Long-Term Consequences of Neonatal Injury

The maturation of the central nervous system’s (CNS’s) sensory connectivity is driven by modality-specific sensory input in early life. For the somatosensory system, this input is the physical, tactile interaction with the environment. Nociceptive circuitry is functioning at the time of birth; however, there is still considerable organization and refinement of this circuitry that occurs postnatally, before full discrimination of tactile and noxious input is possible. This fine-tuning involves separation of tactile and nociceptive afferent input to the spinal cord’s dorsal horn and the maturation of local and descending inhibitory circuitry. Disruption of that input in early postnatal life (for example, by tissue injury or other noxious stimulus), can have a profound influence on subsequent development, and consequently the mature functioning of pain systems. In this review, the impact of neonatal surgical incision on nociceptive circuitry is discussed in terms of the underlying developmental neurobiology. The changes are complex, occurring at multiple anatomical sites within the CNS, and including both neuronal and glial cell populations. The altered sensory input from neonatal injury selectively modulates neuronal excitability within the spinal cord, disrupts inhibitory control, and primes the immune system, all of which contribute to the adverse long-term consequences of early pain exposure.     

Investigation on Amari’s dynamical neural field with global constant inhibition

In this paper, the properties of Amari’s dynamical neural field with global constant inhibition induced by its kernel are investigated. Amari’s dynamical neural field illustrates many neurophysiological phenomena successfully and has been applied to unsupervised learning like data clustering in recent years. In its applications, the stationary solution to Amari’s dynamical neural field plays an important role that the underlying patterns being perceived are usually presented as the excited region in it. However, the type of stationary solution to dynamical neural field with typical kernel is often sensitive to parameters of its kernel that limits its range of application. Different from dynamical neural field with typical kernel that have been discussed a lot, there are few theoretical results on dynamical neural field with global constant inhibitory kernel that has already shown better performance in practice. In this paper, some important results on existence and stability of stationary solution to dynamical neural field with global constant inhibitory kernel are obtained. All of these results show that such kind of dynamical neural field has better potential for missions like data clustering than those with typical kernels, which provide a theoretical basis of its further extensive application.     

Henri Laborit and the inhibition of action

Henri Laborit was one of the founders of modern neuropsychopharmacology, having discovered, or participated in, the discovery of chlorpromazine, gamma-OH, clomethiazole, and minaprine. He also put forward a theory regarding the necessity of counteracting the negative consequences of defense mechanisms during anesthesia or behavioral inhibition. The scope of his work covers neurophysiology, pharmacology, psychiatry, and psychosomatics. His independence of spirit meant that most of his research was not done within university settings.     

Alterations in excitatory and inhibitory brainstem interneuronal circuits in fibromyalgia: Evidence of brainstem dysfunction

ObjectivePatients with fibromyalgia syndrome (FMS) perceive stimuli differently and show altered cortical sensory representation maps following peripheral stimulation. Altered sensory gating may play a causal role.MethodsBlink reflex, blink reflex excitability recovery, and prepulse inhibition of the blink reflex – representing brainstem excitability – were assessed in 10 female patients with FMS and 26 female healthy controls.ResultsUnconditioned blink reflex characteristics (R1 latency and amplitude, R2 and R2c latency and area-under-the-curve) did not differ significantly between patients and controls. Blink reflex excitability recovery was enhanced in patients versus controls at all intervals tested. Prepulses significantly suppressed R2 area and increased R2 latency in patients and controls. However, R2 area suppression was significantly less in patients than in controls (patients: to 80.0 ± 28.9%, controls: to 47.8 ± 21.7%). The general pattern of corresponding changes in R2c was similar.ConclusionsBlink reflex is normal, whereas blink reflex excitability recovery is enhanced and blink reflex prepulse inhibition is reduced in patients with FMS, suggesting functional changes at the brainstem level in FMS.SignificanceReduced blink reflex prepulse inhibition concurs with altered sensory gating in patients with FMS.     

Gaining insight into adolescent vulnerability for social anxiety from developmental cognitive neuroscience

Social anxiety disorder (SAD) markedly impairs daily functioning. For adolescents, SAD can constrain typical development precisely when social experiences broaden, peers’ opinions are highly salient, and social approval is actively sought. Individuals with extreme, impairing social anxiety fear evaluation from others, avoid social interactions, and interpret ambiguous social cues as threatening. Yet some degree of social anxiety can be normative and non-impairing. Furthermore, a temperament of behavioral inhibition increases risk for SAD for some, but not all adolescents with this temperament. One fruitful approach taken to understand the mechanisms of social anxiety has been to use neuroimaging to link affect and cognition with neural networks implicated in the neurodevelopmental social reorientation of adolescence. Although initial neuroimaging studies of adolescent SAD and risk for SAD underscored the role of fear-processing circuits (e.g., the amygdala and ventral prefrontal cortex), recent work has expanded these circuits to include reward-processing structures in the basal ganglia. A growing focus on reward-related neural circuitry holds promise for innovative translational research needed to differentiate impairing from normative social anxiety and for novel ways to treat adolescent SAD that focus on both social avoidance and social approach.     

Social power and approach-related neural activity

It has been argued that power activates a general tendency to approach whereas powerlessness activates a tendency to inhibit. The assumption is that elevated power involves reward-rich environments, freedom and, as a consequence, triggers an approach-related motivational orientation and attention to rewards. In contrast, reduced power is associated with increased threat, punishment and social constraint and thereby activates inhibition-related motivation. Moreover, approach motivation has been found to be associated with increased relative left-sided frontal brain activity, while withdrawal motivation has been associated with increased right sided activations. We measured EEG activity while subjects engaged in a task priming either high or low social power. Results show that high social power is indeed associated with greater left-frontal brain activity compared to low social power, providing the first neural evidence for the theory that high power is associated with approach-related motivation. We propose a framework accounting for differences in both approach motivation and goal-directed behaviour associated with different levels of power.     

A systems model of altered consciousness: integrating natural and drug-induced psychoses

Increasing evidence from neuroimaging and behavioral studies suggests that functional disturbances within cortico-striato-thalamic pathways are critical to psychotic symptom formation in drug-induced and possibly also naturally occurring psychoses. Recent basic and clinical research with psychotomimetic drugs, such as the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, ketamine, and the serotonin-2A (5-HT(2A)) receptor agonist, psilocybin, suggest that the hallucinogenic effects of these drugs arise, at least in part, from their common capacity to disrupt thalamo-cortical gating of external and internal information to the cortex. Deficient gating of sensory and cognitive information is thought to result in an overloading inundation of information and subsequent cognitive fragmentation and psychosis. Cross-species studies of homologues gating functions, such as prepulse inhibition of the startle reflex, in animal and human models of psychosis corroborate this view and provide a translational testing mechanism for the exploration of novel pathophysiologic and therapeutic hypotheses relevant to psychotic disorders, such as the group of schizophrenias.     

Response inhibition subprocesses and dopaminergic pathways: Basal ganglia disease effects

Response inhibition is a component of executive functions, which can be divided into distinct subprocesses by means of event-related potentials (ERPs). These subprocesses are (pre)-motor inhibition and inhibition monitoring, which are probably reflected by the Nogo-N2 and Nogo-P3, respectively. Here we ask, if these subprocesses may depend on distinct basal ganglia subsystems. We examined response inhibition processes in an extended sample of young and elderly subjects, patients with Parkinson's disease (PD) and Huntington’ disease (HD). This combination of groups also allow us to study whether, and to what degree, pathological basal ganglia changes and healthy aging have similar and/or different effects on these processes. We show that subprocesses of response inhibition are differentially modulated by distinct basal ganglia circuits. Processes related to (pre)-motor inhibition appear to be modulated by the nigrostriatal system, and are sensitive to aging and age-related basal ganglia diseases (i.e. PD). Parkinson's disease induces additive effects of aging and pathology. In contrast, inhibition monitoring is most likely modulated by the mesocortico-limbic dopamine system. These processes are equally affected in healthy aging and both basal ganglia diseases (i.e. PD, HD).     

Left temporal low‐frequency rTMS for the treatment of tinnitus: clinical predictors of treatment outcome – a retrospective study

Background: There is increasing evidence that repetitive transcranial magnetic stimulation (rTMS) can reduce chronic tinnitus. However, treatment results are characterized by high interindividual variability. Therefore, the identification of predictors for treatment response is of high clinical relevance. Methods: Clinical data of 194 patients with tinnitus were evaluated. All patients were treated with a standardized rTMS procedure (1 Hz, 10 days, 2000 stimuli/day, over the left temporal cortex). A potential influence on the outcome was analysed for the following parameters: age, gender, depression scores in Beck Depression Inventory (BDI) and tinnitus severity (TQ) before rTMS, lateralization, frequency and duration of tinnitus and extent of hearing loss. Results: An effect of tinnitus laterality was observed. In patients with left‐sided or bilateral tinnitus, rTMS resulted in a statistically significant reduction of TQ scores, whereas patients with right‐sided tinnitus did not show a significant improvement after rTMS treatment. However, in correlation analyses, we found a trend which did not reach statistical significance that in the subgroup of treatment responders tinnitus duration influenced rTMS outcome. In addition, a multiple regression analysis identified the TQ score at baseline as a significant predictor for treatment outcome. For all other investigated parameters, no statistically significant effects were found. Conclusions: This study suggests that left temporal low‐frequency rTMS has beneficial effects in left‐sided and bilateral tinnitus, but not in right‐sided tinnitus. In line with the results from earlier studies involving smaller samples, tinnitus duration was found to influence rTMS outcome.