ABSTRACT
Complex regional pain syndrome (CRPS) is a chronic neuropathic pain disorder. Pain catastrophizing, characterized by magnification, rumination, and helplessness, increases perceived pain intensity and mental distress in CRPS patients. As functional connectivity patterns in CRPS remain largely unknown, we aimed to investigate functional connectivity alterations in CRPS patients and their association with pain catastrophizing using a whole-brain analysis approach. Twenty-one patients with CRPS and 49 healthy controls were included in the study for clinical assessment and resting-state functional magnetic resonance imaging. Between-group differences in whole-brain functional connectivity were examined through a Network-based Statistics analysis. Associations between altered functional connectivity and the extent of pain catastrophizing were also assessed in CRPS patients. Relative to healthy controls, CRPS patients showed higher levels of functional connectivity in the bilateral somatosensory subnetworks (components 1~2), but lower functional connectivity within the prefronto-posterior cingulate (component 3), prefrontal (component 4), prefronto-parietal (component 5), and thalamo-anterior cingulate (component 6) subnetworks (p<0.05, family-wise error corrected). Higher levels of functional connectivity in components 1~2 (β=0.45, p=0.04) and lower levels of functional connectivity in components 3~6 (β=-0.49, p=0.047) were significantly correlated with higher levels of pain catastrophizing in CRPS patients. Higher functional connectivity in the somatosensory subnetworks implicating exaggerated pain perception and lower functional connectivity in the prefronto-parieto-cingulo-thalamic subnetworks indicating impaired cognitive-affective pain processing may underlie pain catastrophizing in CRPS.
ABSTRACT
Sleep is essential to brain function and mental health. Insomnia and obstructive sleep apnea (OSA) are the two most common sleep disorders, and are major public health concerns. Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive method of quantifying neurometabolite concentrations. Therefore, 1H-MRS studies on individuals with sleep disorders may enhance our understanding of the pathophysiology of these disorders. In this article, we reviewed 1H-MRS studies in insomnia and OSA that reported changes in neurometabolite concentrations. Previous studies have consistently reported insomnia-related reductions in γ-aminobutyric acid (GABA) levels in the frontal and occipital regions, which suggest that changes in GABA are important to the etiology of insomnia. These results may support the hyperarousal theory that insomnia is associated with increased cognitive and physiological arousal. In addition, the severity of insomnia was associated with low glutamate and glutamine levels. Previous studies of OSA have consistently reported reduced N-acetylaspartate (NAA) levels in the frontal, parietooccipital, and temporal regions. In addition, OSA was associated with increased myo-inositol levels. These results may provide evidence that intermittent hypoxia induced by OSA may result in neuronal damage in the brain, which can be related to neurocognitive dysfunction in patients with OSA. The current review summarizes findings related to neurochemical changes in insomnia and OSA. Future well-designed studies using 1H-MRS have the potential to enhance our understanding of the pathophysiology of sleep disorders including insomnia and OSA.
ABSTRACT
Sleep is essential to brain function and mental health. Insomnia and obstructive sleep apnea (OSA) are the two most common sleep disorders, and are major public health concerns. Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive method of quantifying neurometabolite concentrations. Therefore, 1H-MRS studies on individuals with sleep disorders may enhance our understanding of the pathophysiology of these disorders. In this article, we reviewed 1H-MRS studies in insomnia and OSA that reported changes in neurometabolite concentrations. Previous studies have consistently reported insomnia-related reductions in γ-aminobutyric acid (GABA) levels in the frontal and occipital regions, which suggest that changes in GABA are important to the etiology of insomnia. These results may support the hyperarousal theory that insomnia is associated with increased cognitive and physiological arousal. In addition, the severity of insomnia was associated with low glutamate and glutamine levels. Previous studies of OSA have consistently reported reduced N-acetylaspartate (NAA) levels in the frontal, parietooccipital, and temporal regions. In addition, OSA was associated with increased myo-inositol levels. These results may provide evidence that intermittent hypoxia induced by OSA may result in neuronal damage in the brain, which can be related to neurocognitive dysfunction in patients with OSA. The current review summarizes findings related to neurochemical changes in insomnia and OSA. Future well-designed studies using 1H-MRS have the potential to enhance our understanding of the pathophysiology of sleep disorders including insomnia and OSA.
ABSTRACT
Transcranial direct current stimulation (tDCS) is a non-invasive and effective neuromodulatory technique to modulate cortical activities by applying 1 to 2 milliamps electric current. The use of tDCS to enhance cognitive function such as executive function and memory has attracted much attention in recent years, and a lot of studies have been carried out to identify neural mechanisms underlying cognitive enhancement effects of tDCS. In this review, we discussed the previous neuroimaging studies on applications of tDCS for cognitive enhancement using functional magnetic resonance imaging (fMRI). Previous tDCS studies for neurological or psychiatric conditions and elderly individuals suggested that cognitive enhancement effects of tDCS were associated with normalizing aberrant brain networks and activities related to pathophysiology. Moreover, tDCS-induced cognitive enhancement in healthy individuals was associated with functional changes in brain activations and network connectivity. Furthermore, cognitive enhancement effects of tDCS were varied depending on the neurological structure and functional characteristics between individuals. The current review may provide critical insights into functional activity and connectivity of the brain regarding cognitive enhancement effects of tDCS, which could give direction for further studies on identifying the specific neural mechanisms and clinical strategies of tDCS.
ABSTRACT
Shift workers experience a disruption in the circadian sleep-wake rhythm, which brings upon adverse health effects such as fatigue, insomnia and decreased sleep quality. Moreover, shift work has deleterious effects on both work productivity and safety. In this review, we present a brief overview of the current literature on the consequences of shift work, especially focusing on attention-associated cognitive decline and related behavioral changes. We searched two electronic databases, PubMed and RISS, using key search terms related to cognitive domains, deleterious effects, and shift work. Twenty studies were eligible for the final review. The consequences of shift work can be classified into the following three categories extracted from the literature review : 1) work accidents ; 2) commuting accidents such as car accidents that occur on the way to and from work ; and 3) attendance management at work (i.e., absenteeism, tardiness, and unscheduled early departure). These cognitive and behavioral consequences of shift work were also found to be associated with sleep disorders in shift workers. Thus, improvements in the shift work system are necessary in order to enhance workers' health conditions, work productivity, and safety.