Speakers can check in at the lounge, submit their final slides, and prepare for presentations throughout NeuPSIG 2023. 

Early Career delegates are invited to stop by and network with colleagues.

Microneurography is the only neurophysiological technique that records neuronal activity directly from nerves in awake patients. Recording from nociceptive fibres provides unrivalled insight into peripheral neuronal activity and how it can relate to chronic neuropathic pain. The unmyelinated nociceptive fibres, tested by microneurography, are not assessed by conventional nerve conduction studies and are important for sensing pain. Nociceptive fibres are heterogenous, they show different stimulus-response functions and some are mechanically-insensitive in the naive state. We still have an incomplete understanding of which nociceptive afferent population and which activity is the key driver of neuropathic pain. Microneurography has the potential to answer these fundamental questions. The application of microneurography to the study of neuropathic pain is under-utilised. We believe that these techniques should be adopted more widely by the neuropathic pain field

 

In our workshop we will provide an introduction to microneurography, and show how this technique can provide new insights into our understanding of neuropathic pain and sensory nerve function. 

Despite major advances in our understanding of the pathophysiology of neuropathic pain, progress in mechanism-based therapies has lagged behind. While a number of different neurophysiological techniques have proven useful to diagnose lesions of the somatosensory system – a prerequisite for the neuropathic pain diagnosis – objective measures of sensitization or spontaneous neural activity are less established. This workshop will focus on the use of pain-related evoked potential, quantitative sensory testing, advanced paradigms of thermosensory integration (thermal grill illusion) and microneurography to close important gaps in our understanding of neuropathic pain mechanisms. In additional to classical applications of diagnosing sensory loss, novel paradigms to reveal sensitization processes will be highlighted. The methods will be presented and critically appraised with regard to research and clinical applications. To this end, "bedside" protocols, which can be integrated into the diagnostic routine in dedicated outpatient clinics will be presented.

Chronic pain affects a significant portion of the global population and poses a major socioeconomic burden. Recent research has shown the importance of data-driven approaches in understanding and treating chronic pain. This workshop will focus on the latest developments and applications of brain imaging and data analysis techniques in the study of Trigeminal Neuralgia (TN). Topics will include the genetics of TN, potential risk factors and comorbidities, new imaging techniques and how these novel methods can be used in the assessment, diagnosis, and management of TN, including prognosis and outcome prediction. The goal of this workshop is to share and integrate new insights in this field to expedite research and improve pain care.

The reproducibility and translatability of pre-clinical studies remains a challenge as we seek to better understand and treat chronic neuropathic pain. In this session, we will offer positive and practical solutions to improve the impact of pre-clinical experiments on the pain field. Alfonso Romero-Sandoval will reflect on his recent efforts to conduct multi-center rodent behavioral experiments. He will consider the lessons we can take from the results and how they might help us further improve how we standardize and validate in vivo outcome measures in pain research. Andrew Rice will discuss the utility of ethologically relevant behavioral measures in animal models; he will focus on diverse tactics for cross laboratory validation of such measures using the innate rodent behaviors of burrowing and predator avoidance as examples. Finally, Dr. Duncan Lascelles will discuss the measurement of pain and the role of clinical studies in non-rodent models, including the potential utility of using owned pet animals with naturally occurring pain conditions.

This session will focus on the diagnosis of and treatment options for pDPN, and the management of the pain. Diabetic neuropathy is a serious diabetes complication that affects many people with diabetes.

Learning Objectives

• Articulate the importance of early diagnosis of pDPN 

• Determine the appropriate tools that can facilitate early diagnosis of pDPN 

• Summarize the range of treatment options available for pDPN 

This session has  been independently planned and developed to be delivered by IASP/NeuPSIG.  Grunenthal has provided a donation for the independent development of this session.  

The primary reason for inadequate analgesic effects of current pharmaceuticals for neuropathic pain is that we do not fully understand the pathophysiological mechanisms that underlie its development. We will discuss the concept that non-neuronal cells residing in the skin (e.g. glia, inflammatory cells) and peripheral mediators (e.g. axon guides) may play a key role in nociceptive signal transduction. This shift in paradigm has opened an exciting field of studies with regard to pain mechanisms. We will present potential implications on clinical practice. Data from preclinical and clinical studies will be discussed critically focusing on Schwann cells and other glia cells, keratinocytes, fibroblasts, mechanoreceptors, ion channels, and axon guidance mechanisms. Lastly, we will present new data on changes in cutaneous sensory and sympathetic vaso- and sudomotor innervation in peripheral and central neuropathic pain conditions. Experimentally- and pathology-induced changes using 8% capsaicin will be related to the clinical (pain) phenotype, and novel insights into potential therapeutic targets showcased.

This workshop will update clinicians and basic researchers about emerging neuroimmunology research to highlight new clinical and research opportunities. Basic research approaches using patient specimens have already proven that specific neuropathies are maintained by pathological antibodies targeting cells in symptom-associated pathways. Rapid, accurate diagnosis enables consideration of targeted mechanism-based therapies available today with clinical-trial efficacy data.  We will mention the classic dysimmune neuropathies but focus on the more recent evidence in painful disorders including peripheral neuropathies and fibromyalgia. We will review the methods and conclusions from experiments analysing samples from patients that demonstrate causality and elucidate pathological mechanisms. These include in vitro studies and passive-transfer models in vivo, where antibodies from patients are administered to mice that develop behavioural, anatomical, and physiological correlates of human pain syndromes. In vitro assays effectively identify putative pathogenic antibodies and targets, and passive-transfer approaches are the gold-standard for proving autoimmune causality. Both have yielded mechanistic advances with high degrees of predictive validity. We will end by discussing less-certain topics including which other chronic pain conditions have lesser evidence of dysimmune contributions, steps in clinical diagnostic pathways, the best-established immunotherapies, when immunotherapy is not appropriate to consider. Emerging research opportunities will be highlighted. 

Fibromyalgia syndrome is a chronic pain condition associated with autonomic symptoms, fatigue and cognitive disturbances. Despite the large body of studies on the topic, the mechanisms underlying this common chronic pain condition are still a matter of debate. However, recent preclinical investigations have indicated that dorsal root ganglia damage, due to circulating autoantibodies, may play a role in fibromyalgia. Accordingly, approximately 50% of patients with fibromyalgia have a reduced intraepidermal nerve fibre density as assessed with skin biopsy. This small nerve fibre loss, commonly defined as small-fibre pathology, may also underlie the multiple symptoms that patients with fibromyalgia experience, such as ongoing burning extremity pain, bladder and bowel disturbances. 

However, the relationship between small-fibre pathology and the symptoms and signs that patients with fibromyalgia experience is still an issue of controversy. Whereas several studies have reported that patients with fibromyalgia have impaired sensory profiles at the quantitative sensory testing and abnormal nociceptive evoked potentials, other studies showed that small-fibre pathology is not associated with clinically meaningful abnormalities of the somatosensory nervous system.

This workshop addresses the two opposite views on fibromyalgia. The first speaker, Jordi Serra, will detail all the evidence supporting a specific role of small-fibre pathology in patients with fibromyalgia. The second speaker, Andrea Truini, will provide evidence that the small-fibre pathology may have a negligible impact on symptoms that patients with fibromyalgia experience. 

The discussion will be led by the chair, Claudia Sommer.

A key question in this topical workshop is whether basic mechanisms being defined for spontaneous activity in nociceptors have useful clinical implications. Spontaneous activity in primary somatosensory neurons has long been associated with non-evoked pain, but the underlying mechanisms have been slow to emerge. However, recent advances have identified electrophysiological and cellular mechanisms of spontaneous activity in rodent and human nociceptors that make therapeutically promising predictions that can be tested in human patients. Dr. Carolina Roza will summarize aberrant electrophysiological behavior of peripheral nerve fibers observed in experimental models, the associated pathophysiological mechanisms, and their relationship to symptoms reported by patients. Dr. Edgar Walters will describe newly characterized irregular depolarizing spontaneous fluctuations of membrane potential in dissociated rodent and human nociceptors that drive spontaneous activity, how these synergize with other electrophysiological alterations that promote ongoing discharge, and the identification of prominent underlying biophysical and cell signaling alterations. Dr. Martin Schmelz will show microneurographic evidence for depolarization of spontaneously active nociceptors in patients and describe how the effects of slow depolarizing electrical stimuli applied to human and pig nociceptors are consistent with new findings from rodent nociceptors, potentially providing improved translational tools to assess alterations of nociceptor excitability in patients.