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Biomedical subjects

Andres M Kanner

Publications and source records attributed to Andres M Kanner.

At least 37 records · Page 2Linked to original sources

Depression in epilepsy: prevalence, clinical semiology, pathogenic mechanisms, and treatment.

Depression is the most frequent comorbid psychiatric disorder in epilepsy. Its lifetime prevalence has been estimated at between 6% and 30% in population-based studies and up to 50% among patients followed in tertiary centers. The risk of suicide has been estimated to be 10 times higher than that in the general population. Although no one questions that epilepsy is a risk for depression, recent studies have also revealed that a history of depression is associated with a 4- to 6-fold greater risk of developing epilepsy. These data suggest either a possible "bi-directional" relationship between these two disorders or the presence of common pathogenic mechanisms that facilitate the occurrence of one in the presence of the other. The clinical presentation of depressive disorders in epilepsy can be identical to that of nonepileptic patients and can include major depression, bipolar and dysthymic disorders, and minor depression. In a significant percentage of cases, however, the clinical features of depression in epilepsy fail to meet any of the DSM-IV Axis I categories. Depression in epilepsy may be iatrogenically induced with various antiepileptic drugs used to treat the seizure disorder or after surgical treatment of intractable epilepsy. Despite its relatively high prevalence, depression remains unrecognized and untreated, and unfortunately its treatment is based on empirical and uncontrolled data.

Brain↗

A past psychiatric history may be a risk factor for topiramate-related psychiatric and cognitive adverse events.

OBJECTIVES: Topiramate (TPM) is a new antiepileptic drug (AED) that has been found to be associated with a high prevalence of cognitive adverse events (CAEs). The prevalence of psychiatric adverse events (PAEs) has yet to be established. The purpose of this study was to determine the prevalence of PAEs related to TPM when used in polytherapy regimens in a large cohort of adult patients with epilepsy, to identify any association between the occurrences of CAEs and PAEs and to identify predictors of PAEs and CAEs. METHODS: Investigators from 16 epilepsy centers (PADS group) prospectively obtained postmarketing safety and efficacy data on 596 patients aged 16 years and older. All data were recorded on standardized data retrieval forms, completed at the initial visit, while follow-up data were obtained every 6 months or at the time of discontinuation. RESULTS: PAEs were identified in 75 (12.6%) patients: 30 (5%) experienced symptoms of depression and 34 (5.7%) of aggressive behavior and irritability, while 9 patients experienced symptoms of psychosis (1.5%). CAEs were reported by 247 (41.5%) patients. There was a significant association between the occurrences of CAEs and PAEs. A past psychiatric history was a predictor of CAEs, while older age and past psychiatric history were predictors of PAEs. CONCLUSIONS: The use of TPM in polytherapy regimens can cause PAEs and CAEs and their occurrence is significantly correlated. Patients with a past psychiatric history may be at a higher risk for experiencing PAEs and CAEs.

Adolescent↗

The impact of mood disorders in neurological diseases: should neurologists be concerned?

Depression is one of the most frequent comorbid psychiatric disorders identified in patients with neurological disorders. The prevalence rates range between 20 and 50% of patients with stroke, epilepsy, multiple sclerosis, and Parkinson's disease. Despite these relatively high prevalence rates, depression remains underrecognized and undertreated in these patients. And yet, depression accounts for poor quality-of-life ratings and has a negative impact on the recovery from neurological symptoms. In this article, we review the epidemiological and clinical characteristics of mood disorders in patients with multiple sclerosis, Parkinson's disease, stroke, and epilepsy, and focus on the impact mood disorders have on the quality of life of these patients and on their recovery from their neurological deficits.

Comorbidity↗

Rates and risk factors for suicide, suicidal ideation, and suicide attempts in chronic epilepsy.

Studies of causes of death among people with epilepsy suggest that the lifetime prevalence rate of suicide is elevated. Although not all of the studies have reported an increased risk for suicide, the collective data yield an average rate of approximately 12% among people with epilepsy, compared with 1.1-1.2% in the general population. The increased risk for suicide appears to affect children and adolescents as well as adults. Rates of suicide attempts have also been reported to be elevated among people with epilepsy. A suicide attempt is a significant risk factor for completed suicide. Certain psychiatric disorders, including primary mood disorders, also increase the risk for suicide. Among people with epilepsy, psychiatric comorbidity is common, and rates of mood disorders, particularly major depression, have consistently been reported to be elevated. Other potential risk factors are family issues, physical health, personality, life stress, previous suicidal behavior, and access to firearms. Assessing severity of risk helps to determine the appropriate level of intervention. The suicidality module of the Mini-International Neuropsychiatric Interview is a practical tool to help quantify current suicide risk.

Chronic Disease↗

When did neurologists and psychiatrists stop talking to each other?

Patients with epilepsy have a significantly higher prevalence of psychiatric comorbid disorders involving depression, anxiety, psychotic, and attention deficit disorders. Accordingly, one would expect that psychiatrists would be actively involved in the evaluation and management of these patients. This, however, is hardly the case. Patients who undergo temporal lobectomies, for example, are known to experience postsurgical depression and occasionally psychotic disorders. Yet, most epilepsy centers in North America do not include a psychiatric evaluation as part of the presurgical work-up. Collaboration between epileptologists and psychiatrists is often sparse, despite the intimate relationship between psychiatric comorbidities and epilepsy. The purpose of this paper is to highlight this bizarre phenomenon and to identify some of the reasons behind it.

Behavioral Symptoms↗

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.

Depression↗

More controversies on the treatment of psychogenic pseudoseizures: an addendum.

There is no shortage of controversies when it comes to psychogenic pseudoseizures (PPS). In this addendum to the Iriarte et al. paper [Epilepsy Behav 4 (2003) 354], I review some controversial issues related to the treatment of PPS. First, I advocate the point that our first goal of therapy is not to attempt to stop the occurrence of PPS, but to ensure that patients and families have accepted that they do not suffer from epilepsy, because the most frequent cause of morbidity and mortality seen in these patients is related to their misdiagnosis as epilepsy patients and the resultant aggressive treatment in intensive care units. Remission of PPS should be our second goal! The second controversial point pertains to how long neurologists should continue to follow up patients after a diagnosis of PPS is reached, and I suggest some parameters to be used in reaching such decision. In the third controversial issue, I review the lack of communication between neurologists and psychiatrists exemplified by the misinterpretation by psychiatrists of the diagnostic value of video-EEG-telemetry studies and resulting mixed messages given to patients and families by neurologists and psychiatrists. The fourth controversial point pertains to the criteria to discontinue antiepileptic drugs after a diagnosis of PPS has been established. Finally, I discuss the timing of introducing a psychogenic cause during the presentation of the diagnosis to patient and family.

Anticonvulsants↗

The diagnostic significance of video-EEG monitoring findings on pseudoseizure patients differs between neurologists and psychiatrists.

PURPOSE: The diagnosis of psychogenic pseudoseizures has improved with the availability of video-electroencephalography (EEG) monitoring; however, the outcome of this difficult disorder has remained poor. In an attempt to elucidate factors contributing to this poor outcome, we hypothesized that neurologists and psychiatrists differ in their views of the diagnosis and management of psychogenic pseudoseizure patients. METHODS: The hypothesis was tested by using a brief anonymous questionnaire administered to neurologists and psychiatrists at continuing medical education (CME) conferences. RESULTS: We found that neurologists and psychiatrists differ significantly in their opinion as to the accuracy of the video-EEG procedure; psychiatrists view video-EEG as often inaccurate in the diagnosis of psychogenic pseudoseizures compared with neurologists (p < 0.001). Neurologists, more frequently than psychiatrists, thought that patients' own psychopathology rather than "doctors dropping the ball" was a predominant factor in contributing to therapeutic failure, but this difference between specialties did not reach statistical significance. CONCLUSIONS: Resolving the differences between neurologists and psychiatrists would be helpful in caring for psychogenic pseudoseizure patients. These results support the need to encourage psychiatrists to have an integral involvement in epilepsy centers and to improve the understanding of psychogenic pseudoseizures in both disciplines.

Attitude of Health Personnel↗

The complex epilepsy patient: intricacies of assessment and treatment.

The aim of treatment of all patients with epilepsy is the same: a complete remission of seizures with minimal or no adverse events. However, the means to reach that common goal may differ among patients, not only because of differences in their epileptic syndrome or type of seizures within the same syndrome, but also because of a variety of comorbid pathologic entities that are commonly identified in patients with epilepsy. In this article, we discuss some of the complexities inherent in the planning of therapeutic regimens for epilepsy patients. Comorbid conditions, whether intrinsic or extrinsic to the epileptic disorder, must play a paramount role in the choice of the therapeutic regimen for seizure control. We review the impact of psychiatric comorbidities on the quality of life of patients with epilepsy, with special attention to the tight relationship between depression and epilepsy. Yet, despite this close relationship, comorbid depression is more often than not underrecognized and undertreated. Next, we review the impact of antiepileptic drugs (AEDs) on comorbid medical disorders and give clear examples of the potentially deleterious impact of several AEDs on the therapeutic effects of concomitant medications used for their treatment. Clearly, treating epilepsy is not only about controlling seizures.

Anticonvulsants↗

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.

Comorbidity↗

Neuropsychiatric complications of epilepsy.

Psychiatric complications of epilepsy are multiple and result from the complex interaction between endogenous, genetic, therapeutic, and environmental factors. The relationship between epilepsy and psychiatric disorders may be much closer than previously appreciated. Recent studies have suggested the existence of a bi-directional relationship between depression and epilepsy, whereby patients with epilepsy have a higher risk than the general population of suffering from depression, not only after, but also before the onset of epilepsy. Furthermore, similar neurotransmitter changes have been identified in depression and epilepsy, suggesting the possibility that these two disorders share common pathogenic mechanisms. Although the clinical manifestations of psychiatric disorders in epilepsy are often indistinguishable from those of nonepileptic patients, certain types of depression and psychotic disorders may present with clinical characteristics that are particular to epilepsy patients. These include the psychosis of epilepsy, postictal psychotic disorders, alternative psychosis (or forced normalization), and certain forms of interictal depressive disorders.

Depression↗

The localizing yield of sphenoidal and anterior temporal electrodes in ictal recordings: a comparison study.

PURPOSE: To compare the localizing yield of sphenoidal electrodes placed under fluoroscopic guidance (SEs) and anterior temporal electrodes (ATEs) in ictal recordings from a group of patients with seizure disorders of anterior temporal origin. METHODS: We compared ictal recordings of 156 seizures obtained with SEs and ATEs from 40 consecutive patients with seizures of anterior temporal origin. Four electroencephalographers reviewed ictal recordings independently and blind to the patients' identity, presurgical data, and inclusion of ATEs or SEs. Outcome variables included (a) number of correctly localized seizures with SE and ATE recordings by at least three raters; (b) number of ictal foci in which all seizures were localized only with SEs; and (c) number of seizures in which SEs identified the ictal onset > or =5 s earlier than ATEs. RESULTS: Interrater agreement among the four raters was significantly greater with SE than with ATE recordings (p < 0.0001). The number of seizures correctly localized was significantly greater with SEs (n = 144) than with ATEs (n = 99; p < 0.0001). All the seizures [n = 36 (23%)] originating from 14 ictal foci (29%) in 11 patients (27.5%) were localized only with SEs. Finally, the ictal onset was detected at SEs > or =5 s earlier than at ATEs in 67 (43%) seizures originating from 33 (69%) foci in 30 (75%) patients. CONCLUSIONS: SEs improve interrater agreement in the localization of seizures of anterior temporal origin, and in about one fourth of patients, SEs add ictal data not identified by ATEs.

Adolescent↗