RESUMEN
In this paper we look at non-pharmaceutical treatments for intractable epilepsy based on neurophysiological methods especially with EEG analysis. In summary, there are a number of limbic and thalamo-cortical related structures involved in the processing of musical emotion (exposure), including the amygdala (arousal, expression of mood, fear), hippocampus (memory, regulation of HPA axis, stress), parahippocampal gyrus (recognition, memory retrieval), insula (valence), temporal poles (connectivity), ventral striatum (expectation and experience of reward), orbitofrontal cortex (valence) and cingulate cortex (autonomic regulation). One method is to audify (a form of sonification) EEG activity to find music by feedback to entrain abnormal EEG activity. We discuss various methods and our use of X-System (https://www.x-system.co.uk/) which is a computational model of the musical brain capable of predicting the neurophysiological effects of music. It models structures and pathways related to responses to music, including the cochlea, brain stem, auditory and motor cortex, as well as basal ganglia, cerebellum and limbic structures. It can predict autonomic and endocrine activity as well as the substrates of electrical activity to select music which can regularise EEG abnormalities to decrease epileptic activity and seizures, especially in those unresponsive to antiepileptic medication or invasive treatments.
Asunto(s)
Epilepsia , Musicoterapia , Música , Humanos , Epilepsia/terapia , Epilepsia/fisiopatología , Musicoterapia/métodos , Electroencefalografía , Encéfalo/fisiopatología , Percepción Auditiva/fisiología , Medicina de Precisión/métodosRESUMEN
The objective of this study was to determine prevalence and predictive risk factors of suicidality in a large sample of epilepsy outpatients. We prospectively examined 193 consecutive adult epilepsy outpatients for depression, including suicidal ideation. Demographic and epilepsy factors, medication toxicity and health-related quality of life were also evaluated. The prevalence of suicidal ideation within the past two weeks was 11.9%. Although medication toxicity, health-related quality of life and BDI scores were each associated with suicidal ideation in the bivariate analyses, only the BDI remained significant in the logistic regression analysis. About one-fourth of the subjects with suicidal ideation had no significant symptoms of depression. Recent thoughts of suicide are a common occurrence in the outpatient epilepsy clinic setting, but these are not predicted by gender, age, seizure factors, medication toxicity or self-perceived quality of life. Although depression is associated with suicidal ideation, about one-fourth of the suicidal subjects were euthymic or only mildly depressed.
Asunto(s)
Depresión/epidemiología , Depresión/psicología , Epilepsia/epidemiología , Epilepsia/psicología , Calidad de Vida , Suicidio/psicología , Adulto , Anticonvulsivantes/uso terapéutico , Epilepsia/tratamiento farmacológico , Femenino , Humanos , Masculino , Persona de Mediana Edad , Escalas de Valoración Psiquiátrica , Análisis de Regresión , Convulsiones/epidemiología , Convulsiones/psicología , Suicidio/estadística & datos numéricos , Encuestas y CuestionariosRESUMEN
The whole-cell patch-clamp technique was used to examine the effect of substance P (SP) on glutamate-induced currents in freshly dissociated rat spinal dorsal horn neurons (LI-III). In 48% of examined cells SP (10(-10)-10(-6) M) at -70 mV, induced in inward current that desensitized in the continued presence of SP. When applied simultaneously with, or prior to L-glutamate, SP caused a potentiation of L-glutamate-induced current in 65% of the tested cells. Since glutamate activates both N-methyl-D-aspartate (NMDA) and non-NMDA receptors in rat dorsal horn neurons, selective agonists, kainate, quisqualate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and NMDA were used to determine which subtype of excitatory amino acid receptors interacted with SP. We found that the responses to quisqualate, kainate, and AMPA were not significantly affected by SP (less than 20% increase). In contrast, the inward currents induced by NMDA (30-300 microM) appear to be reduced and potentiated after the administration of 2-200 nM of SP. These results suggest that post-synaptic mechanisms of action of tachykinins may contribute to the regulation of the strength of glutamate-mediated excitatory transmission in the rat spinal dorsal horn.
Asunto(s)
Glutamatos/farmacología , Neuronas/fisiología , Médula Espinal/fisiología , Sustancia P/farmacología , Animales , Potenciales Evocados/efectos de los fármacos , Ácido Glutámico , Ácido Iboténico/análogos & derivados , Ácido Iboténico/farmacología , Técnicas In Vitro , Ácido Kaínico/farmacología , N-Metilaspartato/farmacología , Neuronas/efectos de los fármacos , Ácido Quiscuálico/farmacología , Ratas , Receptores de N-Metil-D-Aspartato/efectos de los fármacos , Receptores de N-Metil-D-Aspartato/fisiología , Médula Espinal/efectos de los fármacos , Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol PropiónicoAsunto(s)
Canales de Calcio/metabolismo , Guanosina 5'-O-(3-Tiotrifosfato)/farmacología , Ácido Ocadaico/farmacología , Núcleos del Rafe/efectos de los fármacos , Receptores de Serotonina/metabolismo , 8-Hidroxi-2-(di-n-propilamino)tetralin/análogos & derivados , 8-Hidroxi-2-(di-n-propilamino)tetralin/farmacología , Animales , Bario/metabolismo , Electrofisiología , Proteínas de Unión al GTP/metabolismo , Cinética , Masculino , Neuronas/efectos de los fármacos , Fosforilación , Núcleos del Rafe/metabolismo , Ratas , Ratas Wistar , Receptores de Serotonina 5-HT1RESUMEN
Serotonin syndrome usually occurs after treatment with monoamine oxydase inhibitors and drugs that enhance serotoninergic transmission. Serotonin agents, such as Proza, are commonly prescribed drugs; therefore, the serotonin syndrome appears more frequently than before. Clinicians must be able to prevent, recognize, and treat this syndrome in their practice. This review summarizes the literature of case reports of patients who developed the serotonin syndrome.