bluuebunny/crossref_metadata_2025_split huggingface dataset:
Myalgia as a symptom at hospital admission by severe acute respiratory syndrome coronavirus 2 infection is associated with persistent musculoskeletal pain as long-term post-COVID sequelae: a case-control study
Authors: Fernández-de-las-Peñas César , Rodríguez-Jiménez Jorge , Fuensalida-Novo Stella , Palacios-Ceña María , Gómez-Mayordomo Víctor , Florencio Lidiane L. , Hernández-Barrera Valentín , Arendt-Nielsen Lars 
Published: April 2021

Abstract
This study investigated the association between COVID-related myalgia experienced by patients at hospital admission and the presence of post-COVID symptoms. A case-control study including patients hospitalised due to COVID-19 between February 20 and May 31, 2020, was conducted. Patients reporting myalgia and patients without myalgia at hospital admission were scheduled for a telephone interview 7 months after hospital discharge. Hospitalisation and clinical data were collected from medical records. A list of post-COVID symptoms with attention to musculoskeletal pain was evaluated. Anxiety and depressive symptoms, and sleep quality were likewise assessed. From a total of 1200 hospitalised patients with COVID-19, 369 with and 369 without myalgia at hospital admission were assessed 7.2 months (SD 0.6) after hospital discharge. A greater proportion (P = 0.03) of patients with myalgia at hospital admission (20%) showed ≥3 post-COVID symptoms when compared with individuals without myalgia (13%). A higher proportion of patients presenting myalgia (odds Rratio 1.41, 95% confidence interval 1.04-1.90) exhibited musculoskeletal post-COVID pain when compared to those without myalgia. The prevalence of musculoskeletal post-COVID pain in the total sample was 38%. Fifty percent of individuals with preexisting musculoskeletal pain experienced a worsening of their symptoms after COVID-19. No differences in fatigue, dyspnoea, anxiety/depressive levels, or sleep quality were observed between myalgia and nonmyalgia groups. The presence of myalgia at hospital admission was associated with preexisting history of musculoskeletal pain (OR 1.62, 95% confidence interval 1.10-2.40). In conclusion, myalgia at the acute phase was associated with musculoskeletal pain as long-term post-COVID sequelae. In addition, half of the patients with preexisting pain conditions experienced a persistent exacerbation of their previous syndromes.
Central amygdala inflammation drives pain hypersensitivity and attenuates morphine analgesia in experimental autoimmune encephalomyelitis
Authors: Dworsky-Fried Zoë , Faig Christian A. , Vogel Holly A. , Kerr Bradley J. , Taylor Anna M.W. 
Published: April 2021

Abstract
Chronic pain is a highly prevalent symptom associated with the autoimmune disorder multiple sclerosis (MS). The central nucleus of the amygdala plays a critical role in pain processing and modulation. Neuropathic pain alters nociceptive signaling in the central amygdala, contributing to pain chronicity and opioid tolerance. Here, we demonstrate that activated microglia within the central amygdala disrupt nociceptive sensory processing and contribute to pain hypersensitivity in experimental autoimmune encephalomyelitis (EAE), the most frequently used animal model of MS. Male and female mice with EAE exhibited differences in microglial morphology in the central amygdala, which was associated with heat hyperalgesia, impaired morphine reward, and reduced morphine antinociception in females. Animals with EAE displayed a lack of morphine-evoked activity in cells expressing somatostatin within the central amygdala, which drive antinociception. Induction of focal microglial activation in naïve mice via injection of lipopolysaccharide into the central amygdala produced a loss of morphine analgesia in females, similar to as observed in EAE animals. Our data indicate that activated microglia within the central amygdala may contribute to the sexually dimorphic effects of morphine and may drive neuronal adaptations that lead to pain hypersensitivity in EAE. Our results provide a possible mechanism underlying the decreased efficacy of opioid analgesics in the management of MS-related pain, identifying microglial activation as a potential therapeutic target for pain symptoms in this patient population.
From acute to long-term alterations in pain processing and modulation after spinal cord injury: mechanisms related to chronification of central neuropathic pain
Authors: Defrin Ruth , Gruener Hila , Gaidukov Evgeni , Bondi Moshe , Rachamim-Katz Orna , Ringler Erez , Blumen Nava , Zeilig Gabi 
Published: April 2021

Abstract
A severe and debilitating consequence of a spinal cord injury (SCI) is central neuropathic pain (CNP). Our aim was to investigate the processes leading to CNP emergence and chronification by analyzing causal relationship over time between spinothalamic function, pain excitability, and pain inhibition after SCI. This longitudinal follow-up study included 53 patients with acute SCI and 20 healthy controls. Spinothalamic, pain excitability, and intrasegmental and extrasegmental pain inhibition indices were repeatedly evaluated at 1.5, 3, and 6 months post-SCI. Between- and within-group analyses were conducted among those patients who eventually developed CNP and those who did not. Healthy controls were evaluated twice for repeatability analysis. Patients who developed CNP, compared with those who did not, exhibited increased thermal thresholds (P < 0.05), reduced pain adaptation (P < 0.01), and conditioned pain modulation (P < 0.05), early post-injury, and the CNP group's manifestations remained worse throughout the follow-up. By contrast, allodynia frequency was initially similar across SCI groups, but gradually increased in the subacute phase onward only among the CNP group (P < 0.001), along with CNP emergence. Early worse spinothalamic and pain inhibition preceded CNP and predicted its occurrence, and early worse pain inhibition mediated the link between spinothalamic function and CNP. Crossover associations were observed between early and late pain inhibition and excitability. Inefficient intrasegmental and extrasegmental inhibition, possibly resulting from spinothalamic deafferentation, seems to ignite CNP chronification. Pain excitability probably contributes to CNP maintenance, possibly via further exhaustion of the inhibitory control. Preemptive treatment promoting antinociception early post-SCI may mitigate or prevent CNP.
The Relationship Between the Activities-Specific Balance Confidence Scale and Balance Performance, Self-perceived Handicap, and Fall Status in Patients With Peripheral Dizziness or Imbalance
Authors: Herssens Nolan , Swinnen Eva , Dobbels Bieke , Van de Heyning Paul , Van Rompaey Vincent , Hallemans Ann , Vereeck Luc 
Published: April 2021

Objective:
Describe the relationship between the Activities-Specific Balance Confidence (ABC) scale and Dizziness Handicap Inventory (DHI) with balance performance, as well as fall status in patients with peripheral vestibular disorders.

Study Design:
Retrospective.

Setting:
Outpatient balance clinic, tertiary referral center.

Patients:
Data from 97 patients (age: 54.8 ± 12.3 yrs; 48 women) with dizziness or imbalance symptoms of peripheral vestibular origin were used for analysis.

Intervention(s):
/

Main Outcome Measure(s):
ABC-scores, DHI-scores, static and dynamic balance tests, and fall status of the past 4 weeks, 2 months, and 6 months before the time of measurement were collected. Spearman's rho correlations, χ2 with post-hoc testing, and Kruskal–Wallis with post-hoc Mann–Whitney U test results were interpreted.

Results:
The ABC- and DHI-scores show moderate correlations with static balance (ABC: r = 0.44; DHI: r = –0.34) and dynamic balance tests (ABC: r = [–0.47;0.56]; DHI: r = [–0.48;0.39]) and a strong inverse correlation with each other (ABC: 70 ± 25; DHI: 33 ± 26; r = –0.84). Related to fall status, weak correlations were found (ABC: r = [–0.29;–0.21]; DHI: r = [0.29;0.33]). Additional results show that subjects in the low-level functioning (ABC) or severe self-perceived disability (DHI) categories have a poorer balance assessed by standing balance, Timed-Up-and-Go and Functional Gait Assessment and are more likely to have experienced multiple falls.

Conclusions:
The ABC-scale and DHI showed a strong convergent validity, additionally the ABC-scale showed a better concurrent validity with balance performances and the DHI with fall history. In general, patients with peripheral vestibular impairments reporting a lower self-confidence or a more severe self-perceived disability show worse balance performances and a higher fall incidence.
Participation of the Anterior Cingulate Cortex in Sodium Salicylate-induced Tinnitus
Authors: Fan Xin , Song Yu , Du Yali , Liu Junxiu , Xiong Shan , Zhao Gang , Wang Menglin , Wang Jiang , Ma Furong , Mao Lanqun 
Published: April 2021

Hypothesis:
The anterior cingulate cortex (ACC) participates in sodium salicylate (SS)-induced tinnitus through alteration of the disordered neural activity and modulates the neuronal changes in the auditory cortex (AC).

Background:
Although the mechanism underlying tinnitus remains unclear, the crucial roles of the auditory center and limbic system in this process have been elucidated. Recent reports suggest that dysfunction of the ACC, an important component of the limbic system that regulates and controls the conduction of multiple sensations, is involved in tinnitus. Although altered functional connectivity between the ACC and the auditory system has been observed in humans with tinnitus, the underlying neuronal mechanism remains unexplored.

Methods:
SS (350 mg/kg, 10%, i.p.) was used to yield tinnitus model in rats, followed by comparison of the alteration in the spontaneous firing rate (SFR), local field potential (LFP), and extracellular glutamic acid in the ACC. The responses of neurons in the AC to electrical stimulation from the ACC were also observed.

Results:
We determined significant increases in the neuronal SFR and extracellular glutamate level in the ACC after SS injection (p < 0.05). These effects were accompanied by decreased alpha band activity and increased beta and gamma band activity (p < 0.05). In the majority of AC neurons, the SFR decreased in response to ACC stimulation (p < 0.05).

Conclusions:
Our results demonstrated that disordered neural activity in the ACC contributes to SS-induced tinnitus and that ACC activation can modulate AC activity.
How do we identify the crashing traumatic brain injury patient – the intensivist's view
Authors: McCredie Victoria A. , Chavarría Javier , Baker Andrew J. 
Published: April 2021

Purpose of review
Over 40% of patients with severe traumatic brain injury (TBI) show clinically significant neurological worsening within the acute admission period. This review addresses the importance of identifying the crashing TBI patient, the difficulties appreciating clinical neurological deterioration in the comatose patient and how neuromonitoring may provide continuous real-time ancillary information to detect physiologic worsening.

Recent findings
The latest editions of the Brain Trauma Foundation's Guidelines omitted management algorithms for adult patients with severe TBI. Subsequently, three consensus-based management algorithms were published using a Delphi method approach to provide a bridge between the evidence-based guidelines and integration of the individual treatment modalities at the bedside. These consensus statements highlight the serious situation of critical deterioration requiring emergent evaluation and guidance on sedation holds to obtain a neurological examination while balancing the potential risks of inducing a stress response.

Summary
One of the central tenets of neurocritical care is to detect the brain in trouble. The first and most fundamental neurological monitoring tool is the clinical exam. Ancillary neuromonitoring data may provide early physiologic biomarkers to help anticipate, prevent or halt secondary brain injury processes. Future research should seek to understand how data integration and visualization technologies may reduce the cognitive workload to improve timely detection of neurological deterioration.
Immediate postcardiac arrest treatment: coronary catherization or not?
Authors: Dumas Florence , Bougouin Wulfran , Cariou Alain 
Published: April 2021

Purpose of review
Early coronary angiogram (CAG) remains a cornerstone in postcardiac arrest management as coronary disease (CAD)-related cardiac arrest is the leading cause of sudden death in adults. The opportunity to treat the cause early on with immediate CAG may improve outcome in cardiac arrest patients with AMI. Identifying the patients who will benefit from such an early invasive strategy is an unanswered question. Recent and ongoing trials may improve the level of evidence on this problematic, especially for some subgroup; however, current guidelines remain founded upon a very heterogeneous level of evidence.

Recent findings
The key variable to argue for immediate CAD remains the pattern of the ECG monitored after return of spontaneous of circulation (ROSC). ST-segment elevation (STE) on postresuscitation ECG is the strongest argument to rule for an early CAG strategy. In other situations, identifying the best candidates for early CAG is very challenging. Different approaches including elements, such as circumstances of cardiac arrest and expected outcomes. may also drive the strategy.

Summary
This review aims to provide an overview of these different discussion points. The indication for early CAG should rely on multiple factors and an individual approach.
A simple way to manage a chronic ulcer at the cranioplasty titanium implant exposure site by dermal autograft and platelet-rich plasma
Authors: Lee I-Lung , Lin Yun-Nan , Huang Shu-Hung , Chung Chia-Li , Chuang Chieh-Han , Chen Rong-Fu , Kuo Yur-Ren 
Published: April 2021

Abstract

Rationale:
Titanium implant exposure is not a rare complication after cranioplasty. Usually, we apply a free flap or local flap for reconstruction.

Patient concerns:
A 56-year-old male with a medical history of gout, hepatitis and chronic renal disease presented with an ulcer and implant exposure after titanium cranioplasty. The flap around the ulcer was too thin to perform local flap reconstruction. Free flap surgery was rejected by the patient.

Diagnoses:
The ulcer with implant exposure had little exudate without malodor. The underlying wound had epithelial ingrowth and was 1.5 cm × 0.5 cm in size over the left parietal region of the head. The wound culture was staphylococcus lugdunensis-positive.

Interventions:
Oral antibiotics and biofilm decontamination were used to manage peri-implantitis for 6 weeks. Dermal autografts were harvested with a thickness of 0.020 inches. A 2 mm wide area of de-epithelization was created around the ulcer margin. Platelet-rich plasma was locally injected into the periwound skin.

Outcomes:
The patient was followed up by telephone at 9 months postoperatively, and the scar condition was stable without recurrent ulcers.

Lessons:
Dermal autografts with platelet-rich plasma may serve as an alternative method when a local flap is not feasible and the wound defect is smaller than 1 cm2.
Combined treatment with lymphaticovenular anastomosis and ethanol sclerotherapy for femoral lymphocele with lymphedema after oncologic surgery
Authors: Yoshida Shuhei , Koshima Isao , Imai Hirofumi , Sasaki Ayano , Nagamatsu Shogo , Yokota Kazunori 
Published: April 2021

AbstractIntroduction:Several treatment options like sclerotherapy and surgical excision of lymphocele are available for the management of lymphocele, although each modality has its own advantages and disadvantages. Lymphaticovenular anastomosis (LVA) has recently been gaining attention in the field of microsurgery as a minimally invasive form of surgical reconstruction. Combined treatment using surgical excision of lymphocele and LVA for large or long-lasting lymphoceles has been reported, but the combination can be very invasive. Here, we report a combined use of LVA and sclerotherapy in the treatment of a large lymphocele with satisfactory results. Hence this combination can be a complementary minimally invasive treatment of large lymphoceles.Patient concerns:The patient was a 49-year-old man with a refractory lymphocele in the lateral aspect of the left thigh after wide resection of a sarcoma 2 months earlier.Diagnosis:The patient was diagnosed as femoral lymphocele with lymphedema. Percutaneous needle aspiration was performed once weekly, and 2000 to 3000 mL fluid was aspirated each time. On indocyanine green (ICG) lymphography, the actual lymphatic routes flowing into the lymphocele could not be detected because of extensive dermal backflow in the thigh area.Interventions:We performed combined treatment using LVA and ethanol sclerotherapy to treat the lymphocele and reduce the risk of lymphedema progression.Outcomes:The lymphocele resolved and no recurrence was noted. Postoperative ICG lymphography after a follow-up period of 12 months revealed reduced dermal backflow.Conclusion:LVA is an excellent treatment option when the lymphatics flowing into the cyst are detectable or can be targeted. However, this is not always the case, especially for the lymphoceles that are large, long-lasting, or infected. For this reason, we combined LVA with sclerotherapy. This allowed for a relatively less invasive method with closure of the dead space using sclerotherapy without further exacerbating the lymphedema. Hence, combined treatment using LVA with sclerotherapy can be a complementary minimally invasive treatment option for a large or long-lasting lymphocele.
Diagnostic and therapeutic challenges of BRASH syndrome
Authors: Ata Fateen , yasir Muhammad , Javed Saad , Bilal Ammara Bint I , Muthanna Bassam , Minhas Bushra , Chaudhry Hammad Shabir 
Published: April 2021

Abstract

Rationale:
BRASH syndrome is a relatively unknown medical entity in which there is a combination of bradycardia, renal injury, hypoperfusion, and hyperkalemia. It is clinically essential to take these manifestations as a syndrome rather than isolated findings because they are interrelated and have synergistic effects. Bradycardia can result in hypoperfusion, which can cause renal injury. The resultant renal injury causes hyperkalemia (which can also be the initial trigger), which potentiates the bradycardia. Deteriorating patients with the syndrome usually do not respond to regular Advanced Cardiac Life Support resuscitation protocols. Treatment focused on the timely replacement of fluids and electrolytes gives better outcomes. It is vital to keep BRASH syndrome in diagnostic possibilities while seeing patients with refractory bradycardia, hyperkalemia, and renal injury, especially when other diagnoses are ruled out.

Patient concerns:
In this report, we present a 64-years-old gentleman who came with generalized fatigue, non-bloody diarrhea, vomiting, and low oral intake for the past 5 days.

Diagnoses:
The patient was diagnosed with BRASH syndrome.

Interventions:
The patient received intravenous fluids, 2 doses of atropine 0.5 mg and received dextrose 50 percent with insulin regular 10 units, and salbutamol 5 mg for hyperkalemia. He was intubated due to a low Glasgow Coma Scale and received dialysis for resistant hyperkalemia. A transvenous pacemaker was inserted due to bradycardia.

Outcomes:
The patient had 2 cardiac arrests and could not survive the second.

Lessons:
BRASH is a life-threatening yet largely underdiagnosed condition. Physicians should keep a high index of suspicion for BRASH while seeing patients with resistant and self-potentiating bradycardia, hyperkalemia, and renal failure, as a timely diagnosis is crucial in the management. Variable clinical presentations and limited literature create a diagnostic challenge. Further studies are warranted to understand the pathophysiology and develop better and accurate management algorithms. Patients’ risk of developing BRASH syndrome should be considered while prescribing causative medications (Atrioventricular nodal blocking drugs such as beta-blockers) in hospitals and outpatient settings.
FIP1L1- platelet-derived growth factor receptor A -positive chronic eosinophilic leukemia showing dramatic response to imatinib
Authors: Abu-Tineh Mohammad , Aljaloudi Esra’a , Amer Aliaa , Ibrahim Firyal , Ibrahim Wanis H. , Alhasson Hussam , Yassin Mohamed A. 
Published: April 2021

Abstract

Introduction:
Eosinophilia associated with FIP1L1- platelet-derived growth factor receptor A (PDGFRA) rearrangement is one of a subgroup of chronic eosinophilic leukemia, The 2008 World Health Organization classification of tumors of hematopoietic and lymphoid tissues established a new category for myeloid and lymphoid neoplasms with eosinophilia and abnormalities in PDGFRA, platelet-derived growth factor receptor Beta (PDGFRB) or Fibroblast growth factor receptor 1. The number of reported cases is limited worldwide, with limited data on the best modality of treatment of such disease.

Patient concerns:
A 48-year-old male patient with recurrent visits to the hospital presenting with multiple vague symptoms but found to have persistent marked eosinophilia.

Diagnosis:
The patient was diagnosed as a case of Myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA

Interventions:
The patient was started on Tyrosine kinase inhibitor (Imatinib) 100 mg daily.

Outcomes:
The patient eosinophilia has improved markedly, and the patient's eosinophils levels dropped to normal levels within 3 weeks period.

Conclusion:
This case indicates that in the era of Tyrosine Kinase inhibitors such as imatinib, the prognosis of Eosinophilia associated with FIP1L1-PDGFRA rearrangement has significantly improved And Prompt treatment with imatinib can lead to complete hematological response and resolution of any organ damage involved with this disease.
Certolizumab pegol-induced immunoglobulin A vasculitis in a patient with rheumatoid arthritis
Authors: Yamamoto Shintaro , Mukai Tomoyuki , Fujita Shunichi , Morita Yoshitaka 
Published: April 2021

Abstract

Rationale:
Certolizumab pegol (CZP) is a tumor necrosis factor (TNF) inhibitor with the unique characteristic of being a humanized Fab′ fragment. Immunoglobulin A (IgA) vasculitis has been reported to be associated with the use of TNF inhibitors, including infliximab, etanercept, and adalimumab.

Patient concerns:
The case was a 34-year-old Japanese woman with rheumatoid arthritis who had been treated with CZP for 3 years. She had delivered a healthy child 5 months earlier. On presentation, she had a 2-day history of abdominal pain and purpura on the lower extremities.

Diagnoses:
Histological analyses of a skin specimen revealed inflammatory cell infiltrates around the vessel walls and IgA and C3 deposits in the vessel walls of the upper dermis. Computed tomography showed terminal ileitis. The diagnosis was IgA vasculitis, presumably associated with use of CZP.

Intervention:
CZP was discontinued and prednisolone was administered.

Outcomes:
The abdominal pain and purpura promptly improved in response to treatment. No relapse of vasculitis occurred after discontinuation of CZP.

Lessons:
In this case, the cumulative immunomodulatory effects of the TNF inhibitor and the patient postpartum status were considered to be involved in inducing IgA vasculitis. Clinicians should be aware of IgA vasculitis-related symptoms as a possible adverse effect of TNF inhibitors to ensure prompt diagnosis and appropriate treatment.