Allodynia: what is it, causes, treatment, prognosis, complications

What is allodynia?

Official definition allodynia at the time of this writing, "pain due to stimuli that usually do not cause it." An example would be a light touch of a feather that causes pain when it should only cause sensation. Allodynia is different from hyperalgesia, which is an exaggerated response to a usually painful stimulus, although both can and often coexist. Both states are types neuropathic pain.

An example of the difference between allodynia and hyperalgesia on physical examination is rubbing a cotton swab gently against the patient's skin. A light touch of the tampon to the skin will cause mild irritation, but no pain response. A patient who is in pain from an irritant that should only cause sensation may have allodynia. If the doctor increases the pressure significantly, some pain will be part of the normal response. A patient who feels severe pain will have hyperalgesia. Thus, on physical examination, allodynia manifests itself as a decrease in the pain threshold, and hyperalgesia as an increase in the reaction. Although this often means that allodynia and hyperalgesia seem to coexist with the same continuum of stimuli on physical examination, there is still a clear difference in modalities. In allodynia, the response to a stimulus differs from those with normal sensations, while in hyperalgesia, the response to the stimulus is the same as in those who have normal sensations, but it exaggerated.

Allodynia may result from an underlying medical condition such as neuropathic tactile allodynia caused by diabetes, or may be the primary process of the disease itself, for example, in postherpetic neuralgia. It is often further classified by the type of stimulus that induces nociception, such as tactile, thermal, dynamic or static allodynia, or at the main site of nociception, such as cutaneous allodynia.

Causes

The exact etiology of allodynia is unknown. Allodynia is the phenomenon of a painless stimulus that causes a sharp painful reaction, which means an error in neuronal conduction. The mechanism of this error is unclear. The most compelling evidence available suggests that sensory neuronal fibers can stimulate pain pathways, possibly due to an error in long-term potentiation. However, there are studies that suggest that surface sensory components may also have participation, as well as evidence that various mental conditions can influence the perception of allodynia. If we use the crossed fibers analogy, the actual arrangement of the crisscrossing fibers is can vary and can be located almost anywhere on the periphery of the central nervous system systems. Allodynia can affect both the peripheral nervous system and the central nervous system via sensitization, and the mechanism underlying inappropriate pain sensation may over time develop.

A painless stimulus, such as lightly touching the skin, should only activate low-threshold A-beta fibers. In cutaneous allodynia, these A-beta fibers then also bind and activate pain pathways through other types sodium channels than 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 thalamic pain after stroke, the intersection of neurons can occur as high as in the cerebellum ..

Thus, many types of peripheral nerve fibers communicate and travel along various pathways in the central nervous system. Type A nerve fibers are myelinated. They are further subdivided into alpha fibers, which are mainly responsible for proprioception, beta fibers that transmit light touch and delta fibers that carry both pain and temperature sensations. There are also unmyelinated type C nerve fibers that carry sensations of aching pain as well as fever and itching.

Epidemiology

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

- Fibromyalgia.

Fibromyalgia affects 0.5% to 5% of people in general, with different ranges in different countries. Known risk factors for fibromyalgia include age, lupus erythematosus and rheumatoid arthritis. Research shows that women are 2-9 times more likely to be diagnosed with fibromyalgia than men; however, this may have more to do with clinical bias than simply meeting the criteria for fibromyalgia. A recent study of patients with rheumatoid arthritis, which used a rigorous criteria-based scoring system to diagnose fibromyalgia, found that 58% of patients were women. Some studies also support that stress, obesity and family history are risk factors.

- Trigeminal neuralgia.

Trigeminal neuralgia affects 0.01% to 0.02% of the general population. In women, trigeminal neuralgia is diagnosed 1.5-3 times more often than in men. Age is an important factor, with most trigeminal neuralgia occurring after age 40.

- Diabetic neuropathic pain.

Diabetes affects about 10% of people, and this figure increases by about 5% annually. At least 10% (and some sources estimate 100%) of people with diabetes will develop neuropathic pain. Neuropathic pain can include allodynia, hyperalgesia, or other types of pain such as electric shock or burning sensation. The severity of neuropathic pain often does not correlate with the degree of sensory deficit, making it a primary disease rather than a secondary symptom due to neuronal damage. There are no gender differences in the development of diabetic neuropathic pain.

- Allodynia associated with migraine.

Prevalence of cutaneous allodynia among sufferers migraine is about 65%, although according to some estimates it is higher. Severe cutaneous allodynia can occur in about 20% of migraine sufferers.

Diagnostics

Allodynia is a symptom, not a disease. This may be the patient's main complaint, but it is important to do further research to determine the painful process that causes allodynia.

First, one should ask when and how allodynia began. There is often a triggering event such as chemotherapy, herpes, or injury. Sources suggest that allodynia may develop more abruptly, as in trigeminal neuralgia, or may develop more subtly, as in diabetes-related allodynia. Careful medical, surgical and family history is also needed, especially with respect to cancer, diabetes, hypertension, strokes, migraines, rheumatological history, trauma, extreme stress and opioid anamnesis.

- Physical examination.

On physical examination, allodynia is often accompanied by less stimulus than hyperalgesia. It is important to have a complete neurologic examination; it includes light touch, temperature and proprioceptive sensory tests, and motor and strength tests. For comparison, it is very important to check the “unaffected” side, even if the alleged allodynia is present on only one side. It is also important to check all four limbs, especially if allodynia appears to be progressing from distal to proximal areas.

- Analyzes.

Blood tests:

CBC and baseline metabolic panel often help with supplementation ESR and CRP if concomitant rheumatologic disease is suspected. Glycated hemoglobin can be helpful in diagnosing diabetes. B12, thiamine, and TSH can also help diagnose other causes of neuropathy.

Visualization:

Imaging is usually not required for this diagnosis. A CT scan of the head may be helpful in older patients with a high suspicion of stroke. Likewise, an MRI of the brain can help diagnose multiple sclerosisif the clinical picture raises serious suspicions.

- Tests of neuronal function.

Formal tests of neuronal function are not needed to diagnose allodynia or disorders associated with the disorder. They are most useful for quantifying the effectiveness of treatments and conducting research. There are several methods for testing sensory neuronal conduction. These tests usually require referral to specialist clinics, but are summarized below:

Quantitative sensory testing:

Quantitative sensory testing, or QST, is commonly used to test delta and type C fibers. The method exposes the skin to thermal irritants in stages. Plastic monofilaments, needles and vibrometers can be used to examine light touch, pain and vibration, but these methods are often secondary to its ability to isolate the response of type C fibers to thermal irritants.

This test creates a graph with individual perception and pain threshold. It also aims to test small, unmyelinated C fibers that are more difficult to isolate during routine physical examination. However, it still relies on patient participation in the assessment of pain and sensation.

Neural conduction studies:

Neural conduction studies - a type of neurophysiological method that measures time and quality electrical impulse when it passes from the place of stimulation of the neuron to the place of registration of the same neuron. They are often performed on motor neurons in conjunction with electromyography (EMG) to assess motor neuron function. The same applies to sensory neurons. Note that standard neural conduction studies usually stimulate the nerve directly. In addition, standard neural conduction studies only test beta fibers as they have lower thresholds than delta fibers; it directly tests the fiber, but only on a short stretch of the neuron.

Somatosensory evoked potentials:

Somatosensory evoked potentials (ERPs) measure the electrical activity of the brain following a somatosensory stimulus from beta fibers. SSEP evaluates the state of the neuron as a whole and is often useful if you suspect possible problems with the conduction of the central nervous system, for example, in patients with multiple sclerosis or spinal cord injury, and in the neurosurgical operating room for prevent injury.

Laser thermal pulses and contact thermal potentials:

These potentials work similarly to somatosensory evoked potentials. Instead of sensory stimulus, laser-generated heat pulses and contact heat-induced potentials use lasers and heating instruments to test the perception of heat pain, thereby measuring delta fibers.

Skin biopsy:

Perforated skin biopsy allows for quantitative measurement of small neurons. After biopsy, samples are stained to determine the density of intraepidermal nerve fibers by comparing the measured density with a standard.

Electromyography:

Electromyography involves placing electrodes on the skin or in muscle fibers to measure muscle activation. EMG is useful for distinguishing between muscle and neuronal weakness on efferent motor neurons, but not for measuring sensory neuron deficits. EMG is an option if there is concern about motor neuron degeneration. Although EMG does not directly assess nociceptive pathways, it often helps distinguish the sites of neuropathy and assess whether neuropathy has a motor neuron component.

Treatment

- Drug therapy.

Oral medication:

Sodium channel blockers, calcium channel antagonists, and anticonvulsants increase the arousal threshold and are usually effective in the treatment of allodynia and neuropathic pain. Antidepressants such as serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants (TCAs) also appears to help with some types of neuropathic pain, although the evidence is stronger for hyperalgesia than for allodynia. However, selective serotonin reuptake inhibitors (SSRIs) have produced mixed and disappointing results and are not recommended for the treatment of allodynia. A recent Cochrane review found no conclusive evidence for the use of non-steroidal anti-inflammatory drugs (NSAIDs) with neuropathic pain.

Opioids are quite effective in treating pain in general; however, they are not as effective in treating neuropathic pain, and there is only very low quality evidence that oxycodone is helpful in treating neuropathies. In addition, opioids themselves have many potential side effects and can even cause long-term neuropathic pain. There are several strong proponents of cannabis medicines. A recent Cochrane review found minimal evidence of benefits and concluded that on based on current research, the potential side effects of cannabis may outweigh it Benefits. However, he also acknowledged that there is not much research available.

Local application of medicines:

Topical medications seem to help with some 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 are highly concentrated because they do not pass through the skin. Topical menthol works by first activating and then desensitizing nociceptors and can cause cold allodynia. Recent Cochrane research papers have found no good quality randomized controlled trials to support the use of topical lidocaine and topical menthol for neuropathic pain, although many small studies report some efficacy of these funds. The strongest capsaicin cream available on the shelves is 0.1%. A prescription patch with 8% capsaicin is also available, but its use requires careful monitoring in a hospital setting due to the potential for adverse reactions. In a recent Cochrane article, it was found that capsaicin at a high concentration (8%) caused greater pain relief compared to a control or low dose of capsaicin.

Other topical medications include salicylates, fentanyl patches, amitriptyline, gabapentin, and ketamine. Botulinum toxin A (Botox injections) has also been used for peripheral pain. Salicylates can help with underlying inflammation, but are not commonly used for neuropathic pain. Fentanyl patches do not have sufficient data on their effectiveness in neuropathic pain, and their limited local bioavailability requires high concentrations; this is a health hazard as patients are known to swallow their patches frequently instead of just using them topically. Topical amitriptyline and gabapentin represent a new method of delivering systemic drugs that are known to be useful locally. Again, there is limited data to support their topical use, but they can be helpful if patients exhibit negative systemic side effects of oral medications. The use of topical ketamine is relatively recent. Ketamine is well absorbed by the skin and this delivery method appears to mitigate most of the effects on the central nervous system caused by intravenous administration. It has low oral bioavailability, which also reduces the likelihood of overdose. Botulinum Toxin A works by inhibiting muscle contraction, which is believed to reduce biofeedback and muscle pain.

- Non-drug treatment.

Psychological therapy:

A certain level of counseling should accompany the treatment of allodynia. At a minimum, counseling should include goals and expectations for medical therapy. Patients often hope, but mistakenly, believe that drug therapy can completely relieve their symptoms. It should be made clear to practitioners that the goal of drug therapy is not to completely alleviate allodynia, but to reduce pain to an acceptable level. Weekly or monthly sessions with a trained therapist can often be helpful; therapists can help patients explore alternative pain management strategies in general and work on cognitive behavioral therapy to address comorbid psychological problems that often accompany pain.

Physiotherapy:

Physiotherapy uses several psychological methods to help patients with neurological pain. Most of these methods work best for pain without a significant medical component. such as complex regional pain syndrome (CRPS), post-amputation pain and trigeminal neuralgia nerve. One of the methods is desensitization, in which the intensity of a light, harmless stimulus that does not activate the pain response gradually increases as the patient endures. Another physiotherapeutic method of pain relief often used for CRPS and post-amputation pain syndrome is mirror therapy in which the patient sees and interacts with a mirror image of his “healthy” side instead of the sensitive side sides. Biofeedback and exposure therapy are additional ways that physical therapists can help with allodynia.

Complementary Alternative Medicine:

There is very little evidence for the effectiveness of complementary alternative medicine for neuropathic pain. Cupping and acupuncture have the most research data and may be useful in treating various types of neuropathic pain, but more research is needed.

Interventional treatment:

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

Forecast

Allodynia can be caused by many different medical conditions. It can arise from past or present disturbances, be exacerbated or triggered by emotional states, or be idiopathic. The prognosis for the development of allodynia will vary dramatically depending on the underlying underlying disease.

Complications

The course and complications of allodynia depend on the cause of the allodynia. In general, the condition often worsens over time as crossed neuronal synapses create stronger connections. Allodynia can have a significant negative impact on mental and emotional health due to the stress of constant pain. Drug treatment for allodynia also has side effects, especially if the treatment involves opioids.