Variations in Theta/Beta Ratio and Cognitive Performance in Subpopulations of Subjects with ADHD Symptoms: Towards Neuropsychological Profiling for Patient Subgrouping.

ADHD is a neurodevelopmental disorder appearing in childhood but remaining in many cases in adults. There are both pharmacological and non-pharmacological approaches to treating ADHD, but they do not have the same efficacy in all subjects. Better knowledge of the neurophysiological basis of this disorder will allow for the design of more effective treatments. Studies performing qEEG analysis in children suggest the existence of subgroups of ADHD patients with different neurophysiological traits. There are fewer studies in adults, who might have undergone plastic changes allowing them to cope with ADHD symptoms along with brain maturation. Herein, we study cognitive performance and the theta/beta ratio in young adults with ADHD symptoms. We found that subjects with ADHD symptoms and low working memory performance (n = 30) present higher theta/beta ratios than controls (n = 40) at O2 and T6 in the eyes-closed condition, as well as a tendency toward a higher theta/beta ratio at O1 and Cz. Subjects with ADHD and high working memory performance (n = 50) do not differ from the controls in their theta/beta ratios at any derivation. Our results suggest that neuropsychological profiling could be useful for patient subgrouping. Further research will allow for the distinction of neuropsychological profiles and their neurophysiological correlates, leading to a better classification of ADHD subtypes, thus improving treatment selection.

Personalization of Pharmacological Treatments for ADHD: Why it is Advisable and Possible Options to Achieve it.

Attention-deficit hyperactivity disorder is a neurodevelopmental disorder diagnosed primarily in children, although it is also present in adults. Patients present inattention, impulsivity, and hyperactivity symptoms that create difficulties in their daily lives. Pharmacological treatment with stimulants or non-stimulants is used most commonly to reduce ADHD symptoms. Although generally effective and safe, pharmacological treatments have different effects among patients, including lack of response and adverse reactions. The reasons for these differences are not fully understood, but they may derive from the highly diverse etiology of ADHD. Strategies to guide optimal pharmacological treatment selection based on individual patients' physiological markers are being developed. In this review, we describe the main pharmacological ADHD treatments used and their main drawbacks. We present alternatives under study that would allow the customization of pharmacological treatments to overcome these drawbacks and achieve more reliable improvement of ADHD symptoms.

ADHD: Reviewing the Causes and Evaluating Solutions.

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder in which patients present inattention, hyperactivity, and impulsivity. The etiology of this condition is diverse, including environmental factors and the presence of variants of some genes. However, a great diversity exists among patients regarding the presence of these ADHD-associated factors. Moreover, there are variations in the reported neurophysiological correlates of ADHD. ADHD is often treated pharmacologically, producing an improvement in symptomatology, albeit there are patients who are refractory to the main pharmacological treatments or present side effects to these drugs, highlighting the importance of developing other therapeutic options. Different non-pharmacological treatments are in this review addressed, finding diverse results regarding efficacy. Altogether, ADHD is associated with different etiologies, all of them producing changes in brain development, leading to the characteristic symptomatology of this condition. Given the heterogeneous etiology of ADHD, discussion is presented about the convenience of personalizing ADHD treatment, whether pharmacological or non-pharmacological, to reach an optimum effect in the majority of patients. Approaches to personalizing both pharmacological therapy and neurofeedback are presented.

Sexual Behavior and Synaptic Plasticity.

Although sex drive is present in many animal species, sexual behavior is not static and, like many other behaviors, can be modified by experience. This modification relies on synaptic plasticity, a sophisticated mechanism through which neurons change how they process a given stimulus, and the neurophysiological basis of learning. This review addresses the main plastic effects of steroid sex hormones in the central nervous system (CNS) and the effects of sexual experience on the CNS, including effects on neurogenesis, intracellular signaling, gene expression, and changes in dendritic spines, as well as behavioral changes.

El consumo de riesgo de alcohol y el riesgo de dependencia al alcohol presentan correlatos neurofisiológicos diferentes / Hazardous alcohol consumption and risk of alcohol dependence present different neurophysiological correlates

Introducción. El consumo de riesgo de alcohol (CRA) es un patrón de consumo que puede resultar dañino para el usuario o para los demás. Investigaciones previas sugieren que el CRA y la dependencia al alcohol comparten algunas características neurofisiológicas, pero difieren en otras. Objetivo. Determinar si el CRA y la dependencia al alcohol presentan correlatos neurofisiológicos diferentes. Sujetos y métodos. Doscientos sujetos realizaron la prueba de detección de CRA y riesgo de dependencia al alcohol (DEP). Se realizó un estudio de electroencefalografía cuantitativa para determinar la potencia absoluta, la potencia relativa y la frecuencia media de las bandas delta, theta, alfa y beta en sujetos con CRA, con DEP y controles. Resultados. Un total de 114 sujetos cumplió los criterios de inclusión. El grupo con CRA presentó mayor potencia absoluta, mayor potencia relativa y menor frecuencia media de la banda beta en comparación con los controles, mientras que el grupo con DEP presentó menor potencia absoluta de la banda delta que los controles. Conclusiones. El DEP y el CRA presentan diferentes correlatos neurofisiológicos. Hay un efecto importante de la gravedad de la dependencia al alcohol sobre sus correlatos neurofisiológicos. Nuestros resultados apoyan la existencia de dos tipos distintos de desinhibición conductual

Introduction. Hazardous alcohol consumption (HAC) is a pattern of alcohol use that may result in harm for the user and/or for those around them. Prior research has suggested that HAC and alcohol dependence share some neurophysiological features but differ in others. Aim. To determine whether HAC and alcohol dependence presented different neurophysiological correlates. Subjects and methods. Two hundred subjects were screened for HAC or alcohol dependence. A quantitative electroencephalographic analysis of delta, theta, alpha and beta absolute power, relative power and mean frequency in subjects with HAC but not alcohol dependence, subjects with risk of alcohol dependence and controls was performed. Results. One hundred and fourteen subjects met inclusion criteria. The HAC group presented with higher beta absolute power and relative power, as well as a lower beta mean frequency than the control group, while the group with risk of alcohol dependence presented lower delta absolute power than controls. Conclusions. HAC and risk of alcohol dependence present different neurophysiological correlates. There is an important effect of the severity of alcohol dependence on neurophysiological correlates of this condition. Our results support the existence of two different types of behavioral disinhibition

Dopaminergic Modulation of Sleep-Wake States.

The role of dopamine in sleep-wake regulation is considered as a wakefulness-promoting agent. For the clinical treatment of excessive daytime sleepiness, drugs have been commonly used to increase dopamine release. However, sleep disorders or lack of sleep are related to several dopaminerelated disorders. The effects of dopaminergic agents, nevertheless, are mediated by two families of dopamine receptors, D1 and D2-like receptors; the first family increases adenylyl cyclase activity and the second inhibits adenylyl cyclase. For this reason, the dopaminergic agonist effects on sleep-wake cycle are complex. Here, we review the state-of-the-art and discuss the different effects of dopaminergic agonists in sleep-wake states, and propose that these receptors account for the affinity, although not the specificity, of several effects on the sleep-wake cycle.

Quantitative electroencephalography analysis in university students with hazardous alcohol consumption, but not alcohol dependence.

Hazardous alcohol consumption is a pattern of consumption that leads to a higher risk of harmful consequences either for the user or for others. This pattern of alcohol consumption has been linked to risky behaviors, accidents, and injuries. Individuals with hazardous alcohol consumption do not necessarily present alcohol dependence; thus, a study of particular neurophysiological correlates of this alcohol consumption pattern needs to be carried out in nondependent individuals. Here, we carried out a quantitative electroencephalography analysis in health sciences university students with hazardous alcohol consumption, but not alcohol dependence (HAC), and control participants without hazardous alcohol consumption or alcohol dependence (NHAC). We analyzed Absolute Power (AP), Relative Power (RP), and Mean Frequency (MF) for beta and theta frequency bands under both eyes closed and eyes open conditions. We found that participants in the HAC group presented higher beta AP at centroparietal region, as well as lower beta MF at frontal and centroparietal regions in the eyes closed condition. Interestingly, participants did not present any change in theta activity (AP, RP, or MF), whereas previous reports indicate an increase in theta AP in alcohol-dependent individuals. Our results partially resemble those found in alcohol-dependent individuals, although are not completely identical, suggesting a possible difference in the underlying neuronal mechanism behind alcohol dependence and hazardous alcohol consumption. Similarities could be explained considering that both hazardous alcohol consumption and alcohol dependence are manifestations of behavioral disinhibition.

Taste memory formation: latest advances and challenges.

Taste memory has been a useful model for studying memory formation; using different approaches ranging from lesion studies, analysis of receptor and neurotransmitter activity, and measurement of intracellular signaling mechanisms or gene expression, it has been possible to describe processes which may be involved in several types of memory. Taste memory includes the recognition of a taste as well as its characteristics related to the hedonic value, degree of familiarity, and the nutritive or toxic properties associated with that taste. In terms of evolutionary adaptation, taste memory is necessary for the proper identification of available nutritive foods and, of course, is essential to avoid deadly toxins. This review summarizes the current knowledge of taste memory, describing the evidence obtained using non-associative and associative taste learning models by manipulating the different structures involved in the formation and expression of taste memory. Pharmacological, biochemical, and molecular data are shown for each structure and subsequently current theories are presented about possible inter-structural interactions taking part in taste memory formation. Finally, we describe how the study of taste memory can reveal basic mechanisms of learning, raising issues that might apply to learning processes in general.

Activation of hippocampal postsynaptic muscarinic receptors is involved in long-term spatial memory formation.

Spatial memory has been strongly associated with hippocampal function. There are several reports of the participation of this structure in acquisition and consolidation of spatial tasks. In this study, we evaluated the effects of selective and non-selective muscarinic antagonists in the dorsal hippocampus of rats during acquisition and encoding of a spatial task. Rats were trained in a Morris water maze for 4 days with identical daily sessions, and tested for long-term memory (LTM) 1 week after training. The animals were injected bilaterally in the dorsal hippocampus 20 min before the start of every day of training. The results showed that the non-selective muscarinic antagonist, scopolamine, disrupted acquisition of water maze memory formation. Moreover, microinjections of a selective postsynaptic muscarinic antagonist, pirenzepine, disrupted LTM, whereas it did not affect acquisition. Conversely, a selective presynaptic muscarinic antagonist, AFDX-116, did not disrupt either water maze acquisition or LTM formation. Combination of AFDX-116 and pirenzepine had similar effects as scopolamine, partially blocking acquisition and impairing long-term spatial memory. These results support the view that muscarinic receptors are involved in spatial learning and that postsynaptic muscarinic receptors in the dorsal hippocampus are particularly involved in long-term spatial memory formation.