Allodynia

What It Is, Causes, Signs and Symptoms, and More

Author: Emily Miao, PharmD
Editor: Alyssa Haag
Editor: Lily Guo
Editor: Kelsey LaFayette, DNP
Illustrator: Jessica Reynolds, MS
Copyeditor: David G. Walker
Modified: Mar 11, 2024

What is allodynia?

Allodynia, a form of neuropathic pain, is a clinical symptom in which an individual experiences pain or discomfort in response to a stimulus that does not usually provoke pain. Individuals with allodynia may have heightened sensitivity and pain responses to various sensory modalities, including light touch, pressure, pinprick, and temperature. Allodynia can be associated with various medical conditions, including migraines, trigeminal neuralgia (i.e., a chronic pain condition affecting the trigeminal nerve in the face), and fibromyalgia (i.e., a chronic pain condition characterized by widespread pain, tenderness, and sensitivity to pressure).
An infographic detailing the causes, signs and symptoms, diagnosis, and treatment of Allodynia

What causes allodynia?

While the exact etiology of allodynia is poorly understood, it is hypothesized that allodynia is either caused by a dysfunction in neural networks of the nervous system (i.e., central sensitization), nerve damage (e.g., diabetic neuropathy, postherpetic neuralgia), inflammatory conditions (i.e., rheumatologic conditions can cause widespread inflammation, affecting nerve function), complex regional pain syndrome (i.e., a chronic pain syndrome that develops following an injury or prolonged illness), nutritional deficiency (e.g., vitamin B12), or iatrogenic (e.g., medication-induced).

Central sensitization is a neurologic phenomenon in which the central nervous system (i.e., brain and spinal cord) excessively amplifies signals, resulting in hypersensitivity to painful stimuli. The persistent transmission of nociceptive (or pain) signals results in cortical reorganization in sensory and motor regions of the brain and increases the risk of development of chronic pain syndromes, such as fibromyalgia and trigeminal neuralgia. Medication-induced allodynia can also occur, and some medications known to cause neuropathic pain include chemotherapy agents (e.g., carboplatin or cisplatin), antibiotics (e.g. fluoroquinolones), and diabetes medications (e.g., metformin).

There are several subtypes of allodynia, including mechanical allodynia, which is characterized by the perception of pain in response to mechanical stimuli and movement (e.g., clothing rubbing against skin);  tactile allodynia, which occurs with light pressure or touch on the skin; and thermal allodynia, which occurs with hot or cold temperatures. 

What are the signs and symptoms of allodynia?

Signs and symptoms of allodynia include the perception of pain or discomfort in response to typically non-painful stimuli, including light touch, gentle pressure, or mild temperature fluctuations. For example, individuals may experience pain with different textures of clothing brushing against the skin or lightly stroking the skin. 

How is allodynia diagnosed?

Diagnosis of allodynia begins with a thorough medical history and physical examination. Allodynia is a clinical symptom; therefore, “nerve pain” may be the primary chief complaint. It is important to ask about provoking and alleviating factors, the quality, temporality, duration, and location of the nerve pain. Other pertinent information includes medication history and whether the individual has a history of cancer (i.e., chemotherapy), diabetes mellitus, hypertension, stroke, rheumatologic conditions, or trauma as they can all cause allodynia. A thorough neurological examination should be performed to identify the area of hypersensitivity, which can include testing for light touch (e.g., monofilament testing), temperature (e.g., using ice in a glove), and vibration (e.g., tuning fork) in the affected area in addition to reflex, motor, and strength testing. 

Laboratory blood tests may help identify underlying nutritional deficiencies (e.g., vitamin B12), evidence of inflammation in rheumatologic conditions (e.g., ESR, CRP), and diabetes mellitus (e.g., hemoglobin A1c). Imaging is not required for diagnosis; however, magnetic resonance imaging (MRI) can help rule out the possibility of acute or chronic stroke. Similarly, neuronal function testing is not necessary but can help test for sensory neuronal conduction abnormalities. These include electromyography (EMG) (i.e., which involves placing electrodes onto the skin or in muscle fibers to measure muscle activation) and quantitative sensory testing, which uses a device that applies thermal stimuli to the skin and uses data to plot a graph of the individual’s pain perception and thresholds. 

How is allodynia treated?

Treatment of allodynia is aimed at slowing or reversing the progression of the underlying condition or etiology and also includes pharmacologic and non-pharmacologic options for addressing nerve pain. For example, if an individual experiences allodynia or peripheral neuropathy due to advanced progression of diabetes mellitus, the treatment also includes tighter glucose control. If a vitamin B12 nutritional deficiency is suspected, adequate supplementation may potentially reverse the symptoms. Additionally, if allodynia is secondary to a rheumatologic condition (e.g., rheumatoid arthritis or systemic lupus erythematosus), then it is important to control the underlying condition, such as using corticosteroids for acute flares and disease-modifying agents (i.e. methotrexate) and tumor necrosis factor receptor inhibitors (i.e., adalimumab, etanercept, and infliximab) for maintenance therapy.

A combination of topical (e.g., gels, creams, patches) and oral pharmacologic agents can be used to treat allodynia. Topical agents, including local anesthetics (e.g., lidocaine) or capsaicin, a compound derived from chili peppers that block pain receptors, may be used. Oral options such as antiepileptic calcium channel blockers (e.g., gabapentin) and sodium channel blockers (e.g., carbamazepine) which decrease neuronal firing; antidepressants, including serotonin-norepinephrine reuptake inhibitors (SNRIs) (e.g., duloxetine, milnacipran); and tricyclic antidepressants (e.g., nortriptyline, doxepin, imipramine) have also shown to demonstrate analgesic effects. The efficacy of opioid analgesics for allodynia and neuropathic pain is controversial; therefore, the aforementioned options are typically trialed before considering opioids

Non-pharmacologic options include cognitive behavioral therapy (CBT), mind-body strategies, and physical therapy. CBT and mind-body strategies are psychosocial interventions aimed at helping individuals understand their own behaviors and motivations and help the individual gain coping skills for their pain. Physical therapy using desensitization techniques can also provide pain relief. Desensitization techniques are used to modify the sensitivity of the affected area to a particular stimulus and normalize the body’s response to particular sensations. 

What are the most important facts to know about allodynia?

Allodynia, a type of neuropathic pain, is a clinical symptom in which an individual experiences pain or discomfort in response to a stimulus that does not usually provoke pain. Individuals with allodynia may have heightened sensitivity and pain responses to various sensory modalities, including light touch, pressure, pinprick, and temperature. There are several types of allodynia, including mechanical allodynia, tactile allodynia, and thermal allodynia. The exact etiology of allodynia is poorly understood; however, it is hypothesized that it is either caused by central sensitization, nerve damage, inflammatory conditions, complex regional pain syndrome, nutritional deficiency, or iatrogenic causes. Diagnosis is made clinically using a thorough medical history, physical examination, and laboratory tests and diagnostics to aid in identification of any underlying condition. Management includes treating the underlying cause as well as a combination of topical and oral pharmacologic agents (e.g., topical lidocaine, capsaicin, antidepressants, anticonvulsants) and nonpharmacologic modalities (e.g., psychosocial interventions and physical therapy). 

References


Colloca L, Ludman T, Bouhassira D, Baron R, Dickenson AH, et al. Neuropathic pain. Nat Rev Dis Primers. 2017;3:17002. doi: 10.1038/nrdp.2017.2


Finnerup NB, Attal N, Haroutounian S, et al. Pharmacotherapy for neuropathic pain in adults: A systematic review and meta-analysis. Lancet Neurol. 2015;14(2):162-73. doi:10.1016/S1474-4422(14)70251-0


Finnerup NB, Haroutounian S, Kamerman P, et al. Neuropathic pain: An updated grading system for research and clinical practice. Pain. 2016;157(8):1599-1606. doi:10.1097/j.pain.0000000000000492


Jensen TS, Finnerup NB. Allodynia and hyperalgesia in neuropathic pain: Clinical manifestations and mechanisms. Lancet Neurol. 2014;13(9):924-35. doi:10.1016/S1474-4422(14)70102-4

Woolf CJ. Central sensitization: Implications for the diagnosis and treatment of pain. Pain. 2011;152(3 Suppl):S2-S15. doi:10.1016/j.pain.2010.09.030
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