Executive and attentional functions in chronic pain: Does performance decrease with increasing task load?

Contains fulltext : 107817.pdf (publisher's version ) (Open Access)BACKGROUND: Diminished executive function and attentional control has been reported in chronic pain patients. However, the precise pattern of impairment in these aspects of cognition in chronic pain remains unclear. Moreover, a decline in psychomotor speed could potentially influence executive and attentional control performance in pain patients. OBJECTIVE: To examine different aspects of executive and attentional control in chronic pain together with the confounding role of psychomotor slowing. METHODS: Neuropsychological tests of sustained attention, planning ability, inhibition and mental flexibility were administered to 34 participants with chronic pain and 32 control participants. RESULTS: Compared with the controls, participants with chronic pain took longer to complete tests of sustained attention and mental flexibility, but did not perform worse on inhibition or planning tasks. The decreased performance on the mental flexibility task likely reflects a reduction in psychomotor speed. The pattern of performance on the sustained attention task reveals a specific decline in attention, indicated by a disproportionate decline in performance with an increase in task duration and by increased fluctuations in attention during task performance. No additional effect was noted of pain intensity, pain duration, pain catastrophizing, depressive symptoms, reduced sleep because of the pain or opioid use. CONCLUSIONS: Executive and attention functions are not uniformly affected in chronic pain. At least part of the previously reported decline in executive function in this group may reflect psychomotor slowing. Overall, limited evidence was found that executive and attention performance is indeed lower in chronic pain. Therefore, it can be concluded that in chronic pain sustained attention performance is diminished while mental flexibility, planning and inhibition appear to be intact.7 p

Hemispheric Asymmetry in White Matter Connectivity of the Temporoparietal Junction with the Insula and Prefrontal Cortex

The temporoparietal junction (TPJ) is a key node in the brain's ventral attention network (VAN) that is involved in spatial awareness and detection of salient sensory stimuli, including pain. The anatomical basis of this network's right-lateralized organization is poorly understood. Here we used diffusion-weighted MRI and probabilistic tractography to compare the strength of white matter connections emanating from the right versus left TPJ to target regions in both hemispheres. Symmetry of structural connectivity was evaluated for connections between TPJ and target regions that are key cortical nodes in the right VAN (insula and inferior frontal gyrus) as well as target regions that are involved in salience and/or pain (putamen, cingulate cortex, thalamus). We found a rightward asymmetry in connectivity strength between the TPJ and insula in healthy human subjects who were scanned with two different sets of diffusion-weighted MRI acquisition parameters. This rightward asymmetry in TPJ-insula connectivity was stronger in females than in males. There was also a leftward asymmetry in connectivity strength between the TPJ and inferior frontal gyrus, consistent with previously described lateralization of language pathways. The rightward lateralization of the pathway between the TPJ and insula supports previous findings on the roles of these regions in stimulus-driven attention, sensory awareness, interoception and pain. The findings also have implications for our understanding of acute and chronic pains and stroke-induced spatial hemineglect

Cortical thickness analysis – The methods

Over the course of the last century, the cerebral cortex has been of interest for neuroscientists, and the work with mapping and measuring the cortex started in the early 1900s (Brodmann 1909). The advances in medical imaging over the recent decades has given the opportunity to measure the cortex in vivo, and several algorithms and types of software applications has been developed for this purpose. These software applications can be used to execute complex analysis to determine both cortex thickness and density. The algorithms and software applications presented in this paper are the ones most utilized to measure cortical thickness today, and include four software applications and two algorithms. The basic principles of these tools will be outlined, as well as their strengths and weaknesses

Basic research and clinical investigations of the neural basis of orofacial pain

Background: Trigeminal nerve injury or orofacial inflammation causes severe pain in the orofacial regions innervated by uninjured nerves or uninflamed tissues as well as injured or inflamed tissues. Pathological orofacial pain associated with trigeminal nerve injury or inflammation is difficult to diagnose and treat. Highlights: To develop appropriate treatments for patients with orofacial pathological pain, various animal models of trigeminal nerve injury or orofacial inflammation have been developed. Further, the possible mechanisms involving the trigeminal ganglion (TG), trigeminal spinal subnucleus caudalis (Vc), and upper cervical spinal cord (C1-C2) have been studied. Conclusions: 1) Neurotransmitters released from the somata of TG neurons are involved in peripheral sensitization. 2) Neurotransmitter release from TG neurons is decreased by botulinum toxin-type A administration, suggesting that this toxin suppressed neurotransmitter release and alleviated the neuropathic pain-related behavior. 3) Altered states of glial cells and nociceptive neurons, in the Vc and C1-C2 are involved in pathological orofacial pain associated with trigeminal nerve injury or orofacial inflammation. 4) The trigeminal sensory nuclear complex, especially the trigeminal spinal subnucleus oralis, is involved in normal and pathological orofacial pain conditions after peripheral nerve injury. 5) Neuroimaging analyses have suggested functional changes in the central and peripheral nervous systems in neuropathic pain conditions

Central pain modulatory mechanisms of attentional analgesia are preserved in fibromyalgia

Fibromyalgia is a prevalent pain condition that is associated with cognitive impairments including in attention, memory, and executive processing. It has been proposed that fibromyalgia may be caused by altered central pain processing characterised by a loss of endogenous pain modulation. We tested whether attentional analgesia, where cognitive engagement diminishes pain percept, was attenuated in patients with fibromyalgia (n = 20) compared with matched healthy controls (n = 20). An individually calibrated, attentional analgesia paradigm with a 2 × 2 factorial design was used with brain and brainstem-focussed functional magnetic resonance imaging. Patients with fibromyalgia had both lower heat pain thresholds and speeds in a visual attention task. When this was taken into account for both attentional task and thermal stimulation, both groups exhibited an equivalent degree of attentional analgesia. Functional magnetic resonance imaging analysis showed similar patterns of activation in the main effects of pain and attention in the brain and brainstem (with the sole exceptions of increased activation in the control group in the frontopolar cortex and the ipsilateral locus coeruleus). The attentional analgesic effect correlated with activity in the periaqueductal gray and rostral ventromedial medulla. These findings indicate that patients with fibromyalgia can engage the descending pain modulatory system if the attentional task and noxious stimulus intensity are appropriately titrated

Diffusion tensor imaging detects microstructural reorganization in the brain associated with chronic irritable bowel syndrome

Irritable bowel syndrome (IBS) is a common gastrointestinal disorder characterized by recurring abdominal pain associated with alterations in bowel habits. We hypothesized patients with chronic visceral pain associated with IBS may have microstructural differences in the brain compared with healthy control subjects (HCs), indicative of long-term neural reorganization of chronic pain pathways and regions associated with sensory integration. In the current study we performed population-based voxel-wise DTI comparisons and probabilistic tractography in a large sample of phenotyped patients with IBS (n=33) and HCs (n=93). Patients had lower fractional anisotropy (FA) in thalamic regions, the basal ganglia and sensory/motor association/integration regions as well as higher FA in frontal lobe regions and the corpus callosum. In addition, patients had reduced mean diffusivity (MD), within the globus pallidus, and higher MD in the thalamus, internal capsule, and coronal radiata projecting to sensory/motor regions, suggestive of differential changes in axon/dendritic density in these regions. Sex differences in FA and MD were also observed in the patients but not in HCs. Probabilistic tractography confirmed a higher degree of connectivity in patients between the thalamus and pre-frontal cortex, as well as the medial dorsal thalamic nuclei and anterior cingulate cortex, and a lower degree of connectivity between the globus pallidus and thalamus. Together, these results support the hypothesis that patients with chronically recurring visceral pain from IBS have long-term microstructural changes within the brain, particular in regions associated with integration of sensory information and cortico thalamic modulation

Layer- and subregion-specific electrophysiological and morphological changes of the medial prefrontal cortex in a mouse model of neuropathic pain

Chronic neuropathic pain constitutes a serious public health problem, but the disease mechanisms are only partially understood. The involvement of different brain regions like the medial prefrontal cortex has already been established, but the comparison of the role of different subregions and layers is still inconclusive. In the current study, we performed patch-clamp recordings followed by anatomical reconstruction of pyramidal cells from different layers of the prelimbic and infralimbic subregions of the medial prefrontal cortex in neuropathic (spared nerve injury, SNI) and control mice. We found that in the prelimbic cortex, layer 2/3 pyramidal cells from SNI mice exhibited increased excitability compared to sham controls, whereas prelimbic layer 5 pyramidal neurons showed reduced excitability. Pyramidal cells in both layer 2/3 and layer 5 of the infralimbic subregion did not change their excitability, but layer 2/3 pyramidal cells displayed increased dendritic length and branching. Our findings support the view that chronic pain is associated with subregion- and layer-specific changes in the medial prefrontal cortex. They therefore provide new insights into the mechanisms underlying the chronification of pain