ruihua hou

Loss of neuromelanin in the midbrain is known in Parkinson’s disease(PD), which can now be directly detected by neuromelanin-sensitive MRI(NM-MRI). This case-control study was to investigate the distribution of neuromelanin in the substantia nigra(SN) and the locus coeruleus(LC) using NM-MRI technique and evaluate its potential as a diagnostic marker for PD. 10 early PD patients(H&Y stage Ⅰ, Ⅱ), 11 progressive PD patients(H&Y stage Ⅲ-Ⅴ), and 10 healthy controls matched in age and gender were recruited. All participants completed clinical and psychometric assessments as well as NM-MRI scans. Neuromelanin signal intensities in SN and LC were measured by contrast-to-noise ratios(CNRs) derived from NM-MRI scans. There were significant decreases of CNRs in SNpc(including anterior, central, and posterior) and LC in PD patients compared to controls. There were also significant differences of CNR between the left and right sides. CNR in LC had a negative correlation with the Non-Motor Sympt...

1-Methyl-4-phenylpyridinium (MPP+) induces microglial activation and degeneration of dopaminergic (DAergic) neurons. Donepezil is a well-known acetylcholinesterase inhibitor used clinically to treat cognitive dysfunction in Alzheimer's disease (AD). In the present study, we tested the hypothesis that MPP+ promotes microglial M1 polarization and suppresses M2 polarization and that this can be restored by donepezil. Results indicate that MPP+ treatment in microglial BV2 cells promotes microglial polarization toward the M1 state. However, pretreatment with donepezil inhibited MPP+-induced M1 polarization in microglia by suppressing the release of interleukin (IL)-6, IL-1β, or tumor necrosis factor (TNF)-α. Importantly, we found that MPP+ inhibited microglial M2 polarization by suppressing expression of Arg-1, Fizz1, and Ym1, which was also rescued by pretreatment with donepezil. In addition, IL-4-mediated induction of anti-inflammatory marker genes IL-10, IL-13, and transforming gr...

Endothelial dysfunction and disruption of the blood-brain barrier have been found to be associated with Parkinson's disease (PD). However, the mechanisms underlying these effects have yet to be elucidated. It has also been found that activated protein C (APC) displays neuroprotective properties. Presently, the effects of APC on PD remain unknown. Using a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) neurotoxin rodent model of PD, we found that administration of MPTP can reduce expression of endothelial protein C receptor (EPCR), an N-glycosylated type I membrane protein that has the ability to enhance protein C activation. However, the use of MPTP does not alter levels of thrombomodulin. These findings were verified in an in vitro study showing that 1-methyl-4-phenylpyridinium (MPP+) treatment leads to suppression of EPCR along with reduction of protein C activation in human primary endothelial cells. Importantly, our results display that activation of the transcription...

Neuronal loss and tau aggregation in the Locus Coeruleus (LC) are suggested to be among the earliest pathologies in Alzheimer’s Disease (AD). However this remains to be investigated in vivo. Depletion of cortical noradrenaline (NA) concentration as a result of LC degeneration has proinflammatory effects on microglia and likely contributes to the neuroinflammatory changes observed in animal models of AD. However inflammatory changes within the human LC and the relation to inflammation seen in LC projection areas, e.g. the temporal cortex, has not been investigated.

OBJECTIVE Psychological distress is a common complication in patients after Subarachnoid haemorrhage (SAH) which often has significant impact on the prognosis. The objective of this study was to determine the pooled prevalence of anxiety symptoms and depressive symptoms in patients after SAH and identify relevant risk factors. METHODS The study adopted a systematic review and meta-analysis protocol. Multiple databases including EMBASE, Medline, PsychInfo, and Web of Science were searched for publications before 1st January 2020. Screening, data extraction, and quality assessment were undertaken following the PRISMA guidelines for preferred reporting of systematic reviews and meta-analysis. The random-effects model was used to calculate pooled prevalence rates. Meta-analysis was conducted using Comprehensive Meta-analysis software. The review protocol was registered on PROSPERO (CRD42020182594). RESULTS 42 studies reporting anxiety symptoms and 64 studies reporting depressive symptoms were included. The pooled short term(<3 years) and long term(≥3 years) prevalence rates of anxiety symptoms were 31.4%(95% CI: 23.6%, 40.4%) and 40.4%(95% CI: 31.6%, 49.8%), respectively, whereas the pooled short term and long term prevalence rates of depressive symptoms were 25.2%(95%CI: 17.8%, 34.5%) and 35.8%(95%CI: 28.6%, 43.6%), respectively. Gender and pre-existing psychiatric conditions were identified as potential risk factors. CONCLUSIONS The high prevalence of anxiety symptoms and depressive symptoms after SAH highlights the need for appropriate assessment and management of psychological stress in patients after SAH. Further research is warranted to explore potential underlying mechanisms and to develop holistic interventions that incorporate understanding of both the biological and psychological impact of SAH.

BackgroundBackground: Growing evidence from observational studies indicates a high prevalence of anxiety in asthma. However, prevalence rates of coexisting anxiety symptoms and comorbid anxiety disorders vary widely across studies. We aimed to evaluate the associations between anxiety and asthma and provide more precise comorbidity estimates.MethodsWe systematically reviewed the literature from case-controlled studies and conducted a meta-analysis to evaluate the pooled prevalence estimates and risks of anxiety symptoms and anxiety disorders in asthma individuals. Screening, data extraction, and quality assessment were undertaken following PRISMA guidelines for preferred reporting of systematic reviews and meta-analysis. A random-effects model was used to calculate pooled prevalence rates. Meta-analysis was conducted using Review Manager 5.3. Multiple databases including PubMed, ScienceDirect, PsychINFO, and PsycARTICLES were searched for publications before 1 December 2019. The rev...

The locus coeruleus (LC) is the major source of noradrenaline, which plays a key role in cognition. We aimed to detect the extent of the LC signal attenuation in Alzheimer's disease (AD) patients using a neuromelanin (NM)-sensitive MRI and how it may correlate with inflammatory and autonomic measures. An individually matched case-control study design was employed. 24 patients with AD and 24 age and gender matched controls with no cognitive impairment were recruited. The primary outcome measure was the LC signal intensity indicated by the LC contrast ratio (CR) and measured by the NM-sensitive MRI. Secondary outcome measures included neuropsychometric tests of cognitive state, peripheral inflammatory and autonomic measures. Conditional logistic regression analysis revealed a significant 22% LC-CR reduction in the AD group compared with the control group. However, there was no statistical significance from inflammatory or autonomic measures. This is the largest individually-matched case-control study to visualise the LC degeneration in AD patients. The study revealed significant LC degeneration which holds promise to stratify patients who may benefit from treatment targeting noradrenergic dysfunction.

The locus coeruleus (LC), a tiny nucleus in the brainstem and the principal site of noradrenaline synthesis, has a major role in regulating autonomic function, arousal, attention, and neuroinflammation. LC dysfunction has been linked to a range of disorders; however particular interest is given to the role it plays in Alzheimer’s disease (AD). The LC undergoes significant neuronal loss in AD, thought to occur early in the disease process. While neuronal loss in the LC has also been suggested to occur in aging, this relationship is less clear as the findings have been contradictory. LC density has been suggested to be indicative of cognitive reserve and the evidence for these claims will be discussed. Recent imaging techniques allowing visualization of the LC in vivo using neuromelanin-sensitive MRI are developing our understanding of the role of LC in aging and AD. Tau pathology within the LC is evident at an early age in most individuals; however, the relationship between tau accum...

This article reflects on some radical changes made in mental health services in China which include the implementation of the initial triage system and the special isolation ward, the early screening and testing for both patients and staff, the smaller teams working on rotating shifts on-site, and the adequate provision of PPE. These measures would be of great value as a reference to the effective delivery of mental health services in other countries through this pandemic.

BACKGROUND Extensive research into psychoneuroimmunology has led to substantial advances in our understanding of the reciprocal interactions between the central nervous system and the immune system in neuropsychiatric disorders. To date, inflammation has been implicated in the pathogenesis of depression and anxiety. The immunomodulating effects of antidepressants on depression have been reported, however, there is no evidence of the similar effects of antidepressants on anxiety. The aim of the study was to investigate the effects of selective serotonin reuptake inhibitors (SSRIs) on peripheral inflammatory cytokines in patients with first episode generalized anxiety disorder (GAD). METHODS A prospective cohort design was employed: 42 patients with first episode GAD were treated with either escitalopram or sertraline for 12 weeks. Anxiety was measured by the Generalized Anxiety Disorder Scale and the State Trait Anxiety Inventory, serum pro-inflammatory cytokine levels were measured by the enzyme-linked immunosorbent assay (ELISA), and CRP determined by an immunoturbidimetric method before and after SSRIs treatment RESULTS: Baseline levels of anxiety and pro-inflammatory cytokines including IL-1α, IL-6, IL-8, IL-12, IFN-γ, and CRP were significantly reduced after treatment of SSRIs (p < 0.05 in all cases). In addition, the change of anxiety measures co-vary with the change of peripheral cytokine levels (p < 0.05 in all cases). The regression model revealed that log transformed baseline levels of CRP and IL-6 predicted treatment response (p < 0.05 in both cases). CONCLUSIONS This study is the first to investigate the effects of SSRIs on pro-inflammatory cytokines in patients with first episode GAD. The findings indicate moderate acute anti-inflammatory effects of SSRIs in GAD, and suggest that these anti-inflammatory effects may underlie anxiolytic effects of SSRIs. The study also indicates that serum levels of CRP and IL-6 may predict treatment response. However, data from randomized controlled trials is warranted to confirm these findings.

Many pharmacological and psychological approaches have been found efficacious in patients with generalized anxiety disorder (GAD), but many treatment-seeking patients will not respond and others will relapse despite continuing with interventions that initially had beneficial effects. Other patients will respond but then stop treatment early because of untoward effects such as sexual dysfunction, drowsiness, and weight gain. There is much scope for the development of novel approaches that could have greater overall effectiveness or acceptability than currently available interventions or that have particular effectiveness in specific clinical subgroups. 'Experimental medicine' studies in healthy volunteers model disease states and represent a proof-of-concept approach for the development of novel therapeutic interventions: they determine whether to proceed to pivotal efficacy studies and so can reduce delays in translating innovations into clinical practice. Investigations in ...

To investigate the effect of salt intake on the circadian rhythm of blood pressure and the characteristics of ambulatory blood pressure (ABP) in salt-sensitive (SS) subjects. Twenty-three normotensive subjects and forty-three patients with essential hypertension were included in this study. Salt sensitivity was determined with a chronic dietary salt loading test and an acute venous saline loading test, respectively. 24-hour ABP measurements were performed twice in normotensive subjects when they were on a high salt diet and when they had a low salt diet. Blood and urine samples were collected for measurement of plasma norepinephrine concentration (PNE), plasma renin activity (PRA), angiotensin II, aldosterone, erythrocyte sodium content and urinary sodium excretion. 24-hour ABP readings were also obtained in patients with essential hypertension when antihypertensive drugs were discontinued for at least 2 weeks. High salt intake attenuated the circadian rhythm of blood pressure in SS normotensive subjects, and the nocturnal decline in blood pressure was smaller in SS patients with essential hypertension than in salt-resistant (SR) patients. The level of PNE was higher and the suppression of PRA was smaller in SS subjects than in SR subjects when they had a high salt diet, and the urinary sodium excretion decreased and the erythrocyte sodium content increased significantly in SS subjects on high salt intake. High salt intake caused an abnormal circadian rhythm of blood pressure in SS subjects. The blunted nocturnal decline in blood pressure may be a characteristics of SS patients with essential hypertension.

Introduction. Histaminergic neurones are located in the tuberomammillary nucleus (TMN) of the posterior hypothalamus and project to most areas of the cerebral cortex, cerebellum, hypothalamus, and many brain stem nuclei (1,2). The central histaminergic neurones have important roles in the regulation of arousal, endrocrine and autonomic functions. The ascending histaminergic projection exerts a powerful alerting effect on the neocortex, via the activation of H1 histamine receptors (1,2,3). Recently it has been shown that the ascending histaminergic system is one of the most important alerting systems of the brain, mediating the sedative effects of GABAergic (e.g, muscimol, propofol and pentobarbitone) (4) and of noradrenergic (e.g, dexmedetomidine) (5) anaesthetics. It has been proposed that the activity of the TMN is essential to the maintenance of wakefulness. In sleep, the activity of the TMN is switched off by a GABAergic input originating from the ventrolateral preoptic nucleus (VLPO) of the hypothalamus. In fact, in order to maintain wakefulness, it is important to switch off the activity of the VLPO: this is accomplished by the activation of a noradrenergic inhibitory input from the locus coeruleus (5). GABAergic anaesthetics act by activating inhibitory GABA receptors in the TMN, whereas noradrenergic anaesthetics act by switching off the locus coeruleus via the activation of inhibitory alpha-2 adrenoceptors (autoreceptors) on locus coeruleus neurones (6). The orexinergic neurones of the lateral hypothalamic area (LHA) play an important role in the maintenance of wakefulness, possibly by activating the TMN either directly (7), or indirectly via the locus coeruleus (8). The activation of the locus coeruleus would enhance the noradrenergic inhibition of the VLPO, which in turn would lead to the disinhibition of the TMN by the VLPO. The importance of the TMN in the maintenance of arousal is demonstrated by clinical observations: the hypersomnia observed in encephalitis lethargica by von Economo in the 1920s could be related to a discrete lesion of the posterior hypothalamus involving the TMN (1,3). Furthermore, the blockade of excitatory H1 receptors in the cerebral cortex may underlie the sedative effects of a number of drugs with affinity for H1 histamine receptors (e.g, first generation antihistamines, phenothiazine antipsychotics, tricyclic antidepressants). The central histaminergic system also plays a role in autonomic regulation: it has been shown that the activation of central H1 and H2 histamine receptors results in an increase in sympathetic outflow (2,9). Although the first generation antihistamines have well-documented sedative properties in humans, their effects on autonomic functions have not been studied in detail. In particular, it was of interest to examine how pupillary function is affected by these drugs, since the pupil is under a well-mapped-out dual sympathetic/parasympathetic regulation (6). Therefore, we have examined the pupillary effects of one such drug, diphenhydramine, and compared them with those of diazepam, a sedative drug with little effect on autonomic functions. It should be noted that diphenhydramine, like most first generation antihistamines, also block muscarinic cholinoceptors, an effect that may modify pupillary function. Methods. Fifteen healthy male volunteers participated in three experimental sessions at weekly intervals in which they received (i) diphenhydramine 75 mg, (ii) diazepam 10 mg, (iii) placebo. The three treatments were administered in a balanced order according to a double-blind protocol. Pupil diameter was measured with a binocular pupillometer (Procyon, UK) under four light intensities (darkness, 6, 91, 360 Cd m). Light reflex responses were evoked by green (peak wavelength 565 nm) light flashes (200 ms, 0.43 mW cm); recordings were made with a binocular infrared television pupillometer (TVP 1015B, Applied Science Laboratories Waltham, MA. USA). The level of

There is a close relationship between arousal and pupil diameter, decrease in the level of arousal being accompanied by constriction of the pupil (miosis), probably reflecting the attenuation of sympathetic outflow as sedation sets in. Paradoxically, sedation induced by benzodiazepines is not accompanied by miosis. The objective of this study was to examine the hypothesis that diazepam may attenuate both the sympathetic and the opposing parasympathetic outflow to the iris, which may mask the miosis. Dapiprazole (sympatholytic) and tropicamide (parasympatholytic) were applied topically, together with the cold pressor test (CPT), to manipulate the sympathetic/parasympathetic balance. Sixteen healthy male volunteers participated in four weekly sessions according to a balanced double-blind protocol. Diazepam 10 mg (two sessions) and placebo (two sessions), associated with either 0.01% tropicamide or 0.5% dapiprazole eyedrops, were administered orally. Pupil diameter, light and darkness reflexes and pupillary sleepiness waves were recorded with infrared video pupillometry, alertness was measured by critical flicker fusion frequency (CFFF) and visual analogue scales (VAS), blood pressure and heart rate by conventional methods. CPT was applied after post-treatment testing. Data were analysed by analysis of variance, with multiple comparisons. Diazepam caused sedation (reduction in VAS alertness scores and CFFF, increase in sleepiness waves), dapiprazole had a sympatholytic and tropicamide a parasympatholytic effect on the pupil. Diazepam had no effect on pupil diameter and reflexes or their modifications by the antagonists. CPT increased pupil diameter, blood pressure and heart rate, and the increase only in systolic blood pressure was attenuated by diazepam. Diazepam-induced sedation is not accompanied by any change in either the sympathetic or parasympathetic influence on the iris.

Classical fear conditioning involves pairing a neutral conditional stimulus (CS) with an aversive unconditional stimulus (US). Subsequent presentation of the CS alone induces fear responses. Acquisition of conditioned fear is thought to involve learning of the CS/US association, followed by memory consolidation. Recently we reported that the N1/P2 auditory evoked potential was enhanced by fear conditioning in humans. Diazepam 10mg, given before CS/US pairing, prevented subsequent expression of fear potentiation when the response was elicited, 1 week later, in the presence of the CS. In this experiment, we examined whether this effect of diazepam was caused by disruption of the formation of CS/US associations or by disruption of consolidation. The benzodiazepine antagonist flumazenil was used to block the effect of diazepam either during the association period or during subsequent consolidation. Forty-two male volunteers (18-35 years) participated in two sessions separated by 7 days....

The noradrenergic locus coeruleus is a major wakefulness-promoting nucleus of the brain, which is also involved in the regulation of autonomic and endocrine functions. The activity of the locus coeruleus is believed to be tonically enhanced by a mesocoerulear dopaminergic pathway arising from the ventral tegmental area of the midbrain. Both modafinil, a wakefulness-promoting drug, and pramipexole, a D2/D3receptor agonist with sedative properties, may act on this pathway, with modafinil increasing and pramipexole decreasing locus coeruleus activity. The aim of this study was to compare the two drugs on alertness, autonomic and endocrine functions in healthy volunteers. Pramipexole (0.5mg), modafinil (200mg), and their combination were administered to 16 healthy males in a double-blind, placebo-controlled design. Methods included tests of alertness (pupillographic sleepiness test, critical flicker fusion frequency, visual analogue scales), autonomic functions (resting pupil diameter, ...

A significant proportion (15-30%) of patients with mild traumatic brain injury (MTBI) are at risk of developing postconcussional syndrome (PCS). The aim of this study was to investigate the contributions of cognitive, emotional, behavioural and social factors to the development of PCS and identify early predictors. A prospective cohort design was employed. 126 MTBI patients completed baseline questionnaire assessments within 2 weeks of the injury and 107 completed follow-up questionnaire assessments at 3 and 6 months. A series of self-report measures were used to assess cognitive, behavioural and emotional responses to MTBI. The primary outcome was the ICD-10 diagnosis for PCS. Demographic and clinical characteristic variables were compared between PCS cases and non-cases using independent sample t tests and χ(2) tests. Individual and multivariate logistic regression analyses were used to detect predictors of PCS. Of 107 MTBI patients, 24 (22%) met the criteria for PCS at 3 months and 22 (21%) at 6 months. Individual logistic regression analysis indicated that negative MTBI perceptions, stress, anxiety, depression and all-or-nothing behaviour were associated with the risk of PCS. Multivariate analysis revealed that all-or-nothing behaviour was the key predictor for the onset of PCS at 3 months while negative MTBI perceptions predicted PCS at 6 months. The study provides good support for the proposed cognitive behavioural model. Patients' perceptions of their head injury and their behavioural responses play important roles in the development of PCS, indicating that cognitive and behavioural factors may be potential targets for early preventive interventions.

ObjectiveThe aim of this study was to investigate the contributions of cognitive, emotional and behavioural factors to the development of Post Concussional Syndrome (PCS) after mild traumatic brain injury (MTBI), particularly the role of attentional bias (AB).Methods80 MTBI patients completed baseline questionnaire assessments and 39 completed computer tasks. 42 patients completed the follow-up assessments. A series of self-report measures were used to assess cognitive, behavioural and emotional responses, and the visual probe task was adopt to measure reaction time (RT) and assess attentional bias (AB). The main outcomes were measured by the Rivermead Postconcussion Symptoms Questionnaire (RPQ).ResultsPCS symptoms at 3 months were positively correlated with measures of stress response (r = 0.397, p = 0.011), particularly stress avoidance (r = 0.497, p = 0.001), anxiety (r = 0.33, p = 0.035), illness perception (r = 0.528, p = 0.000), and all or nothing behaviour (r = 0.422, p = 0.0...

Adherence to medication is essential for achieving good outcomes for patients with bipolar affective disorder. This study tested whether treatment and illness beliefs are important predictors of adherence to medication. Results indicate that beliefs are predictive, and may be a suitable target for modification in efforts to change behaviour.

ABSTRACT Attentional bias is an important psychological mechanism that has been extensively explored within the anxiety literature and more recently in chronic pain. Cognitive behavioural models of chronic fatigue syndrome (CFS) and chronic pain suggest an overlap in the mechanisms of these two conditions. The current study investigated attentional bias towards health-threat stimuli in individuals with CFS, compared to healthy controls. The study also examined whether individuals with CFS have impaired executive attention, and how it was related to attentional bias.Methods Two participant groups, CFS (n = 27) and healthy control (n = 35), completed a Visual Probe Task measuring attentional bias towards health-threat stimuli (words and pictures) presented at 500ms and 1250ms, and an Attention Network Test measuring alerting, orienting and executive attention. Participants also completed a series of standard self-report measures.ResultsWhen compared to the control group, the CFS group showed greater attentional bias towards threat-words, but not pictures, regardless of stimulus duration. This was not related to anxiety or depression. The CFS group was also significantly impaired on executive attention compared to the controls. Post-hoc analyses indicated that only CFS individuals with poor executive attention showed a threat-word bias when compared to controls and CFS individuals with good executive attention.Conclusions The findings from this study suggest that CFS individuals show enhanced attentional biases for health-threat stimuli, which may contribute to the perpetuation of the condition. Moreover, the attentional biases in CFS are dependent on an individual's capacity to voluntarily control their attention.

Background: Traumatic brain injury is one of the most common neurological conditions. However, the majority of cases 90% are actually mild. Mild traumatic brain injury (MTBI) remains a major, unrecognized public health issue and has been called a “silent epidemic” (1). A significant proportion (15-30%) of patients are at risk of developing Post Concussional Syndrome (PCS) (2)(3), which is a symptom cluster including a number of physical, cognitive, emotional?and behavioural symptoms. Objective: The aim of this study was to investigate the contributions of cognitive, emotional and behavioural factors to the development of PCS based on a cognitive-behavioural model. Methods: A prospective cohort design was employed. 126 patients met the diagnosis of MTBI (mean age 38.32 years; male 63%) completed baseline questionnaire assessments within 2 weeks after injury, and 108 patients completed follow-up questionnaire assessments at both 3 and 6 months after injury. A series of self-report measures including the Brief Illness Perception Questionnaire, the Behavioural Response to Illness Questionnaire, the Impact of Event Scale, the Hospital Anxiety and Depression Scale, the Brief Social Support Questionnaire, and the Rivermead Postconcussion Symptoms Questionnaire were used to assess baseline somatic, cognitive, behavioural and emotional responses. The primary outcome measures were the ICD-10 Diagnosis for PCS and the Rivermead Postconcussion Symptoms Questionnaire. Data from 107 patients were entered into final analysis. Demographic and clinical characteristic variables were compared between the PCS cases and non-cases using independent-sample t tests and ?² tests. Significant variables from the individual regression analysis were subjected to multiple logistic regression modelling with PCS outcome entered as the dependent variable. A stepwise backward logistic regression procedure was used to derive the model. The Likelihood Ratio Test was used to select predictor variables in the logistic regression model. Fit of the model was assessed by the Hosmer-Lemeshow ‘‘goodness of fit statistic’’ for significance. Results: Of 107 participants, 24 (23%) patients met the criteria for PCS at 3 months, and 23 (22%) at 6 months. Somatic symptoms such as headache, fatigue, sleep disturbance, were most prevalent at two follow-ups. Significant predictors indicated by individual logistic regression analysis including illness perceptions, stress, HADS anxiety and depression, and all-or-nothing behaviour, were then entered into two separate multiple regression analysis. The resultant model for PCS at 3 months included all-or-nothing behaviour, and the resultant model at 6 months included all-or-nothing behaviour and negative illness perceptions. All-or-nothing behaviour was found to be an independent predictor for PCS at 3 months (Odds Ratio 1.141, 95% confidence interval 1.050 to 1.240, p = 0.002), while negative illness perceptions was an independent predictor at 6 months after injury (Odds Ratio 1.053, 95% confidence interval 1.008 to 1.101, p = 0.021). Conclusions: The study provides good support for the proposed cognitive behavioural model for PCS. Patients’ negative illness beliefs and certain behavioural response play important roles in the development of PCS, indicating that they may be important early intervention targets.