Una revisión de los programas de intervención grupal con víctimas de violencia de género / A review of group intervention programs with victims of gender violence

La violencia de género es un problema personal y social grave, con múltiples consecuencias para las mujeres maltratadas. Los estudios de intervención para ayudar a estas personas son escasos y desde aproximaciones diversas. Se ha realizado aquí una revisión sistemática de los tratamientos aplicados en grupo a mujeres que han sido objeto de violencia de género. Se han revisado las bases de datos de Scopus, Web of Science, Google Scholar, ResearchGate, además de literatura gris. Del total de trabajos se han seleccionado 34 de ellos que sí eran estudios con datos de efica-cia, agrupados por el tipo de intervención: terapias cognitivo-conductuales (22), terapias contextuales (4) y programas diversos (8). Los resultados muestran que las terapias cognitivo-conductuales son eficaces para reducir las conductas de ansiedad, estrés y trastorno de estrés postraumático, con distintos tamaños del efecto y seguimientos hasta 12 meses. Las terapias contextuales son prometedoras en este campo y permiten una aplicación adaptada a la persona. Las demás terapias muestran eficacia en algunos casos, aunque partan de teorías diferentes utilizan también técnicas de la terapia cognitivo-conductual. Se concluye sobre la necesidad de investigar los componentes específicos de las terapias, y realizar estudios con diseños de grupos aleatorizados (AU)~

Gender violence is a serious personal and social problem, with multiple consequences for abused women. Inter-vention studies to help these people, are scarce and from different approaches. We have carried out a systematic review of the treatments applied in groups to women who have been in gender violence. The data bases of Scopus, Web of Science, Google Scholar, Dialnet and grey literature were reviewed. From the papers found, 34 of them have been select because they were studies with data about efficacy, grouped by the type of intervention: cognitive-behavioural therapies (22), contextual therapies (4), and diverse programmes (8). The results showed that cognitive-behavioural therapies are effective in reducing anxiety, stress, and PTSD behaviours, with varying effect sized and follow-ups to 12 months. Contextual therapies are promising in this field and can be addressed in an individualized way. The other therapies sowed efficacy in some cases, although each is based on different theories, they also use techniques from cognitive-behavioural therapies. We concluded that there is a need for research on the specific components of the therapies, and more studies with randomized group designs (AU)

Encefalopatías y encefalitis durante la infección aguda por SARS-CoV2. Registro de la Sociedad Española de Neurología SEN COVID-19 / Encephalopathy and encephalitis during acute SARS-CoV-2 infection. Spanish Society of Neurology COVID-19 Registry

OBJETIVOS: Desde el inicio de la pandemia por el virus SARS-CoV2 la Sociedad Española de Neurología (SEN) creó un registro de afectación neurológica para informar al neurólogo clínico. Las encefalopatías y encefalitis fueron una de las complicaciones más descritas. Analizamos las características de las mismas. PACIENTES Y MÉTODOS: Estudio descriptivo retrospectivo, observacional multicéntrico, de pacientes con sintomatología compatible con encefalitis o encefalopatía, introducidos en el Registro SEN COVID-19 desde el 17 de marzo hasta el 6 de junio de 2020. RESULTADOS: Se han registrado 232 casos con síntomas neurológicos, 51 casos de encefalopatía/encefalitis (21,9%). Ningún paciente era trabajador sanitario. Los síndromes más frecuentes fueron: cuadro confusional leve-moderado (33%) y encefalopatía grave o coma (9,8%). El tiempo medio entre el inicio de la infección y la clínica neurológica fue de 8,02 días. Punción lumbar en el 60,8% de pacientes; solo hubo un caso con PCR positiva. Resonancia craneal en el 47% de los pacientes (alterada en el 7,8% de ellos). Se realizó electroencefalograma en el 41,3% de los casos (alterado en el 61,9% de los mismos). CONCLUSIONES: Las encefalopatías y encefalitis son dos de las complicaciones más frecuentes descritas en el SEN COVID-19. Más de un tercio de los pacientes presentó un cuadro de síndrome confusional leve o moderado. El tiempo medio de aparición de la sintomatología neurológica desde el inicio de la infección fue de 8 días (hasta 24 h antes en mujeres que en hombres). El electroencefalograma fue la prueba más sensible en estos pacientes, encontrando muy pocos casos con alteraciones en las pruebas de neuroimagen. Todos los pacientes que recibieron tratamiento con bolos de corticoides o inmunoglobulinas tuvieron una evolución favorable

OBJECTIVES: Since the beginning of the COVID-19 pandemic, the Spanish Society of Neurology has run a registry of patients with neurological involvement for the purpose of informing clinical neurologists. Encephalopathy and encephalitis were among the most frequently reported complications. In this study, we analyse the characteristics of these complications. PATIENTS AND METHODS: We conducted a retrospective, descriptive, observational, multicentre study of patients with symptoms compatible with encephalitis or encephalopathy, entered in the Spanish Society of Neurology's COVID-19 Registry from 17 March to 6 June 2020. RESULTS: A total of 232 patients with neurological symptoms were registered, including 51 cases of encephalopathy or encephalitis (21.9%). None of these patients were healthcare professionals. The most frequent syndromes were mild or moderate confusion (33%) and severe encephalopathy or coma (9.8%). The mean time between onset of infection and onset of neurological symptoms was 8.02 days. Lumbar puncture was performed in 60.8% of patients, with positive PCR results for SARS-CoV-2 in only one case. Brain MRI studies were performed in 47% of patients, with alterations detected in 7.8% of these. EEG studies were performed in 41.3% of cases, detecting alterations in 61.9%. CONCLUSIONS: Encephalopathy and encephalitis are among the complications most frequently reported in the registry. More than one-third of patients presented mild or moderate confusional syndrome. The mean time from onset of infection to onset of neurological symptoms was 8 days (up to 24 hours earlier in women than in men). EEG was the most sensitive test in these patients, with very few cases presenting alterations in neuroimaging studies. All patients treated with boluses of corticosteroids or immunoglobulins progressed favourably

Encephalopathy and encephalitis during acute SARS-CoV-2 infection. Spanish Society of Neurology COVID-19 Registry. / Encefalopatías y encefalitis durante la infección aguda por SARS-CoV2. Registro de la Sociedad Española de Neurología SEN COVID-19.

OBJECTIVES: Since the beginning of the COVID-19 pandemic, the Spanish Society of Neurology has run a registry of patients with neurological involvement for the purpose of informing clinical neurologists. Encephalopathy and encephalitis were among the most frequently reported complications. In this study, we analyse the characteristics of these complications. PATIENTS AND METHODS: We conducted a retrospective, descriptive, observational, multicentre study of patients with symptoms compatible with encephalitis or encephalopathy, entered in the Spanish Society of Neurology's COVID-19 Registry from 17 March to 6 June 2020. RESULTS: A total of 232 patients with neurological symptoms were registered, including 51 cases of encephalopathy or encephalitis (21.9%). None of these patients were healthcare professionals. The most frequent syndromes were mild or moderate confusion (33%) and severe encephalopathy or coma (9.8%). The mean time between onset of infection and onset of neurological symptoms was 8.02 days. Lumbar puncture was performed in 60.8% of patients, with positive PCR results for SARS-CoV-2 in only one case. Brain MRI studies were performed in 47% of patients, with alterations detected in 7.8% of these. EEG studies were performed in 41.3% of cases, detecting alterations in 61.9%. CONCLUSIONS: Encephalopathy and encephalitis are among the complications most frequently reported in the registry. More than one-third of patients presented mild or moderate confusional syndrome. The mean time from onset of infection to onset of neurological symptoms was 8 days (up to 24hours earlier in women than in men). EEG was the most sensitive test in these patients, with very few cases presenting alterations in neuroimaging studies. All patients treated with boluses of corticosteroids or immunoglobulins progressed favourably.

Reduced sedation and increased ethanol consumption in knock-in mice expressing an ethanol insensitive alpha 2 subunit of the glycine receptor.

Previous studies have shown the presence of several subunits of the inhibitory glycine receptor (GlyR) in the reward system, specifically in medium spiny neurons (MSNs) of the nucleus Accumbens (nAc). It was suggested that GlyR α1 subunits regulate nAc excitability and ethanol consumption. However, little is known about the role of the α2 subunit in the adult brain since it is a subunit highly expressed during early brain development. In this study, we used genetically modified mice with a mutation (KR389-390AA) in the intracellular loop of the GlyR α2 subunit which results in a heteromeric α2ß receptor that is insensitive to ethanol. Using this mouse model denoted knock-in α2 (KI α2), our electrophysiological studies showed that neurons in the adult nAc expressed functional KI GlyRs that were rather insensitive to ethanol when compared with WT GlyRs. In behavioral tests, the KI α2 mice did not show any difference in basal motor coordination, locomotor activity, or conditioned place preference compared with WT littermate controls. In terms of ethanol response, KI α2 male mice recovered faster from the administration of ataxic and sedative doses of ethanol. Furthermore, KI α2 mice consumed higher amounts of ethanol in the first days of the drinking in the dark protocol, as compared with WT mice. These results show that the α2 subunit is important for the potentiation of GlyRs in the adult brain and this might result in reduced sedation and increased ethanol consumption.

Changes in neuronal excitability and synaptic transmission in nucleus accumbens in a transgenic Alzheimer's disease mouse model.

Several previous studies showed that hippocampus and cortex are affected in Alzheimer's disease (AD). However, other brain regions have also been found to be affected and could contribute with new critical information to the pathophysiological basis of AD. For example, volumetric studies in humans have shown a significant atrophy of the striatum, particularly in the nucleus Accumbens (nAc). The nAc is a key component of the limbic reward system and it is involved in cognition and emotional behaviors such as pleasure, fear, aggression and motivations, all of which are affected in neurodegenerative diseases such as AD. However, its role in AD has not been extensively studied. Therefore, using an AD mouse model, we investigated if the nAc was affected in 6 months old transgenic 2xTg (APP/PS1) mice. Immunohistochemistry (IHC) analysis in 2xTg mice showed increased intraneuronal Aß accumulation, as well as occasional extracellular amyloid deposits detected through Thioflavin-S staining. Interestingly, the intracellular Aß pathology was associated to an increase in membrane excitability in dissociated medium spiny neurons (MSNs) of the nAc. IHC and western blot analyses showed a decrease in glycine receptors (GlyR) together with a reduction in the pre- and post-synaptic markers SV2 and gephyrin, respectively, which correlated with a decrease in glycinergic miniature synaptic currents in nAc brain slices. Additionally, voltage-clamp recordings in dissociated MSNs showed a decrease in AMPA- and Gly-evoked currents. Overall, these results showed intracellular Aß accumulation together with an increase in excitability and synaptic alterations in this mouse model. These findings provide new information that might help to explain changes in motivation, anhedonia, and learning in the onset of AD pathogenesis.

High ethanol sensitive glycine receptors regulate firing in D1 medium spiny neurons in the nucleus accumbens.

Inhibitory glycine receptors (GlyRs) are widely expressed in spinal cord and brain stem. They are also expressed in the nucleus Accumbens (nAc) where they have been implicated in the release of dopamine from the ventral tegmental area to the nAc in the presence of ethanol. One of the major types of neurons in the nAc are the Dopamine 1 receptor-expressing (D1+) medium spiny neurons (MSNs) that are activated when addictive drugs, like ethanol, are administrated. Thus, D1(+) MSNs are a relevant target for the study of ethanol effects. Here, using electrophysiological recordings, we report that GlyRs in D1(+) MSNs are highly sensitive to ethanol, with potentiation starting at 5 mM (26 ± 5%). Single channel recordings in D1(+) MSNs showed that 10 mM ethanol increased the open probability of the channel (0.22 ± 0.05 versus 0.66 ± 0.16), but did not affect channel conductance (~40 pS). A glycinergic mediated tonic current in D1(+) MSNs was potentiated by 10 and 50 mM ethanol causing a reduction in the excitability of these cells. A 34 ± 7% reduction in action potential firing was observed in these neurons in the presence of 50 mM ethanol. Interestingly, no effects of ethanol were detected in the presence of strychnine or in D1(-) MSNs in the nAc. These results indicate that GlyRs present in D1(+) MSNs are sensitive to low concentrations of ethanol, and that potentiation of this inhibitory current regulates the activation of nAc, acting as a homeostatic signal that would prevent over-activation of the reward system when drugs like ethanol are consumed.

Role of membrane GM1 on early neuronal membrane actions of Aß during onset of Alzheimer's disease.

The ability of beta-amyloid peptide (Aß) to disrupt the plasma membrane through formation of pores and membrane breakage has been previously described. However, the molecular determinants for these effects are largely unknown. In this study, we examined if the association and subsequent membrane perforation induced by Aß was dependent on GM1 levels. Pretreatment of hippocampal neurons with D-PDMP decreased GM1 and Aß clustering at the membrane (Aß fluorescent-punctas/20µm, control=16.2±1.1 vs. D-PDMP=6.4±0.4, p<0.001). Interestingly, membrane perforation with Aß occurred with a slower time course when the GM1 content was diminished (time to establish perforated configuration (TEPC) (min): control=7.8±2 vs. low GM1=12.1±0.5, p<0.01), suggesting that the presence of GM1 in the membrane can modulate the distribution and the membrane perforation by Aß. On the other hand, increasing GM1 facilitated the membrane perforation (TEPC: control=7.8±2 vs. GM1=6.2±1min, p<0.05). Additionally, using Cholera Toxin Subunit-B (CTB) to block the interaction of Aß with GM1 attenuated membrane perforation significantly. Furthermore, pretreatment with CTB decreased the membrane association of Aß (fluorescent-punctas/20µm, Aß: control=14.8±2.5 vs. CTB=8±1.4, p<0.05), suggesting that GM1 also plays a role in both association of Aß with the membrane and in perforation. In addition, blockade of the Aß association with CTB inhibited synaptotoxicity. Taken together, our results strongly suggest that membrane lipid composition can affect the ability of Aß to associate and subsequently perforate the plasma membrane thereby modulating its neurotoxicity in hippocampal neurons.

Presence of ethanol-sensitive glycine receptors in medium spiny neurons in the mouse nucleus accumbens.

KEY POINTS: The nucleus accumbens (nAc) is involved in addiction-related behaviour caused by several drugs of abuse, including alcohol. Glycine receptors (GlyRs) are potentiated by ethanol and they have been implicated in the regulation of accumbal dopamine levels. We investigated the presence of GlyR subunits in nAc and their modulation by ethanol in medium spiny neurons (MSNs) of the mouse nAc. We found that the GlyR α1 subunit is preferentially expressed in nAc and is potentiated by ethanol. Our study shows that GlyR α1 in nAc is a new target for development of novel pharmacological tools for behavioural intervention in drug abuse. ABSTRACT: Alcohol abuse causes major social, economic and health-related problems worldwide. Alcohol, like other drugs of abuse, increases levels of dopamine in the nucleus accumbens (nAc), facilitating behavioural reinforcement and substance abuse. Previous studies suggested that glycine receptors (GlyRs) are involved in the regulation of accumbal dopamine levels. Here, we investigated the presence of GlyRs in accumbal dopamine receptor medium spiny neurons (MSNs) of C57BL/6J mice, analysing mRNA expression levels and immunoreactivity of GlyR subunits, as well as ethanol sensitivity. We found that GlyR α1 subunits are expressed at higher levels than α2, α3 and ß in the mouse nAc and were located preferentially in dopamine receptor 1 (DRD1)-positive MSNs. Interestingly, the glycine-evoked currents in dissociated DRD1-positive MSNs were potentiated by ethanol. Also, the potentiation of the GlyR-mediated tonic current by ethanol suggests that they modulate the excitability of DRD1-positive MSNs in nAc. This study should contribute to understanding the role of GlyR α1 in the reward system and might help to develop novel pharmacological therapies to treat alcoholism and other addiction-related and compulsive behaviours.

Tromboprofilaxis farmacológica en paciente crítico y la acumulación de heparinas de bajo peso molecular / Drug thromboprophylaxis in critical patients and the accumulation of low molecular weight heparins

No disponible

ATP leakage induces P2XR activation and contributes to acute synaptic excitotoxicity induced by soluble oligomers of ß-amyloid peptide in hippocampal neurons.

Recent studies suggest that the toxic effects of Aß can be attributed to its capability to insert in membranes and form pore-like structures, which are permeable to cations and molecules such as ATP. Our working hypothesis is that Aß increases extracellular ATP causing activation of P2X receptors and potentiating excitatory synaptic activity. We found that soluble oligomers of ß-amyloid peptide increased cytosolic Ca(2+) 4-fold above control (415 ± 28% of control). Also, ATP leakage (157 ± 10% of control) was independent of extracellular Ca(2+), suggesting that ATP traveled from the cytosol through an Aß pore-mediated efflux and not from exocytotic mechanisms. The subsequent activation of P2XR by ATP can contribute to the cytosolic Ca(2+) increase observed with Aß. Additionally, we found that ß-amyloid oligomers bind preferentially to excitatory neurons inducing an increase in excitatory synaptic current frequency (248.1 ± 32.7%) that was blocked by the use of P2XR antagonists such as PPADS (Aß + PPADS: 110.9 ± 18.35%) or Apyrase plus DPCPX (Aß + inhibitors: 98.97 ± 17.4%). Taken together, we suggest that Aß induces excitotoxicity by binding preferentially to excitatory neuron membranes forming a non-selective pore and by increasing intracellular calcium by itself and through P2XR activation by extracellular ATP leading to an augmention in mEPSC activity. All these effects were blocked with a non-specific P2XR antagonist, indicating that part of the neurotoxicity of Aß is mediated by P2XR activation and facilitation of excitatory neurotransmitter release. These findings suggest that P2XR can be considered as a potential new target for the development of drugs or pharmacological tools to treat Alzheimer's disease. This article is part of the Special Issue entitled 'Synaptopathy--from Biology to Therapy'.

Rapamycin protects against Aß-induced synaptotoxicity by increasing presynaptic activity in hippocampal neurons.

The mammalian target of rapamycin (mTOR) is involved in the regulation of learning and memory. Recently, rapamycin has been shown to be neuroprotective in models for Alzheimer's disease in an autophagy-dependent manner. Here we show that rapamycin exerts neuroprotection via a novel mechanism that involves presynaptic activation. Rapamycin increases the frequency of miniature excitatory postsynaptic currents and calcium transients of rat hippocampal primary neurons by a mechanism that involves the up regulation of SV2, a presynaptic vesicular protein linked to neurotransmitter release. Under these conditions, rapamycin-treated hippocampal neurons are resistant to the synaptotoxic effect induced by Aß oligomers, suggesting that enhancers of presynaptic activity can be therapeutic agents for Alzheimer's disease.

An extracellular mechanism that can explain the neurotoxic effects of α-synuclein aggregates in the brain.

Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), and Dementia with Lewy bodies (DLB), display an accumulation of proteins including α-synuclein aggregates in cortical and subcortical regions of the brain. PD is a complex, progressive disease which involves damage of motor and cognitive brain regions, as well as autonomic and sensory areas. Since α-synuclein is a neuronal cytosolic protein, it is assumed that pathogenic changes induced by α-synuclein aggregates occur only at the cytoplasmic level. However, recent studies have identified the presence of extracellular α-synuclein, suggesting that the pathogenic action of this protein may also occur in the extracellular milieu through an unknown mechanism. One of the hypotheses is that extracellular α-synuclein aggregates or oligomers may directly disrupt the neuronal membrane by the formation of a pore reminiscent to the ones formed by ß-amyloid aggregates. Here, we will review some evidence that support this mechanism, analyzing the interactions of α-synuclein with components of the plasma membrane, the formation of pore/perforated structures, and the implications on ionic dyshomeostasis. Furthermore, we will also discuss how this mechanism can be integrated into a general phenomenon that may explain the synaptotoxicity and neurotoxicity observed in different neurodegenerative diseases.

Aß oligomers induce glutamate release from hippocampal neurons.

Soluble oligomers of the amyloid-ß peptide (AßOs) accumulate in Alzheimer's disease (AD) brain and have been implicated in mechanisms of pathogenesis. The neurotoxicity of AßOs appears to be, at least in part, due to dysregulation of glutamate signaling. Here, we show that AßOs promote extracellular accumulation of glutamate and d-serine, a co-agonist at glutamate receptors of the N-methyl-d-aspartate subtype (NMDARs), in hippocampal neuronal cultures. The increase in extracellular glutamate levels induced by AßOs was blocked by the sodium channel blocker tetrodotoxin (TTX), by the NMDAR blocker (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) and by removal of Ca(2+) from the extracellular medium, indicating dependence on excitatory neuronal activity. AßOs enhanced both the release of pre-synaptic vesicles labeled by FM1-43 and spontaneous post-synaptic activity measured by whole-cell patch-clamp. Activation of inhibitory GABA(A) receptors by taurine blocked the increase in extracellular glutamate levels, suggesting that selective pharmacological inhibition of neuronal activity can counteract the impact of AbOs on glutamate dyshomeostasis. Results reveal a novel mechanism by which Ab oligomers promote abnormal release of glutamate in hippocampal neurons, which may contribute to dysregulation of excitatory signaling in the brain.

Regulation of glycinergic and GABAergic synaptogenesis by brain-derived neurotrophic factor in developing spinal neurons.

Brain-derived neurotrophic factor (BDNF) effects on the establishment of glycinergic and GABAergic transmissions in mouse spinal neurons were examined using combined electrophysiological and calcium imaging techniques. BDNF (10 ng/ml) caused a significant acceleration in the onset of synaptogenesis without large effects on the survival of these neurons. Amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) associated to activation of glycine and GABA(A) receptors were augmented in neurons cultured with BDNF. The neurotrophin effect was blocked by long term tetrodotoxin (TTX) addition suggesting a dependence on neuronal activity. In addition, BDNF caused a significant increase in glycine- and GABA-evoked current densities that partly explains the increase in synaptic transmission. Presynaptic mechanisms were also involved in BDNF effects since triethylammonium(propyl)-4-(2-(4-dibutylamino-phenyl)vinyl)pyridinium (FM1-43) destaining with high K(+) was augmented in neurons incubated with the neurotrophin. The effects of BDNF were mediated by receptor tyrosine kinase B (TrkB) and mitogen-activated protein kinase kinase (MEK) activation since culturing neurons with either (9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3',2',1'- kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester (K252a) or 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) blocked the augmentation in synaptic activity induced by the neurotrophin.

Anti-homeostatic synaptic plasticity of glycine receptor function after chronic strychnine in developing cultured mouse spinal neurons.

In this study, we describe a novel form of anti-homeostatic plasticity produced after culturing spinal neurons with strychnine, but not bicuculline or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Strychnine caused a large increase in network excitability, detected as spontaneous synaptic currents and calcium transients. The calcium transients were associated with action potential firing and activation of gamma-aminobutyric acid (GABA(A)) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors as they were blocked by tetrodotoxin (TTX), bicuculline, and CNQX. After chronic blockade of glycine receptors (GlyRs), the frequency of synaptic transmission showed a significant enhancement demonstrating the phenomenon of anti-homeostatic plasticity. Spontaneous inhibitory glycinergic currents in treated cells showed a fourfold increase in frequency (from 0.55 to 2.4 Hz) and a 184% increase in average peak amplitude compared with control. Furthermore, the augmentation in excitability accelerated the decay time constant of miniature inhibitory post-synaptic currents. Strychnine caused an increase in GlyR current density, without changes in the apparent affinity. These findings support the idea of a post-synaptic action that partly explains the increase in synaptic transmission. This phenomenon of synaptic plasticity was blocked by TTX, an antibody against brain-derived neurotrophic factor (BDNF) and K252a suggesting the involvement of the neuronal activity-dependent BDNF-TrkB signaling pathway. These results show that the properties of GlyRs are regulated by the degree of neuronal activity in the developing network.

Historical and current perspectives of neuroactive compounds derived from Latin America.

Plants and invertebrates in Latin America have contributed to a great extent in the use, discovery and development of novel neuroactive tools. Significantly, these neuroactive drugs have proven to be particularly important for our current understanding of the physiology and pharmacology of the nervous system. In addition, these discoveries have helped to build the modern and successful pharmacological business that we know today. For example, curare helped to introduce the use of muscle relaxing agents into modern surgical techniques. The discovery of cocaine from the leaves of Peruvian coca plants was instrumental in the discovery of local anesthetics. The search and discovery for useful neuroactive compounds derived from Latin America has also been ongoing in other areas and new applications for quinine, capsaicin and epibatidine were recently described. Besides these organic compounds, several peptides produced by spiders and other invertebrates to hunt their prey also induce effects in channels and membrane receptors at very low concentrations, indicating their high potency and selectivity. It is likely that new pharmaceutics will be developed from these molecules. The interest to renew the search for new compounds is timely, since largely unexplored lands, such as the Amazon and Patagonia, hold an important number of plants and animals that contain exciting new active compounds. With the introduction of new techniques to isolate, identify and characterize the molecular targets and actions of chemical entities, together with the need for more potent and selective compounds to treat neurological conditions, it is necessary to broaden the current exploratory effort in order to find more beneficial uses.

Evaluación de un servicio de salud mental: análisis de la demanda y datos epidemiológicos / The assessment of a public mental health service: epidemiological data and analysis of demand

Los servicios públicos de salud mental atienden a una gran cantidad de pacientes al día. La evaluación de estos servicios es necesaria para mejorar la atención profesional y la eficiencia de los tratamientos. En este artículo presentamos los datos de una evaluación externa durante cuatro años. El centro evaluado es un Equipo de Salud Mental de Distrito (ESMD) del Servicio Andaluz de Salud en Málaga, formado por un equipo multiprofesional que atienden la demanda de varios cientos de nuevos casos clínicos cada año. La evaluación se centra en: 1) datos epidemiológicos sobre la incidencia de trastornos en la población, 2) trabajo de los profesionales, y 3) diagnóstico psicopatológico según las categorías del CIE-10. La evaluación se realizó cada año, desde 1993 a 1997, sobre los datos de entrevistas clínicas semiestructuradas que permitían cuantificar una serie de variables para su posterior análisis en un programa informático (SISMA) diseñado para el trabajo específico de los equipos de salud mental en Andalucía. Se presentan los datos globales de los 4 años que reflejan como perfil de paciente más frecuente, el de una persona diagnosticada de ansiedad o depresión con un nivel socio-cultural medio-bajo. Se analizan en detalle las diferencias entre pacientes hombre-mujer y adultos-niños (AU)

[Cognitive constructs related to depression in children]. / Evaluación de constructos cognitivos relacionados con la depresión en niños.

UNLABELLED: Hopelessness, anhedonia and automatic thoughts have all been related to major depression and depressive symptoms. Few research has been done on these constructs in children, specially together. AIM: The aim of this study was to translate into Spanish and validate the hopelessness scale for children, the pleasure scale for children, the automatic thoughts scale and the Kovak's child depression inventory, and then to relate the cognitive constructs to depressive symptoms in a sample of normal children. METHODS: Children were recruited from the Federal Primary School Mexican Air Forces of Mexico City. All Children from the 3rd to 6th grades were included. RESULTS: 256 children were included, 53% male and 46% female, mean age 9.8 1.15 years. Internal consistencies for instruments were as follows: anhedonia scale 0.91, hopelessness scale 0.63, automatic thoughts 0.87 and depression 0.80. The factor structures of the translated versions were similar to those reported by their original authors. Interinstruments correlations ranged from 0.17 to 0.39. Automatic thoughts and depressive symptoms reached the highest significant value (r= 0.39). 6th graders rated significantly lower in all instruments than their 5th and 3rd peers. CONCLUSIONS: All measures studied demonstrate moderate to high internal reliability and the factor structures predicted. Depressive symptoms among normal children related weakly but significantly to the cognitive constructs studied, just as seen in normal adults.

Evaluación de constructos cognitivos relacionados con la depresión en niños / Cognitive constructs related to depression in children

La anhedonia, la desesperanza y los pensamientos automáticos se han relacionado con la presencia de depresión mayor y de síntomas depresivos.Objetivo. El propósito de este trabajo fue traducir al español y obtener las propiedades psicométricas de las escalas de desesperanza, de pensamientos automáticos, de anhedonia y de sintomatología depresiva para niños, así como determinar la relación entre estos constructos cognoscitivos y los síntomas depresivos en infantes normales.Método. Fueron evaluados niños de ambos sexos de tercero y sexto grado de primaria de la Escuela Primaria Federal 'Fuerzas Armadas de México'.Resultados. La muestra de estudio fue de 256 niños, 53 por ciento chicos y 46 por ciento chicas, con una edad promedio de 9,8 ñ 1,15 años. Las consistencias internas de los instrumentos fueron, para la escala de anhedonia 0,91; para la de desesperanza 0,63; para la de pensamientos automáticos 0,87; y para la de síntomas de depresión 0,80. Las estructuras factoriales de los instrumentos fueron similares a las reportadas por sus autores originales. Las correlaciones entre los instrumentos variaron entre 0,17 y 0,39. La escala de pensamientos automáticos y los síntomas depresivos mostraron la correlación más alta (r= 0,39). Se encontraron diferencias significativas entre grados escolares, con menores valores promedio a mayor escolaridad.Conclusión. Los instrumentos evaluados demostraron consistencia interna de mediana a alta y las estructuras factoriales que se había predicho. Los síntomas depresivos en población infantil normal se relacionan débil pero significativamente con los constructos cognoscitivos estudiados, tal y como se ha reportado en adultos normales (AU)