Kelin Cristine Martin

Prevalence of psychiatric comorbidities in temporal lobe epilepsy: the value of structured psychiatric interviews

BackgroundAlthough many studies have demonstrated a high prevalence of psychiatric disorders in epileptic patients, most have used unstructured psychiatric interviews for diagnosis, which may lead to significant differences in results. Here we present a study evaluating the prevalence of major psychiatric comorbidities in a cohort of South Brazilian patients with temporal lobe epilepsy using a structured clinical interview.MethodsNeuropsychiatric symptoms were analyzed in 98 patients (39 men and 59 women) with temporal lobe epilepsy. Patient mean age was 43 years old, and mean duration of epilepsy was 25 years. Patients were diagnosed according to the ILAE Classification of Epileptic Syndromes using clinical, EEG, and neuroimaging criteria. All patients participated in the Structured Clinical Interview for DSM-IV (SCID).ResultsFifty-three patients (54.1%) presented major psychiatric comorbidities. Mood disorders were observed in 42 patients (42.9%), the most common being neuropsychiatric disorders. Anxiety disorders were the second most frequent disorders, observed in 18 patients (18.4%). Psychotic disorders and substance abuse were each observed in six patients (6.1%). There were no clinical variables regarding epilepsy characteristics (age of onset, duration, response to antiepileptic drugs) and no MRI features associated with psychiatric disorders. A seven-fold increased risk of mood disorders was identified in patients with inter-ictal EEG abnormalities associated with the left hemisphere.ConclusionRelative to previous reports, we identify a high prevalence of psychiatric disorders in TLE patients, although our data is similar to that observed in other studies which have used similar structured interviews in populations of epileptic patients attending tertiary centres. The wide variation in percentages is probably attributable to the different patient groups investigated and to the even greater variety of diagnostic methods. Structured psychiatric interviews may contribute to a better evaluation of the true prevalence of psychiatric comorbidities in temporal lobe epilepsy.

Serotonin gene polymorphisms and psychiatry comorbidities in temporal lobe epilepsy

OBJECTIVE Neuropsychiatric comorbidities are frequent in temporal lobe epilepsy (TLE). It is biologically plausible that alterations in serotonin-related genes may be involved in higher susceptibility to psychiatric disease in these individuals. Here we report results of an association study of serotonin gene polymorphisms and psychiatry comorbidities in TLE. METHODS Case-control study of 155 patients with temporal lobe epilepsy. We evaluate the influence of 5-HTTLPR and 5-HTTVNTR polymorphisms in the 5-HTT gene and the C-1019G polymorphism in the 5-HT1A gene in psychiatric comorbidities of TLE. RESULTS After logistic regression, female sex (OR=2.34; 95% CI 1.06-5.17; p=0.035) and the presence of C allele of 5-HT1A C-1019G polymorphism (OR=2.77; 95% CI 1.01-7.63; p=0.048) remained independent risk factors for anxiety disorders in temporal lobe epilepsy. CONCLUSION C allele of 5-HT1A C-1019G polymorphism might be an independent risk factor for anxiety disorders in temporal lobe epilepsy. We believe that other studies in this venue will shade some light on molecular mechanisms involved in psychiatric comorbidities in epilepsy.

Serotonin transporter gene (5HTT) polymorphisms and temporal lobe epilepsy.

OBJECTIVE Preclinical and clinical studies have shown that serotonin levels might modulate susceptibility to seizures. Here we evaluated an association between 5HTTLPR and 5HTTVNTR allele variants in serotonin transporter gene and epileptogenesis in temporal lobe epilepsy (TLE). METHODS A case-control candidate gene study evaluating the frequencies of 5HTTLPR biallelic and 5HTTVNTR allele variants in patients and healthy subjects. Genotypes were grouped according to transcriptional efficiency. Cases were 175 patients with TLE selected from the Epilepsy Outpatient Clinic of Hospital de Clínicas de Porto Alegre, classified according to the electroclinical classification of the ILAE and neuroimaging findings. The control group consisted of 155 healthy unrelated subjects selected from the same population. RESULTS We observed that less efficient transcriptional genotypes for 5-HTT polymorphisms were more frequent in epileptic patients (O.R.=3.24; 95% C.I.=1.08-9.73; p=0.036). Our results suggest that less efficient transcriptional genotypes for serotonin transporter gene are associated with TLE. CONCLUSION In this study we observed an association between the presence of 5HTTLPR and 5-HTTVNTR less transcriptional efficient combined genotypes and TLE. Our results suggest that modulation of the serotoninergic system might be implied in epileptogenesis in TLE.

Prevalence of psychiatric comorbidities in temporal lobe epilepsy in a Southern Brazilian population

A great prevalence of psychiatric disorders in epilepsy is well demonstrated, although most studies have used unstructured psychiatric interviews for diagnosis. Here we present a study evaluating the prevalence of psychiatric comorbidities in a cohort of Southern Brazilian patients with temporal lobe epilepsy (TLE) using a structured clinical interview. We analyzed 166 patients with TLE regarding neuropsychiatric symptoms through the Structured Clinical Interview for DSM-IV. One hundred-six patients (63.9%) presented psychiatric comorbidities. Mood disorders were observed in 80 patients (48.2%), anxiety disorders in 51 patients (30.7%), psychotic disorders in 14 (8.4%), and substance abuse in 8 patients (4.8%) respectively. Our results agree with literature data where most authors detected mental disorders in 10 to 60% of epileptic patients. This wide variation is probably attributable to different patient groups investigated and to the great variety of diagnostic methods. Structured psychiatric interviews might contribute to a better evaluation of prevalence of psychiatric comorbidities in TLE.

Nasu–Hakola disease and primary microglial dysfunction

in their article (Microglia in neurodegenerative disease. Nat. Rev. Neurol. 6, 193–201; 2010)1 Perry et al. provide a comprehensive review of the involvement of microglia in neurodegenerative disease. the authors highlight the substantial interest that exists regarding the possible roles of activated microglia in disease pathogenesis, and question whether activated microglia exacerbate pathology or aid tissue repair in neurodegenerative diseases. in all of the diseases used as examples by the authors, microglial activation is secondary to other pathological processes that affect the Cns. in order to contribute to this discussion, we would like to highlight the interesting example of nasu–Hakola disease, and discuss how microglial dysfunction might cause substantial brain damage.2–6 this example of microglial dysfunction causing brain damage is important because it might offer insights into the importance of microglial homeostasis in the brain. nasu–Hakola disease—also known as polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOsL)—is a genetic disorder characterized by progressive presenile dementia and bone cysts.2–7 Patients with nasu–Hakola disease develop a variant of frontotemporal dementia associated with cyst-like bone lesions (Figure 1). the disease usually starts during the 4th decade of life, leading to death after only a few years.2–7 in contrast to other diseases, evidence strongly suggests that in nasu–Hakola disease Cns damage is directly caused by microglial dysfunction.2,3,8,9 Histological examination of brains from patients with nasu–Hakola disease shows that neuronal loss, and astrocyte proliferation and hypertrophy, occurs mainly in the white matter of the frontotemporal lobe and basal ganglia.3,10 nevertheless, the most interesting feature of this disease is a well-documented activation of microglia in the cerebral white matter of patients with this condition, and this prominent microglial activation might be the primary underlying factor responsible for nasu–Hakola disease.3,11 Genetic studies have shown that mutations in the genes TREM2 and TYROBP, which encode the proteins treM2 and tYrOBP, respectively, are responsible for the phenotypic abnormalities in homozygous patients with this condition.5,12 the treM2– tYrOBP protein complex regulates the differentiation and function of osteoclasts, which are bone-resorbing cells.6,13 in the brain, treM2–tYrOBP has been shown to be expressed mainly—or even exclusively—by microglia, and is thought to regulate cell function.3,7,10,14,15 takahashi et al. showed that knockdown of treM2 in microglia inhibited phagocytosis of apoptotic neurons and increased proinflammatory responses,15 a finding important for understanding

Impact of the chronic use of benzodiazepines prescribed for seizure control on the anxiety levels of patients with epilepsy

In a cross-sectional study, we evaluated the impact of the chronic use of benzodiazepines (BDZ) prescribed for seizure control on the anxiety levels of patients with temporal lobe epilepsy. We assessed the anxiety level of 99 patients with temporal lobe epilepsy with (n=15) or without (n=84) BDZ for seizure control, using the Beck Anxiety Inventory (BAI) or the Hamilton Anxiety Scale (HAMA). Independent risk factors for high anxiety levels were being a female patient (O.R.=2.93; 95% C.I.=1.05-8.16; p=0.039), having uncontrolled seizures (O.R.=4.49; 95% C.I.=1.66-12.11; p=0.003) and having a history of a psychiatric disorder (O.R.=4.46; 95% C.I.=1.63-12.21; p=0.004). However, there were no statistically significant differences in anxiety levels between patients utilizing or not utilizing BDZ prescribed exclusively for seizure control. We concluded that in our study, patients with chronic use of BDZ prescribed exclusively for seizure control showed similar anxiety levels than patients who were not using this class of drug. Additional studies are needed to define better strategies for the treatment of anxiety disorders in epilepsy.

Abstract TP314: Comparison of Patient-centered Outcome Measures of the International Consortium for Health Outcomes Measurements (ICHOM) Between Private and Public Healthcare System in Brazil

Introduction: An international experts panel was assembled to create a standard set of outcome measures for use in both low and high-income countries. Additionally, the panel intended to represent the most relevant outcomes for subsequent cost-effectiveness analysis. For implementing the tool, it was necessary to make it feasible in different healthcare systems. The objective of this study was to implement and compare the ICHOM outcome measures between two different stroke centers: a university public hospital and a private hospital. Methods: the medical data of all patients with stroke diagnosis consecutively admitted in the two hospitals were registered. ICHOM outcomes in the 3-month follow-up were measured by interviews in person, by phone or by e-mail, and the results were compared between the hospitals. Results: 90-day outcome measurements were available for 328 patients (169 in the private hospital and 159 in the public), corresponding to 87% of the patients admitted with stroke diagnosis in these hospitals. The mean age was 68 years in the private vs. 65 in the public, with a mean NIHSS of 7, and 90% had ischemic strokes (18% received IV thrombolysis in the private setting vs. 16% in the public). Public hospital inpatients had a greater number of comorbidities. The mortality rate was 14% in both hospitals, and functional independence (mRS 0-2) occurred in 51% of private setting patients and 39% of the public. The greater proportion of patients needing help for dressing or toileting, as well as having language issues, was in the public setting. Better outcomes were measured in the private hospital regarding the resumption of the social role (64% vs 40%), satisfaction with social activities (65% vs 57%) and good quality of life (66% vs 57%). In both hospitals, 34% had access to physiotherapy after hospital discharge. Conclusions: In patients with acute stroke from private and public hospitals the thrombolysis eligibility are similar, without increasing the mortality rates in the public setting. However, better functional outcomes were found in private patients, probably due to less comorbidities, better prevention and post-discharge rehabilitation care.