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Doctors think the pain caused by RSD comes from problems in your sympathetic nervous system. Your sympathetic nervous system controls blood flow movements that help regulate your heart rate and blood pressure.

Complex regional pain syndrome (CRPS) is a form of chronic pain that usually affects an arm or a leg. complex regional pain syndrome (CRPS) typically develops after an injury, a surgery, a stroke or a heart attack. The pain is out of proportion to the severity of the initial injury.

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If you experience constant, severe pain that affects a limb and makes touching or moving that limb seem intolerable, see your health care provider to determine the cause. It's important to treat CRPS early.

RSD is an older term used to describe one form of Complex Regional Pain Syndrome (CRPS). Both RSD and CRPS are chronic conditions characterized by severe burning pain, most often affecting one of the extremities (arms, legs, hands, or feet). There are often pathological changes in bone and skin, excessive sweating, tissue swelling and extreme sensitivity to touch, known as allodynia.

RSD is sometimes called Type I CRPS, which is triggered by tissue injury where there is no underlying nerve injury, while Type II CRPS refers to cases where a high-velocity impact (such as a bullet wound) occurred at the site and is clearly associated with nerve injury. Type II used to be called "causalgia" and was first documented over 100 years ago by doctors concerned about the pain that Civil War veterans suffered even after their wounds had healed. RSD is unusual in that it affects the nerves, skin, muscles, blood vessels and bones at the same time.

The key symptom is, chronic, intense pain that is out of proportion to the severity of the injury (if an injury occurred) and which gets worse over time rather than better. It most often affects the arms, legs, hands or feet and is accompanied by:

For most people with RSDS symptoms will go away over time, but sometimes symptoms spread away from the initial site and affect a whole limb or even the whole body. In rare cases, the pain, skin changes and motor symptoms can persist for years and become debilitating.

The nociceptive flexion reflex (NFR) is a physiological, polysynaptic reflex allowing for painful stimuli to activate an appropriate withdrawal response. NFR is easily measurable in clinical setting, and is a reliable and objective tool for measurement of an individual's pain experience. An exhaustive review of the literature, covering multiple search engines, indicates that the NFR method is valuable in studying the impact of diverse pharmacological and non-pharmacological interventions on the flexion reflex, in conditions of acute pain and in healthy volunteers. More recently, the NFR method has gained particular attention as a research tool in studies of central sensitization and persistent or chronic pain.

The withdrawal response (reflex), also known as the nociceptive flexion reflex, is an automatic response of the spinal cord that is critical in protecting the body from harmful stimuli. The first known definition of a reflex dates back to 1649 when Ren Descartes noted that specific bodily movements occurred instantaneously and independent of the process of thought. Modern definitions state that a reflex is an involuntary response of effector tissue caused by the stimulation of specific receptors.[1]

The reflex arc is the basic unit of a reflex, which involves neural pathways acting on an impulse before that impulse has reached the brain. Instead of directly traveling to the brain, sensory neurons of a reflex arc synapse in the spinal cord. This is an important evolutionary adaptation for survival, which allows faster actions by activating spinal motor neurons instead of delaying reaction time by signals first having to go to the brain.

The withdrawal reflex can occur in either the upper or lower limbs and is a polysynaptic reflex, which means that interneurons mediate the reflex between the afferent (sensory) and efferent (motor) signals. In contrast, the deep tendon reflex is monosynaptic and does not utilize interneurons to transmit information. Additionally, the withdrawal response is an intersegmental reflex arc, meaning that the outcomes of the reflex are mediated by the stimulation or inhibition of motor neurons from multiple levels of the same spinal cord.[2]

A sensory neuron that gets excited via its nociceptors delivers this excitation through pain fibers to the central nervous system (CNS). Notably, these fibers transmit excitation to the cell body of the sensory neuron, which resides in the dorsal root ganglia (DRG) of the spinal cord. The specific fibers that communicate mechanical, thermal, and chemical pain are the A-delta and C fibers. Once these fibers relay the action potential to the cell body of the sensory neuron in the DRG, the sensory neuron sends excitatory postsynaptic potentials (EPSPs) to motor neurons and interneurons, as previously explained. The sensory neuron accomplishes this by releasing neurotransmitters, with glutamate being the primary excitatory neurotransmitter in the CNS. Some interneurons involved in the withdrawal reflex are inhibitory and relay inhibitory postsynaptic potentials (IPSPs) by releasing inhibitory neurotransmitters, with the primary inhibitory neurotransmitters in the CNS being GABA and glycine.[5]

The excited somatic motor neurons complete the withdrawal reflex by depolarizing and contracting their targeted muscles. This depolarization travels along the motor neuron, which exits the spinal cord and enters the peripheral nervous system (PNS). Within the PNS, the motor neuron releases the excitatory neurotransmitter acetylcholine (ACh), which binds to the nicotinic acetylcholine receptors on the sarcolemma of the muscle, initiating an action potential that travels down the T-tubules. The sarcoplasmic reticulum (SR) then releases calcium ions and binds troponin, changing its conformation. This change reveals the active site on actin by removing tropomyosin, and myosin can now form a cross-bridge with actin to induce contraction. ATP then powers the release of myosin from actin, calcium ions are actively transported back into the SR, and tropomyosin returns to its site to block actin. The somatic motor neurons inhibited in the spinal cord will not be depolarized, resulting in no contraction of their targeted muscle groups.[6]

The withdrawal reflex is mediated by the PNS and CNS, the epidermis, and the musculoskeletal system. The epidermis is central to the reflex initiation because, when damaged, it releases chemicals to induce the activation of the sensory neurons that further the completion of the reflex. The PNS includes the sensory neurons stimulated by noxious input and the somatic motor neurons that target muscles. The CNS is involved because the sensory neuron communicates through the spinal cord to relay the withdrawal reflex. Lastly, the extensor and flexor muscles of the body accomplish the actual movement of the limb away from the stimulus. For example, suppose the reflex was to occur in the upper limb. In this case, the flexor muscles involved include the biceps brachii and coracobrachialis, with the primary extensor of the arm at the elbow joint being the triceps brachii. In the lower limb, there are flexors at the knee, which include the biceps femoris, semimembranosus, and semitendinosus muscles. Extensors of the knee include the rectus femoris, vastus lateralis, vastus medius, and vastus intermedius, collectively known as the quadriceps muscle group.

The withdrawal reflex is polysynaptic, meaning that, in addition to the sensory and motor neurons, this response utilizes interneurons which pass signals between the sensory and motor neurons, ultimately creating multiple synaptic connections.[7] The steps of a polysynaptic withdrawal reflex are outlined below, resulting in a limb pulling away from the noxious stimulus within half a second.

The withdrawal reflex can be tested using an electromyogram (EMG). This device measures the electrical activity of peripheral nerves and striated skeletal muscles and includes a needle EMG and nerve conduction studies (NCS). The EMG was first described in 1943 by Weddell et al., who pioneered its use in examining muscles.[10]

A loss of function of sensory neurons may prevent the withdrawal reflex from being initiated. Different pathologies can affect peripheral sensation, such as multiple sclerosis and stroke. Congenital insensitivity to pain is a rare disease that impairs an individual's ability to perceive pain[12]. Insensitivity to pain makes a patient vulnerable to severe injuries due to the absence of protective reactions to noxious stimuli such as the withdrawal reflex. Genetic variances can alter an individual's perception of pain by modifying the sodium ion channels in sensory neurons.[13]

The withdrawal reflex may also be impacted if motor neurons or their synapses with musculature are damaged, as can be seen in amyotrophic lateral sclerosis (ALS).[14] Autoimmune diseases such as myasthenia gravis (MG) and Lambert-Eaton myasthenic syndrome (LEMS) negatively impact the communication between lower motor neurons and the muscles they act upon, which theoretically can alter the withdrawal reflex.[15] A loss of the withdrawal reflex can also be seen in transverse myelitis, a demyelinating condition of the spinal cord with multiple causes, including multiple sclerosis, fungal infections (Mycoplasma pneumoniae), and viruses (CMV, HSV, and enterovirus). Patients with transverse myelitis will experience motor weakness, autonomic nervous system (ANS) and sensory dysfunction, and diminished reflexes.[16] Overriding of the withdrawal reflex can be seen in drugged, drunk, or unconscious patients. These patients will not exhibit this reflex.

Specific modulators of the withdrawal reflex have long been topics of research, which has revealed that the reflex pattern may undergo modulation by running, different phases of walking, stimulus intensity, and even the load on the leg. In fact, the particular phase of walking has been found to reverse the reflex. Classical conditioning involving the cerebellum as a structure for procedural learning has also been found to affect the withdrawal reflex.[17] Non-invasive vagal nerve stimulation has also been found to increase the threshold of the withdrawal reflex to a single stimulus.[18] Stroke is the fifth leading cause of morbidity and mortality in the United States, with stroke patients frequently exhibiting spasticity as a complication, which can affect the withdrawal reflex. Research also demonstrates that injecting botulinum toxin A modifies the withdrawal reflex in stroke patients by reducing spasticity, suggesting that this may be a valuable tool in treating post-stroke spasticity.[19] 2351a5e196