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Статті в журналах з теми "Nerve trauma and disease"
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Khalilzadeh, Omid, Laura M. Fayad, and Shivani Ahlawat. "3D MR Neurography." Seminars in Musculoskeletal Radiology 25, no. 03 (June 2021): 409–17. http://dx.doi.org/10.1055/s-0041-1730909.
Повний текст джерелаАнотація:
AbstractHigh-resolution isotropic volumetric three-dimensional (3D) magnetic resonance neurography (MRN) techniques enable multiplanar depiction of peripheral nerves. In addition, 3D MRN provides anatomical and functional tissue characterization of different disease conditions affecting the peripheral nerves. In this review article, we summarize clinically relevant technical considerations of 3D MRN image acquisition and review clinical applications of 3D MRN to assess peripheral nerve diseases, such as entrapments, trauma, inflammatory or infectious neuropathies, and neoplasms.
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Koenig, Ralph W., Maria T. Pedro, Christian P. G. Heinen, Thomas Schmidt, Hans-Peter Richter, Gregor Antoniadis, and Thomas Kretschmer. "High-resolution ultrasonography in evaluating peripheral nerve entrapment and trauma." Neurosurgical Focus 26, no. 2 (February 2009): E13. http://dx.doi.org/10.3171/foc.2009.26.2.e13.
Повний текст джерелаАнотація:
High-resolution ultrasonography is a noninvasive, readily applicable imaging modality, capable of depicting real-time static and dynamic morphological information concerning the peripheral nerves and their surrounding tissues. Continuous progress in ultrasonographic technology results in highly improved spatial and contrast resolution. Therefore, nerve imaging is possible to a fascicular level, and most peripheral nerves can now be depicted along their entire anatomical course. An increasing number of publications have evaluated the role of high-resolution ultrasonography in peripheral nerve diseases, especially in peripheral nerve entrapment. Ultrasonography has been shown to be a precious complementary tool for assessing peripheral nerve lesions with respect to their exact location, course, continuity, and extent in traumatic nerve lesions, and for assessing nerve entrapment and tumors. In this article, the authors discuss the basic technical considerations for using ultrasoniography in peripheral nerve assessment, and some of the clinical applications are illustrated.
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Rukmana Tri Pratistha, Indra, Nyoman Gede Bimantara, I. Gede Mahardika Putra, Made Bramantya Karna, Anak Agung Gde Yuda Asmara, and Putu Feryawan Meregawa. "Nerves Transfer Procedure in Patients with Left Upper Extremities Weakness Following Gunshot Wounds: A Case Report." Open Access Macedonian Journal of Medical Sciences 9, no. C (September 5, 2021): 140–45. http://dx.doi.org/10.3889/oamjms.2021.6393.
Повний текст джерелаАнотація:
BACKGROUND: Gunshot wounds (GSWs) to the extremities can result in damage to the neurovascular structure which results in high morbidity and loss of function. According to the Centers for Disease Control report, the incidence of non-fatal GSWs has increased in the past decade. Trauma to the brachial plexus is a type of peripheral nerve trauma that is most difficult to treat due to its complex surgical procedures. Early exploration and reconstruction of peripheral nerve trauma are still being debated to this day. However, most recommend surgical exploration when the suspicion of neurovascular trauma is very high based on clinical findings. Nerve transfer is one of the recommended methods of nerve reconstruction even in pre-ganglionic lesions. We report a case of a patient with weakness of the upper limb after a gunshot wound to his left shoulder. Based on clinical considerations and investigations, nerve transfer procedure is carried out to restore patient’s shoulder function. CASE REPORT: Male, 32 years old, working as a policeman, complained difficulty on moving his shoulder for 3 months. Patients had a history of GSWs to the left shoulder which also results in a left clavicular fracture. First aid, debridement, and fracture management were performed at Bhayangkara Hospital, Palu. Physical examination revealed winging scapula positive on his left shoulder, shoulder abduction 5/1, and hypoesthesia at left C5 level. Electromyographic examination revealed lesions on the left posterior chord and left brachial plexus. Based on clinical findings and supporting examination, we performed nerve transfers procedure from the accessory nerve to suprascapular notch. In the previous study, 63% of cases GSWs associated with nerve dysfunction. About 75% of patients with nerve palsy are associated with nerve lacerations during surgical exploration. However, many surgeons continue to recommend early exploration after GSWs to the upper extremities, especially in patients who will undergo surgical treatment for other indications. Based on this, we suggest the probable cause of brachial plexus lesions in this case resulted from gunshot wound which injures the brachial plexus or as a complication from previous procedures. Surgery that is too early can interfere with the spontaneous reinnervation process, but late surgical procedures can result in failure of reinnervation. In general, optimal time is set between 3 and 6 months after trauma. Nerve transfer is one method of reconstructing peripheral nerve lesions that can be applied to pre-ganglionic or post-ganglionic lesions. CONCLUSION: This procedure has several benefits, namely, the proximity of the donor and the recipient nerve anatomy, shorter operating time and does not require grafts. Brachial plexus trauma due to trauma or non-trauma together has an impact on the patient’s quality of life. However, advances in surgical techniques and further understanding of nerve physiology have led clinicians and patients to better outcomes. The current trend of treatment strategies for brachial plexus trauma is surgical reconstruction with the nerve transfer procedure.
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Zheng, Tong, Shuoke Qiu, Lei Li, Binglong Li, and Meng Zhang. "Polymers containing natural plant phenolic compounds for peripheral nerve injury." Biomaterials and Biosensors 1, no. 1 (December 30, 2022): 48–61. http://dx.doi.org/10.58567/bab01010004.
Повний текст джерелаАнотація:
Peripheral nerve injury is a serious and disabling disease prevalent in the world. It caused by trauma is often accompanied with soft tissue injuries, fractures, infections, etc., and can cause permanent damage. The treatment methods of peripheral nerve injury mainly include traditional microsurgical repair, neurotrophic drug treatment, as well as cuttingedge nerve conduit treatment, nerve stimulation, cell therapy, etc. However, more than 30% of patients with peripheral nerve injury still have poor recovery, including partial loss or complete loss of motor and/or sensory function, muscle atrophy，chronic pain and severe disability, among can lead to permanent disease. Phenolic compounds are secondary metabolites which is the most abundant in plants, consisting of an aromatic ring and one or more hydroxyl substituents, the main groups including flavonoids, phenolic acids, tannins, stilbene and lignans. A lot of studies have shown that natural phenolic compounds have various properties, such as antioxidant, anti-infective, anticancer, anti-inflammatory, etc., and have broad applications in the prevention of heart disease, cancer, diabetes, oxidative stress-related diseases, and neuroprotection prospect. This review discusses the potential applications and molecular mechanisms of natural phenolic compounds its polymer derivatives in the treatment of peripheral nerve injury.
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Motswaledi, M. H. "Herpes zoster (Shingles)." South African Family Practice 60, no. 4 (August 28, 2018): 28–30. http://dx.doi.org/10.4102/safp.v60i4.4898.
Повний текст джерелаАнотація:
Herpes zoster or Shingles is caused by varicella-zoster virus (VZV), the same virus that causes chicken-pox (varicella).Primary infection with varicella-zoster virus causes chicken-pox (varicella), then the virus persists in nerve ganglia of sensory but rarely motor nerves, in a latent stage.If the virus gets reactivated it causes herpes zoster, which presents as painful vesicles following a dermatome. It is more common in the elderly and the immunocompromised.Herpes zoster is a common skin and mucous membrane disease caused by reactivation of latent varicella zoster virus, which had lodged previously in nerve ganglia.Trigeminal nerve nuclei and thoracic spinal ganglia are the most commonly affected.Reactivation of latent varicella-zoster virus can be triggered by old age, that is why herpes zoster is common in the elderly, above 60 years of age. This is due to age related decline in specific cell mediated immune response to VZV. Other triggering factors are malignancies malnutrition, emotional stress, physical trauma, chronic diseases like diabetes mellitus and immunosuppression from drugs and HIV.¹,²
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Hasan, Syed Asif, Abdulrahman Saad Aljammaz, Mosleh Motesh AlGhamdi, Mohamed Jasim ALQattan, Abdulrahman Hussain Alsalman, Wafaa Sulaiman Alhifzi, Hassan Ahmed Aljudia, et al. "The different causes of branchial plexus injuries." International Journal Of Community Medicine And Public Health 8, no. 8 (July 27, 2021): 4119. http://dx.doi.org/10.18203/2394-6040.ijcmph20213052.
Повний текст джерелаАнотація:
Many etiologies have been reported to account for injuries to the brachial plexus, peripheral nerves and trauma. Additionally, many diseases have also been reported to cause the injury with many different pathophysiologies. For instance, some diseases have been classified as the primary diseases of the peripheral nerves including hereditary neuropathy. In the same context, brachial plexus damage or injury might also result secondary to a systemic disease, leading to a significant peripheral nerve injury as in cases with most metabolic neuropathies, which may result secondary to renal insufficiency, diabetes, amyloidosis and many other diseases. Furthermore, toxic and iatrogenic causes were also reported as potential causes for brachial plexus injuries. However, traumatic events are the most commonly reported, owing to motorcycle accidents, being the most common etiology. Although evidence is now abundant regarding the etiology, further studies are needed to furtherly validate the evidence and for more specification of the etiology and the underlying mechanisms.
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Soman, Soja, and Sanjairaj Vijayavenkataraman. "Perspectives on 3D Bioprinting of Peripheral Nerve Conduits." International Journal of Molecular Sciences 21, no. 16 (August 12, 2020): 5792. http://dx.doi.org/10.3390/ijms21165792.
Повний текст джерелаАнотація:
The peripheral nervous system controls the functions of sensation, movement and motor coordination of the body. Peripheral nerves can get damaged easily by trauma or neurodegenerative diseases. The injury can cause a devastating effect on the affected individual and his aides. Treatment modalities include anti-inflammatory medications, physiotherapy, surgery, nerve grafting and rehabilitation. 3D bioprinted peripheral nerve conduits serve as nerve grafts to fill the gaps of severed nerve bodies. The application of induced pluripotent stem cells, its derivatives and bioprinting are important techniques that come in handy while making living peripheral nerve conduits. The design of nerve conduits and bioprinting require comprehensive information on neural architecture, type of injury, neural supporting cells, scaffold materials to use, neural growth factors to add and to streamline the mechanical properties of the conduit. This paper gives a perspective on the factors to consider while bioprinting the peripheral nerve conduits.
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Placheta-Györi, Eva, Lea Maria Brandstetter, Jakob Zemann-Schälss, Sonja Wolf, and Christine Radtke. "Myelination, axonal loss and Schwann cell characteristics in axonal polyneuropathy compared to controls." PLOS ONE 16, no. 11 (November 4, 2021): e0259654. http://dx.doi.org/10.1371/journal.pone.0259654.
Повний текст джерелаАнотація:
Introduction Polyneuropathy is a debilitating condition characterized by distal sensory and motor deficits. Schwann cell dysfunction and axonal loss are integral factors in pathophysiology and disease progression of polyneuropathy. Aims The aim of this study was the assessment of Schwann cell characteristics, nerve fibers and myelination parameters in polyneuropathy patients compared to controls. Methods Nerve tissue was obtained from polyneuropathy patients (n = 10) undergoing diagnostic sural nerve biopsies. Biopsies of healthy peripheral nerves (n = 5) were harvested during elective sural nerve grafting for chronic peripheral nerve lesions. Exclusion criteria for the healthy control group were recent neurological trauma, diabetes, neurological and cardiovascular disease, as well as active malignancies and cytotoxic medication within the last 12 months. The over-all architecture of nerve sections and myelination parameters were histomorphometrically analyzed. Immunofluorescent imaging was used to evaluate Schwann cell phenotypes, senescence markers and myelination parameters. Results Histomorphometric analysis of nerve biopsies showed significant axonal loss in polyneuropathy patients compared to controls, which was in accordance with the neuropathological findings. Immunofluorescent staining of Schwann cells and myelin basic protein indicated a significant impairment of myelination and lower Schwann cell counts compared to controls. Phenotypic alterations and increased numbers of non-myelinating p75-positive Schwann cells were found in polyneuropathy patients. Discussion This study provided quantitative data of axonal loss, reduced myelination and Schwann cell dysfunction of polyneuropathy patients compared to neurologically healthy controls. Phenotypic alterations of Schwann cells were similar to those seen after peripheral nerve injury, highlighting the clinical relevance of Schwann cell dysfunction.
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Guyennet, Eloïse, Jean-Laurent Guyomard, Emilie Barnay, Franck Jegoux, and Jean-François Charlin. "Cephalic Tetanus from Penetrating Orbital Wound." Case Reports in Medicine 2009 (2009): 1–3. http://dx.doi.org/10.1155/2009/548343.
Повний текст джерелаАнотація:
Tetanus is a neurologic disorder caused by tetanospasmin, a protein toxin elaborated by Clostridium tetani. Cephalic tetanus is a localized form of the disease causing trismus and dysfunction of cranial nerves. We report the case of a man who presented with facial trauma, complete ophthalmoplegia, exophthalmos, areactive mydriasis, and periorbital hematoma. An orbital CT revealed air bubbles in the right orbital apex. The patient was given a tetanus toxoid booster and antibiotherapy. After extraction of a wooden foreign body, the patient developed right facial nerve palsy, disorders of swallowing, contralateral III cranial nerve palsy, and trismus. Only one case of cephalic tetanus from penetrating orbital wound has been reported in literature 20 years ago. When a patient presents with an orbital wound with ophthalmoplegia and signs of anaerobic infection, cephalic tetanus should be ruled out.
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Sparapani, Fabio Veiga de Castro, Marcela Fernandes, Leonardo Favi Bocca, Luis Renato Nakachima, and Sergio Cavalheiro. "Acute handlebar syndrome: Two extremes of a challenging diagnosis." Surgical Neurology International 11 (October 29, 2020): 366. http://dx.doi.org/10.25259/sni_606_2020.
Повний текст джерелаАнотація:
Background: Ulnar nerve mononeuropathy diagnosis can be challenging depending on where neural lesion is present. Repetitive trauma during cycling is a rare cause of ulnar neuropathy. Case Description: We describe two patients who developed the handlebar syndrome, an ulnar nerve palsy at Guyon’s canal after cycling. The first patient had the syndrome after a short-distance ride and she was treated surgically, while the second patient developed the classical syndrome after a long ride and received conservative treatment. Surgical treatment of the first patient led to functional recovery. Conclusion: Handlebar syndrome is a neuropathy caused by extrinsic repetitive compression of ulnar nerve at wrist. Increasing incidence of this disease can be expected after increasing popularity of cycling sports. Avoid of repetitive trauma is the main management goal, with surgical treatment reserved for failure of conservative treatment.
Дисертації з теми "Nerve trauma and disease"
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Payette, Daniel. "Neuronal dysfunction and degeneration in Alzheimer's disease and brain trauma." Oklahoma City : [s.n.], 2008.
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Sahar, Muhammad Sana Ullah. "Development of a nerve stretching device to facilitate peripheral nerve repair." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/396190.
Повний текст джерелаАнотація:
Advancements in biomedical engineering have improved medical technology by redefining surgical standards and developing medical devices to carry out complex repairs at a tissue level; however, effective surgical management for segmental defects (nerve gaps) in peripheral nerves clinically, remains a challenging endeavour. Traditional nerve gap management surgical techniques cannot bridge longer defects effectively, while contemporary techniques using a variety of nerve conduits to facilitate nerve regeneration have consistently failed to reproduce reliable results. One of the root causes of these inconsistent results lies in the nerve’s inability to regrow expediently after injury and hence the ‘slow rate of nerve regeneration’ is one of the main factors in unsuccessful nerve gap management.
This situation demands a satisfactory approach to address the aforementioned problem. In the past, researchers have attempted to increase the growth rate of axons by stretching them mechanically outside the body and have proved that axons can respond to mechanical stimulus where their growth rate depends on the type and degree of mechanical strain. These promising findings, however, are difficult to translate to in-vivo applications, because stretching a nerve in-vivo is not analogous to pulling it ex-vivo, and need appropriate resources to provide such translation, which limits the effectiveness of this technique clinically.
This thesis aimed to address the slow rate of peripheral nerve regeneration post-trauma and presents a solution to expedite nerve growth rate. During this research work, a novel method of stretching a whole nerve in a conduit using a controlled negative pressure (vacuum) was developed. The rationale behind proposing negative pressure as a stretching agent was that, it would promote angiogenesis by drawing more blood, from the microvessels coursing in the epineurium, to nourish growing sprouts of axons.
Appropriate bioengineering tools were fabricated to carry out the in-vivo nerve stretch which included building a vacuum generating device (nerve stretcher) and fabricating a synthetic T-shaped conduit to hold and stretch the transected nerve stumps using the generated vacuum.
Firstly, safe limits of applying vacuum to nerve stumps were ascertained during a pilot study on cadaveric rats (Chapter 3), where, a surgical procedure was also developed to implant T-shaped conduits, and ability of the nerve stretcher in generating a stable vacuum was tested at various vacuum levels. Secondly, the developed technique for in-vivo nerve stretching was then preliminarily tested on live rats (Chapter 4) and based on the experimental observations, the strategy for implanting the nerve conduit for a longer post-surgical period was revised. Finally, the modified approach was tested on 30 rats to study the in-vivo mechanotransduction effect of the injured peripheral nerves in response to vacuum. These in-vivo experiments involved transecting sciatic nerves of rats, placing the respective nerve ends into T-shaped conduits and then applying vacuum. Nerve stumps were tractioned at various negative pressure levels for seven days. After seven days, nerves were excised, and each nerve stump was sectioned and stained using histological and immuno-histochemical staining methods, slides were analysed qualitatively and quantitatively to measure the extent of nerve growth in response to negative pressure.
The results of in-vivo nerve stretch-growth showed that the three treatment groups displayed better outcomes in terms of absolute growth of nerve stumps, higher rates of angiogenesis, and a greater quantity of nissl substance in cytoplasm over the control group. First, absolute growth of the nerve stumps in all three treatment groups provided direct quantitative evidence of enhanced growth in sciatic nerves in response to mechanical stress acting in the form of negative pressure. Second, a higher quantity of blood vessels in the treatment group confirmed the efficacy of negative pressure in promoting angiogenesis. Third, the presence of nissl substance in greater amounts in the treatment groups signalled that the effect of nerve injury has started to resolve (on injury to a nerve, neurons deploy macrophages to clear up the cell debris to make room for Schwann cells that perform myelination of axons). During result analysis, each treatment group was compared against each other and the control group, and it was found that a negative pressure of 20 mmHg displayed the most superior outcomes, favouring both nerve lengthening and angiogenesis. The results of this research work successfully justified the hypothesis of this thesis (Chapter 2), that an in-vivo application of negative pressure acting directly to transected rat sciatic nerves will enhance nerve regrowth by promoting angiogenesis and nerve lengthening.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Eng & Built Env
Science, Environment, Engineering and Technology
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Bruno, Martin. "Nerve Growth Factor, Aging and Alzheimer's disease." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18741.
Повний текст джерелаАнотація:
Since the cholinergic hypothesis of geriatric memory dysfunction was proposed by Bartus and colleagues in 1982, studies conducted in animals and humans so far have failed to obtain evidence for the involvement of NGF in normal Aging and/or in the pathophysiology of Alzheimer's disease (AD). It has been hypothesized that age-related degeneration of basal forebrain cholinergic neurons (BFCN) may be caused by the altered endogenous NGF maturation either by reduced responsiveness to NGF, by reduced NGF transport or by the failure in coupling to second messengers. NGF administered in the CNS of AD patients led to undesirable side effects, most likely mediated by p75 neurotropin receptor (p75NTR) rather than through its specific TrkA receptor. Thus, we decided to treat behaviorally characterize age-impaired (AI) rats with small proteolytic- resistant peptide mimetic of the TrkA receptor, named D3. This selective partial agonist of the TrkA receptor reversed the atrophy of the BFCN, ameliorating the cognitive decline observed in AI rats. The realization that the precursor of NGF (proNGF) might play a biological role in the CNS, raised questions regarding the regulatory mechanisms leading to its release, as well as the control of the proNGF to NGF ratio and, ultimately, the degradation of the NGF molecule. To answer these questions, we performed in vitro and in vivo studies aimed at elucidating the preferential NGF form released from the cerebral cortex, and the biochemical pathway leading to NGF maturation and degradation. These studies have revealed that proNGF is the main releasable form of the neurotrophin and that the maturation and degradation of NGF largely occurs in the extracellular space with the involvement of a complex protease cascade. The newly described mechanism for NGF conversion and degradation was found compromised in Alzheimer's disease. In brief, we found a failure in the conversion of proNGF to NGF, which was exacerbated by an increased NGF degradDepuis que l'hypothèse cholinergique sur la dysfonction de la mémoire chez la personne âgée a été proposée par Bartus et collègues en 1982, toutes les études cherchant à mettre en évidence l'implication du NGF chez les sujets normaux âgés et ceux atteints de la Maladie D'Alzheimer (MDA) ont échoué à la fois chez l'homme et chez l'animal. L'hypothèse émise fût que la dégénérescence des Neurones Cholinergiques du Cerveau Antérieur Basal (NCCAB) liée à l'âge pourrait être due soit à une maturation altérée du NGF endogène soit à une réponse réduite au NGF, par un transport déficient, ou bien encore à un défaut de couplage aux seconds messagers. Le NGF administré dans le SNC de patients atteints de MDA conduit à des effets secondaires indésirables principalement causés par p75 ou le récepteur neurotropique (p75NTR) plutôt qu'à travers son récepteur spécifique, TrkA. Par conséquent, nous avons décidé de traiter des rats caractérisés comme âgé-déficients (AD) avec de petits peptides résistant à la protéolyse appelés D3 et mimant l'action du NGF sur les récepteurs TrkA. Cet agoniste partiel du récepteur TrkA remédie à l'atrophie des neurones cholinergiques du CAB, réduisant le déclin cognitif observé chez les rats AD. Le fait que le précurseur du NGF (proNGF) pourrait jouer un rôle biologique, soulève des questions quant aux mécanismes régulant sa libération, ainsi que ceux contrôlant le ratio proNGF/NGF et enfin ceux contrôlant la dégradation finale du NGF. Pour répondre à ces questions, nous avons réalisé des expériences in vitro et in vivo afin de savoir sous quelle forme préférentielle le NGF était libéré dans le cortex cérébral, et afin de connaitre les chemins biochimiques menant à la maturation et la dégradation du NGF. Ces études ont révélé que le proNGF représentait la forme principale de libération de cette neurotrophine et que la maturation et la dégradation du NGF$
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Sander, Anthony. "Penetrating Abdominal Trauma: Spectrum of disease in a Level 1 Trauma Centre." Master's thesis, Faculty of Health Sciences, 2019. http://hdl.handle.net/11427/31208.
Повний текст джерелаАнотація:
Background: Penetrating abdominal trauma (PAT) in South Africa represents a significant burden of disease. The current global trend has seen management shift towards selective conservatism. The purpose of this study is to describe the presentation, management and outcomes of PAT in a level I trauma unit, which routinely practices selective non-operative management (SNOM). Methods: This was a retrospective descriptive audit of prospectively collected data. The Setting was Groote Schuur Hospital Trauma Centre, Cape Town, South Africa over 24 months (1 May 2015 to 30 April 2017). All patients presenting to the centre with PAT during the study period were included. The data captured and analysed included: basic demographics; admission vital signs; blood investigations; number of traumatic insults; penetrating wound positions; radiological investigations and interventions; indication for laparotomy; operative or nonoperative management; laparotomy findings: negative, therapeutic or non-therapeutic; abdominal visceral injuries and associated injuries. The Revised Trauma Score (RTS); Injury Severity Score (ISS); Penetrating Abdominal Trauma Index (PATI); and Kampala Trauma Score (KTS) were then calculated. The descriptive end points included the following: Length of hospital stay (LOS); ICU admission time; relaparotomy; readmission; mortality; and in-hospital complications. Results: During the study period, 805 patients with penetrating abdominal trauma were managed. There were 502 (62.4%) and 303 (37.6%) patients with gunshot and stab wounds, respectively. The majority were young men (762 – 94.7%) with a mean age of 28.3 (95%CI: 27.7-28.9) years. The median trauma scores were as follows: RTS – 7.84 (IQR: 7.00-7.84); ISS: 13 (IQR: 9-22), PATI: 6 (IQR: 1-14); and KTS: 14 (IQR: 14-15). Abdominal penetration was thoracoabdominal in 332 (41.2%), abdominal in 694 (86.5%), and pelvic in 192 (23.9%) patients. Immediate laparotomy was performed in 446 (55.4%) patients for: haemodynamic instability – 42 (5.2%); peritonism – 296 (36.8%); evisceration - 27 (3.4%); unreliable clinical evaluation – 24 (3.0%); and positive radiological findings – 57 (7.1%). There were 406 (50.4%) therapeutic laparotomies; 18 (2.3%) negative laparotomies; and 22 (2.7%) nontherapeutic laparotomies in the immediately operated group. Initial SNOM was performed in 359 (44.5%) patients, of which 208 (68.7%) sustained stab wounds and 151 (30.1%) gunshot wounds. Thirty-five (4.3%) patients failed SNOM and underwent delayed laparotomy. Should a policy of mandatory laparotomy have been implemented in this series, 206 (68.0%) SW and 163 (32.5%) GSW patients would have underwent unnecessary exploration. Overall non-fatal complications were 179 (22.2%) which were then further classified according to the Clavien-Dindo grading system. The median hospital stay was 4.5 (IQR: 3-7) and 7 (IQR: 5-12) days for SW and GSW, respectively. Overall 114 (14.2%) patients required admission to critical care unit for a median stay of 3 (IQR: 2-5) days. Total mortality was 7.2% (n=58). Conclusion: Clinical evaluation (haemodynamic instability, peritonism and evisceration) was remarkably accurate in determining the need for early laparotomy. The unnecessary laparotomy rate of this group was 5.0% (negative: 2.3% and nontherapeutic: 2.7%) overall. Selective nonoperative management was performed in 44.5% of patients with a successful SNOM rate of 90.3%. The overall mortality was 7.2 %.
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Yang, In Hong. "The study of the neurophysiology of high strain rate nerve injury." Texas A&M University, 2003. http://hdl.handle.net/1969.1/416.
Повний текст джерелаАнотація:
The study of the mechanism of traumatic brain injury (TBI) processes at the cellular level is vital to obtain characterization of nerve cell damage after mechanical deformation. This understanding is needed to find feasible therapeutic targets for mechanically damaged neurons. To study the cellular level of TBI damage, development of a new in vitro cellular model of TBI might be done to simulate in vivo cellular TBI.
In this research, two studies were performed: (1) the design and construction of an in vitro cell stretching device to mechanically injure cells and (2) the characterization of the molecular and cellular level of the TBI mechanism. The cell stretching device design allows for the precise control of cell strain and duration of stretching cells such that TBI can be mimicked. Analysis of the cellular and molecular level mechanisms of TBI in the proposed in vitro model might help in the design of therapeutic strategies for the treatment of TBI. Our proposed mechanism of injury due to TBI is as follows: after the cell is stretched, a cellular signaling molecule is released to activate the cellular signaling pathway. The activated cell signal may activate kinases which phosphorylate proteins and initiate new protein synthesis. Newly phosphorylated and synthesized proteins may activate the apoptotic process.
Using a variety of pharmacological agents, one could block steps in the hypothesized mechanism and examine the effect of those agents on downstream cellular processes and cell apoptosis. For example, the inhibitions of calcium transport, protein synthesis, and caspases were performed to examine the initial activation of the signaling pathway and the role of both in the apoptosis process. Proteomics of TBI may help the understanding of the mechanism of TBI related protein expression. This work will contribute to the discovery of new therapeutic targets and better treatments for TBI.
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Ogilvie, Alan L. "Vagal function in oesophageal disease." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262775.
Повний текст джерела
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Fidler, Larry E. "Gas bubble trauma in fish." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/28659.
Повний текст джерелаАнотація:
Fish exposed to gas supersaturated water often experience a form of stress known as Gas Bubble Trauma (GBT). GBT is an acute condition involving various forms of bubble growth both internal and external to the animal. Theoretical models are developed which establish thresholds for bubble growth. These models apply to:
1. ) Bubble growth in the vascular systems of fish.
2. ) Bubble growth in the environmental water that can occur in the buccal cavity and between gill lamella.
4.) Overinflation of the swimbladder.
3. ) Sub-dermal bubbles that occur on external skin surfaces such as the opercular flaps, between fin rays and in the lining of the mouth.
In order to develop the models for general use, it was necessary to establish the effective size of nucleation sites and other physiological parameters contained in the bubble growth threshold equations. This was accomplished through a review of data from the scientific literature and a two phase experimental program.
The literature review resulted in the compilation of a database containing over 1000 records of supersaturation data on salmonids. Various filters based on length, species, total gas pressure (TGP), partial pressure of oxygen (PO₂) and other criteria were applied to the database. The filtering operations established the existence of GBT mortality thresholds and identified relationships between other experimental parameters. The results of this analysis suggest that a lower threshold occurs at a water TGP of 1.10 Atms. and a higher threshold occurs at 1.15 to 1.18 Atms. However, it was not established that the apparent mortality thresholds correspond to thresholds for bubble growth predicted by the theoretical models.
To make this correlation, a preliminary experimental study examined the physiological response of fish exposed to supersaturated water. It was found that arterial PO₂, hematocrit and blood pressure yield unique responses to bubble growth over specific ranges of water TGP. The results of these experiments also indicate that the lower mortality threshold of the database analyses is associated with a combination of sub-dermal bubble growth in the mouth and extracorporeal bubbles growing between gill lamella.
The second phase of experimental study included surveys of blood PO₂, hematocrit and pH along with microscopic studies of intravascular and extracorporeal bubble growth in gills. The results of these experiments confirm the source of mortality for the lower threshold at a water TGP of 1.1 Atms. In addition, the data demonstrate that the upper TGP threshold of 1.15 to 1.18 Atms. of the database analysis corresponds to the threshold for intravascular bubble growth. The results further confirm that, as predicted by the theoretical model, intravascular bubble growth thresholds are dependent on water PO₂ .
Combining the results of the database analysis and the experimental studies permitted the effective size of nucleation sites responsible for bubble growth to be back calculated from the theoretical equations. This completed the development of the bubble growth threshold equations. The equations can now be used to predict thresholds for the various forms of bubble growth and mortality that occur in fish exposed to supersaturated water. The experimental results also provide valuable information regarding the physiological response of fish to gas supersaturated water.Science, Faculty of
Zoology, Department of
Graduate
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De’Ath, Henry D. I. "Trauma associated cardiac injury & dysfunction." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8466.
Повний текст джерелаАнотація:
The existence of a trauma induced secondary cardiac injury (TISCI) remains in doubt. The risk factors and pathological processes that lead to its development are not known, whilst the effects of TISCI on injured patient outcome are uncertain. Concurrently, the incidence of coronary heart disease (CHD) in a trauma population and its influence on mortality are inconclusive. The aim of this research project was to address these specific areas of uncertainty. Critically injured patients (n=135) were retrospectively investigated for the incidence and nature of adverse cardiac events (ACEs), and levels of the cardiac specific biomarkers Troponin I, B-type Natriuretic Peptide and Heart-type Fatty Acid Binding Protein were measured. Biomarkers and cardiac events were evaluated against outcome. Thereafter, the relationship of pro-inflammatory cytokines with TISCI was explored. A prospective cohort study of 199 trauma patients followed, to confirm the existence of TISCI and describe its clinical features, risk factors and outcomes. Finally, coronary artery calcium, as a marker of CHD, was evaluated on 432 CT scans of the chest of trauma patients aged 45 years or over, and its association with survival after injury was established. ACEs and early biomarker rises occurred in trauma patients and both were unrelated to the severity of chest injury. Each was associated with higher mortality, and confirmed the existence of TISCI. Risk factors for the development of the condition included increasing age, worsening tissue injury and shock. A relationship with cytokines was demonstrated, and implicated acute inflammation in the pathogenesis of TISCI. Calcification on CT scans revealed the incidence of CHD in an injured cohort approached 70%, although its presence did not impact survival. There exists a trauma induced secondary cardiac injury which was related to poorer outcome. The condition was associated with inflammation. CHD was widespread in older trauma patients but was not associated with increased in-hospital mortality.
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Friberg, Danielle. "Nerve lesions in pharynx - an aetiology of obstructive sleep apnoea /." Stockholm, 1997. http://diss.kib.ki.se/1997/91-628-2721-9.
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Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.
Повний текст джерелаКниги з теми "Nerve trauma and disease"
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Venu, Akuthota, and Herring Stanley A. 1954-, eds. Nerve and vascular injuries in sports medicine. New York: Springer, 2009.
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D, Lewis Benjamin, and Davies Charlie James, eds. Optic nerve disease research perspectives. New York: Nova Science, 2008.
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Justin, Mowchun, and Grudem Jon, eds. Peripheral nerve and muscle disease. New York: Oxford University Press, 2009.
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Convery, Ian, Maggie Mort, Josephine Baxter, and Cathy Bailey. Animal Disease and Human Trauma. London: Palgrave Macmillan UK, 2008. http://dx.doi.org/10.1057/9780230227613.
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Kline, David G. Nerve injuries: Operative results for major nerve injuries, entrapments, and tumors. Philadelphia: W.B. Saunders, 1995.
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Franz, Hefti, Fondation IPSEN pour la recherche thérapeutique., and Colloque médecine et recherche (6th : 1990 : Strasbourg, France), eds. Growth factors and Alzheimer's disease. Berlin: Springer-Verlag, 1991.
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1950-, Gage F., Privat A. 1943-, Christen Yves, and Colloque médecine et recherche (3rd : 1988 : Montpellier, France), eds. Neuronal grafting and Alzheimer's disease. Berlin: Springer-Verlag, 1989.
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Pandav, Surinder, Parul Ichhpujani, and Michael A. Coote, eds. The Optic Nerve Head in Health and Disease. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6838-5.
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Slavin, Konstantin V. Peripheral nerve stimulation. Basel: Karger, 2011.
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Vrbová, Gerta, Olga Hudlicka, and Kristin Schaefer Centofanti. Application of Muscle/Nerve Stimulation in Health and Disease. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-8233-7.
Повний текст джерелаЧастини книг з теми "Nerve trauma and disease"
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Rana, Abdul Qayyum, Ali T. Ghouse, and Raghav Govindarajan. "Nerve Trauma." In Neurophysiology in Clinical Practice, 75–77. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39342-1_9.
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Penkert, Götz. "Focal Nerve Trauma." In Focal Peripheral Neuropathies, 365–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-54780-5_11.
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Hanna, Amgad S. "Case IX: Trauma 3." In Nerve Cases, 97–100. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39694-1_19.
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Hanna, Amgad S. "Case VIII: Trauma 1." In Nerve Cases, 37–42. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39694-1_8.
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Hanna, Amgad S. "Case IX: Trauma 2." In Nerve Cases, 43–46. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39694-1_9.
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Marshall, Benjamin, and Rachel Brakke Holman. "Nerve." In Sports-related Fractures, Dislocations and Trauma, 675–81. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-36790-9_38.
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Fujinaga, Yasunari, Tomoharu Watanabe, Satoshi Kawakami, Masumi Kadoya, Hideaki Hamano, and Shigeyuki Kawa. "Nerve Lesions." In IgG4-Related Disease, 119–22. Tokyo: Springer Japan, 2013. http://dx.doi.org/10.1007/978-4-431-54228-5_18.
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Deiler, Stephan, and Helen Vester. "Nerve Injury in Adults." In Acute Elbow Trauma, 127–34. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-97850-5_11.
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Perkin, G. D. "Peripheral nerve disease." In Diagnostic Tests in Neurology, 180–201. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-3320-1_8.
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Penkert, Götz, and Hisham Fansa. "Trauma-Related Limb Nerve Lesions." In Peripheral Nerve Lesions, 69–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-09232-3_6.
Повний текст джерелаТези доповідей конференцій з теми "Nerve trauma and disease"
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Rapkin, Jeffrey S., and Julian J. Nussbaum. "Spectral Laminography of Subretinal Neovascular Membranes." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/navs.1988.wc3.
Повний текст джерелаАнотація:
Subretinal neovascularization occurs in association with age-related maculopathy, histoplasmosis, angioid streaks, trauma and myopia.1 Other less common associations include optic nerve head drusen, choroidal tumors, pigment epithelial hamartomas, photocoagulation, rubella retinopathy and various inflammatory disorders such as multifocal posterior pigment epitheliopathy and Harada's disease.1 The clinical appearance of subretinal neovascularization is a dirty gray or green discoloration at the level of the retinal pigment epithelium.1,2 New vessel growth may be accompanied by a serous, exudative or hemorrhagic detachment of the retinal pigment epithelium or neurosensory retina. Early treatment of neovascular membrane by laser photocoagulation has been shown to be of benefit in limiting vision loss for some patients.3,4 Prompt recognition and localization of the neovascular process is essential for successful treatment. Fluorescein angiography is the standard method used to confirm the presence and anatomical location of subretinal neovascular membranes.1,2,5,6
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Gaudencio, Julia Loureiro, Hilton Mariano Mariano da Silva Júnior, and Pedro Neves Fortunato. "Ramsay Hunt Syndrome complicated by Cerebral venous thrombosis (case report)." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.222.
Повний текст джерелаАнотація:
Context: Ramsay Hunt syndrome is a condition caused by the Varicella-Zoster Virus in the geniculate ganglion and leads to peripheral facial nerve palsy and erythematous vesicular rash in the affected area. It is a rare disorder but is the second most common cause of peripheral facial nerve palsy without trauma. Cerebral venous thrombosis is a rare cerebrovascular disease and responsible for only 0.5% of all strokes. Among its causes are oral contraceptives, infection in the central nervous system, systemic inflammations, and thrombophilia. Case report: We report the case of a previously healthy 29 years old woman diagnosed with Ramsay Hunt syndrome followed by cerebral venous thrombosis two weeks later. Her first admission to the hospital was due to pain in the face and a pulsing type right hemicranial headache. It started in the cervical region and was irradiated to the right retroorbital and auricular area, with difficulty contracting the right eyelid, otalgia, and vertigo. She used oral contraceptives, had two cesarean deliveries, and quitted smoking at 20 years old. She had multidirectional and bilateral nystagmus with fast phase to the left, right peripheral face paralysis, and crusts in the right ear canal. The patient was treated with aciclovir and prednisone, with good recovery. Two weeks later, she returned because of two episodes of convulsion and headache. Brain CTA (computed tomography angiography) showed cerebral venous thrombosis. Conclusion: Cerebral venous thrombosis is a rare complication of Ramsay Hunt Syndrome. It is important to stay alert to the development of vascular complications in these patients.
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Marin, Carolina Maria, Gustavo Carvalho Costa, Emilia Correa Souto, Icaro França Navarro Pinto, Igor Braga Farias, Bruno de Mattos Lombardi Badia, Roberta Ismael Lacerda Machado, Paulo Victor Sgobbi Souza, Wladimir Bocca Vieira de Rezende Pinto, and Acary Souza Bulle Oliveira. "Charcot arthropathy in the elbow caused by hydrosiringomyelia." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.148.
Повний текст джерелаАнотація:
Introduction: Syringomyelia is a chronic disease of the spinal cord that leads to damage to nerve fibers in the spinothalamic tract. The changes in these structures responsible for the thermal and painful sensitivity lead to an abnormal innervation of the joints, which can lead to neuropathic arthropathy, called Charcot arthropathy. Syringomyelia is the main cause of Charcot arthropathy in the upper limbs, and the most involving joints are the shoulder and elbow. It is a rare condition and its recognition allows for early diagnosis and proper management. Case report: A 50-year-old female patient, with a previous history of spinal cord trauma, who has been in a wheelchair since then, started with edema in the left upper limb, mainly in the elbow, evolved with local ulcer and presence of serosanguinolent secretion, weakness and paresthesia in the left hand. Magnetic resonance imaging of the elbow showed signs of neuroarthropathy and the study of the thoracic cervical spine showed enlargement of the cerebrospinal fluid space and tapering of the spinal cord. Conclusions: Charcot’s arthropathy should be considered as a differential diagnosis of pain, edema and limitation of joint movements. When present in the upper limbs, an investigation should be carried out to exclude syringomyelia.
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Camelo Filho, Antonio Edvan, Diego Sant’Ana Sodré, Halisson Flamini Arantes, and Carlos Otto Heise. "Covid-19 Brachial plexopathy: a case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.518.
Повний текст джерелаАнотація:
Context: The understanding of neuromuscular manifestations secondary to infection by SARS-CoV-2 is scarce. Peripheral neuropathies are a heterogeneous group of diseases affecting the peripheral nervous system, with a variable motor, sensitive and autonomic involvement. There are recent descriptions of atypical patterns of neuropathies after COVID-19. In this study we aim to report a brachial plexopathy secondary to COVID-19 with its clinical and electrophysiological characterization. We performed a cross-sectional, observational, descriptive, case report type, using medical record review. Case report: A 42 year-old female was hospitalized for 2 months due to severe respiratory syndrome due to COVID-19. She remained in the ICU for 20 days. During her stay in the ward she complained of weakness and pain in his right upper limb. Physical examination revealed weakness in the right shoulder abduction and elbow flexion. Nerve conduction studies demonstrated involvement of the upper trunk of the right brachial plexus. There was no report of trauma. Her BMI was 50 kg/m2. Conclusions: Recent studies bring atypical descriptions of focal neuropathies, multiple mononeuropathies and plexopathies, opening a new field of study in addition to the description of neuromuscular weakness following ICU stay after COVID-19. From an electrophysiological point of view, there is a recent interest in better characterization of patients with axonal neuropathies suggesting a possible vasculitic mechanism of neuronal damage after COVID-19. Further investigations are necessary to improve the characterization of this particular group, helping its diagnosis and early treatment to reduce complications and disabilities.
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"Nerve Growth Factor Receptors in Cardiovascular Disease." In International Conference on Food, Biological and Medical Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2014. http://dx.doi.org/10.15242/iicbe.c0114519.
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McLeod, G. "ESRA19-0606 High frequency microultrasound and photoacoustics for analysing nerve trauma using regional anaesthesia." In Abstracts of the European Society of Regional Anesthesia, September 11–14, 2019. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/rapm-2019-esraabs2019.14.
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Madhukar, Budagavi, I. S. N. Murthy, and A. G. Ramakrishnan. "Modelling of compound nerve action potentials health and disease." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761607.
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Hood, D. C., and X. Zhand. "Ganglion cell/optic nerve disease and the multifocal VEP." In Vision Science and its Applications. Washington, D.C.: OSA, 2001. http://dx.doi.org/10.1364/vsia.2001.fa3.
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Chandra, Anu, Graeme McLeod, Judy Yan, Yohannes Soenjaya, Brandon Morningstar, and Christine Demore. "In Vivo Microultrasound Visualisation of Nerve Trauma Due to Regional Anaesthesia Needle Insertion and Injection." In 2018 IEEE International Ultrasonics Symposium (IUS). IEEE, 2018. http://dx.doi.org/10.1109/ultsym.2018.8579830.
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Nicholson, Kristen J., Taylor M. Gilliland, and Beth A. Winkelstein. "Duration of Nerve Root Compressive Trauma Modulates the Subsequent Thermal Hyperalgesia and Spinal Expression of the Glutamate Transporter, GLT1." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14110.
Повний текст джерелаАнотація:
Mechanical compression of the cervical nerve roots is a common injury modality [1] and a frequent source of neck pain, affecting 30–50% of adults each year [2]. Since the nerve root is viscoelastic in compression (Fig. 1) [3,4], its response to loading from different injury scenarios is also likely a function of the duration of the applied tissue insult, which varies with the type of injury. For example, the nerve root undergoes brief periods of compression during sports and auto-related trauma, whereas a more prolonged compression occurs for a bulging disc or foraminal stenosis [1]. Similarly, mechanical sensitivity (i.e. pain) after root compression is has been shown to be duration-dependent [3,4]. Compression of the cervical nerve root is only sufficient to induce mechanical sensitivity in a rat model if the compression is applied for more than 3 minutes [3]. Yet, mechanical sensitivity is only one behavioral sequelae of radicular pain and it is not known whether the duration dependent response is similar for other types of evoked pain, such as thermal sensitivity.
Звіти організацій з теми "Nerve trauma and disease"
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Hu, XinYi, JingXuan Hao, and HangYue Wang. Improvement of Environmental enrichment on Cognitive Functions in Patients and animals : A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2022. http://dx.doi.org/10.37766/inplasy2022.12.0014.
Повний текст джерелаАнотація:
Review question / Objective: To study the relationship between environmental enrichment and cognitive function through a meta-analysis of the literature, analyze its effects on the improvement of cognitive function in patients and animals, and evaluate the effects of different environmental enrichment measures on cognitive function improvement. Condition being studied: Cognitive decline refers to an individual's memory, language, reasoning and other aspects of cognitive function showing obvious, measurable decline or abnormal. The causes of cognitive decline are various, including neurodegeneration, cerebrovascular disease, infection, trauma, and depression. Alzheimer's disease and stroke are the most common.
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Zhang, Yingrong, Sanchun Tan, Jieyu Wang, Yanji Zhang, Mengyuan Huang, Hongjie Xia, Yaxin Hu, Yinyue Rao, and Zhongyu Zhou. A scoping review protocol of systematic reviews and meta-analyses to acupuncture for the treatment of peripheral facial paralysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0084.
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Review question / Objective: To conduct a systematic comprehensive review for Acupuncture treatment of peripheral facial paralysis and to evaluate the efficacy and safety of acupuncture therapy for peripheral facial paralysis. Condition being studied: Peripheral facial paralysis, known as peripheral facial never palsy, includes Bell’s palsy and Ramsay Hunt syndrome.Any medical conditions such as infection, malignancy and autoimmune issues can result it. Idiopathic Bell's palsy is the most common disease causing peripheral facial nerve palsy, which clinical features include unilateral weakness of the facial nerve, hyperacusis, dysgeusia, dry eye or uncontrollable tears, but the etiology of it is unclear. Ramsay Hunt syndrome, less common than Bell’s palsy, is often caused by herpes zoster virus, which clinical features are unilateral weakness of face with ear herpes, tinnitus and dizziness. Facial paralysis patients with ear herpes can be diagnosed with Ramsay Hunt syndrome. Peripheral facial paralysis not only result the dyskinesia of facial muscles but also affect the quality of patient’s life.There are lot of evidence shows that Acupuncture can be used in any period and any kind of peripheral facial paralysis.However, we still lack systematic reviews to assess the efficacy and safety of acupuncture therapy. As a result, we conduct a scoping review of systematic reviews and meta-analyses to address this gap.
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Totten, Annette, Dana M. Womack, Marian S. McDonagh, Cynthia Davis-O’Reilly, Jessica C. Griffin, Ian Blazina, Sara Grusing, and Nancy Elder. Improving Rural Health Through Telehealth-Guided Provider-to-Provider Communication. Agency for Healthcare Research and Quality, December 2022. http://dx.doi.org/10.23970/ahrqepccer254.
Повний текст джерелаАнотація:
Objectives. To assess the use, effectiveness, and implementation of telehealth-supported provider-to-provider communication and collaboration for the provision of healthcare services to rural populations and to inform a scientific workshop convened by the National Institutes of Health Office of Disease Prevention on October 12–14, 2021. Data sources. We conducted a comprehensive literature search of Ovid MEDLINE®, CINAHL®, Embase®, and Cochrane CENTRAL. We searched for articles published from January 1, 2015, to October 12, 2021, to identify data on use of rural provider-to-provider telehealth (Key Question 1) and the same databases for articles published January 1, 2010, to October 12, 2021, for studies of effectiveness and implementation (Key Questions 2 and 3) and to identify methodological weaknesses in the research (Key Question 4). Additional sources were identified through reference lists, stakeholder suggestions, and responses to a Federal Register notice. Review methods. Our methods followed the Agency for Healthcare Research and Quality Methods Guide (available at https://effectivehealthcare.ahrq.gov/topics/cer-methods-guide/overview) and the PRISMA reporting guidelines. We used predefined criteria and dual review of abstracts and full-text articles to identify research results on (1) regional or national use, (2) effectiveness, (3) barriers and facilitators to implementation, and (4) methodological weakness in studies of provider-to-provider telehealth for rural populations. We assessed the risk of bias of the effectiveness studies using criteria specific to the different study designs and evaluated strength of evidence (SOE) for studies of similar telehealth interventions with similar outcomes. We categorized barriers and facilitators to implementation using the Consolidated Framework for Implementation Research (CFIR) and summarized methodological weaknesses of studies. Results. We included 166 studies reported in 179 publications. Studies on the degree of uptake of provider-to-provider telehealth were limited to specific clinical uses (pharmacy, psychiatry, emergency care, and stroke management) in seven studies using national or regional surveys and claims data. They reported variability across States and regions, but increasing uptake over time. Ninety-seven studies (20 trials and 77 observational studies) evaluated the effectiveness of provider-to-provider telehealth in rural settings, finding that there may be similar rates of transfers and lengths of stay with telehealth for inpatient consultations; similar mortality rates for remote intensive care unit care; similar clinical outcomes and transfer rates for neonates; improvements in medication adherence and treatment response in outpatient care for depression; improvements in some clinical monitoring measures for diabetes with endocrinology or pharmacy outpatient consultations; similar mortality or time to treatment when used to support emergency assessment and management of stroke, heart attack, or chest pain at rural hospitals; and similar rates of appropriate versus inappropriate transfers of critical care and trauma patients with specialist telehealth consultations for rural emergency departments (SOE: low). Studies of telehealth for education and mentoring of rural healthcare providers may result in intended changes in provider behavior and increases in provider knowledge, confidence, and self-efficacy (SOE: low). Patient outcomes were not frequently reported for telehealth provider education, but two studies reported improvement (SOE: low). Evidence for telehealth interventions for other clinical uses and outcomes was insufficient. We identified 67 program evaluations and qualitative studies that identified barriers and facilitators to rural provider-to-provider telehealth. Success was linked to well-functioning technology; sufficient resources, including time, staff, leadership, and equipment; and adequate payment or reimbursement. Some considerations may be unique to implementation of provider-to-provider telehealth in rural areas. These include the need for consultants to better understand the rural context; regional initiatives that pool resources among rural organizations that may not be able to support telehealth individually; and programs that can support care for infrequent as well as frequent clinical situations in rural practices. An assessment of methodological weaknesses found that studies were limited by less rigorous study designs, small sample sizes, and lack of analyses that address risks for bias. A key weakness was that studies did not assess or attempt to adjust for the risk that temporal changes may impact the results in studies that compared outcomes before and after telehealth implementation. Conclusions. While the evidence base is limited, what is available suggests that telehealth supporting provider-to-provider communications and collaboration may be beneficial. Telehealth studies report better patient outcomes in some clinical scenarios (e.g., outpatient care for depression or diabetes, education/mentoring) where telehealth interventions increase access to expertise and high-quality care. In other applications (e.g., inpatient care, emergency care), telehealth results in patient outcomes that are similar to usual care, which may be interpreted as a benefit when the purpose of telehealth is to make equivalent services available locally to rural residents. Most barriers to implementation are common to practice change efforts. Methodological weaknesses stem from weaker study designs, such as before-after studies, and small numbers of participants. The rapid increase in the use of telehealth in response to the Coronavirus disease 2019 (COVID-19) pandemic is likely to produce more data and offer opportunities for more rigorous studies.