We would like to express our appreciation to Dr. Roger Goucke for the invaluable input, suggestion, and language editing of the manuscript.
Pain has recently been redefined as “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.” Pain is not only an undesirable experience, but also is associated with many consequences, including lower patient satisfaction, delayed recovery from surgery, and increased perioperative mortality and morbidity. Moreover, a prolonged period of pain can lead to long-term detrimental effects on quality of life, psychological and social function, and the economy.
Even though pain can cause the aforementioned consequences, improper pain management can lead to even more harmful complications such as an overdose or death from opioids as evidenced by the opioid crisis in some countries. , Pain is the most common reason that patients seek medical care, and the surgeon will encounter various types, both in the outpatient and inpatient setting. Thus, a fundamental understanding of pain management is an essential part of education for all surgeons, including otolaryngologists.
This chapter will describe the pain conditions that can be commonly found in the otolaryngologist’s practice from acute perioperative pain, chronic noncancer pain, and chronic cancer pain.
Acute perioperative pain in otolaryngology
In the United States, more than 50 million inpatient operations are performed annually; however, less than half of these patients report adequate postoperative pain relief.
Inadequate pain control causes physiological changes in multiple systems and can lead to delayed recovery, morbidity, and mortality as follows:
Cardiovascular system: increased sympathetic output, increased blood pressure, heart rate and myocardial oxygen demand, and cardiac arrhythmias
Respiratory system: increased risk for atelectasis, pneumonia, and respiratory failure secondary to splinting
Gastrointestinal system: increased postoperative ileus
Nervous system: increased risk of postoperative delirium, increased risk of chronic postsurgical pain
Endocrine system: increased cortisol levels, elevated blood glucose, sodium and water retention, and protein catabolism
Immune system: immunosuppression and increased risk of postoperative infection, increased potential for cancer recurrence
Hematological system: increased risk for deep vein thrombosis due to immobilization
Magnitude of pain in otolaryngology surgery
Otolaryngology surgery can be associated with a variable degree of postoperative pain. A study showed groups of patients who underwent otolaryngology surgery have a 48%–58% incidence of moderate-to-severe pain after surgery in the oral region, pharynx, larynx, neck, and salivary glands, 4–10 times higher than when compared to ear surgery. Moreover, contrary to the general understanding that endoscopic procedures are quite painless, they have been associated with a 30%–35% incidence of moderate to severe pain on postoperative day zero.
The type of surgery is not the only predicting factor for the degree of acute postoperative pain. Besides the operative site, preoperative pain and pain catastrophizing (an exaggerated negative mental set brought to bear during an actual or anticipated painful experience) are independent risk factors of moderate-to-severe pain after surgery.
Management of perioperative pain
Pain assessment and measurement
The first step of successful pain management is the recognition and assessment of pain (RAT model; recognition, assess, and treat). The recognition starts from understanding the high incidence of pain and asking or noticing if the patient has pain, especially during the perioperative period (recognition). Recording pain intensity as “the fifth vital sign”—originally intended to improve recognition and acute pain management—contributed to unrealistic goals, such as being pain-free and excessive opioid use leading to overdoses, deaths from opioids, and the opioid crisis in North America. In 2018, the USA Joint Commission on Accreditation of Healthcare Organizations (JCAHO) implemented new and revised pain assessment and management standards, by focusing more on the impact of pain on patients’ physical function, rather than pain intensity.
Pain assessment should be obtained from a thorough medical history and physical examination, pain history, functional impact, and adverse effects of treatment. Pain history can be obtained by the acronym PAIN: place (site of pain), amplitude (intensity), intensifier, and nullifier. At the end of taking the history, physicians should have a clear understanding of the type of pain, pain intensity, and individual physical and psychological factors contributing to the pain to determine a treatment plan.
Types of pain
There are many ways to classify pain (acute/chronic, cancer/noncancer, nociceptive/neuropathic). However, classifying by pathophysiology into nociceptive and neuropathic will help the clinician choose from the correct group of medications for treatment. The differences between nociceptive and neuropathic pain are shown in Table 2.1 .
|Pain that arises from nonneural tissue and is due to the activation of nociceptors
|Pain caused by a lesion or disease of the somatosensory nervous system
|Acute: fracture, incisional pain
Chronic: bone metastasis
|Acute: nerve injuries, stump pain
Chronic: chronic postsurgical pain
|Dull aching pain
|Sharp shooting pain
Numbness, hyperalgesia, allodynia
|Acetaminophen Nonsteroidal anti-inflammatory drugs (NSAIDs)
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
Contrary to a general understanding that nociceptive pain is the exclusive type of pain in acute postoperative pain, acute postoperative pain can be a mixed component of nociceptive and neuropathic pain. Additionally, the concept of mixed pain has been studied in many chronic pain conditions, which were previously recognized as purely nociceptive pain. The prevalence of neuropathic pain in chronic low back pain is 20%–55% and 19%–39% in cancer pain.
As acute postoperative pain is mixed pain by nature, neuropathic pain medications such as gabapentinoids also have roles in acute postoperative pain. However, the high dose of gabapentinoids can be associated with sedation, and specific studies of gabapentinoids for otolaryngologic surgery are still limited. Finally, because opioids can alleviate both acute nociceptive and neuropathic pain, opioids have been popular analgesics in the acute pain setting (but not recommended as the first line for chronic noncancer pain).
The pain intensity or severity will determine the strength of treatment, according to the analgesic ladder. Many pain measurement tools have been applied in clinical practice. However, self-reporting tools such as the Visual Analog Scale or Verbal Numerical Rating Scale (0–10 or 0–100) are the gold standard measurement of pain intensity and are most commonly used. Typically, the pain scale from 0 to 10 is classified into mild (0–3), moderate (4–6), or severe (7–10) pain.
There is little evidence that one pain assessment tool is superior to others. However, for certain patient populations where self-report is difficult or impossible, adapted scales or behavioral tools may be used instead. Examples of pain measurement tools for these specific populations include
Face, Legs, Activity, Cry, Consolability Scale for children ages between 1 and 6 years old (However, Face Pain Scale, which provides images from smiling to crying faces for the children to choose, is a self-reporting tool and is suitable for children ages more than 6 years old.)
Critical Care Pain Observation Tool for critically ill patients who are incapable of reporting their pain
Pain Assessment in Advanced Dementia Scale for cognitively impaired patient
Factors contributing to pain management
There are a number of factors that have been shown to have significant effects on pain management. These include
Physical factors such as allergies and comorbidities, especially any conditions that might affect pharmacological choice, such as a history of gastrointestinal (GI) bleeding, history of cardiovascular disease, kidney and liver function
Psychological factors such as depression, anxiety, and catastrophizing
Treatment of acute postoperative pain
The options for pain treatment include both nonpharmacological and pharmacological treatment.
Nonpharmacologic treatment can commence preoperatively with good education about the surgery and continue postoperatively with good communication and reassurance. There are many additional techniques to attenuate pain, such as distraction for children, application of cold, transcutaneous electrical nerve stimulation (TENS), relaxation therapy, music therapy, meditation, and acupuncture.
The World Health Organization’s (WHO’s) analgesic ladder originally intended to provide a stepped approach to the management of cancer pain ( Fig. 2.1A ); however, clinicians also apply it for acute pain. The model starts with nonopioids (acetaminophen, NSAIDs) for mild pain, then escalates to weak opioids (codeine, tramadol) for moderate pain, and strong opioids (morphine, fentanyl) for severe pain. Remembering that it is appropriate to start at the top of the ladder for acute severe nociceptive pain. As postoperative pain is usually acute and severe and tends to improve over time, the reverse ladder approach, which starts with strong opioids and steps down subsequently, has been applied for acute pain ( Fig. 2.1B ).
Nonopioid analgesics including nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, ketamine, local anesthetics (systemic, local infiltration, and regional block), clonidine, and gabapentin. Commonly used nonopioid analgesics, mechanism of action, route, and precaution are listed in Table 2.2 . The combination of two or more medications or techniques (such as combination with local anesthetic infiltration or regional anesthesia) that act by different mechanisms for providing analgesia is termed multimodal analgesia.
|Mechanism of actions
|Unknown, may involve cyclooxygenase, endocannabinoid, TRPV1, and serotonin
|PO, PR, IV
|Minimal, unless overdose (recommended dose less than 3–4 g/day)
|Traditional NSAIDs (e.g., ibuprofen, naproxen,
|Central and peripheral COX inhibitors
|Allergy to NSAIDs. Decrease dose in renal impairment, elderly or bodyweight <50 kg
|GI bleeding, renal failure and surgical bleeding, possible risk of anastomotic leakage after colorectal surgery
|COX-2 inhibitors (e.g., celecoxib)
|Cross allergy with sulfonamides
|Fewer GI side effects. Minimal effect on platelets. Similar renal risk but increased cardiovascular events with long-term use
|Sodium channel blockers
|IV (lidocaine), local infiltration nerve block
|Allergy to local anesthetic
|Local anesthetic systemic toxicity
|NMDA receptor antagonist
|IV, IM, PO
|Patient with psychosis
|Hallucination, delirium, hypertension, tachycardia
|Calcium channel blockers
|Adjust dose for renal function (CrCl <60 mL/min), elderly
Multimodal analgesia improves pain control, reduces opioid requirements, reduces opioid-related side effects, and has the potential to reduce costs in patients undergoing surgery. Strong evidence shows that NSAIDs, gabapentin, pregabalin, systemic lidocaine, and ketamine are opioid-sparing medications and reduce opioid-related adverse effects.
Opioids are strong analgesics, acting at μ-opioid receptors in the brain and spinal cord, which inhibits transmission of the nociceptive signal. Opioids can be administered by many routes, including oral and intravenous, intramuscular, subcutaneous, buccal, transdermal, or neuraxial (spinal, epidural). Commonly used opioids in the perioperative period and comments are shown in Table 2.3 .
|Weak μ agonist
|Need CYP2D6 enzyme that converts codeine to morphine; poor metabolizers (8%–10%) do not respond, whereas ultrarapid metabolizers (3%–5%) are at risk of toxicity
|Transdermal route (fentanyl patch) results in 12 h of onset and offset delay, not recommended for acute pain, but useful for basal delivery in opioid-tolerant patients
|Associated with an increased risk of delirium in the postoperative period compared to other opioids
|Contraindicated in end-stage renal disease
|May produce less nausea and vomiting than morphine in some patients
|μ agonist (L-isomer),
NMDA antagonist (D-isomer)
|Long half-life, analgesic dose is twice or thrice a day and once daily as methadone maintenance therapy for the management of opioid addiction. May also have NMDA antagonist effect, thus decreasing opioid tolerance
|Often coformulated with acetaminophen (Percocet), requiring caution in patients where there is a potential to take a larger than recommended dose, and patients should be warned about not also taking tylenol (acetaminophen) simultaneously when these coformulations are used.
|Often coformulated with acetaminophen (Vicodin), see caution above.
|Contraindicated in chronic opioid users (precipitating withdrawal).
Used in labor and delivery due to lower risk of neonatal respiratory depression. Low dose (5 mg IV) used for the treatment of pruritus (side effect) from other narcotics.
|Partial μ agonist,
|Lower risk of respiratory depression. Use in patients with previous problems with opioid addiction. High affinity to mu receptor, preventing euphoric/analgesic effect from other opioids, should stop 3–5 days before a major operation and monitor for withdrawal symptoms.
Even if opioids are effective in managing postoperative pain, they are often associated with adverse events, including nausea, vomiting, itching, ileus and constipation, sedation, dizziness, confusion, urinary retention, respiratory depression and tolerance, and dependence. Nausea is dose related and the most common side effect (32%).
Postsurgical patients who experienced an opioid-related adverse event had a 55% longer length of hospital stay, 47% higher costs, 36% increased risk of readmission, and 3.4 times higher risk of inpatient mortality. As discussed, nonopioid analgesics have been administrated as part of multimodal analgesia to reduce opioid use and the aforementioned side effects.
Benefits of early pain control
Intense nociceptive stimulation leads to peripheral and central sensitization, which affects pain in the short and long term. Early and adequate pain control may decrease central sensitization, thus allowing better pain control and preventing persistent pain.
The strategy of early pain control by the administration of an analgesic before an acute nociceptive stimulus is called preemptive analgesia. Even though the laboratory studies found preemptive analgesia effectively minimized dorsal horn changes, which are associated with central sensitization more than if the same analgesic is given after the pain state was established, clinical studies have shown conflicting results.
Preventive analgesia is a subsequent strategy that focuses on preventing central sensitization, rather than time. As postoperative pain relates not only to the skin incision but also to intraoperative tissue and nerve injuries and postoperative effects; preventive analgesia initiates analgesics or interventions not only before a nociceptive stimulus but also continues until the majority of nociceptive stimuli have abated. Preventive analgesia provides the persistence of analgesic efficacy beyond its pharmacological duration, including long-term outcomes such as any effect on chronic postsurgical pain. Local anesthetics (systemic, local, or regional block) and ketamine demonstrate a preventive analgesic effect in the perioperative period, whereas studies on gabapentinoids have shown conflicting results.
Perioperative management for chronic opioid users
Perioperative management of patients receiving opioid therapy is quite challenging. Several studies have suggested that these patients have an increased risk of poor surgical outcome, inadequate pain control, and perioperative opioid-related adverse events, which require particular attention and multidisciplinary treatment. Evidence shows that preoperative opioid misuse is associated with considerable postoperative morbidity and mortality, such as surgical site infection, respiratory failure, and pneumonia.
Before the operation, patients should be assessed for the likelihood of opioid-related adverse events. This depends on the dosage and the duration of preoperative opioid use combined with other factors, such as uncontrolled psychiatric comorbidities, a history of a substance use disorder, and surgery likely to give a high incidence of severe postoperative pain. Generally, patients receiving more than 60 oral morphine milligram equivalents (MME) per day in the 7-day period before surgery are considered high risk. For elective surgery, it is recommended to wean down opioids preoperatively to the minimum effective dose, where possible, as there is a correlation between preoperative opioid dose and poor surgical outcomes. In addition, these patients should be educated to promote shared pain management expectations, and a perioperative pain specialist should be consulted before surgery. If psychological comorbidity is present, it should be optimized preoperatively.
Perioperatively, it is strongly recommended to use individualized multimodal pain management strategies, with analgesic drugs from different classes and analgesic techniques that target different mechanisms being combined. Nonopioid analgesics, such as paracetamol and NSAIDs, should be routinely prescribed—if there is no contraindication. Several nonopioid analgesics can also be used as part of a comprehensive multimodal analgesia, and these include ketamine and lidocaine infusion, anticonvulsants, α-2 agonists, and nefopam. Strong evidence shows that regional anesthesia is superior to the use of opioid analgesia and usually reduces opioid consumption during the perioperative period. , Regional anesthesia techniques commonly used for head and neck surgery include blockade of the trigeminal nerve, maxillary nerve, mandibular nerve, and cervical plexus. Nonpharmacological methods, such as TENS, distraction therapy, and hypnosis, may be considered postoperatively in some patients.
Regarding perioperative opioid management, it is recommended to use the lowest effective dose of opioid during the perioperative period, while avoiding opioid dose escalation postoperatively. A patient’s typical dose of prescribed opioid should be continued on the morning of surgery. Although opioid-free anesthesia is possible, there is insufficient data to recommend this method.
For patients receiving medication-assisted therapy, such as methadone or buprenorphine, careful analgesic regimens may be required. It is suggested that methadone should be continued on the same dose throughout the perioperative period. For buprenorphine, perioperative management depends on several factors, including the extent of surgery, elective or emergency surgery, buprenorphine preparation, and indication for buprenorphine therapy. Several strategies have been proposed. Generally, for patients expected to have mild-to-moderate pain, buprenorphine should be continued, while supplementing with a titrated high affinity pure μ-opioid receptor agonist (such as fentanyl) or buprenorphine itself for acute postoperative pain control. Alternatively, switching to a full opioid agonist before surgery is recommended for patients expected to have moderate-to-severe pain. For these patients, buprenorphine should be discontinued 3–5 days before the operation, and a pure opioid agonist may be needed for the management of withdrawal symptoms.
Postoperatively, the dosage of opioids should be deescalated to the preoperative dose. Physicians should limit opioid prescriptions to the expected duration of pain that is severe enough to require opioids. If opioid use is continued beyond the expected duration of acute pain, consultation with a pain specialist and coordination with the patient’s outpatient provider may be necessary.
Chronic pain in otolaryngology
Chronic pain is the pain that persists past the normal healing time and usually lasts or recurs for more than 3 months. In the United States, the prevalence of chronic pain ranges from 19% to 43% of the population, which often results in patients’ suffering, demoralization, and functional impairment and has led to a national economic burden. However, the difference between acute and chronic pain is not only time but also the pathophysiology, goal of treatment, and prognosis ( Table 2.4 ).
|Tissue, nerve injuries
|Tends to improve over time
|Persists more than 3–6 months
|Goal of treatment
|Pain intensity reduction
|Improve function with multidisciplinary approach
Chronic pain itself can be classified into cancer and noncancer pain. The important difference is not only the cause of pain but also the role of strong opioids as a treatment.
Opioids are strong analgesics, and long-term use inevitably produces physical tolerance; opioids are indispensable for the relief of severe pain during short-lived painful events such as postoperative periods and at the end of life such as advanced cancer. However, the long-term benefit of strong opioids for chronic noncancer pain is still unclear, but the risk of abuse, overdose, and death is evident from the “opioid crisis” in North America. The role of strong opioids for a long-lived painful event such as chronic noncancer pain is very limited in current practice.
In otolaryngology, patients may present with various types of chronic pain, for example, chronic orofacial pain, chronic otalgia, and chronic neck pain. Even though the data about the exact prevalence of chronic pain in otolaryngology is still lacking, this problem is commonly encountered in otolaryngology clinics. Therefore, an understanding of pathophysiology, presentation, and management of these conditions is extremely beneficial for otolaryngologists.
Chronic noncancer pain
Chronic postsurgical pain
The majority of the patients who undergo surgery recover without consequences. However, up to 40% of these patients, can develop persistent pain beyond the healing period. Moreover, in some procedures (such as thoracotomy, mastectomy, amputation), 5%–10% of patients reported severe pain 1 year after the surgery and had impacted quality of life, psychological and social function, and led to disability. The persistent pain beyond the period of wound healing is now recognized as a disease by itself called chronic postsurgical pain syndrome (CPSP). Even though it can be a common consequence of surgery and can have a considerable negative impact on the patients’ quality of life, CPSP is still underdiagnosed and undertreated.
Definition of chronic postsurgical pain
The official definition of CPSP was defined by the International Association for the Study of Pain (IASP) in 2017 as “chronic pain developing or increasing in intensity after a surgical procedure and persisting beyond the healing process, i.e., at least 3 months after surgery. The pain is either localized to the surgical field, projected to the innervation territory of a nerve situated in this area, or referred to a dermatome (after surgery/injury to deep somatic or visceral tissues). Other causes of pain including infection, malignancy, etc. need to be excluded as well as pain continuing from a preexisting pain problem”. As a disease by itself, in the upcoming version of the International Classification of Diseases (ICD-11), CPSP has its own code as MG30.21 (chronic postsurgical pain). CPSP is a growing area of study within pain medicine due to the increasing number of patients undergoing surgery each year. Amplified by the variable reported incidence depending on the operation (5%–85%), producing an increased number of patients with new chronic pain. A survey of the prevalence of CPSP in a large tertiary care pain center found this diagnosis in 8% of total visits, the fourth ranked of the most common out-patient diagnoses in their pain clinic.
Pathophysiology of chronic postsurgical pain
The mechanism by which CPSP develops is not completely understood, but a likely mechanism includes the maladaptation of acute pain to chronic pain (neuroplasticity), nerve injuries, and opioid-induced hyperalgesia. The neuroplasticity change is believed to be the result of inflammation and intense nociceptive stimuli from surgery leading to the alteration of the gene expression involving molecular and cellular level changes from the peripheral to central nerve pathways. This change in the somatosensory pathway leads to hyperalgesia, central sensitization, and chronic pain, the maladaptive version of sensitization. This concept is supported by the clinical evidence that poor acute postoperative pain control is associated with a higher incidence of CPSP. As such, it is important that there is a strategy to control pain early and in a proactive way to prevent central sensitization. Additional strategies to prevent CPSP according to pathophysiology includes the modification of surgical technique to lessen nerve injuries and the application of opioid-sparing strategies to prevent opioids induced hyperalgesia.
Risk factors of chronic postsurgical pain
Risk factors for CPSP include surgical factors (type of surgery especially thoracotomy and mastectomy have the highest incidence of CPSP), patients’ characteristics (younger age, presence of preoperative pain either at the surgical site or other sites), psychological factors (lower SF-12 mental score, presence of depression, or catastrophizing ideas), and poor postoperative pain control. As CPSP is common and has a high impact on patients’ quality of life, the identification of patients at risk, to discuss the risks of CPSP as part of the consent for surgery, is necessary for all surgeons. Additionally, recognizing the risk factors to help stratify risk and tailor preventive measures for the high-risk patients including the following: changing the surgical technique to minimally invasive surgery, aggressive acute postoperative pain control, and preventive analgesia. Moreover, the administration of some analgesics such as ketamine, lidocaine infusion, or the application of regional anesthesia may be beneficial for the prevention of CPSP.
Persistent postoperative opioid use
One of the most concerning long-term effects after surgery is persistent postoperative opioids use, which is defined as the use of opioids for more than 90 days after surgery in opioid-naïve patients. The prevalence of new persistent opioid use was 5.9% for minor surgeries and 6.5% for major surgeries. The similar prevalence between minor and major surgeries (OR 1.04, [0.93, 1.18]) suggests that prolonged opioid use after surgery cannot be simply explained by the extent of surgical injury. The multivariable analysis found that significant risk factors for persistent opioid use included tobacco use, alcohol and substance abuse disorders, mood disorder, anxiety and preoperative chronic pain. Similar to the risk of CPSP, the risk of persistent postoperative opioid use should be addressed and discussed before the operation.
Clinical evidence shows opioid use for acute pain, after even minor surgical procedures is associated with long-term opioid use, and that a greater amount of early opioid exposure is associated with greater risk for long-term use. Preventive measures, especially for high-risk patients include minimizing postdischarge opioid use with a multimodal analgesic care plan and prescribing the lowest effective dose of immediate-release opioids, with no greater quantity than needed for the expected duration of pain that is severe enough to require opioids.
Management of chronic postsurgical pain
CPSP is categorized as chronic noncancer pain, the principal of management includes patient education and using a multidisciplinary approach with the surgeon, pain physician, psychiatrist, and rehabilitation medicine physician. As the majority of the patients with common types of CPSP suffer from neuropathic pain (45%, 65%, and 80% in thoracotomy, mastectomy, and amputation, respectively), the commonly used analgesics for CPSP are those used for neuropathic pain.
The first line recommended analgesics for neuropathic pain are tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors, and gabapentinoids ( Table 2.5 ). Neuropathic pain is generally difficult to treat by itself. The number needed to treat among the first-line medication range from 3.6 (tricyclic antidepressant) to 7.7 (pregabalin) and a combination of the first-line medications is quite common in practice.
|Mechanism of actions
|Tricyclic antidepressants (TCAs)
|Inhibit catecholamine reuptake (increases serotonin and norepinephrine in descending inhibitory pathway).
|Precaution in elderly due to risk of fall, delirium, urinary retention (avoid dose more than 25 mg/day in elderly)
|Anticholinergic effect (dry mouth, difficult urination, sedation, increase risk of delirium), cardiac arrhythmia
|Serotonin and norepinephrine reuptake inhibitors (SNRIs)
|Duloxetine Venlafaxine Desvenlafaxine
|Increase norepinephrine in descending inhibitory pathway
|Fewer than TCAs, but includes dry mouth, nausea, and hypertension (high-dose venlafaxine)
|Blocks calcium channels, alpha2-delta subunit. (No interaction with GABA receptors)
|Need dose adjustment in patients with renal impairment
|Dizziness, sedation, peripheral edema, weight gain
There is no evidence of the long-term benefit of strong opioids for chronic noncancer conditions, and both weak and strong opioids are not recommended as first line. Opioids may be considered as second- and third-line medications for chronic noncancer neuropathic pain; however, the initiation of opioids in chronic noncancer patients needs careful consideration of the risks and benefits, screening for potential abuse and close monitoring. Opioids should be stopped if there is evidence of abuse, overdose, or no clinically meaningful improvement in pain and function.
Chronic orofacial pain
Orofacial pain (OFP) is considered one of the major problems in otolaryngology that has a significant impact on quality of life. It is defined as pain occurring mainly or exclusively under the orbitomeatal line, anterior to the pinnae, and above the neck, including the oral cavity. It can be caused by disorders of the orofacial structures, by dysfunction of the nervous system, or through a referral from distant sources. Dental issues are considered common causes of acute or subacute OFP, and these are well managed by dentists. However, chronic OFP can originate from a wide range of etiologies, which can be either odontogenic or nonodontogenic causes.
From a survey in the United Kingdom, about a quarter of the general population reported OFP during the 1-month period before the interview. The prevalence was higher in women than in men. The reported prevalence of chronic OFP varies from 10% to 62% of the patients affected with OFP, depending on study populations. ,
Chronic OFP can be classified in several ways. According to the IASP and the ICD-11, it can be either primary or secondary. Chronic primary OFP is defined as OFP that occurs on at least 15 days per month for longer than 3 months, where the pain is not better accounted for by another condition. One of the common causes of chronic primary OFP is associated with temporomandibular joint disorders, accounting for almost 5% of the US population. In contrast, chronic secondary OFP is pain that may be conceived as a symptom secondary to an underlying disease, such as cranial and regional neuralgias and neuropathies.
In 2020, the comprehensive, internationally accepted classification of OFP was published as the first edition of the International Classification of Orofacial Pain (ICOP). This classification is modeled on the third edition of the International Classification of Headache Disorders (ICHD-3), joining the ICHD-3 and the ICD-11 in establishing clear terminology that will allow better communication and data sharing. Additionally, the criterion of a 4-hour duration per day has been added when defining chronicity in OFP. In this system, OFP is classified according to Table 2.6 . Apart from OFP diagnosis, the ICOP committee also recommends integrating a psychosocial assessment to understand and manage OFP more comprehensively.