The functional neuroanatomy of the evolving parent–infant relationship

Infant survival and the development of secure and cooperative relationships are central to the future of the species. In humans, this relies heavily on the evolving early parent–infant social and affective relationship. While much is known about the behavioural and psychological components of this relationship, relatively little is known about the underlying functional neuroanatomy. Affective and social neuroscience has helped to describe the main adult brain networks involved, but has so far engaged very little with developmental findings. In this review, we seek to highlight future avenues for research by providing a coherent framework for describing the parent–infant relationship over the first 18 months. We provide an outline of the evolving nature of the relationship, starting with basic orienting and recognition processes, and culminating in the infant's attainment of higher socio-emotional and cognitive capacities. Key social and affective interactions, such as communication, cooperative play and the establishment of specific attachments propel the development of the parent–infant relationship. We summarise our current knowledge of the developing infant brain in terms of structure and function, and how these relate to the emergent abilities necessary for the formation of a secure and cooperative relationship with parents or other caregivers. Important roles have been found for brain regions including the orbitofrontal, cingulate, and insular cortices in parent–infant interactions, but it has become clear that much more information is needed about the developmental time course and connectivity of these regions.     

The pain matrix reloaded: a salience detection system for the body

Neuroimaging and neurophysiological studies have shown that nociceptive stimuli elicit responses in an extensive cortical network including somatosensory, insular and cingulate areas, as well as frontal and parietal areas. This network, often referred to as the "pain matrix", is viewed as representing the activity by which the intensity and unpleasantness of the perception elicited by a nociceptive stimulus are represented. However, recent experiments have reported (i) that pain intensity can be dissociated from the magnitude of responses in the "pain matrix", (ii) that the responses in the "pain matrix" are strongly influenced by the context within which the nociceptive stimuli appear, and (iii) that non-nociceptive stimuli can elicit cortical responses with a spatial configuration similar to that of the "pain matrix". For these reasons, we propose an alternative view of the functional significance of this cortical network, in which it reflects a system involved in detecting, orienting attention towards, and reacting to the occurrence of salient sensory events. This cortical network might represent a basic mechanism through which significant events for the body's integrity are detected, regardless of the sensory channel through which these events are conveyed. This function would involve the construction of a multimodal cortical representation of the body and nearby space. Under the assumption that this network acts as a defensive system signaling potentially damaging threats for the body, emphasis is no longer on the quality of the sensation elicited by noxious stimuli but on the action prompted by the occurrence of potential threats.     

Effects of incremental exercise on cerebral oxygenation measured by near-infrared spectroscopy: A systematic review

We conducted a systematic review and meta-regression analysis to quantify effects of exercise on brain hemodynamics measured by near-infrared spectroscopy (NIRS). The results indicate that acute incremental exercise (categorized relative to aerobic capacity (VO₂peak) as low – <30% VO₂peak; moderate – ≥30% VO₂peak to <60% VO₂peak; hard – ≥60% VO₂peak to <VO₂peak; and very hard – ≥VO₂peak intensities) performed by 291 healthy people in 21 studies is accompanied by moderate-to-large increases (mean effect, dz ± 95% CI) in the prefrontal cortex of oxygenated hemoglobin (O₂Hb) or other measures of oxygen level (O₂Hbdiff) or saturation (SCO₂) (0.92 ± 0.67, 1.17), deoxygenated hemoglobin (dHb) (0.87 ± 0.56, 1.19), and blood volume estimated by total hemoglobin (tHb) (1.21 ± 0.84, 1.59). After peaking at hard intensities, cerebral oxygen levels dropped during very hard intensities. People who were aerobically trained attained higher levels of cortical oxygen, dHb, and tHb than untrained people during very hard intensities. Among untrained people, a marked drop in oxygen levels and a small increase in dHb at very hard intensities accompanied declines in tHb, implying reduced blood flow. In 6 studies of 222 patients with heart or lung conditions, oxygenation and dHb were lowered or unchanged during exercise compared to baseline. In conclusion, prefrontal oxygenation measured with NIRS in healthy people showed a quadratic response to incremental exercise, rising between moderate and hard intensities, then falling at very hard intensities. Training status influenced the responses. While methodological improvements in measures of brain oxygen are forthcoming, these results extend the evidence relevant to existing models of central limitations to maximal exercise.     

Anesthesia and perioperative stress: Consequences on neural networks and postoperative behaviors

Anesthesia is a state of drug-induced unconsciousness with suppression of sensory perception, and consists of both hypnotic and analgesic components. The anesthesiologist monitors the clinical response to noxious stimuli and adjusts drug dosage(s) to achieve an adequate depth of anesthesia, with the aim of reducing operative stress. Acute stress in the perioperative period has four major contributors: anxiety, pain, the surgical stress response, and the potential neurotoxicity of anesthetic agents. Any or all of these may act deleteriously on multiple systems in the brain and have known significant effects on brain regions such as the hippocampus and the hypothalamic-pituitary–adrenal axis. Perioperative stress on the nervous system and the resultant central nervous system (CNS) changes are likely to be causative for altered behaviors that are seen postoperatively, including chronic pain, posttraumatic stress disorder, and learning difficulties. Improving the ability of the anesthesiologist to control all four components of acute perioperative stress could potentially reduce the negative impact of surgery on the brain. Currently, there is no objective measurement for any of these stressors. The development and application of objective measures for perioperative stressors is the first step towards controlling these risk factors and eliminating or reducing their serious postoperative consequences. In this paper we review known and likely effects of perioperative stressors on brain systems and how they may play a significant role in altered postoperative behaviors. We discuss the role of current (and developing) measures of brain function and their potential for monitoring perioperative stress, with an emphasis on functional neuroimaging.     

Ammonia metabolism,the brain and fatigue; revisiting the link

This review addresses the ammonia fatigue theory in light of new evidence from exercise and disease studies and aims to provide a view of the role of ammonia during exercise. Hyperammonemia is a condition common to pathological liver disorders and intense or exhausting exercise. In pathology, hyperammonemia is linked to impairment of normal brain function and the onset of the neurological condition, hepatic encephalopathy. Elevated blood ammonia concentrations arise due to a diminished capacity for removal via the liver and lead to increased exposure of organs, such as the brain, to the toxic effects of ammonia. High levels of brain ammonia can lead to deleterious alterations in astrocyte morphology, cerebral energy metabolism and neurotransmission, which may in turn impact on the functioning of important signalling pathways within the neuron. Such changes are believed to contribute to the disturbances in neuropsychological function, in particular the learning, memory, and motor control deficits observed in animal models of liver disease and also patients with cirrhosis. Hyperammonemia in exercise occurs as a result of an increased production by contracting muscle, through adenosine monophosphate (AMP) deamination (the purine nucleotide cycle) and branched chain amino acid (BCAA) deamination prior to oxidation. Plasma concentrations of ammonia during exercise often achieve or exceed those measured in liver disease patients, resulting in increased cerebral uptake. In this article we propose that exercise-induced hyperammonemia may lead to concomitant disturbances in brain function, potentially through similar mechanisms underpinning pathology, which may impact on performance as fatigue or reduced function, especially during extreme exercise.