Tactile Discrimination, Praxis and Cognitive Impulsivity in ADHD Children: A Cross-Sectional Study.

BACKGROUND: The study of attention deficit hyperactivity disorder (ADHD) has traditionally focused on deficit of inhibitory control and cognitive impulsivity. However, the pathophysiology of ADHD has also been associated with the somatosensory cortex. The aim of this study was to explore if there were differences in tactile discrimination and praxis between neurotypical and ADHD children and whether these differences could be explained by cognitive impulsivity. METHODS: A cross-sectional study was conducted. The sample comprised 74 children aged 7 to 11 years divided in two groups: 43 with neurotypical development, 31 with ADHD. To assess tactile discrimination, the finger localization and the graphestesia tests were used. Praxis was assessed with the Kaufman Assesment Battery for Children (K-ABC) hand movement subtest, the action program and the Zoo Map subtests of the Behavioral Assessment of Dysexecutive Syndrome, and the complex figure of Rey-Osterrieth test (ROCF). Cognitive impulsivity was assessed using the Magallanes Computerized Impulsivity Scale test (EMIC). RESULTS: Children with ADHD showed greater cognitive impulsivity (p = 0.038) and scored lower in Zoo Map (p = 0.023) and hand-movement subtests (p = 0.002), and in ROCF test (p = 0.004). Differences in praxis skills still remained after controlling by gender and cognitive impulsivity. CONCLUSION: Praxis deficit might have repercussions not only on the characterization of ADHD but also on its treatment.

Assessment of Sensory Processing and Executive Functions in Childhood: Development, Reliability, and Validity of the EPYFEI.

The aim of this study was to determine the psychometric properties of the "Assessment of Sensory Processing and Executive Functions in Childhood" (EPYFEI), a questionnaire designed to assess the sensory processing and executive functions of children aged between 3 and 11 years. The EPYFEI was completed by a sample of 1,732 parents of children aged between 3 and 11 years who lived in Spain. An exploratory factor analysis was conducted and showed five main factors: (1) executive attention, working memory, and initiation of actions; (2) general sensory processing; (3) emotional and behavioral self-regulation; (4) supervision, correction of actions, and problem solving; and (5) inhibitory. The reliability of the analysis was high both for the whole questionnaire and for the factors it is composed of. Results provide evidence of the potential usefulness of the EPYFEI in clinical contexts for the early detection of neurodevelopmental disorders, in which there may be a deficit of executive functions and sensory processing.

Corrigendum: Assessment of Sensory Processing Characteristics in Children between 3 and 11 Years Old: A Systematic Review.

[This corrects the article on p. 57 in vol. 5, PMID: 28424762.].

Assessment of Sensory Processing Characteristics in Children between 3 and 11 Years Old: A Systematic Review.

The assessment of sensory perception, discrimination, integration, modulation, praxis, and other motor skills, such as posture, balance, and bilateral motor coordination, is necessary to identify the sensory and motor factors influencing the development of personal autonomy. The aim of this work is to study the assessment tools currently available for identifying different patterns of sensory processing. There are 15 tests available that have psychometric properties, primarily for the US population. Nine of them apply to children in preschool and up to grade 12. The assessment of sensory processing is a process that includes the use of standardized tests, administration of caregiver questionnaires, and clinical observations. The review of different studies using PRISMA criteria or Osteba Critical Appraisal Cards reveals that the most commonly used tools are the Sensory Integration and Praxis Test, the Sensory Processing Measure, and the Sensory Profile.

A peripheral adrenoceptor-mediated sympathetic mechanism can transform stress-induced analgesia into hyperalgesia.

BACKGROUND: Stress has paradoxical effects on pain, causing stress-induced analgesia but also exacerbating pain via poorly understood mechanisms. Adrenergic neurotransmission is integral in pathways that regulate the response to both pain and stress. Hyperalgesia is often associated with enhanced adrenergic sensitivity of primary afferents, but sympathetic nervous system outflow has not been demonstrated to exacerbate pain perception after stress. METHODS: Rats or C57/BL6 wild-type mice treated with α-2 receptor antagonists or α-2A receptor knockout mice were exposed to ultrasonic noise stress or footshock stress and subsequently tested for hotplate paw withdrawal latencies. The sensory sensitivity of α-2A knockout mice to electrical and chemical stimuli was tested neurophysiologically and behaviorally. The effects of sympatholytic treatments were investigated. RESULTS: Noise and footshock stressors induced thermal hyperalgesia in rats pretreated systemically with α-2 antagonists. Wild-type mice pretreated with α-2 antagonists and α-2A knockout mice also exhibited thermal hyperalgesia induced by noise stress. Local spinal or intraplantar injection of an α-2 antagonist counteracted stress-induced analgesia without causing hyperalgesia. The α-2A knockout mice had decreased thresholds for peripheral sensitization with sulprostone and for windup of the dorsal horn neuronal response to repetitive electrical stimuli. Stress-induced hyperalgesia was abolished and the sensitization was attenuated by sympathectomy or systemic administration of an α-1-adrenergic antagonist. CONCLUSIONS: Sympathetic postganglionic nerves can enhance pain sensation via a peripheral α-1-adrenoceptor mechanism when sympathetic outflow is disinhibited. The net effect of stress on pain sensation reflects a balance between descending spinal inhibition and sympathetic outflow that can shift toward pain facilitation when central and peripheral α-2-adrenoceptor inhibitory mechanisms are attenuated.

Hippocampal focal knockout of CBP affects specific histone modifications, long-term potentiation, and long-term memory.

To identify the role of the histone acetyltransferase (HAT) CREB-binding protein (CBP) in neurons of the CA1 region of the hippocampus during memory formation, we examine the effects of a focal homozygous knockout of CBP on histone modifications, gene expression, synaptic plasticity, and long-term memory. We show that CBP is critical for the in vivo acetylation of lysines on histones H2B, H3, and H4. CBP's homolog p300 was unable to compensate for the loss of CBP. Neurons lacking CBP maintained phosphorylation of the transcription factor CREB, yet failed to activate CREB:CBP-mediated gene expression. Loss of CBP in dorsal CA1 of the hippocampus resulted in selective impairments to long-term potentiation and long-term memory for contextual fear and object recognition. Together, these results suggest a necessary role for specific chromatin modifications, selectively mediated by CBP in the consolidation of memories.

Membrane-associated glucocorticoid activity is necessary for modulation of long-term memory via chromatin modification.

Glucocorticoid hormones enhance the consolidation of long-term memory of emotionally arousing training experiences. This memory enhancement requires activation of the cAMP-dependent kinase pathway and the subsequent phosphorylation of cAMP response-element binding (CREB) protein. Here, we demonstrate that glucocorticoids enhance the consolidation of hippocampus-dependent and hippocampus-independent aspects of object recognition memory via chromatin modification. More specifically, systemic corticosterone increases histone acetylation, a form of chromatin modification, in both the hippocampus and insular cortex following training on an object recognition task. This led us to examine whether increasing histone acetylation via histone deacetylase (HDAC) inhibition enhances memory in a manner similar to corticosterone. We found a double dissociation between posttraining HDAC inhibitor infusion into the insular cortex and hippocampus on the enhancement of object recognition and object location memory, respectively. In determining the molecular pathway upstream of glucocorticoids' effects on chromatin modification, we found that activation of membrane-associated glucocorticoid receptors (GRs) and the subsequent interaction between phospho-CREB and CREB-binding protein (CBP) appear to be necessary for glucocorticoids to enhance memory consolidation via chromatin modification. In contrast, mineralocorticoid receptors (MRs) do not appear to be involved. The findings also indicate that glucocorticoid activity has differential influences on hippocampus-dependent and hippocampus-independent components of memory for objects.

Automated scoring of fear-related behavior using EthoVision software.

Fear conditioning is a frequently used paradigm for assessing learning and memory in rodents. Traditionally researchers have relied upon scoring of fear-related behavior by human observation, which can be difficult and subjective and thus vary among investigators. The goal of this study was to evaluate the ability of EthoVision tracking software (Noldus Information Technology Inc.) to reliably and accurately score fear-related behavior in mice. Specifically, we were interested in its ability to accurately track mice and score immobility as a fear-related behavior during contextual and cued fear conditioning. Contextual and cued fear conditioning were performed in modified PhenoTyper chambers (Noldus Information Technology Inc.) fitted with grid floors to deliver a scrambled foot shock. Our results demonstrate that we have identified parameters in EthoVision that can accurately track mice and be used for automated scoring of immobility that is nearly identical to scoring by human observation. Together, EthoVision software and the modified PhenoTyper chambers provide an excellent system for the reliable and accurate measurement of fear-related behavior in a high-throughput manner.

Histone deacetylase inhibitors enhance memory and synaptic plasticity via CREB:CBP-dependent transcriptional activation.

Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance both memory and synaptic plasticity. The current model for the action of HDAC inhibitors assumes that they alter gene expression globally and thus affect memory processes in a nonspecific manner. Here, we show that the enhancement of hippocampus-dependent memory and hippocampal synaptic plasticity by HDAC inhibitors is mediated by the transcription factor cAMP response element-binding protein (CREB) and the recruitment of the transcriptional coactivator and histone acetyltransferase CREB-binding protein (CBP) via the CREB-binding domain of CBP. Furthermore, we show that the HDAC inhibitor trichostatin A does not globally alter gene expression but instead increases the expression of specific genes during memory consolidation. Our results suggest that HDAC inhibitors enhance memory processes by the activation of key genes regulated by the CREB:CBP transcriptional complex.

Selective lesions of the nucleus basalis magnocellularis impair cognitive flexibility.

The authors tested the hypothesis that the cholinergic nucleus basalis magnocellularis (NBM) is involved in solving problems requiring cognitive flexibility. Rats with 192 IgG-saporin lesions of the NBM were assessed for perseveration (i.e., cognitive inflexibility) in the serial reversal of an operant discrimination and during subsequent extinction testing. It was hypothesized that the NBM lesion and control groups would not differ in the acquisition of the initial, simple discrimination, because this task does not demand cognitive flexibility. In contrast, it was hypothesized that the NBM lesion group would show perseveration during serial reversal and extinction testing. Results generally supported these hypotheses, suggesting that the NBM plays an important role in mediating cognitive flexibility.