears to be pivotal. Furthermore, a lifetime history of depression preceding the onset of epilepsy appears to be predictive of worse seizure control with pharmacotherapy and epilepsy surgery. These data are likely to change the way the relation between depression and epilepsy is conceptualized, to enhance the early recognition and treatment of this disorder and to generate further research on the impact of depressive disorders on seizure response to pharmacologic and surgical treatments.

Depression in epilepsy: a frequently neglected multifaceted disorder

Depressive disorders (DDs) are frequent psychiatric comorbidities of neurological disorders like multiple sclerosis, stroke, dementia, migraine, Parkinson’s disease, and epilepsy. The clinical manifestations of DDs in these neurological disorders are identical to those of idiopathic mood disorders. In epilepsy, however, DDs can frequently also present with clinical characteristics that differ from those of idiopathic depression and fail to meet the criteria included in the Diagnostic and Statistical Manual of Psychiatric Disorders—Fourth Edition. Despite their multifaceted clinical expressions and their relatively high prevalence in epilepsy, DDs very often go unrecognized and untreated. The aim of this article is to review some of the more relevant aspects of DDs in epilepsy, to highlight their various clinical expressions, and their impact on the quality of life of patients with epilepsy, and to review the basic principles of treatment.

Mechanisms of depression in epilepsy from a clinical perspective

The epilepsies are a complex group of disorders commonly associated with brain dysfunction, social isolation, and vocational difficulty. Each of these factors may contribute to increased prevalence of depressive disorders in epilepsy, but the specific mechanisms are not completely understood. The brain regions commonly involved in various types of epilepsies, such as the hippocampus and amygdala in temporal lobe epilepsy and subcortical nuclei in idiopathic generalized epilepsies, are important components of current models of depression. Increased understanding of mechanisms of depression in epilepsy is not only crucial for improving care of many persons with seizures, but may also yield useful information about principal mechanisms underlying both depression and epileptogenesis.

Depression and epilepsy: how closely related are they?

Article abstract Depressive disorders (DDs) are the most common type of psychiatric co-morbidity in patients with epilepsy. They are more likely to occur in patients with partial seizure disorders of temporal and frontal lobe origin and are more frequent among patients with poorly controlled seizures. Despite their relatively high prevalence, DDs remain unrecognized and untreated in a large proportion of patients. This article highlights the evidence of a close association between DDs and epilepsy, beginning with the bi-directional relationship between the two disorders. Not only are patients with epilepsy more likely to experience a DD, but a history of DD preceding the onset of the seizure disorder is more likely to be identified in patients with epilepsy than in a control group. In support of these observations, we review data from animal models of epilepsy showing that decreased activity of serotonin, norepinephrine, dopamine, and GABA facilitate the kindling process of seizure foci, worsen seizure frequency and severity, and are reversed or blocked by antidepressant drugs. Decreased activity of these neurotransmitters is a pivotal pathogenic mechanism of DDs and forms the basis of their pharmacotherapy. Thus, DDs and epilepsy may share common pathogenic mechanisms that facilitate the occurrence of one in the presence of the other. Contrary to long-held beliefs by patients and clinicians alike, in the sense that DDs are a "normal reaction" to the obstacles posed by epilepsy, we review evidence that points to their biologic or endogenous nature. We find a genetic predisposition to DDs, as evidenced by the frequent family history of mood disorders in these patients. Neuroimaging and neuropsychological data support a frontal lobe dysfunction in DDs, and a recent study documents concomitant dysfunction of mesial temporal structures. Depressive disorders have various clinical presentations, some typical of the different types of mood disorders in non-epileptic patients, others constituting rather frequent atypical presentations that can easily go unrecognized. A review of the pharmacologic treatment of DDs in epilepsy highlights the lack of scientific data and points to the empirical form in which these patients have been treated up to the present time. Contrary to clinicians' fears, most antidepressant drugs are safe in patients with epilepsy.