Sympathetic Pain Syndromes

This chapter is a brief overview of the major sympathetic pain syndromes and their clinical characteristics, treatment, and preventative measures. It offers a concise overview of distinguishing characteristics, pathogenetic mechanisms, available treatment options for major sympathetic pain syndromes, and in-depth discussion pertaining to complex regional pain syndrome (CRPS) and the influence of specific surgical procedures on the development of this syndrome. Risk factors and pathogenetic mechanisms related to the emergence of CRPS after orthopedic and spine surgeries have been analyzed, as well as therapies and practices used preemptively to prevent new CRPS and worsening of chronic pain and disability in the affected limb. Finally, possible therapies for the postsurgical period are discussed to facilitate rehabilitation and speed up recovery after orthopedic and spinal surgeries in this patient population.

The Concept of Cotransmission: Focus on ATP as a Cotransmitter and its Significance in Health and Disease

The concept of cotransmission, including sympathetic nerve release of noradrenaline and ATP, was formalised in 1976, which challenged the accepted view known as ‘Dale's Principle’ that one nerve released only one transmitter. ATP was also shown to be a cotransmitter with acetylcholine in parasympathetic nerves supplying the urinary bladder and as a cotransmitter with nitric oxide in non-adrenergic, non-cholinergic inhibitory nerves supplying the intestine. It is now recognised that ATP is a cotransmitter in most, if not all, nerves in the peripheral and central nervous systems. The physiological significance of cotransmission will be considered. In pathophysiology, the role of ATP as a cotransmitter appears to increase as shown, for example, in the parasympathetic nerves supplying the diseased human bladder and in sympathetic nerves in spontaneously hypertensive rats. ATP is likely to be involved in sympathetic pain, causalgia and reflex sympathetic dystrophy. Purinergic signalling also appears to be enhanced in inflammatory and stress conditions.

Fibromyalgia: When Distress Becomes (Un)sympathetic Pain

Fibromyalgia is a painful stress-related disorder. A key issue in fibromyalgia research is to investigate how distress could be converted into pain. The sympathetic nervous system is the main element of the stress response system. In animal models, physical trauma, infection, or distressing noise can induce abnormal connections between the sympathetic nervous system and the nociceptive system. Dorsal root ganglia sodium channels facilitate this type of sympathetic pain. Similar mechanisms may operate in fibromyalgia. Signs of sympathetic hyperactivity have been described in this condition. Genetic factors and/or distressful lifestyle may lead to this state of sympathetic hyperactivity. Trauma and infection are recognized fibromyalgia triggers. Women who suffer from fibromyalgia have catecholamine-evoked pain. Sympathetic dysfunction may also explain nonpain-related fibromyalgia symptoms. In conclusion, in fibromyalgia, distress could be converted into pain through forced hyperactivity of the sympathetic component of the stress response system.