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Cough is a common respiratory complaint driving patients to seek medical advice. Besides being a fundamental respiratory sign, it is also a crucial neurological sign. There are three main types of coughs: Reflex cough (type I), voluntary cough (type II), and evoked cough (type III). Cough is a reflex predominantly mediated by control centers in the respiratory areas of the brainstem, modulated by the cerebral cortex. Cough reflex sensitivity could be increased in many neurological disorders such as brainstem space-occupying lesions, medullary lesions secondary to Chiari type I malformations, tics disorders such as Tourette's syndrome, somatic cough, cerebellar neurodegenerative diseases, and chronic vagal neuropathy due to allergic and non-allergic conditions. Meanwhile, cough sensitivity decreases in multiple sclerosis, brain hypoxia, cerebral hemispheric stroke with a brainstem shock, Parkinson's disease, dementia due to Lewy body disease, amyotrophic lateral sclerosis, and peripheral neuropathy as diabetic neuropathy, hereditary sensory and autonomic neuropathy type IV, vitamin B12, and folate deficiency. Arnold's nerve ear-cough reflex, syncopal cough, cough headache, opioids-associated cough, and cough-anal reflex are signs that could help diagnose underlying neurological conditions. Cough reflex testing is a quick, easy, and cheap test performed during the cranial nerve examination. In this article, we reviewed the role of cough in various neurological disorders that increase or decrease cough sensitivity.

Background Chronic urticaria exerts a profound impact on quality of life. Recent guidelines recommend its evaluation in all chronic urticaria patients. Currently, the Chronic Urticaria Quality of Life Questionnaire (CU-Q2oL) is the only validated tool to assess chronic urticaria-specific quality of life. Objective To validate and adapt the CU-Q2oL to the Bengali language for its widespread use. Methods The CU-Q2oL questionnaire was translated into Bengali. Its internal consistency and reliability were tested by asking 42 chronic urticaria patients to complete this version. They completed the validated Bengali Dermatology Life Quality Index and Urticaria Control test questionnaires, and their scores were correlated with CU-Q2oL score to assess the validity of our Bengali version. Results The mean CU-Q2oL score of our patients (mean age 38.41 ± 13.4 years, male: female 29:13) was 48.8 ± 16.5. Domain 4 (sleep problems) was worst affected, followed by domain 1 (pruritus), while domain 2 (swelling) was least affected. We detected an excellent overall internal consistency (Cronbach's alpha = 0.93) of our version and nearly complete agreement (intra-class correlation coefficient = 0.91) between the test-retest scores. We found a significant positive correlation between the overall CU-Q2oL and Dermatology Life Quality Index scores (rs = 0.53, P = 0.0002), thus implying the validity of our version. Additionally, we noted a significant negative correlation between the overall CU-Q2oL and Urticaria Control test scores (rs = -0.48, P = 0.0007), suggestive of a more severe impairment of quality of life with poorer disease control. Limitations Small sample size, observational design and bias in test-retest reliability analysis due to the use of rescue therapy in-between assessment sessions were important limitations of our study. Conclusion The Bengali version of CU-Q2oL questionnaire is a valid and reliable tool suitable for both clinical and research use in Bengali speaking chronic urticaria patients.

Postoperative abdominal adhesions (PAAs) represent a frequent condition occurring in more than 90% of patients undergoing abdomen and pelvic surgeries, which can cause chronic abdominal pain, female infertility, and repeated bowel obstruction, requiring repetitive surgical interventions causing morbidity and mortality, as well as high costs. It is therefore of paramount clinical importance and significance to develop practical and reliable strategies for preventing the occurrence of PAAs.

To investigate the therapeutic efficacy, feasibility, and safety of total parathyroidectomy (tPTX) in the treatment of secondary hyperparathyroidism (SHPT).

Chemotherapy-induced neuropathy (CIN) is one of the most common complications of cancer treatment with sensory dysfunctions which frequently include pain. The mechanisms underlying pain during CIN are starting to be uncovered. Neuroimaging allows the identification of brain circuitry involved in pain processing and modulation and has recently been used to unravel the disruptions of that circuitry by neuropathic pain. The present study evaluates the effects of paclitaxel, a cytostatic drug frequently used in cancer treatment, at the neuronal function in the anterior cingulate cortex (ACC), hypothalamus and periaqueductal grey (PAG) using manganese-enhanced magnetic resonance imaging (MEMRI). We also studied the metabolic profile at the prefrontal cortex (PFC) and hypothalamus using ex vivo spectroscopy. Wistar male rats were intraperitoneal injected with paclitaxel or vehicle solution (DMSO). The evaluation of mechanical sensitivity using von Frey test at baseline (BL), 21 (T21), 28 (T28), 49 (T49) and 56 days (T56) after CIN induction showed that paclitaxel-injected rats presented mechanical hypersensitivity from T21 until T56 after CIN induction. The evaluation of the locomotor activity and exploratory behaviors using open-field test at T28 and T56 after the first injection of paclitaxel revealed that paclitaxel-injected rats walked higher distance with higher velocity at late point of CIN accompanied with a sustained exhibition of anxiety-like behaviors. Imaging studies performed using MEMRI at T28 and T56 showed that paclitaxel treatment increased the neuronal activation in the hypothalamus and PAG at T56 in comparison with the control group. The analysis of data from ex vivo spectroscopy demonstrated that at T28 paclitaxel-injected rats presented an increase of N-acetyl aspartate (NAA) levels in the PFC and an increase of NAA and decrease of lactate (Lac) concentration in the hypothalamus compared to the control group. Furthermore, at T56 the paclitaxel-injected rats presented lower NAA and higher taurine (Tau) levels in the PFC. Together, MEMRI and metabolomic data indicate that CIN is associated with neuroplastic changes in brain areas involved in pain modulation and suggests that other events involving glial cells may be happening.

Emerging research has revealed that the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasomes contribute to the development of inflammatory and neuropathic pains. In addition, microglia are involved in the central nervous system (CNS) pain conduction. However, the relationship between NLRP3 inflammasome and dental inflammatory pain conduction is yet to be established. Therefore, this study aimed to investigate the roles of P2X7 and NLRP3/Caspase-1 (CASP1) in the inflammatory pain caused by pulpitis using a rat experimental pulpitis model. We discovered that the decreased pain threshold was inversely correlated with the increased expression of NLRP3, Caspase-1, P2X7, interleukin-1β (IL-1β), and IL-18 in the trigeminal ganglion and dorsal horn of the medulla after dental pulp exposure. Furthermore, the pain threshold of rats caused by pulpitis was increased by intraperitoneal injection of Brilliant Blue G (BBG), a P2X7 inhibitor, and the expression levels of NLRP3 and related inflammatory factors IL-1β and IL-18 were decreased. Moreover, treatment with 130nM KCl, a P2X7 inhibitor, significantly reduced the expression of NLRP3, IL-1β, IL-18, Caspase-1, and P2X7 in microglia after lipopolysaccharide(LPS) stimulation. In conclusion, our findings suggest that NLRP3/ CASP1 plays a vital role in the conduction of dental pain; the P2X7regulates NLRP3 pathway in the context of dental inflammatory pain conduction, and inhibiting P2X7 may be a potential strategy for dental inflammatory pain relief.

This guideline provides recommendations for clinicians providing pain care, including those prescribing opioids, for outpatients aged ≥18 years. It updates the CDC Guideline for Prescribing Opioids for Chronic Pain – United States, 2016 (MMWR Recomm Rep 2016;65[No. RR-1]:1-49) and includes recommendations for managing acute (duration of <1 month), subacute (duration of 1-3 months), and chronic (duration of >3 months) pain. The recommendations do not apply to pain related to sickle cell disease or cancer or to patients receiving palliative or end-of-life care. The guideline addresses the following four areas: 1) determining whether or not to initiate opioids for pain, 2) selecting opioids and determining opioid dosages, 3) deciding duration of initial opioid prescription and conducting follow-up, and 4) assessing risk and addressing potential harms of opioid use. CDC developed the guideline using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework. Recommendations are based on systematic reviews of the scientific evidence and reflect considerations of benefits and harms, patient and clinician values and preferences, and resource allocation. CDC obtained input from the Board of Scientific Counselors of the National Center for Injury Prevention and Control (a federally chartered advisory committee), the public, and peer reviewers. CDC recommends that persons with pain receive appropriate pain treatment, with careful consideration of the benefits and risks of all treatment options in the context of the patient's circumstances. Recommendations should not be applied as inflexible standards of care across patient populations. This clinical practice guideline is intended to improve communication between clinicians and patients about the benefits and risks of pain treatments, including opioid therapy; improve the effectiveness and safety of pain treatment; mitigate pain; improve function and quality of life for patients with pain; and reduce risks associated with opioid pain therapy, including opioid use disorder, overdose, and death.

There are concerns that cannabis use disorder (CUD) may develop in chronic pain patients prescribed medical cannabis (MC). The criteria for CUD according to the Statistical Manual for Mental Disorders Version 5 (DSM-5) were not developed for identification of patients using cannabis for therapeutic reasons. In addition, some items of CUD might be attributed to the desire of the patient to relieve the pain. Therefore, alternative strategies are needed to identify the true prevalence of CUD in persons with chronic pain being treated with MC.The prevalence of CUD in chronic pain patients according to the DSM-5 criteria was assessed using an anonymous questionnaire in 187 consecutive patients attending three German pain centres in 2021. Questionnaires were rated as follows: 1) all criteria included; 2) removal of items addressing tolerance and withdrawal; 3) removal of positive items if associated with the desire to relieve pain. Abuse was assessed by self-report (use of illegal drugs; diversion and illegal acquisition of MC) and urine tests for illegal drugs Physicians recorded any observation of abuse.CUD according to the DSM-5 criteria was present in 29.9%; in 13.9% when items of tolerance and withdrawal were removed; in 2.1% when positive behaviour items were removed. In 10.7% at least one signal of abuse was noted. Urine tests were positive for non-prescribed drugs (amphetamines, tranquilizer) in 4.8% of subjects. Physicians identified abuse in one patient. In this study, the DSM-5 criteria overestimated and physicians underestimated the prevalence of CUD in patients prescribed MC for chronic pain.