Rejected

Growing evidence suggests that the interactions between astrocytes and neurons exert important functions in the central sensitization of the spinal cord dorsal horn in rodents with diabetes and neuropathic pain (DNP). However, it still remains unclear how signal transmission occurs in the spinal cord dorsal horn between astrocytes and neurons, especially in subjects with DNP. Chemokine CXC receptor 4 (CXCR4) plays critical roles in DNP, and connexin 43 (CX43), which is also primarily expressed by astrocytes, contributes to the development of neuropathy. We thus postulated that astrocytic and neuronal CXCR4 induces and produces inflammatory factors under persistent peripheral noxious stimulation in DNP, while intercellular CX43 can transmit inflammatory stimulation signals. The results showed that streptozotocin-induced type 1 diabetic rats developed heat hyperalgesia and mechanical allodynia. Diabetes led to persistent neuropathic pain. Diabetic rats developed peripheral sensitization at the early phase (2 weeks) and central sensitization at the late phase (5 weeks) after diabetes induction. Both CXCR4 and CX43, which are localized and coexpressed in neurons and astrocytes, were enhanced significantly in the dorsal horn of spinal cord in rats undergoing DNP during late phase of diabetes, and the CXCR4 antagonist AMD3100 reduced the expression of CX43. The nociceptive behavior was reversed, respectively, by AMD3100 at the early phase and by the antioxidant N-acetyl-L-cysteine (NAC) at the late phase. Furthermore, rats with DNP demonstrated downregulation of glial fibrillary acidic protein (GFAP) as well as upregulation of c-fos in the spinal cord dorsal horn at the late phase compared to the controls, and upregulation of GFAP and downregulation of c-fos were observed upon treatment with NAC. Given that GFAP and c-fos are, respectively, makers of astrocyte and neuronal activation, our findings suggest that CXCR4 as an inflammatory stimulation protein and CX43 as an intercellular signal transmission protein both may induce neurons excitability and astrocytes dysfunction in developing DNP.

Posttraumatic stress symptoms (PTSS) are common after whiplash injury and are associated with poor recovery. The acute stress response may lead to pain sensitization and widespread pain, thereby compromising recovery. To our knowledge, no longitudinal study has assessed the associations between early PTSS and pain sensitization over time using quantitative sensory testing (QST). The aim of this study was to compare participants with different levels of PTSS, as measured by the impact of event scale (IES; subclinical 0-8, mild 9-25, and clinical ≥ 26) at baseline (<10-day post-injury) and at a follow-up of 1, 3, 6, and 12-month post-injury on pain sensitivity, neck mobility, pain distribution, and pain intensity. In total, 740 participants were recruited from emergency units or general practitioners with acute neck pain after a whiplash injury. The clinical PTSS group showed increased pain sensitivity on all QSTs at all time points compared to the subclinical PTSS group. Also, the clinical PTSS group showed significantly lower neck mobility at all time points except for a 3-month follow-up compared to the subclinical PTSS group. Moreover, the clinical PTSS group showed more widespread pain and self-reported headache and neck pain intensity at all time points compared to the subclinical PTSS group. This study emphasizes that participants with clinical levels of PTSS constitute a high-risk group that is sensitized to pain early after the injury. Hence, screening for PTSS within the 1st week after whiplash injury for those who experience high levels of pain intensity and distress may be an important clinical procedure in the assessment and treatment of whiplash-associated disorders (WAD).

The treatment of neuropathic pain (NPP) is considered challenging, while the search for alternative medication is striving. NPP pathology is related with the expression of both the purinergic 2X7 (P2X7) receptor and the transient receptor potential vanilloid 1 receptor (TRPV1). Bufalin is a traditional Chinese medication derived from toad venom with pronounced antitumor, analgesic, and anti-inflammatory properties. However, poor solubility, rapid metabolism, and the knowledge gap on its pain alleviation mechanism have limited the clinical application of bufalin. Hence, the purpose of this study is to illustrate the NPP alleviation mechanism of bufalin chronic constriction injury (CCI). To address the concern on fast metabolism, bufalin-PLGA microspheres (MS) were prepared membrane emulsification to achieve prolonged pain-relieving effects. Western blot, real-time PCR, immunofluorescence, and molecular docking were employed to demonstrate the therapeutic action of bufalin on NPP. The results showed enhanced thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) after the administration of both bufalin and bufalin-PLGA MS in the CCI rats. Prolonged pain-relieving effects for up to 3 days with reduced dose frequency was achieved bufalin-PLGA MS. In the CCI rats treated with bufalin-PLGA MS, the expression levels of protein and mRNA in TRPV1 and P2X7, both localized in the dorsal root ganglion (DRG), were reduced. Moreover, bufalin-PLGA MS effectively reduced the levels of IL-1β, IL-18, IL-6, and TNF-α in the CCI group. The results from molecular docking suggested a possible mechanism of NPP alleviation of bufalin through binding to P2X7 receptors directly. The administration of bufalin-PLGA MS prepared by membrane emulsification demonstrated promising applications for sustained effect on the alleviation of NPP.

Data on potential side effects of COVID-19 vaccines remains limited. This study aims to evaluate the relationship between the clinical presentations and imaging findings of emergency room (ER) patients presenting with suspected side effects or complications of recent COVID-19 vaccination.

Primary osteosarcoma of the breast (POB) is an extremely aggressive and heterogeneous neoplasm that originates from nonepithelial elements of the mammary gland and accounts for fewer than 1% of breast cancers and fewer than 5% of all sarcomas.

Acute renal infarction is a rare condition that can progress to renovascular hypertension, chronic kidney disease, and end-stage kidney disease, depending on the severity. We present a case of a 30-year-old man with no significant past medical history who presented with sudden onset right flank pain. Initially pyelonephritis was suspected but it was later found to be acute renal infarction secondary to cardioemboli from atrial fibrillation.

This review is the second part of the critical analysis of recent papers of Russian and other authors devoted to the study of the stabilometric parameters in postural control biofeedback training and rehabilitation, associated with psychological functions. The review presents the studies of postural control features in chronic pain syndrome, chronic fatigue syndrome, Parkinson's disease, multiple sclerosis, and depression. The leading role of Russian researchers in the development and application of stabilometric biofeedback in the training of optimal functioning, rehabilitation, and correction of neurological disorders is noted. The paradigm of stabilometric biofeedback training of the cognitive and affective functions is offered.

Concussion is a growing public health concern. No uniformly established therapy exists; neurofeedback studies report treatment value. We use infralow frequency neuromodulation (ILF) to remediate disabling neurological symptoms caused by traumatic brain injury (TBI) and noted improved outcomes with a novel concussion protocol. Postconcussion symptoms (PCS) and persistent postconcussion symptoms (PPCS; >3 months post head injury) are designated timelines for protracted neurological complaints following TBI. We performed a retrospective study to explore effectiveness of ILF in PCS/PPCS and investigated the value of using this concussion protocol.

Healthcare workers were prioritized in vaccination campaigns globally because they are exposed to the highest risk of contamination by SARS-CoV-2. This study evaluated the self-reported post-vaccination side effects of inactivated (BBIBP-CorV and CoronaVac) and adenoviral vector-based (AZD1222, Gam-COVID-Vac and Ad26.COV2.S) vaccines among Algerian healthcare workers using a validated questionnaire. The final analysis included 721 healthcare workers, with a predominance of females (59.1%) and younger individuals 20-30 years old (39.4%). Less than half (49.1%) of the respondents reported at least one local side effect, while 53.8% reported at least one systemic side effect. These side effects were more prevalent among viral vector vaccinees than inactivated virus vaccinees. The most common local side effects were injection site pain (39%) and arm pain (25.4%), while fatigue (34.4%), fever (28.4%), headache (24.8%) and myalgia (22.7%) were the most prevalent systemic side effects. The side effects appeared earlier among inactivated virus vaccines recipients and generally lasted for 2 to 3 days for the two vaccinated groups. The risk factors associated with a higher prevalence of side effects included female gender, allergic individuals, individuals with regular medication, those who contracted the COVID-19 disease and those who received two doses for both inactivated and viral-based vaccines groups. Despite the higher prevalence of post-vaccination side effects among adenoviral vector vaccines recipients, both vaccines groups were equally effective in preventing symptomatic infections, and no life-threatening side effects were reported in either vaccine group.

As the world embarks on mass vaccination against SARS-CoV2 to alleviate the spread of this highly contagious novel coronavirus, there are growing anecdotal reports on immune-related neurological complications following immunisation. Similarly, we encountered 2 cases of central nervous system demyelination at our centre with Comirnaty (BNT162b2), a mRNA-based COVID-19 vaccine. Our first patient had typical clinical-radiological manifestations of acute disseminated encephalomyelitis (ADEM) after his COVID-19 vaccination. This was the sixth reported case to date. Our second patient presented with an unusual complaint of trigeminal neuralgia, with an identifiable demyelinating lesion observed in the pons on neuroimaging. Both cases responded well to immunotherapy. However, larger prospective controlled studies and formal registries are much needed to ascertain a possible relationship between COVID-19 vaccines and acute central nervous system demyelination.