Meralgia Paresthetica

Stimulation of Dorsal Root Ganglia for the Management of Complex Regional Pain Syndrome: A Prospective Case Series

“…Skin biopsies from the affected limbs of patients diagnosed with CRPS‐1 show degeneration of cutaneous nociceptors (reductions in C‐ and Aδ‐nerve endings in the epidermis). As with other neuropathic pain conditions, sensitization of primary afferent, spinal, and/or supraspinal neurons occurs in CRPS . This may indicate that maladaptive feedback loops and neuroplasticity are established after the initiating insult.…”

A Comprehensive Outcome‐Specific Review of the Use of Spinal Cord Stimulation for Complex Regional Pain Syndrome

“…It is important to recognize the intricacy of known CRPS pathophysiology, however, as this may have some practical implications when considering a minimally invasive therapy like SCS that can provide efficacious treatment for several outcomes simultaneously, as compared to many other therapeutic options which carry their own treatment-specific adverse effects while targeting only one component of CRPS pathology. Identified components of CRPS pathophysiology include genetic predisposition, 28,29 minor or major trauma, [30][31][32] ischemic injury, 33,34 nitric oxide signaling, 30 neuronal injury, 30,[35][36][37] inflammatory cascade activation, [38][39][40][41][42][43][44][45][46] autoimmune antibody-mediated neuronal and vascular tissue damage, 46,48 tissue edema, 30 autonomic nervous system and adrenergic receptor perturbations, 47 motor atrophy and trophic changes, 29 sensory disturbances, 49,50 peripheral and central nervous system sensitization, 37,51-54 psychological sequelae, [55][56][57] and financial and socioeconomic implications secondary to both morbidity and disability from this syndrome. [58][59][60] Of similar complexity, a similarly diverse and multimodal array of mechanisms has been identified to underlie the effects of spinal cord stimulation.…”

The inflammasome in fibromyalgia and CRPS: a microglial hypothesis?

“…11 Microglia have been highly studied as key contributors to pathological and chronic pain mechanisms, 12 and are involved in hyper algesia and allodynia in both fibromyalgia and chronic fatigue syndrome, as well as pain in CRPS. 13,14 Microglial inflammasome activation promotes the recruitment of peripheral innate immune cells (macrophages) and adaptive immune cells (T cells and B cells), as well as further activating nearby glial cells, which could be responsible for the peripheral effects proposed by Littlejohn. 1 Of note, this Review article mentions that downregulation of activated glial cells is a potential strategy for targeting neurogenic neuroinflammation in fibromyalgia and CRPS, so an inflammasome-induced microglial a ctivation hypothesis could be plausible.…”