Pain experiences are often complex with catastrophic cognitions, emotions, and behaviors. Cognitive behavioral therapists share the work of unraveling these complex experiences with their patients. ...However, the change process underlying the unraveling of the pain experience have not yet been quantified. We used an interrelationship-focused network model to examine the way an undifferentiated conceptualization between cognition and pain experience changed via group cognitive-behavioral therapy (CBT). Overall, 65 participants (77.4% of all patients who entered the intervention) were included in the analysis; they attended the total of 12 weekly group CBT and filled the Short-Form McGill Pain Questionnaire and the pain catastrophizing questionnaire. Before treatment, there were no edges in the partial correlation-based network because of large covariation across items. After treatment, many edges appeared and, particularly strong couplings were found between items within the same subscale. The formative shift from a non-edged pre-treatment network to a mature post-treatment network may indicate that patients were able to conceptualize these symbolic constructs better. These results are probably of interest to clinicians and would be consistent with the fundamental monitoring process of CBT.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
It has been reported that various clinical criteria indicate computed tomography (CT) examination for mild head injury (MHI). However, the decision to perform CT for MHI largely depends on the ...physician. Data on severe head injuries is available in sources such as the Japan Neurotrauma Data Bank, but only a few data has been collected on MHI. A total of 1688 patients with MHI (Glasgow Coma Scale 14 and 15) treated at our hospital from June 2017 to May 2019 were reviewed. CT was performed in 1237 patients (73.28%), and intracranial hemorrhage was detected in 50 patients. Three patients deteriorated, and all were surgically treated. Statistical analysis of the presence or absence of acute intracranial hemorrhage and "risk factors for complications of intracranial lesions in MHI" showed significant differences in unclear or ambiguous accident history (p = 0.022), continued post-traumatic amnesia (p < 0.01), trauma above the clavicles including clinical signs of skull fracture (skull base or depressed skull fracture) (p = 0.012), age <60 years (p < 0.01), coagulation disorders (p < 0.01), and alcohol or drug intoxication (p < 0.01). The 453 patients who did not satisfy these risk factors included only one patient with intracranial hemorrhage, so the negative predictive value was 99.78%. This study shows that the "risk factors for complications of intracranial lesions in MHI" are effective criteria for excluding acute intracranial hemorrhage and CT should be actively considered for patients with the above factors that showed significant differences.
In this study, we aimed to evaluate the longitudinal changes in the cranial shape of healthy Japanese infants using a three-dimensional scanner and construct a normal values database for the growth ...process. Preterm infants (gestational age < 37 weeks), infants with neonatal asphyxia (5-minute Apgar score of <7), and patients who started helmet therapy for deformational plagiocephaly were excluded from this study. The first scan was performed at approximately 1 month of age, followed by two scans conducted at 3 and 6 months of age. The parameters considered were as follows: cranial length, width, height, circumference, volume, cranial vault asymmetry index, and cephalic index. A cranial vault asymmetry index >5% was defined as deformational plagiocephaly. Changes in each parameter were examined using repeated-measures analysis of variance classified by sex and deformational plagiocephaly status. The rate of increase in each parameter was also examined. In total, 88 infants (45 boys and 43 girls) were included in this study. All growth-related parameters were noted to increase linearly with time. Sex differences were observed in all parameters except cranial length. Deformational plagiocephaly was found to have no effect on growth-related parameters. Cranial volume increased by 60% from 1 to 6 months of age. The growth almost uniformly influenced the rate of increase in volume in each coordinate axis direction. Overall, the mean trends in three-dimensional parameters in infants up to 6 months of age were obtained using a three-dimensional scanner. These trends could be used as a guide by medical professionals involved in cranioplasty.
Since optimal treatment at an early stage leads to remission of symptoms and recovery of function, putative biomarkers leading to early diagnosis and prediction of therapeutic responses are desired. ...The current study aimed to use a metabolomic approach to extract metabolites involved in both the diagnosis of major depressive disorder (MDD) and the prediction of therapeutic response for escitalopram. We compared plasma metabolites of MDD patients (n = 88) with those in healthy participants (n = 88) and found significant differences in the concentrations of 20 metabolites. We measured the Hamilton Rating Scale for Depression (HRSD) on 62 patients who completed approximately six-week treatment with escitalopram before and after treatment and found that kynurenic acid and kynurenine were significantly and negatively associated with HRSD reduction. Only one metabolite, kynurenic acid, was detected among 73 metabolites for overlapped biomarkers. Kynurenic acid was lower in MDD, and lower levels showed a better therapeutic response to escitalopram. Kynurenic acid is a metabolite in the kynurenine pathway that has been widely accepted as being a major mechanism in MDD. Overlapping biomarkers that facilitate diagnosis and prediction of the treatment response may help to improve disease classification and reduce the exposure of patients to less effective treatments in MDD.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
In Japan, a range of patients with traumatic brain injury (TBI) has been recorded in a nationwide database (Japan Neurotrauma Data Bank; JNTDB). This study aimed to externally validate three ...international prediction models using JNTDB data: Trauma and Injury Severity Score (TRISS), Corticosteroid Randomization After Significant Head Injury (CRASH), and International Mission for Prognosis and Analysis of Clinical Trials in TBI (IMPACT). We also aimed to validate the applicability of these models in the Japanese population. Of 1,091 patients registered in the JNTDB from July 2009 to June 2011, we analyzed data for 635 patients. We examined factors associated with mortality in-hospital and unfavorable outcomes 6 months after TBI by applying the TRISS, CRASH, and IMPACT models. We also conducted an external validation of these models based on these data. The patients' mean age was 60.1 ±21.1 years, and 342 were alive at the time of discharge (53.9%). Univariate analysis revealed eight major risk factors for mortality in-hospital: age, Glasgow Coma Scale (GCS), Injury Severity Score (ISS), systolic blood pressure, heart rate, mydriasis, acute epidural hematoma (AEDH), and traumatic subarachnoid hemorrhage. A similar analysis identified five risk factors for unfavorable outcomes at 6 months: age, GCS, ISS, mydriasis, and AEDH. For mortality in-hospital, the TRISS had a satisfactory area under the curve value (0.75). For unfavorable outcomes at 6 months, the CRASH (basic and computed tomography) and IMPACT (core and core extended) models had satisfactory area under the curve values (0.86, 0.86, 0.81, and 0.85, respectively). The TRISS, CRASH, and IMPACT models were suitable for application to the JNTDB population, indicating these models had high value in Japanese patients with neurotrauma.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The aim of the current study was to determine the effects of cerebral contusion injury with purinergic adenosine triphosphate Y1 (P2Y1) receptor blockers on postinjury inflammatory responses. ...Adenosine triphosphate (ATP) is released into the extracellular space in several in vivo models, including traumatic brain injury. Released ATP triggers neuroinflammation via activation of microglial cells. P2Y1 receptor blockers were reported to suppress extracellular ATP elevation in several disease models through inhibition of cellular ATP release. In addition to the beneficial effects of inflammation, excess inflammatory reactions cause secondary damage and aggravate outcomes. Here, we assessed the effect of the selective P2Y1 receptor blocker MRS2179 on its potential to prevent posttraumatic inflammation in a rat cerebral contusion model. Cerebral contusion injury was induced in the rat cerebral cortex. Either MRS2179 or artificial cerebral spinal fluid as a control was administered in situ into the center of contused tissue via a subcutaneously implanted osmotic pump. Galectin 3, a marker of microglia and proinflammatory cytokines, was measured 1, 3 and 7 days following injury. Another group of rats was assessed for behavioral performance up to 28 days after injury, including the beam walk test, neurological response test and plus maze test. The Galectin 3 levels in the cortex around the contusion cavity and in the cortex far from the contusion cavity were significantly suppressed by MRS2179 administration on postinjury Days 1 and 3 (p < 0.05). However, administration of MRS2179 failed to improve behavioral outcome. Administration of MRS2179 successfully suppressed microglial activation in a traumatic brain injury model, which will be a potent treatment option in the future. Further study is required to conclude its therapeutic effects.
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•The effect of the selective P2Y1 receptor blocker MRS2179 in a rat cerebral contusion model.•Suppression of the Galectin 3 levels in the cortex around the contusion cavity by MRS2179.•Suppression of the subsequent inflammatory response in a traumatic brain injury model.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Anticipation of pain engenders anxiety and fear, potentially shaping pain perception and governing bodily responses such as peripheral vasomotion through the sympathetic nervous system (SNS). ...Sympathetic innervation of vascular tone during pain perception has been quantified using a peripheral arterial stiffness index; however, its innervation role during pain anticipation remains unclear. This paper reports on a neuroimaging-based study designed to investigate the responsivity and attribution of the index at different levels of anticipatory anxiety and pain perception. The index was measured in a functional magnetic resonance imaging experiment that randomly combined three visual anticipation cues and painful stimuli of two intensities. The peripheral and cerebral responses to pain anticipation and perception were quantified to corroborate bodily responsivity, and their temporal correlation was also assessed to identify the response attribution of the index. Contrasting with the high responsivity across levels of pain sensation, a low responsivity of the index across levels of anticipatory anxiety revealed its specificity across pain experiences. Discrepancies between the effects of perception and anticipation were validated across regions and levels of brain activity, providing a brain basis for peripheral response specificity. The index was also characterized by a 1-s lag in both anticipation and perception of pain, implying top-down innervation of the periphery. Our findings suggest that the SNS responds to pain in an emotion-specific and sensation-unbiased manner, thus enabling an early assessment of individual pain perception using this index. This study integrates peripheral and cerebral hemodynamic responses toward a comprehensive understanding of bodily responses to pain.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Brain activity associated with pain perception has been revealed by numerous PET and fMRI studies over the past few decades. These findings helped to establish the concept of the pain matrix, which ...is the distributed brain networks that demonstrate pain-specific cortical activities. We previously found that peripheral arterial stiffness Formula: see text responds to pain intensity, which is estimated from electrocardiography, continuous sphygmomanometer, and photo-plethysmography. However, it remains unclear whether and to what extent Formula: see text aligns with pain matrix brain activity. In this fMRI study, 22 participants received different intensities of pain stimuli. We identified brain regions in which the blood oxygen level-dependent signal covaried with Formula: see text using parametric modulation analysis. Among the identified brain regions, the lateral and medial prefrontal cortex and ventral and dorsal anterior cingulate cortex were consistent with the pain matrix. We found moderate correlations between the average activities in these regions and Formula: see text (r = 0.47, p < 0.001). Formula: see text was also significantly correlated with self-reported pain intensity (r = 0.44, p < 0.001) and applied pain intensity (r = 0.43, p < 0.001). Our results indicate that Formula: see text is positively correlated with pain-related brain activity and subjective pain intensity. This study may thus represent a basis for adopting peripheral arterial stiffness as an objective pain evaluation metric.
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IZUM, KILJ, NUK, PILJ, PNG, SAZU, UL, UM, UPUK
Abstract
Background
Conjunctival chemosis (CC) is an extremely rare symptom of pituitary neuroendocrine tumor (PitNET). We report an extremely rare case of PitNET manifesting as severe CC.
Case ...presentation
A 48-year-old male was admitted to our hospital with severe CC, proptosis, and ptosis of the right eye. Magnetic resonance imaging demonstrated the tumor mass invading the cavernous sinus (CS) with cystic lesion. The patient underwent emergent endoscopic transsphenoidal surgery, and the pathological diagnosis was PitNET. CC of the right eye remarkably improved after the surgery. Glucocorticoid therapy was performed for right oculomotor nerve palsy, which rapidly improved. The postoperative course was uneventful and the patient was discharged from our hospital without hormone replacement.
Conclusions
CC caused by CS invasion of PitNET can be cured by early surgical treatment. Therefore, PitNET is important to consider in the differential diagnosis of CC.
•PD pain is treated with SCS.•The mechanism of pain relief by SCS is uncertain.•Measured the nociceptive thermal pain threshold.•SCS increased the pain threshold.•The action mechanism of pain relief ...by SCS is thought to be segmental inhibition.
Parkinson's disease (PD)-related pain or PD pain is a frequent non-motor symptom and is treated with pharmacotherapy and non-pharmacologic therapies such as deep brain stimulation (DBS) and spinal cord stimulation (SCS). The mechanism of PD pain relief by DBS is thought to involve increased pain threshold to nociceptive stimulation, whereas the mechanism of SCS has not been elucidated.
PD pain relief by SCS may involve modulation of the pain thresholds in the spinal cord segments and supra-spinal actions. Therefore, we investigated the effect of SCS in patients who underwent SCS for intractable PD pain in the lower extremities by measuring pain thresholds to thermal nociceptive stimulation of the lower (leg) and upper (hand) parts of the stimulated spinal segment during SCS-off and SCS-on using quantitative sensory testing to determine the pain threshold.
Seven PD patients with SCS in the lower thoracic spinal cord underwent measurements of cold sensory threshold, warm sensory threshold, cold pain threshold (CPT), and heat pain threshold (HPT).
In upper part of the stimulated spinal segment, CPT was significantly decreased during SCS-on compared to SCS-off (p < 0.01); whereas HPT was not significantly different. In lower part of the stimulated spinal segment, CPT was significantly increased during SCS-on compared to SCS-off (p < 0.05); and HPT was also increased (p < 0.05).
This study shows that SCS raises the pain threshold to thermal nociception in PD patients. The primary mechanism of pain relief by SCS is thought to be segmental inhibition at the level of the stimulated spinal segments.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP