Pain is a signal in your nervous system that something may be wrong. It is an unpleasant feeling, such as a prick, tingle, sting, burn, or ache. Pain may be sharp or dull. It may come and go, or it may be constant. You may feel pain in one area of your body, such as your back, abdomen, chest, pelvis, or you may feel pain all over

Pain can be helpful in diagnosing a problem. If you never felt pain, you might seriously hurt yourself without knowing it, or you might not realize you have a medical problem that needs treatment.

There are two types of pain: acute and chronic. Acute pain usually comes on suddenly, because of a disease, injury, or inflammation. It can often be diagnosed and treated. It usually goes away, though sometimes it can turn into chronic pain. Chronic pain lasts for a long time, and can cause severe problems.

Pain is not always curable, but there are many ways to treat it. Treatment depends on the cause and type of pain. Pain relievers and other medicines, acupuncture, physical therapy, and sometimes surgery may be helpful.

Pain is an unpleasant signal to us that something hurts. It is a complex experience and differs greatly from individual to individual, even between those with similar injuries and/or illnesses. Pain can be very light, almost unnoticeable, or explosive. Some people experience pain as pricking, tingling, stinging, burning, shooting, aching, or electric. Pain warns us that something is not quite right in our body and can cause us to take certain actions and avoid others. Pain also can significantly impact our quality of life—by adversely affecting our physical and emotional well-being; upsetting relationships with family, coworkers, and friends; and limiting our mobility and participation in daily activities.

Hundreds of pain syndromes or disorders make up the spectrum of pain. For example, there is the pain of childbirth, the pain of a heart attack, the pain of a headache or backache, and the pain that sometimes follows amputation of a limb. There also is pain that accompanies cancer and the pain that follows severe trauma, such as head and spinal cord injuries.

Pain is often a debilitating symptom of many diseases and is considered a disease itself when it persists beyond recovery from an injury or illness. Pain often goes away on its own or with treatment, but it can persist and develop into long-term chronic pain. Millions of Americans have pain every day. Chronic pain is one of the most common reasons adults in the U.S. seek medical care, affecting 50 million people.

Pain is an unpleasant experience that involves both physical and psychological components. Feeling pain is quite adaptive because it makes us aware of an injury, and it motivates us to remove ourselves from the cause of that injury. In addition, pain also makes us less likely to suffer additional injury because we will be gentler with our injured body parts.

Generally speaking, pain can be considered to be neuropathic or inflammatory in nature. Pain that signals some type of tissue damage is known as inflammatory pain. In some situations, pain results from damage to neurons of either the peripheral or central nervous system. As a result, pain signals that are sent to the brain get exaggerated. This type of pain is known as neuropathic pain. Multiple treatment options for pain relief range from relaxation therapy to the use of analgesic medications to deep brain stimulation. The most effective treatment option for a given individual will depend on a number of considerations, including the severity and persistence of the pain and any medical/psychological conditions.

Some individuals are born without the ability to feel pain. This very rare genetic disorder is known as congenital insensitivity to pain (or congenital analgesia). While those with congenital analgesia can detect differences in temperature and pressure, they cannot experience pain. As a result, they often suffer significant injuries. Young children have serious mouth and tongue injuries because they have bitten themselves repeatedly. Not surprisingly, individuals suffering from this disorder have much shorter life expectancies due to their injuries and secondary infections of injured sites (U.S. National Library of Medicine, 2013).

Introduction

The official IASP definition of allodynia at the time of this article is "pain due to a stimulus that does not normally provoke pain." An example would be a light feather touch (that should only produce sensation) causing pain. Allodynia is different from hyperalgesia, which is an exaggerated response from a normally painful stimulus, although both can and often do co-exist. Both are types of neuropathic pain.

An example of the difference between allodynia and hyperalgesia on the physical exam would be softly rubbing a cotton-tipped swab against a patient’s skin. Lightly brushing a swab against the skin would cause a low-level stimulus, but should not elicit a pain response. A patient who experiences pain with a stimulus that should only cause sensation may have allodynia. If the clinician significantly increases the degree of pressure, some pain would be part of a normal response. A patient who feels an excessive amount of pain would be noted to have hyperalgesia. Thus, on physical exam, allodynia presents as a lowering of the pain threshold, while hyperalgesia presents as a heightening of response. While this often means that allodynia and hyperalgesia seem to exist along the same continuum of stimuli on physical exam, there is still a clear difference in modalities. With allodynia, the response to the stimulus differs from those who have normal sensation, while in hyperalgesia, the response to the stimulus is the same as those who have normal sensation, but it is an exaggerated response.

Allodynia can be due to an underlying disease such as diabetes-induced neuropathic tactile allodynia or can be the primary disease process itself, such as in postherpetic neuralgia. It is often further classified by the type of stimulus causing the nociception, such as tactile, thermal, dynamic or static allodynia, or by the principal site of nociception, such as cutaneous allodynia.

Etiology

The exact etiology behind allodynia is unknown. Allodynia is the phenomenon of a non-painful stimulus producing a sharp pain response, which implies an error in neuronal conduction. The mechanism behind this error is unclear. The strongest existing evidence suggests that sensory neuronal fibers may stimulate pain pathways, possibly due to an error in long-term potentiation. However, studies exist that suggest that superficial sensory components may also have involvement, as well as evidence that different mental states can affect the perception of allodynia. If we use the analogy of crisscrossed fibers, the actual location of the crisscrossing can vary and may be located almost anywhere along the peripheral to the central nervous system tract. Allodynia can involve both the peripheral nervous system and central nervous system via sensitization, and the mechanism behind the inappropriate pain sensations can evolve over time; this might partially explain the existing contradictory studies - they may all be measuring allodynia with neuronal confusion at different locations.

A non-painful stimulus such as light skin touch should only activate the low threshold A-beta fibers. In cutaneous allodynia, these A-beta fibers then also communicate with and activate pain pathways, through different sodium channel types than the Nav1.7 sodium channels usually associated with pain, as well as through the modification of dorsal ganglia. However, allodynic pain is multifactorial, and as people suffering from post-thalamic stroke pain can attest, the crisscrossing of neurons can happen as high as in the cerebellum.

In summary, many types of peripheral nerve fibers communicate with and travel via different central nervous system pathways. Type A nerve fibers are myelinated. They further categorize into alpha fibers, which are mostly responsible for proprioception, beta fibers, which transmit light touch, and delta fibers, which carry both pain and temperature sensations. There are also unmyelinated type C nerve fibers, which carry sensations of aching pain, as well as temperature and pruritus.

Epidemiology

Neuropathic pain affects 0.9% to 17.9% of the general population, depending on the study and the exact inclusion criteria for neuropathic pain, with the best estimate between 6.9% and 10% of the population. Allodynia is estimated to affect 15% to 50% of people with neuropathic pain. The exact prevalence and epidemiology of allodynia are difficult to determine, as it is a symptom associated with many diseases. Listed below is the epidemiology of the most common diseases associated with allodynia:

Fibromyalgia

Fibromyalgia affects 0.5% to 5% of people in the general public, with varying ranges across different countries. Known risk factors for fibromyalgia include age, lupus, and rheumatoid arthritis. Studies report that women appear to be 2-9 times more likely to be diagnosed with fibromyalgia than men; however, this may be due more to clinical bias than merely meeting fibromyalgia criteria. A recent study of rheumatoid patients which used a strict criteria-based scoring system to diagnose fibromyalgia found that women composed 58% of the sufferers. Some research also supports stress, obesity, and family history as risk factors; however, the literature is not conclusive.

Trigeminal Neuralgia

Trigeminal neuralgia affects 0.01% to 0.02% of the general population. Women are 1.5-3 times more likely to carry a diagnosis of trigeminal neuralgia than men. Age is a strong factor, with most cases of trigeminal neuralgia occurring at over 40 years of age.

Diabetic Neuropathic Pain

Diabetes affects roughly 10% of people in the US, and this rate is increasing by about 5% each year. At least 10% (and some sources estimate 100%) of people who have diabetes will develop neuropathic pain. The neuropathic pain can include allodynia, hyperalgesia, or other kinds of pain like feelings of electric shocks or burning. The severity of neuropathic pain often does not correlate with the degree of sensory deficit, making this a primary illness, and not a secondary symptom due to neuronal damage. There does not appear to be a sex-specific difference in the development of diabetic neuropathic pain.

Migraine Associated Allodynia

The prevalence of cutaneous allodynia among migraine sufferers is around 65%, although some estimate it to be higher. Severe cutaneous allodynia may occur in roughly 20% of migraine sufferers.

History and Physical

HPI

Allodynia is a symptom, not a disease. It may be a patient’s chief complaint, but it is important to investigate further to determine the disease process causing the allodynia.

First, one should inquire when and how the allodynia started. Often, there is an instigating event, e.g., chemotherapy, herpes, or trauma. Sources suggest allodynia can develop more abruptly, as in trigeminal neuralgia, or may develop more insidiously, as in allodynia associated with diabetes. Other questions to ask the patient: Is the allodynia progressive? Does the pain wax and wane, or is it fairly constant? What is the quality of the pain? What have they tried for the pain? What makes it better, and what makes it worse? Is the pain associated with tactile stimuli, with movement, with temperature, or something else?

A thorough examination of past medical, surgical, and family history is also warranted, particularly for cancer, diabetes, hypertension, strokes, migraines, rheumatological history, trauma, extreme stress, and opioid history. Be sure to have an updated list of medications to spot possible iatrogenic neuropathy. Please refer to the differential diagnosis section for a list of diseases that can cause allodynia. Lastly, the IASP has published an article to assist clinicians in identifying the type and extent of neuropathic pain with which a patient is presenting.

Physical Exam

On physical exam, allodynia is often present with a smaller stimulus than compared to hyperalgesia. Performing a complete neurological exam is essential; this includes isolating light touch vs. temperature vs. proprioception sensory exams, along with motor and strength testing. It is critical to test the “unaffected” side, even if the professed allodynia is only on one side, for comparison. It is also important to test all four extremities, especially if the allodynia seems to be progressive from distal to proximal areas. COverage of EMGs and other neurological tests will be under the “Evaluation" section.

An example of a focused exam on an area of allodynia is below:

General:

First, perform a visual inspection of the area of allodynia. Compare it to the other side for asymmetry. Is muscle wasting present? How is the skin appearance? Are there any rashes, lesions, skin defects, or vesicles? Any scars from prior surgeries?

Light touch:

A cotton-tipped swab is a simple way to deliver a light touch. A monofilament has the added advantage of being able to objectively quantify the amount of pressure the light touch is exerting. Tell the patient to close their eyes while you perform the test, and to tell you when they sense something. Lightly stroke the unaffected side, then the affected side, and then both sides. The patient should be able to articulate which side you stroked. Sometimes patients are so sensitive that even a light breeze will elicit subjective pain. Document if the allodynia follows cutaneous dermatomes, if it is symmetrical and if it is bilateral.

Pain:

A broken wooden cotton-tipped swab is often used to test for the sensation of pain. Use the sharp tip and repeat as above for light touch. The patient should be able to articulate from where the sensation is coming. The distribution of pain sensation and hyperalgesia may be the same or different than the distribution of allodynia.

Temperature:

Some patients experience thermal, rather than tactile, allodynia. You can use the back of any cold metallic device, such as a metal tuning fork, or ice in a glove, to measure sensation to cold. Again, test various cutaneous dermatomes, and examine both sides.

Proprioception and Vibration:

These sensory tests rarely elicit allodynia. However, it is still vital to consider these tests to discern if any other neuronal sensory loss has occurred.

Motor Neurons:

Test bilateral proximal and distal muscles. Testing for coordination will often reveal subtle motor neuron deficits. If the patient is testing poorly on strength, try to ascertain if it is genuinely due to muscle weakness, or if it is due to pain leading to decreased effort.

Reflexes:

Test bilateral reflexes. Make note if the patient is hyper- or hyporeflexive and if reflexes are symmetrical.

Other

Many different diseases can cause allodynia. There should be a further investigation for an underlying cause depending upon history and examination.

Evaluation

Allodynia is a symptom and physical finding. It is imperative to find and diagnose the underlying disease that is associated with or is causing the allodynia. The history and physical should guide clinicians as to whether more invasive (and expensive) evaluations are appropriate.

General Tests

Blood tests:

CBC and BMP are often helpful, with the addition of ESR and CRP if a concurrent rheumatologic condition is suspected. A hemoglobin A1C can be useful to help diagnose diabetes. B12, thiamine, and TSH can also help diagnose other causes of neuropathy.

Imaging:

Imaging is not typically necessary for this diagnosis. CT of the head may be in order in an older patient with a high suspicion for stroke. Similarly, an MRI of the brain may help diagnose MS if the clinical picture suggests high suspicion.

Neuronal Function Tests

Formal neuronal function tests are unnecessary for the diagnosis of allodynia or allodynia related diseases. They are most helpful for quantifying the efficacy of treatment and in research. There are several methods of testing for sensory neuronal conduction. These tests usually require referrals to specialty clinics, but are briefly summarized below:

Quantitative Sensory Testing:

Quantitative sensory testing, or QST, is generally used to test delta and type C fibers. A device applies thermal stimuli to the skin in a graded manner. Plastic monofilaments, needles, and vibrometers can be used to test light touch, pain, and vibration, but those methods are often secondary to its ability to isolate C fiber response to thermal stimuli.

This test creates a graph with an individual's perception and pain thresholds. It also focuses on testing the small unmyelinated C fibers, which are more challenging to isolate during a routine physical exam. However, it still relies on the patient to participate in the measurement of pain and sensation.

Neuron Conduction Studies:

Neuron conduction studies are a type of neurophysiological technique, which measures the time and quality of an electrical impulse as it travels from the stimulation site of a neuron to the recording site of the same neuron. They are often performed on motor neurons along with electromyography (EMG) to assess motor neuron function. The same concept applies to sensory neurons. Note that standard neuron conduction studies usually directly stimulate the nerve. Also, standard neuron conduction studies only test beta fibers, as they have lower thresholds compared to delta fibers; this directly tests the fiber, but only along a short stretch of a neuron.

Somatosensory Evoked Potentials:

Somatosensory evoked potentials measure electrical activity in the brain after a somatosensory stimulus to beta fibers. This test assesses the health of a neuron as a whole and is often useful when possible CNS conduction issues are suspected, such as in patients with multiple sclerosis or spinal cord injury, and in the neurosurgical operating room to prevent injury.

Laser-Generated Heat Pulses and Contact-Heat-Evoked Potentials:

These potentials work similarly to somatosensory evoked potentials. Instead of a sensory stimulus, laser-generated heat pulses and contact-heat evoked potentials use lasers and heated instruments, testing thermal pain perception, thereby measuring delta fibers.

Skin Biopsies:

Punch skin biopsies can quantitatively measure small neurons. After the biopsy, samples are stained to detect intraepidermal nerve fiber (IENF) density, comparing the measured density to a standard.

EMGs:

Electromyography involves placing electrodes on the skin or in muscle fibers to measure muscle activation. EMGs are useful for distinguishing muscular versus neuronal weakness on efferent motor neurons but do not measure sensory neuron deficits. EMG is an option if there is a concern for motor neuron degeneration. Although EMGs do not directly assess nociceptive pathways, they are often helpful in distinguishing locations of neuropathy, and assessing if the neuropathy has a motor neuron component.

Treatment / Management

First, it is important to treat the underlying disease associated with allodynia. Usually, allodynia has an underlying disorder that requires action to slow, stop, or reverse the progression of the disease. However, allodynia by itself is often a progressive disease that worsens, even after the initial insult is over. The effective methods of treating allodynia will differ with each underlying disease state. This article will focus solely on the treatment of general allodynia, from prevention of allodynia’s progression and chronification to medical and other methods of treating allodynia.

Initiation, Progression, and Chronification:

Allodynia appears to be mediated by inflammation. NSAIDs and antiepileptic calcium channel blockers such as gabapentin have helped slow or prevent allodynia in animal models, but more human data is needed. If a preventative component exists, both animal and human research suggest that it would be for the prevention of long-term allodynia, and not to improve immediate post-operative pain relief. Opioids do not seem to prevent allodynia, and in fact can be a cause of allodynia.

Medical Treatment

Oral Medical Pain Management:

Sodium channel blockers, calcium channel antagonists, and anticonvulsants act to increase firing thresholds and are generally effective in treating allodynia and neuropathic pain. Antidepressants such as serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) also seem to help some types of neuropathic pain, although the evidence is stronger for hyperalgesia than for allodynia. However, selective serotonin reuptake inhibitors (SSRIs) have yielded mixed to disappointing results, and are not a recommendation for the treatment of allodynia. A recent Cochrane review found no good evidence for NSAID use in neuropathic pain.

Opioids are quite effective at treating pain in general; however, they are not as effective in treating neuropathic pain, and there is only very low-quality evidence that oxycodone helps in the treatment of neuropathies. Furthermore, opioids themselves have many potential side effects and can even cause long-term neuropathic pain. There are some strong proponents for cannabis-based medicines. A recent Cochrane review found minimal evidence for benefits and concluded that based on the current research, the potential side effects of cannabis might outweigh its benefits. However, it also acknowledged that there is not much existing research.

Topical Medical Pain Management:

Topical medications seem to help with certain types of allodynia, such as postherpetic neuralgia. Typical over the counter topical medications include lidocaine, menthol, and capsaicin. Lidocaine is a local anesthetic. Topical preparations have high concentrations because it does not easily pass through the skin. Topical menthol asserts its actions through initially activating, then desensitizing nociceptors, and may cause cold allodynia. Recent Cochrane evidence articles found no good-quality randomized controlled trials to support the use of topical lidocaine and topical menthol for neuropathic pain, although many small studies have reported some effectiveness. The strongest capsaicin cream available over the counter is 0.1%. There is also a prescription 8% capsaicin patch that is available, but its use requires close supervision in a hospital setting due to the potential for adverse reactions. A recent Cochrane article did find that high-concentration (8%) capsaicin generated more pain relief compared to control or low dose capsaicin.

Other topical medications include salicylates, fentanyl patches, amitriptyline, gabapentin, and ketamine. Botulinum toxin A (Botox injections) have also been used for peripheral pain. Salicylates may help the underlying inflammation but are generally not used for neuropathic pain. Fentanyl patches have poor data as to their efficacy in neuropathic pain, and their limited topical bioavailability makes high concentrations necessary; this presents a health hazard as patients have been known to ingest their patches instead of just using them topically. Topical amitriptyline and gabapentin present a novel way to deliver systemic medications that are known to be beneficial in a localized way. Again, there is limited data to support their topical use, but they may be useful if patients show negative systemic side effects to the oral preparations. The use of topical ketamine is relatively new. Ketamine has good skin absorption, and this delivery method seems to mitigate most CNS effects caused by IV delivery. It has poor oral bioavailability, which also lessens the chances of overdose. Botulinum toxin A works by inhibiting muscle contraction, which is thought to decrease biofeedback and muscularly induced pain.

Summary of Medical Pain Management:

Currently, IASP guideline recommendations are "first-line treatment in neuropathic pain for tricyclic antidepressants, serotonin-noradrenaline reuptake inhibitors, pregabalin, and gabapentin. A weak recommendation for use and proposal as the second-line are lidocaine patches, capsaicin high-concentration patches, and tramadol. Lastly, a weak recommendation for use and proposal as the third-line for strong opioids and botulinum toxin A. Topical agents and botulinum toxin A are recommended for peripheral neuropathic pain only."

Non-medical Treatment

Psychological Therapy:

Some level of counseling should accompany the medical management of allodynia. At a minimum, counseling should include the goals and expectations of medical therapy. Patients often hopefully but erroneously believe that medical therapy can completely alleviate their symptoms. Healthcare practitioners need to clearly communicate that the goal of medical therapy is not to completely alleviate allodynia but to decrease the pain to an acceptable level. Weekly or monthly sessions with a trained therapist can often be helpful; therapists can assist patients with learning alternate coping strategies for pain in general and work on cognitive behavioral therapy to address comorbid psychological issues that often accompany pain.

Physical Therapy:

Physical therapy has adopted several psychology techniques to help patients with neurologic pain. Most of these techniques work best on pain without a large underlying medical component, such complex regional pain syndrome (CRPS), post-amputation pain, and trigeminal neuralgia. One technique is desensitization, where a light, innocuous stimulus that does not activate a pain response is gradually increased in intensity, as the patient tolerates. Another physical therapy pain management technique, often used with CRPS and post-amputation pain syndrome is mirror therapy, where a patient sees and interacts with a mirrored image of their “good” side in place of their sensitive side. Biofeedback and exposure therapy are additional ways physical therapists can help with allodynia.

Complementary Alternative Medicine:

There is scant evidence for the efficacy of complementary alternative medicine in neuropathic pain. Cupping and acupuncture have the most study data and may be beneficial in treating different types of neuropathic pain, but additional research is needed.

Interventional Treatment:

Neuropathic pain, including allodynia, is difficult to treat. Interventional treatment may be a consideration if a patient has failed more conservative treatment. One option is the use of nerve blocks. The most common sites for nerve blocks for chronic pain are intercostal nerves and the trigeminal nerve. They can be quite effective but often are of relatively limited duration, in the order of hours to months. Spinal cord stimulators/peripheral nerve stimulators attempt to stimulate sensory and innocuous neurons enough to prevent a strong signal from reaching the thalamus, and can represent a permanent long-term solution to pain; however, they require minor surgery and implantation of an electrical device. Lastly, surgical ligation of nerves is another option and may be a permanent solution to focal allodynia, such as post-vasectomy allodynia.

Differential Diagnosis

Allodynia is a clinical symptom and not a disease. It can occur due to a known medical disorder, be the result of past trauma or injury, or present idiopathically by itself. Anything that causes neuropathy may also have an association with allodynia. Allodynia is often due to diabetes, fibromyalgia, migraine syndromes, or postherpetic neuralgia. Below is a noncomprehensive list with brief descriptions of diseases and traumas that can cause or have known associations with allodynia in alphabetical order:

Alcoholic polyneuropathy: Slow, progressive, associated with past or present alcohol use. Allodynia is often associated with other sensory abnormalities and may be caused mostly by nutritional deficiencies.

Central poststroke pain (also known as thalamic pain syndrome, also known as Dejerine Roussy syndrome): The patient will have a history of stroke. Classically, the stroke is located in the thalamus, although it can also be in other brain locations, such as the spinothalamocortical tract. Onset has been noted anywhere from 1 month to years after the initial stroke. Abnormalities in temperature sensation often accompany this condition.

Complex regional pain syndrome: Often starts with surgery or other trauma, though the instigating trauma may be mild. It can have associations with edema and changes in skin and blood perfusion. Disease progression varies widely.

Diabetes mellitus-associated allodynia (with neuralgia): Patients will have a history of diabetes, and the allodynia may or may present with accompanying sensory deficits.

Envenomation: Some animals, such as snakes and scorpions, have toxins that can cause allodynia.

Fibromyalgia: Allodynia is a hallmark of fibromyalgia, along with fatigue and nonrestorative sleep.

Medication toxicity: Chemotherapy drugs are significant contributors to medication toxicity.

Migraine-associated allodynia: Patients generally will have a history of migraine, with allodynia occurring during their attacks.

Nutritional deficiencies: There is some evidence that vitamin D deficiency can potentiate allodynia. B-vitamin deficiencies also contribute to neuropathy and allodynia and can be a driving cause behind alcoholic polyneuropathy.

Persistent post-surgical pain (also known as chronic post-surgical pain): Pain, including allodynia, persisting for months after surgery. Generally, more extensive surgeries are more likely to cause persistent post-surgical pain. Other risk factors are female gender and age.

Poisoning: Some poisons can cause allodynia. For example, ciguatera fish poisoning can cause a curious cold-induced allodynia, where cold temperature elicits burning and painfully hot sensations. A history of ingesting fish and accompanying gastrointestinal and possible cardiac signs may be present.

Post-amputation stump pain: Occurs after amputation. Unlike phantom limb pain, the pain is proximal to the amputation. Incidence can be as high as 74%, and the pain can persist for years.

Postherpetic neuralgia: Postherpetic neuralgia is a neuropathic pain that occurs after a herpes zoster rash. It can persist for years after the inciting rash.

Post-radiation pain: Patients can develop pain after radiation. The onset of pain can start anywhere between 1 to 10 years after radiation. The differential for such pain must include possible cancer recurrence.

Trigeminal neuralgia: Patients with trigeminal neuralgia have stimulus-evoked allodynia in the distribution of the trigeminal nerve. Generally, it is sharp and unilateral, although documentation exists of rare cases of bilateral trigeminal neuralgia. The pain can go into remission, or stop, or even change sides of the face with time.

Prognosis

Many different diseases can cause allodynia. It can occur with a past or present insult, be exacerbated or triggered by emotional states, or occur idiopathically. The prognosis of the allodynia will vary dramatically with the associated underlying disease. Please see the differential diagnosis section for a noncomprehensive list of the primary conditions associated with allodynia.

Complications

The course and complications of allodynia will vary depending upon the cause of allodynia. In general, allodynia often worsens over time as crisscrossed neuronal synapses make stronger connections. Allodynia can have a substantial negative impact on mental and emotional health, due to the distress caused by continual pain. Medical treatments for allodynia also have side effects, especially if the treatment involves opioids.

Deterrence and Patient Education

Patient education is critical in the treatment of allodynia, to manage the goals and expectations of medical therapy. As mentioned above, often patients hope for complete and immediate resolution of their pain, which is rarely achievable. Allodynia often becomes persistent, no matter how much medical and alternative therapy a patient receives. Healthcare practitioners need to clearly communicate that the goal of medical therapy is not to completely alleviate allodynia, but to decrease the pain to an acceptable level and to improve functioning.

Many patients erroneously believe opioids are effective for chronic neuropathic pain. Clinicians should educate patients that opioids are considered by the IASP as third-line agents for neuropathic pain as they are not very effective and can cause addiction and worsen long-term pain; the recommendation is to defer starting opioids if possible.

Enhancing Healthcare Team Outcomes

The burden of allodynia has multifactorial components, and an interprofessional healthcare team offers the best approach to management. Therapists and psychologists provide services that can ease fibromyalgia pain in adults, chronic long term pain in children and adolescents,and help in decreasing the development and severity of persistent post-surgical pain. There is Level I evidence for the benefits of psychological treatment on pain, although some types of pain are more resistant to this therapy. Physical therapy also has shown benefits in chronic regional pain syndrome and fibromyalgia (Level II evidence). Many chronic pain clinics work in an interprofessional team of doctors and nurses who assess patients and administer medications, physical therapists who provide movement and physical therapy, and psychologists and therapists, who provide psychological therapy.

Pain is the name given to nociception, which is the neural processing of injurious stimuli in response to tissue damage. Pain is caused by true sources of injury, such as contact with a heat source that causes a thermal burn or contact with a corrosive chemical. But pain also can be caused by harmless stimuli that mimic the action of damaging stimuli, such as contact with capsaicins, the compounds that cause peppers to taste hot and which are used in self-defense pepper sprays and certain topical medications. Peppers taste “hot” because the protein receptors that bind capsaicin open the same calcium channels that are activated by warm receptors.

Nociception starts at the sensory receptors, but pain, inasmuch as it is the perception of nociception, does not start until it is communicated to the brain. There are several nociceptive pathways to and through the brain. Most axons carrying nociceptive information into the brain from the spinal cord project to the thalamus (as do other sensory neurons) and the neural signal undergoes final processing in the primary somatosensory cortex. Interestingly, one nociceptive pathway projects not to the thalamus but directly to the hypothalamus in the forebrain, which modulates the cardiovascular and neuroendocrine functions of the autonomic nervous system. Recall that threatening—or painful—stimuli stimulate the sympathetic branch of the visceral sensory system, readying a fight-or-flight response.

Pain can be classified as acute or chronic, and the two kinds differ greatly.

• Acute pain usually results from a specific injury, disease, and/or inflammation. It generally comes on suddenly, for example, after physical trauma or surgery, and can be accompanied by anxiety or emotional distress. Normally, acute pain is a protective response to tissue damage resulting from injury, disease, overuse, or environmental stressors. The cause of acute pain usually can be diagnosed and treated. The pain is self-limiting, meaning it is confined to a given period of time and severity. Acute pain, however, can become chronic.
  
• Chronic pain is a medical disease that can be made worse by environmental and psychological factors. Chronic pain persists over a long period and can be challenging to manage. People with chronic pain often suffer from more than one painful condition. They also have an increased risk for developing problems with physical functioning, cognition, and emotional reactions. There may be common mechanisms that put some people at higher risk for developing multiple pain disorders. It is not known whether these disorders share a common cause.

Nociceptors

To sense pain, thousands of specialized sensory nerve cells or neurons—called nociceptors— throughout the body trigger a series of responses to a noxious (painful) stimulus. The stimulus triggers an electrical impulse that travels through nerves from the site of the injury or diseased area to the spinal cord and up to the brain. Nociceptors in the head and face relay pain signals directly to the brain stem, where pain pathways converge.

Brain Regions

One brain region that receives pain signals is the thalamus. The thalamus is a relay station that distributes sensory signals to many other brain regions, including those in the cortex—which process the nociceptive (reacting to or causing pain) information from the body and generates the complex experience of pain. This has multiple components including the: 1) sensory-discriminative aspect which helps us localize where on our body an injury has occurred, 2) affective-motivational aspect which conveys just how unpleasant the experience is, and 3) cognitive-evaluative aspect which involves thoughtful planning on how to avoid the pain.

Brain Systems

Many of the characteristics of pain have been associated with specific brain systems, although much remains to be learned. Additionally, researchers have found that many of the brain systems involved with the experience of pain overlap with the experience of basic emotions. Consequently, when people experience undesirable emotions (e.g., fear, anxiety, anger), the same brain systems responsible for these emotions also amplify the experience of pain.

Fortunately, there also are systems in the brain that help to dampen or decrease pain. For example, there are descending signals from the brain that are sent back down the spinal cord that can inhibit (block or interfere with) the intensity of incoming nociceptive signals and reduce the pain experience. One way these descending signals result in pain reduction is by releasing molecules (such as endogenous or self-produced opioids) into the spinal cord that can prevent pain signals from being relayed to the brain from the nerves outside of the brain and spinal cord (peripheral nervous system).

Neurotransmitters

Our ability to perceive pain involves intricate connections among many different brain regions. The nervous system uses a set of chemicals, called neurotransmitters, to communicate between neurons within and across these stations in the pain pathway. These chemicals are released by neurons in tiny packets (vesicles) into the space between two cells. When they reach their target, they bind to special proteins on the surface of the cells called receptors. The transmitter then activates the receptor, which functions much like a gate. The gate will either close to block (inhibitory receptor) the signal or open to send (excitatory receptor) the signal along to the next station. This is known as the gate control theory of pain.

There are many neurotransmitters in the human body and they play a role in normal function as well as in disease. In the case of nociception and pain, they act in various combinations at all levels of the nervous system to transmit and modify signals generated by noxious stimuli.

• Glutamate. Glutamate plays a major role in nervous system function and in pain pathophysiology. It heightens the process called central sensitization (see below) and contributes to making pain persist. Much attention has been given to developing molecules/drugs that block certain receptors for glutamate because of their potential in reducing pain.
• GABA. GABA (or gamma-aminobutyric acid) generally decreases or blocks the activity of neurons. Most of what is known of its role in pain is related to its function in inhibiting spinal cord neurons from transmitting signals and therefore dampening pain. Chemicals that are similar to GABA have been explored as possible analgesics, but because GABA is so widespread in the nervous system it is difficult to make a GABA-like drug without affecting other nervous system functions.
• Norepinephrine and Serotonin. Norepinephrine and serotonin dampen the incoming signals from painful stimuli from the site of the injury or inflammation. Drugs that modulate the activity of these transmitters, such as some antidepressants, are effective in treating some chronic pain conditions, likely by enhancing the availability of the transmitters through a recycling and reuse process. Serotonin receptors also are present on the nerves that supply the surface of the brain involved in migraines, and their modulation by a class of drugs called “triptans” is effective in acutely treating migraine.
• Opioids. Opioids are involved in pain control, as well as pleasure and addiction. Their receptors are found throughout the body and can be activated by endogenous opioid peptides (two or more amino acids that work together to interfere with pain signals) that are released by neurons in the brain. Enkephalins, dynorphins, and endorphins are some of the body’s own natural pain killers. Endorphins may be familiar for their role in the feeling of well-being during exercise. Opioid receptors also can be activated by morphine, which mimics the effect of our endogenous opioids. Morphine is naturally produced by the body and like similar synthetic opioids, is a very potent, but potentially addictive pain killer that is widely used for severe acute and chronic pain management. However, there is limited research suggesting that the long-term use of opioids for chronic pain is an effective pain management tool. In addition, research suggests that opioid-induced hyperalgesia (an enhanced pain response) can occur with frequent and/or long-term use of opioids, which can result in a person becoming more sensitive to pain.

Central Sensitization

Central sensitization refers to changes in the nervous system that are associated with the development and maintenance of chronic pain. When this occurs, the nervous system goes through a process called wind-up and is in a continued state of high reactivity. This persistent state of reactivity lowers the threshold for a sensation to evoke a pain response and subsequently maintains pain even after the initial injury might have healed. People who experience allodynia and/or hyperalgesia may have a heightened sensitivity to pain and touch. Allodyniaoccurs when someone experiences pain as a result of stimuli that aren’t normally painful. Hyperalgesiaoccurs when a stimulus is more painful than it should be.

The link between the nervous and immune systems also is important. Cytokines, a group of proteins found in the nervous system, are also part of the immune system—the body's shield for fighting off disease and responding to injury. Cytokines can trigger pain by promoting inflammation, even in the absence of injury or damage. After a trauma, cytokine levels rise in the brain and spinal cord and at the site of the injury. Improvements in our understanding of the precise role of cytokines in producing pain may lead to new classes of drugs that can block the action of these substances to produce analgesia.

Neural Circuits and Chronic Pain

The pain that we perceive when we have an injury or infection alerts us to the potential for tissue damage. Sometimes this protective pain persists after the healing occurs or may even appear when there was no apparent cause. This persistent pain is linked to changes in our nervous system, which responds to internal and external change by reorganizing and adapting throughout life. This phenomenon is known as neuronal plasticity, a process that allows us to learn, remember, and recover from brain injury. Following an injury or disease process, the nervous system sometimes undergoes a structural and functional reorganization that is not a healthy form of plasticity. Long-term, inappropriate, or inadequate changes in both the peripheral and central nervous system can make us hypersensitive to pain and can make it persist after injuries have healed. For example, sensory neurons in the peripheral nervous system, which normally detect noxious/painful stimuli, may alter the electrical or molecular signals they send to the spinal cord. This in turn triggers genes to alter production of receptors and chemical transmitters in spinal cord neurons, setting up a chronic pain state. Increased activity of neurons in the spinal cord, in turn enhance pain signaling pathways to the brain stem and in the brain. This central sensitization is difficult to reverse and makes pain persist beyond its protective role.

Differences in our genes highlight how differently we experience pain. Scientists believe that genetic variations can determine our risk for developing chronic pain, how sensitive we are to painful stimuli, whether certain therapies will reduce our pain, and how we experience acute and/or chronic pain. Many genes contribute to pain perception, and mutations in one or more pain-related genes account for some of the variability of pain experiences. Some people born insensate to pain—meaning they cannot feel pain—have a mutation in part of a gene that plays a role in electrical activity of nociceptors and other types of neurons. A different mutation in that same gene can cause a severe and disabling pain condition. Scientists have identified many genes involved in pain by screening large numbers of people with pain conditions for shared gene mutations. While genes play a role in determining our sensitivity to pain, they only account for a portion of this variability. Ultimately, our individual sensitivity to pain is governed by a complex interaction of genes, cognitions, mood, our environment, and early life experiences.

According to the Institute of Medicine’s (IOM) 2011 report: Relieving Pain in America (https://www.nap.edu/catalog/13172/relieving-pain-in-america-a-blueprint-for-transforming-prevention-care), women often report a higher prevalence of chronic pain than men and are at a greater risk for many pain conditions. Women also are likely to have more pain from certain diseases, such as cancer. In addition, some chronic pain disorders occur only in women while others occur predominantly in women. These include chronic fatigue syndrome, endometriosis, fibromyalgia, interstitial cystitis, vulvodynia, and temporomandibular disorders.

The IOM report notes three theories that might explain the gender differences in pain experience:

• A gender-role theory that assumes that it is more socially acceptable for women to report pain;
• An exposure theory that suggests that women are exposed to more pain risk factors; and
• A vulnerability theory proposing that women are more vulnerable to developing certain types of pain, such as musculoskeletal pain.

Of these, the vulnerability theory is best supported by scientific evidence.

According to the 2011 IOM report, cultural perspectives and identification in a specific racial or ethnic group can influence a patient’s report of pain. Initial research also indicates that healthcare providers’ expectations of a person’s pain can be influenced by race or ethnicity. People of different races/ethnicities often experience different rates of clinically painful conditions. Some research has shown that African Americans, Asians, and Hispanics demonstrate lower pain tolerance compared to Caucasians. Stereotypes also have resulted in the undertreatment of racial/ethnic minorities. Some studies suggest that there are such disparities in pain management for a variety of conditions and treatment settings. They indicate that African Americans and Hispanics are more likely to have their pain undertreated than Caucasians.

According to the 2011 IOM report, the likelihood of experiencing pain and the type of care one receives differs for children and the very old, compared to young and middle-aged adults.

Older people

Pain is the number one medical complaint of older Americans. Research suggests that more severe pain and pain that interferes with activities increases with age. Evidence also shows that older people are more vulnerable to severe or persistent pain and that the inability to tolerate severe pain also increases with age. Some of the most common causes of pain in older adults include joint pain, post-surgical pain, chronic disease, and conditions associated with aging.

Pain management in the older population differs from that in younger people. For example, older people are much more likely to experience medication-related side effects than younger people.

Children

Pain in children also requires special attention. Identifying the problem and getting a proper diagnosis can be particularly difficult because young children often are not able to describe the degree of pain that they are experiencing. Also, a child’s pain is often undertreated for various reasons, one being there are few evidence-based recommendations regarding medication-prescribing practices for children and adolescents. Although treating pain in children poses challenges to physicians and parents alike, children should never be undertreated. Specific tools and questionnaires for measuring pain in children have been developed that, when combined with feedback from parents, can help physicians select the most effective treatments.

There is no way to objectively measure pain. Only the person experiencing pain can describe how much pain he/she is feeling. After learning about a patient’s pain history and other medical concerns, a healthcare provider may conduct physical exams, clinical assessments, and order diagnostic tests and imaging to assess pain intensity and diagnose or rule out any conditions.

Healthcare providers have many approaches and technologies to help identify the cause of a patient’s pain. Primarily these include:

• A musculoskeletal and neurological examination in which the physician tests movement, reflexes, sensation, balance, and coordination.
• Laboratory tests (e.g., blood, urine, cerebrospinal fluid) can help the physician diagnose infection, cancer, nutritional problems, endocrine abnormalities, and other conditions that may cause pain.
• Electrodiagnostic procedures including electromyography (EMG), nerve conduction studies, evoked potential (EP) studies, and quantitative sensory testing measure the electrical activity of muscles and nerves. They help physicians evaluate muscle symptoms that may result from a disease or an injury to the body’s nerves or muscles. EMG tests muscle activity and identifies which muscles or nerves are affected by weakness or pain. Nerve conduction studies (usually performed along with an EMG) record how nerves are functioning. EP studies measure electrical activity in the brain in response to sight, sound, or touch stimulation. Quantitative sensory testing can establish thresholds for sensory perception which can then be compared to normal values. These tests are used to detect abnormalities in sensory function and nerve disorders.
• Imaging, especially magnetic resonance imaging or MRI, provides a look inside the body's structures and tissues, such as the brain and spinal cord. MRI uses magnetic fields and radio waves to differentiate between healthy and diseased tissue. Ultrasound imaging uses high-frequency sound waves to obtain images inside the body.
• Nerve blocks not only can treat but also can help to diagnose the cause of pain. A person’s response to a nerve block may the help provider to determine what is causing the pain or where it is coming from, since pain signals can spread throughout the body.
• Psychological assessments often are performed when assessing chronic pain. There is a high prevalence of depression, anxiety, and emotional distress associated with chronic pain (and vice versa), and often the diagnoses can be hard to separate. A provider may ask a patient to complete psychological questionnaires or ask how the person is feeling emotionally.
• X-rays produce pictures of the body's structures, such as bones and joints. Bone scans can help diagnose and track infection, fractures, or other bone disorders.

The goal of pain management is to improve function—enabling individuals to work, attend school, and participate in daily activities. The many treatment options will vary depending on the type of pain, its duration, and patient access.

The best way to prevent, assess, and treat people who experience chronic pain is the biopsychosocial treatment model. This model allows patients, healthcare providers, and caregivers to view pain as a dynamic interaction among and within the biological, psychological, and social factors unique to that individual. It provides the best foundation for tailoring the most comprehensive pain management program for each person.
Interdisciplinary treatment—which involves team members from different healthcare specialties working collaboratively to set goals, make decisions, and share resources and responsibilities—is based on the biopsychological model that is important when assisting chronic pain sufferers.

For the most part, the medications, procedures, interventions, and therapies listed below have been shown in clinical trials to help relieve or manage pain associated with a specific condition(s), but none have been proven fully effective in relieving all types of pain. Discuss with your healthcare provider which treatment, or combination of treatments, will be most effective for you and your pain condition. It is important to remember that, while not all pain is curable, all pain can be treated. Common treatments include:

Acupuncture involves the application of needles to precise points on the body to relieve pain. It is part of a category of healing called traditional Chinese medicine. Evidence of the effectiveness of acupuncture for pain relief is conflicting and clinical studies to investigate its benefits are ongoing.

Analgesic refers to the class of drugs that includes most “painkillers.” This includes classes of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen, as well as acetaminophen and opioids (which have a narcotic effect and can induce sedation and pain relief). Nonprescription or over-the-counter pain relievers are generally used for mild to moderate pain. Prescription opioid pain relievers, sold through a pharmacy under the direction of a physician, are used for moderate to severe acute pain and are usually prescribed for short periods of time.

Anticonvulsants are used to treat seizure disorders because they dampen abnormally fast electrical impulses. They also are prescribed by physicians to treat various pain conditions, particularly neuropathic pain

Antidepressants are often used to treat chronic pain and are particularly used to help manage musculoskeletal pain, neuropathic pain, and headache-related pain.

Anti-inflammatory diets (nutrition) are another approach to chronic pain management. Research suggests that some people with chronic pain can benefit from eating anti-inflammatory foods to help reduce their level of pain with limited negative side effects.

Beta-blockers are medications which inhibit one arm of the sympathetic nervous system and adrenal “fight or flight” hormones. Propranolol and timolol are used to prevent migraine headaches.

Biofeedback is used to treat many common pain problems, most notably headache and back pain. Biofeedback enables individuals to learn how to change physiological activity for the purpose of improving health and performance. The biofeedback machine provides rapid and accurate feedback that helps people become aware of, follow, and gain control over certain bodily functions, including muscle tension, heart rate, breath rate, and skin temperature. Feedback in conjunction with changes in thinking, emotions, and behavior leads to physiological changes that can be sustained over time without continued use of the biofeedback machine. Biofeedback is often used in combination with other treatment methods, generally without side effects.

Botox(botulinum toxin) is a Food and Drug Administration (FDA)-approved treatment for chronic migraines—those that last for or occur for 15 or more days a month. Botox is injected around pain fibers that are involved in headaches. Botox enters the nerve endings and blocks the release of chemicals involved in pain transmission.

Calcitonin gene-related peptide (CGRP) monoclonal antibodies are a class of FDA-approved medications to help prevent frequent migraines. Some of the new medications include Aimovig, Ajovy, and Emgality.

Chiropractic care may ease back pain, neck pain, headaches, and musculoskeletal conditions. It involves "hands-on" therapy designed to adjust the relationship between the body's structure (mainly the spine) and its functioning. Chiropractic spinal manipulation includes the adjustment and manipulation of the joints and adjacent tissues. Such care also may involve therapeutic and rehabilitative exercises. A review of numerous clinical trials to assess the effectiveness of spinal manipulations concludes that there is only low-quality evidence of their benefit for acute and sub-acute low back pain. For chronic back pain however, there is evidence of small to moderate treatment relief.

Cognitive-behavioral therapy is a well-established treatment for pain that involves helping an individual improve coping skills—pacing day-to-day activities, addressing negative thoughts and emotions that can amplify pain, and learning relaxation methods to help prepare for and cope with pain and changes in the nervous system. It is used for chronic pain, postoperative pain, cancer pain, and with transitions from acute to chronic pain.

Counseling can give an individual pain sufferer much needed support, whether it comes from family, group, or individual counseling. Support groups can provide an important supplement to drug or surgical treatment. Psychological treatment also can help people learn how to better handle physiological changes produced by pain.

Electrical stimulation, including implanted electric nerve stimulation, and deep brain or spinal cord stimulation, is the modern-day version of age-old practices in which the nerves or muscles are stimulated by heat or massage. The following techniques require specialized equipment and trained personnel:

• TENS (transcutaneous electrical stimulation) uses tiny electrical pulses, delivered through the skin to nerve fibers, to cause changes in muscles, such as numbness or contractions. This in turn produces temporary pain relief. TENS can activate subsets of peripheral nerve fibers that can block pain transmission at the spinal cord level.
• Peripheral nerve stimulation uses electrodes placed surgically or percutaneously (injected through the skin) on a peripheral nerve. The individual is then able to send an electrical current as needed to the affected nerve, using a controllable electrical generator.
• Spinal cord stimulation uses electrodes surgically or percutaneously inserted between the spine's protective covering (the dura) and the spinal column. The individual can send a pulse of electricity to the spinal cord using an implanted electrical pulse generator that resembles a cardiac pacemaker.
• Deep brain stimulation is considered a more extreme treatment and involves surgical stimulation of the brain, usually the thalamus or motor cortex. It treats chronic pain in cases that do not respond or have stopped responding to less invasive or conservative treatments.
• Exercise also may be part of the pain treatment regime for most people with pain. A physician or physical therapist can recommend an appropriate routine. Participation in some form of exercise, physical activity, and stretching may help individuals with pain better manage their symptoms, handle daily activities, and maintain flexibility and muscle strength. Exercise, sleep, and relaxation can all help reduce stress, thereby helping to alleviate pain. Supervised exercise has been proven to help many people with low back pain.

Hypnosis, in general, is used to control physical function or response—that is, the amount of pain an individual can withstand. How hypnosis works is not fully understood, and there is limited research suggesting its effectiveness. Some believe that hypnosis enables individuals to improve their ability to concentrate and/or relax.

Injectionsare sometimes used to deliver pain relief medication locally.

• Facet injections target the facet joints (small stabilizing joints in the spine between and behind vertebrae). A person may get pain relief from the local anesthetic and may notice longer lasting relief starting two to five days after injection.
• Steroid injections work by decreasing inflammation and reducing the activity of the immune system. Injecting steroids into one or two local areas allows doctors to directly deliver a high dose of medication.
• Sacroiliac joint injection is used to diagnose the source of a person’s pain, as well as to provide therapeutic pain relief associated with sacroiliac joint dysfunction. The injection provides pain relief by reducing inflammation within the joint.
• Trigger point injections involve injecting a small amount of local anesthetic, sometimes with a steroid medication, directly into a painful trigger point (a specific site on the muscles that causes pain when pressed during an exam).

Low-power lasers have been used by some healthcare providers as a treatment for pain. This low intensity light therapy (not thermal) triggers biochemical changes within cells and may have an effect on pain, inflammation, and tissue repair, but this method is considered controversial.

Marijuana (cannabis) continues to remain highly controversial as a medical treatment to manage pain. Scientific studies are underway to test the safety and usefulness of cannabis for treating different medical conditions. Although marijuana has not been approved for any medical use at the federal level, several states and the District of Columbia permit the use of medical marijuana as a treatment.

• Marinol is an FDA-approved medication with the active ingredient dronabinol, a synthetic form of tetrahydrocannabinol (THC) used to treat chemotherapy-induced nausea and vomiting. Initial research has found that Marinol was no more effective than placebo for post-surgical and nerve-related pain, and only slightly more effective than placebo for chronic non-cancer pain.

Muscle relaxants are used to relax and reduce tension in muscles. Muscle relaxants are not a class of drugs, which means that they do not all have the same chemical structure or work the same way in the brain. The term “muscle relaxers” describes a group of drugs that act as central nervous system depressants and have sedative properties for musculoskeletal pain.

• Anxiolytics include medications in the class of benzodiazepines, used to decrease central nervous system activity. These drugs can act as muscle relaxants and are sometimes used to manage anxiety.

Nerve blocks use drugs, chemical agents, or surgical techniques to interrupt the relay of pain messages between specific areas of the body and the brain. Nerve blocks may involve local anesthesia, regional anesthesia or analgesia, or surgery, and are routinely used for traditional dental procedures. Nerve blocks also can be used to prevent or even diagnose pain and may involve injection of local anesthetics to numb the nerve and/or steroids to reduce inflammation.

A local nerve block may use one of several local anesthetics such as lidocaine or bupivacaine. Peripheral nerve blocks involve targeting a nerve or group of nerves that affect a part of the body. Nerve blocks also may take the form of what is commonly called an epidural, in which a drug is administered into the space between the dura and the spinal column. This procedure is best known for its use during childbirth. However, it is also used to treat acute or chronic leg or arm pain due to an irritated spinal nerve root.

• Neurolytic blocks employ injection of chemical agents such as alcohol, phenol, or glycerol, or the use of radiofrequency energy, to kill nerves responsible for transmitting nociceptive signals. Neurolytic blocks are most often used to treat cancer pain or pain in the cranial nerves.
• Sympathectomy, also called sympathetic blockade, typically involves injecting local anesthetic next to the sympathetic nervous system (involved with regulating heart rate, breathing, blood pressure, and response to stressful or dangerous situations). The procedure is often performed to treat neuropathic pain of a limb (e.g., complex regional pain syndrome) as well as vascular disease pain and other conditions.
• Surgical blocks are performed on cranial, peripheral, or sympathetic nerves. They are most often used to relieve cancer pain and extreme facial pain, such as that experienced with trigeminal neuralgia. There are several types of surgical nerve blocks and they are not without problems and complications. Nerve blocks can cause muscle paralysis and, in many cases, result in partial numbness. For that reason, the procedure should be reserved for a select group of individuals and should only be performed by skilled surgeons. Types of surgical nerve blocks include:
  • Spinal dorsal rhizotomy, in which the surgeon cuts the root or rootlets of one or more of the nerves radiating from the spinal cord. Other rhizotomy procedures include cranial rhizotomy and trigeminal rhizotomy, performed as a treatment for extreme facial or cancer pain.

Physical therapy and rehabilitation may help to decrease pain and improve mobility. by increasing function, controlling pain, and aiding recovery. Individuals may engage in a number of physical therapy treatments simultaneously. A few of the most common forms (in addition to exercise, electrical stimulation, and ultrasound) are:

• Traction sometimes is used to decrease pain and improve mobility in the spine.
• Joint mobilization can occur when a physical therapist passively moves the joints of the body in specific directions to help decrease pain and improve mobility.
• Heat and ice are often used in physical therapy. Heat can increase circulation to the injured tissues, relax the muscles, and provide pain relief. Ice typically is used to help decrease pain and control inflammation.
• Kinesiology taping uses a flexible tape to support body parts and muscles to reduce bruising/swelling and provide pain relief.

Placebos are defined as substances without any therapeutic effect that are typically used as a control factor in clinical studies to determine the effectiveness of a medical treatment. Placebos are inactive substances, such as sugar pills, or harmless procedures such as saline injections, and may be prescribed more for the psychological benefit to the patient than for any physiological effect. Placebos, however, do offer some individuals pain relief. Although placebos have no direct effect on the underlying causes of pain, evidence from clinical studies suggests that many conditions such as migraine headache, back pain, post-surgical pain, rheumatoid arthritis, angina, and depression sometimes respond well to them. This is known as the placebo response, which is defined as the observable or measurable change that can occur after administration of a placebo. One significant component responsible for the effect of placebo is the degree to which people expect the treatment to work. Placebos work in part by stimulating the brain's own analgesics.

Relaxation and mindfulness are ways for people to respond to the physical sensation of pain, which can have a major impact on how the body’s nervous system creates and perceives pain. An individual’s automatic reactions to pain, often unconsciously, can amplify the pain-generating activity of the nervous system. Relaxation strategies (e.g., imagery, progressive muscle relaxation, autogenic relaxation) and mindfulness techniques (e.g., exercises that help the individual observe physical, cognitive, and emotional reactions and make skillful choices to relieve pain) are evidence-based practices to help shift the nervous system back toward a normal non-pain state.

R.I.C.E.—Rest, Ice, Compression, and Elevation—are four components prescribed by many orthopedists, coaches, trainers, nurses, and other professionals for temporary muscle or joint injuries, such as sprains or strains.

Radiofrequency ablation (RFA)uses an electrical current produced by a radio wave to heat up a small area of nerve tissue, thereby decreasing pain signals from that specific area. The degree of pain relief can vary depending on the cause and location of the pain. Some individuals can experience pain relief for up to 6-12 months.

Serotonergic agonists—the triptans (including sumatriptan, naratriptan, and zolmitriptan)—are used specifically for acute migraine headaches because they block pain pathways in the brain. Taken as pills, shots, or nasal sprays, they can relieve many symptoms of migraine.

Surgery may be recommended for some people with pain that significantly impacts their daily functioning. Surgery may be considered when less invasive treatments have not been helpful. However, surgical procedures are not always successful and may not be appropriate for all people.

Topical pain creams/gels are sprayed on or rubbed into the skin over painful muscles or joints. Although they are all designed to relieve pain, they have different ingredients. Topical pain creams and gels (e.g., compounded pain creams to treat specific pain) are sometimes prescribed by a physician, while others can be bought over the counter. There is limited evidence about the effectiveness of such creams. Below are the most common ingredients in products available without a prescription.

• Capsaicin (pronounced cap-SAY-sin) is a chemical found in chili peppers and is also a primary ingredient in prescription or over-the-counter pain-relieving creams as a treatment for several pain conditions, including shingles. This topical cream may be helpful for deep pain. It works by reducing the amount of substance P—a compound thought to be involved in the synaptic transmission of pain and other nerve impulses—that is found in nerve endings and interferes with the transmission of pain signals to the brain. Individuals can become desensitized to the compound, however, perhaps because of long-term capsaicin-induced damage to nerve tissue. Some people cannot tolerate the burning sensation they experience when using capsaicin cream.
• Counterirritants include ingredients such as menthol, methylsalycylate (oil of evergreen), and camphor. They are called counterirritants because they create a burning or cooling sensation that distracts the person from the pain.
• Salicylates are the same ingredients that give aspirin its pain-relieving quality and are found in some creams. When absorbed into the skin, they may help with pain, particularly in joints close to the skin, such as fingers, knees, and elbows.