Healthcare attendance styles among long-term unemployed people with substance-related and mood disorders.

BACKGROUND: Both increased and decreased health service usage and unmet care needs are more prevalent among unemployed people than in the general population. STUDY DESIGN: This study investigates the associations of substance-related and mood disorders among long-term unemployed people with styles of healthcare attendance in Finland. METHODS: The study material consisted of the health register information on 498 long-term unemployed people in a project screening for work disabilities. The data were analysed by mixed methods: qualitative typological analysis was applied to identify differential healthcare attendance styles, and the associations of the obtained styles with mental health disorders were analysed quantitatively by multinomial logistic regression. RESULTS: Three styles, characterized as smooth, faltering and marginalized, were identified. Compared with participants with the smooth attendance style without mental disorders, those with the faltering style had tenfold relative risk for substance-related disorder and fourfold relative risk for mood disorder. Those with the marginalized style had fivefold relative risk for substance-related disorder and twofold relative risk for mood disorder. Adjusting for background characteristics did not alter the statistical significance of substance-related disorder. In the case of mood disorders, the statistical significance persisted throughout the adjustments in the faltering style. CONCLUSION: Dysfunctional use of health services is more common among people with substance-related or mood disorders, who are at risk of drifting towards long-term unemployment and work disabilities. The early detection of those with faltering or marginalized healthcare attendance style may prevent prolonged unemployment, enable rehabilitation measures and reduce the risk of disability pensions.

The benefit of active drug trials is dependent on aetiology in refractory focal epilepsy.

BACKGROUND: Earlier studies have shown that aetiology makes a difference in the outcome of epilepsy, but there is a paucity of follow-up studies to evaluate the possibilities of achieving seizure freedom in initially refractory epilepsy. METHODS: We evaluated the cause of epilepsy based on high-resolution brain MRI and patient history in 119 consecutive thoroughly examined adult patients with refractory focal epilepsy followed up in our centre. We also evaluated the influence of aetiology and duration of epilepsy in this patient cohort on the chances of achieving 12-month remission in a 2-year follow-up. RESULTS: The major finding was that a substantial group of patients achieved remission; 30 (25%) initially refractory patients achieved at least 12 months remission during follow-up. A total of 40.0% of the patients with cryptogenic aetiology had achieved 12-month remission compared with the 16.2% patients with symptomatic aetiologies (age-adjusted OR 3.74, 95% CI 1.54 to 9.07, p = 0.004). Aetiologies often considered for surgical treatment (hippocampal sclerosis, cortical dysplasia, vascular malformation, tumour and dual pathology) carried an almost six-fold risk of persistent seizures compared with cryptogenic epilepsy (age-adjusted OR 5.85, 95% CI 2.00 to 17.11, p = 0.001). CONCLUSIONS: Patients with vascular malformation and dual pathology as aetiology were most refractory, none being in remission for 12 months. There were also patients achieving 12-month remission after a long period of active epilepsy. These results encourage physicians to continue with new drug trials, especially on patients with no possibilities of epilepsy surgery, as well as on those still having seizures after epilepsy surgery.

Enhanced GABAergic inhibition preserves hippocampal structure and function in a model of epilepsy.

Extensive electrical stimulation of the perforant pathway input to the hippocampus results in a characteristic pattern of neuronal death, which is accompanied by an impairment of cognitive functions similar to that seen in human temporal lobe epilepsy. The excitotoxic hypothesis of epileptic cell death [Olney, J. W. (1978) in Kainic Acid as a Tool in Neurobiology, eds. McGeer, E., Olney, J. W. & McGeer, P. (Raven, New York), pp. 95-121; Olney, J. W. (1983) in Excitotoxins, eds. Fuxe, K., Roberts, P. J. & Schwartch, R. (Wenner-Gren International Symposium Series, Macmillan, London), Vol. 39, pp. 82-96; and Rothman, S. M. & Olney, J. W. (1986) Ann. Neurol. 19, 105-111] predicts an imbalance between excitation and inhibition, which occurs probably as a result of hyperactivity in afferent pathways or impaired inhibition. In the present study, we investigated whether the enhancement of gamma-aminobutyric acid (GABA)-mediated (GABAergic) inhibition of neurotransmission by blocking the GABA-metabolizing enzyme, GABA transaminase, could influence the histopathological and/or the behavioral outcome in this epilepsy model. We demonstrate that the loss of pyramidal cells and hilar somatostatin-containing neurons can be abolished by enhancing the level of synaptically released GABA, and that the preservation of hippocampal structure is accompanied by a significant sparing of spatial memory as compared with placebo-treated controls. These results suggest that enhanced GABAergic inhibition can effectively block the pathophysiological processes that lead to excitotoxic cell death and, as a result, protect the brain from seizure-induced cognitive impairment.