Oro Facial Pain

Slide 1 : ??? ???? ?????? ??????

Oro facial Pain : Oro facial Pain Magdy Abdel Naby Associate professor Cairo University

Slide 3 : Oro facial pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damaged, or described in term of tissue damaged. Oro facial pain (OFP) is the presenting symptom of a broad spectrum of diseases. As a symptom, it may be due to disease of the Oro facial structures, generalized musculoskeletal or rheumatic disease, peripheral or central nervous system disease, or psychological abnormality; or the pain may be referred from other sources

Slide 4 : Pain, in the medical model, is considered a symptom of disease, to be diagnosed and treated. Unfortunately, a cause and a diagnosis cannot always be established. Repeated attempts to identify a physical cause may result in unnecessary and sometimes harmful investigations and treatments. Establishing a precise diagnosis and providing effective treatment have become major challenges in medicine and dentistry.

Slide 5 : physical, psychological, and social factors are viewed as mutually influential forces with the potential to create an infinite number of unique pain experiences. The biologic system deals with the anatomic, structural, and molecular substrates of disease. The psychological system deals with the effects of motivation and personality on the experience of illness and on reactions to illness. The social system deals with cultural, environmental, and familial influences on the expression and experience of illness. Each system affects and is affected by all of the others.

Slide 6 : Anatomic Considerations Cranial nerve V (CN V), the trigeminal nerve, is the dominant nerve that relays sensory impulses from the Oro facial area to the central nervous system. The facial (CN VII), glossopharyngeal (CN IX), and vagus (CN X) nerves and the upper cervical nerves (C2 and C3) also relay sensory information from the face and surrounding area Primary sensory neurons associated with pain (nociceptors) are characterized by small-diameter axons with slow conduction velocities (i.e., finely myelinated A delta fibers and unmyelinated C fibers) Nociceptors are activated by intense or noxious stimuli. Some are unimodal and respond only to thermal or mechanical stimuli; others are polymodal and respond to mechanical, thermal, and chemical stimuli.Nociceptors encode the intensity, duration, and quality of a noxious stimulus.

Slide 7 : Observable Pain Behaviors Behavior Observations 1-Guarding : Abnormally slow, stiff, or interrupted movement 2-Bracing : Stiff, pain-avoidant posturing while in a static position 3-Rubbing : Touching, rubbing, or holding of the painful area 4-Sighing : Pronounced exhalation of air 5-Grimacing : Obvious facial expression of pain Assessments of disability related to a pain disorder and psychological status are important parts of any evaluation of chronic pain. Disability is defined as “a lack of the ability to function normally, physically or mentally.” There is no universally accepted method of assessing pain-related disability, but pain-related interference with activities and psychological impairments associated with pain are important aspects.

Slide 8 : The prevalence of depression is substantially higher in chronic pain patients compared to individuals without pain, but the majority of chronic pain patients are not depressed. An association between chronic pain and depression exists, but no one hypothesis has emerged or has been proven to explain the relationship. Theories proposed include the following: 1. Depression causes hypersensitivity to pain. 2. Pain is a “masked” form of depression. 3. Depression is caused by the stress of chronic pain. The literature suggests that in general, pain is more likely to cause emotional disturbances than to be precipitated by them

Slide 9 : Pain reduction is a primary goal, but it is not always achieved. Published studies of pain reduction after treatment in pain clinics report pain reduction ranges of from 1438 to 60%,39 with an average pain reduction of between 20 and 30%.40 Other treatment outcome criteria include reductions in addictive medication, reductions in the use of health care services, increased activity (including return to work), and closures of disability claims.41 Providing effective treatment of chronic pain is challenging, and many of the treatments that are effective for acute pain fail to relieve chronic pain.

Slide 10 : 1-COGNITIVE THERAPY 2-RELAXATION THERAPY 3-DRUG THERAPY Choosing the analgesic group (or groups) and the specific drugs is the first step in management. Drug therapy requires the individualizing of regimens for the greatest effect. In chronic pain management, a drug should also be selected to deal with “breakthrough” pain, an episode of increased pain that the regular regimen is not able to control. This drug is usually a µ-receptor agonist (e.g. oxycodone) with a relatively rapid rate of onset for a brief period. The oral route is preferred for compliance and convenience, and the drug dose requires titration to establish the appropriate regimen. An analgesic is most likely to be effective when given before pain increases and is usually best prescribed with a fixed dose schedule that does not require an increase in pain to signal the need for analgesia. Treatment

Slide 11 : Non-opioid Analgesics. This group consists primarily of acetaminophen and the large group of nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are thought to work primarily at the site of injury by inhibiting the enzyme cyclo-oxygenase (COX), which is required for the synthesis of prostaglandins, substances that sensitize peripheral sensory nerves and contribute to the experience of pain. NSAIDs are available that selectively inhibit only one of the isoforms of COX, namely, COX-2. The inhibition of COX-2 seems to be related to the anti-inflammatory and analgesic effects whereas the inhibition of COX-1 is thought to be responsible for many of the side effects. The COX-2 inhibitors celecoxib and rofecoxib pose less risk of GI bleeding and do not inhibit platelet aggregation.

Slide 12 : Opioids. The largest group of opioids that are commonly used for analgesia consists of the morphine-like agonists. Their most important effects are on the central nervous system and GI system. These drugs bind to µ opioid receptors, resulting in actions that lead to the analgesic effects. Adjuvant Drugs. This group of drugs has been approved for use in conditions other than pain. Alone or in combination with other analgesics and adjuvant, they have been found to be of value in pain management.

Slide 13 : Anticonvulsant drugs are effective in the treatment of trigeminal neuralgia and diabetic neuropathy and for migraine prophylaxis.57 There have been no clinical trials for the treatment of other OFP disorders with anticonvulsants. These drugs frequently produce side effects (including sedation, dizziness, ataxia, and mood changes) that can limit their usefulness. Newer anticonvulsants (specifically felbamate,58 lamotrigine,59 and gabapentin60,61) are receiving attention as possible therapies for pain. Gabapentin has become commonly used in pain management partly because of its relatively few side effects.

Slide 14 : Topical Medications. Topical analgesic therapy on the skin or oral mucosa has the advantage of reduced systemic absorption and thus a reduced risk of side effects. Capsaicin used as a topical cream has been the most researched drug in this field. It is effective in treating post herpetic neuralgia. The therapeutic effect is thought to be due to the depletion of substance P in C fibers,68 decreasing their input to the central nervous system (CNS) neurons. Topical NSAIDs have been demonstrated to be effective for musculoskeletal pain. Doxepin, clonidine, ketamine, cyclobenzaprine, and carbamazepine have been used topically in a variety of vehicles

Slide 15 : Drug therapy for chronic pain is complex and often involves multiple drugs with different routes of administration. Patients often express anxiety about dependence on medication and may sometimes feel that drug therapy is used or recommended in place of “getting to the real cause” of the pain. When using drug therapy to treat the pain as the disorder, patients need information and education about the potential value of drug therapy as part of the comprehensive management of chronic pain.

Slide 16 : Atypical Odontalgia (Atypical Facial Pain) A classification that includes the diagnoses of atypical odontalgia (AO) and atypical facial pain (AFP) is controversial, and many workers in the field of facial pain believe that these terms should be discarded because they are often used either as catchalls to denote patients who have not been adequately evaluated or because they imply that the pain is purely psychological in origin. ETIOLOGY AND PATHOGENESIS There are several theories regarding the etiology of AO and AFP. One theory considers AO and AFP to be a form of de-afferentation or phantom tooth pain.

Slide 17 : Others have theorized that AO is a form of vascular, neuropathic, or sympathetically maintained pain. Other studies support the concept that at least some of the patients in this category have a strong psychogenic component to their symptoms and that depressive, somatization, and conversion disorders have been described as major factors in some patients. There is often strong disagreement between facial pain experts who stress the biologic basis of AO and AFP and others who stress the emotional basis, but the etiology remains unknown at this time.

Slide 18 : A thorough history and examination including evaluation of the cranial nerves, oropharynx, and teeth must be performed to rule out dental, neurologic, or nasopharyngeal disease. Examination of the masticatory muscles should also be performed to eliminate pain secondary to undetected muscle dysfunction. Laboratory tests should be carried out when indicated by the history and examination. Patients with AO or AFP have completely normal radiographic and clinical laboratory studies. MANAGEMENT Once the diagnosis has been made and other pathologies have been eliminated, it is important that the symptoms are taken seriously and are not dismissed as imaginary. Patients should be counseled regarding the nature of AO and reassured that they do not have an undetected life-threatening disease and that they can be helped without invasive procedures.

Slide 19 : Burning Mouth Syndrome (Glossodynia) Burning sensations accompany many inflammatory or ulcerative diseases of the oral mucosa, but the term “burning mouth syndrome” (BMS) is reserved for describing oral burning that has no detectable cause. The burning symptoms in patients with BMS do not follow anatomic pathways, there are no mucosal lesions or known neurologic disorders to explain the symptoms, and there are no characteristic laboratory abnormalities. ETIOLOGY AND PATHOGENESIS The cause of BMS remains unknown, but a number of factors have been suspected, including hormonal and allergic disorders, salivary gland hypo function, chronic low-grade trauma, and psychiatric abnormalities.

Slide 20 : The drug therapies that have been found to be the most helpful are low doses of TCAs, such as amitriptyline and doxepin, or clonazepam (a benzodiazepine derivative). It should be stressed to the patient that these drugs are being used not to manage psychiatric illness, but for their well-documented analgesic effect. Burning of the tongue that results from parafunctional oral habits may be relieved with the use of a splint covering the teeth and/or the palate.

Slide 21 : The somatosensory system serves the valuable function of warning the individual of actual or potential tissue damage. Nociceptors, specialized receptors that signal tissue damage, terminate in a highly ordered manner in the dorsal horn of the spinal cord and its homologous subnucleus caudalis in the spinal trigeminal nucleus. Information is transferred directly or through relay to the ventrobasal thalamus and then to the cortex. In the spinal cord, other pathways from the dorsal horn pass to the ventral horn and activate flexor motor neurons, generating the withdrawal flexion reflex. This model draws attention to the protective aspect of the sensation of pain and is consistent with the qualities of acute pain.

Slide 22 : Chronic pain is now recognized as a complex disorder that is influenced by biologic factors and by a range of psychosocial factors, including emotion, psychological distress, family and work environment, cultural background, the meaning of the pain Chronic pain has been defined as pain that persists past the normal time of healing Recently, pain lasting longer than 3 months has been used to define chronic pain. In the IASP publication on classification, Merskey describes chronic pain as “a persistent pain that is not amenable, as a rule, Orofacial Pain and Temporomandibular Disorders to treatments based on specific remedies, or to the routine methods of pain control such as non-narcotic analgesics. In situations in which no ongoing peripheral injury was present to explain the pain, it was assumed that the pain was psychological.

Slide 23 : Pathophysiology The gate-control theory, introduced by Melzak and Wall in 1965,26 articulated a model that explained the pain experience as a multidimensional process with many modulating influences. The proposed explanation for the persistence of pain after healing relates to changes (neuroplasticity) in the central nervous system.27 Neurons are thought to be capable of altering their structure and function in response to stimuli, resulting in new stimulus-response relationships. This sensitization does not require ongoing peripheral input but is a consequence of changes in the sensitivity of neurons in the spinal cord. These changes include the following: 1. A reduction of the stimulation threshold, with the result that the neurons no longer require a noxious stimulus in order to be activated 2. An alteration in the temporal pattern of the response, so that a transient stimulus evokes a sustained burst of activity 3. An increase in the general responsiveness of the motor neurons, so that a noxious stimulus produces a greater effect 4. The expansion of receptive fields, with the result that responses are evoked over a much wider area.

Slide 24 : The clinical manifestations of these changes include: hyperalgesia ;(an increased response to a stimulus that is normally painful); allodynia ; (pain due to a stimulus that does not normally provoke pain); and spontaneous, radiating, and referred pain. The interaction between the sympathetic and somatosensory nervous systems has been associated with chronic pain and thought to be the cause of many but not all cases of complex regional pain syndrome (CRPS). The relationship may be a coupling mediated by the neurotransmitter noradrenaline, which is released from sympathetic nerve endings acting on a- adrenoreceptors in the membrane of afferent neurons, causing depolarization. The mechanism is thought to be more likely a sensitivity of the somatosensory system than a hyperactivity of the sympathetic efferent system.

Slide 25 : Most of the present classifications are based on a consensus of existing knowledge and on unstructured examination findings or assumptions about the consistency of signs and symptoms. Current Classification Schemes Chronic pain classifications that address the physical, psychological, and social aspects of chronic pain provide a more comprehensive view of the disorder.

Slide 26 : ?EXAMINATION AND ASSESSMENT OF THE PATIENT WITH CHRONIC OROFACIAL PAIN The examination and assessment of patients with chronic OFP is challenging for all clinicians. In most disorders, no specific biologic marker, validated diagnostic criteria, or “gold standard” exists. Biologic markers, including tyramine,87 oxygen free radicals,88 and metabolites of neurotransmitters in lumbar cerebrospinal fluid,89 have been studied in a limited manner in regard to OFP and are not applicable in diagnosis. Even test procedures that are considered objective, such as local anesthetic nerve blocking and the testing of sensation after nerve damage, have yielded inconsistent results. A systematic approach for collecting diagnostic information is needed to minimize the risk of missing critical information.

Slide 27 : History, physical examination, and behavioral assessment usually serve as the basis for diagnosis. Frequent re-evaluation, including assessment of the effects of treatment, is an important part of this process. Even when a diagnosis is uncertain or when previous treatment has failed, the clinician can make a valuable contribution by coordinating the further use of medical and dental services and by being available to advise the patient about possible treatments. Validating patients’ feelings and symptoms in these times is critically important and serves to reduce suffering.

Slide 28 : History Evaluation of OFP symptoms must include all of the standard components of a medical interview: chief complaint, history of present illness, past medical history, medications, review of systems, and family and social history. A diagnosis can sometimes be made on the basis of the history, or the possibilities can be significantly narrowed. Since there are a number of OFP disorders that do not produce physical abnormalities, the history and description of pain may serve as the basis for the diagnosis.

Slide 29 : HISTORY OF THE PRESENT ILLNESS A history of the present illness should include a detailed description of the pain and its location. The VAS or numeric scale described above can be used to assess intensity, and a questionnaire such as the MPQ can capture the multidimensional experience of the pain. Details of previous injuries, surgeries, and radiation therapy should be obtained. Questions about habits such as gum chewing and tooth clenching or grinding may reveal important contributing factors of which the patient is unaware. The effects of eating, opening the mouth wide, rest, exercise, and heat and cold on pain should be explored. Referred pain to the Orofacial region is an important clinical consideration.

Slide 30 : Pain Characteristics Intensity Quality Location Onset Associated events at onset Duration and timing of pain Course of symptoms since onset Activities or experiences that increase pain Activities or experiences that decrease pain Associated symptoms (eg, altered sensation, swelling) Previous treatments and their effects

Slide 31 : PAST MEDICAL HISTORY AND REVIEW OF SYSTEMS The past medical history and review of systems should help provide an insight into the general health of the patient and may provide clues regarding the present pain complaint. Pain may be a presenting feature or an ongoing complaint in systemic disease (eg, connective-tissue disease,demyelinating disease of the CNS, metastatic disease). The patient’s use of medication (including over-the counter preparations, naturopathic and homeopathic remedies, and prescription drugs) should be recorded. Prescription medication is often used incorrectly; therefore, the directions as well as the actual usage should be determined. The medication list may uncover a medical condition that the patient failed to mention in other questioning. Drug effects such as fatigue, dizziness, anxiety, insomnia, or depression may affect the patient’s pain complaints. The use of tobacco, alcohol, caffeine, or illicit drugs should be explored.

Slide 32 : FAMILY, SOCIAL, AND OCCUPATIONAL HISTORY Chronic pain can have disastrous effects on one’s ability to maintain daily activities and fulfill responsibilities. Pain has profound and often negative effects on family and social relationships, and it is important to assess the level of dysfunction that may have occurred. Traumatic events or emotional distress prior to the onset of pain, a history of other close family members with chronic illness or pain, and changes in work and or marital status should be explored because these can be significant stressors.

Slide 33 : Physical Examination The physical examination may identify an abnormality that explains the cause of pain. It can also help eliminate from diagnosis the presence of serious disease related to the pain. The examination should include the following: 1. Inspection of the head and neck, skin, topographic anatomy, and swelling or other orofacial asymmetry 2. Palpation of masticatory muscles, tests for strength and provocation 3. Assessment and measurement of the range of mandibular movement 4. Palpation of soft tissue (including lymph nodes) 5. Palpation of the temporomandibular joint 6. Palpation of cervical muscles and assessment of cervical range of motion 7. Cranial nerve examination. 8. General inspection of the ears, nose, and oropharyngeal areas 9. Examination and palpation of intraoral soft tissue 10. Examination of the teeth and periodontium (including occlusion)

Slide 34 : MUSCLE EXAMINATION Pain that is reproduced or increases as a result of muscle palpation may point to the source of the pain and to a diagnosis. The degree of finger pressure will influence the result of the palpation examination, and patients’ responses to palpation may vary with time. Pressure algometers have been used in research to help standardize examination procedures97 but are not commonly used in clinical practice. Muscle palpation has been shown to yield reliable scores among examiners, but the diagnostic validity and reliability of muscle palpation has not been established. The masseter and temporalis muscles can be palpated bilaterally to identify differences in size or firmness. The suprahyoid muscles, mylohyoid, and anterior belly of the digastric should be included in the palpation examination. Intraoral techniques have been described for palpating the medial and lateral pterygoids. The ability to perform a meaningful palpation examination of the lateral pterygoid has been questioned.98 Palpation techniques have been described, but it may be difficult to distinguish tenderness associated with the procedure from an actual muscle abnormality.

Slide 35 : INTRAORAL EXAMINATION A systematic intraoral inspection looking for changes in form, symmetry, color, and surface texture should be carried out. The examination should include manipulation of the tongue and mandible to clearly visualize all areas. Pooling of saliva on the floor of the mouth should be observed. The palate and tongue should be examined at rest and during function to detect underlying masses that might displace or alter the normal structures. The examiner’s finger should palpate the alveolar processes, lateral and posterior parts of the tongue, floor of the mouth, buccal mucosa, and hard and soft palate to identify abnormalities that may not be readily observed. The finger should not meet significant resistance as it moves across a normally lubricated mucosa. The openings of the submandibular and parotid salivary gland ducts should be isolated and dried with cotton; the glands should then be “milked” to verify a clear flow of saliva.

Slide 36 : The dentition should be examined for wear, damaged teeth, and evidence of caries. This inspection should be followed by probing, palpation for tooth mobility, and percussion of teeth. If a pulpal problem is suspected, thermal and vitality tests should be included. Applying differential pressure on the teeth by having the patient bite down on cotton rolls, wooden bite sticks, or one of the commercially available instruments designed to apply concentrated pressure on cusps may identify pain associated with a vertical crown or root fracture. Periodontal structures should be examined for color changes suggestive of inflammation, altered gingival architecture that occurs with chronic disease, swelling, or other surface changes. Periodontal probing should be performed to identify bleeding points and pocket depths. Tooth contacts in the maximum intercuspal position, in centric relation, and during excursive movements should be identified.

Slide 37 : Pain-Related Disability and Behavioral Assessment An interview most often serves as the basis for a behavioral assessment. Self-report questionnaires and instruments that include methods of scoring are also in use to assess disability and psychological factors. The assessment should explore the following: 1. Events that precede and follow exacerbation of pain 2. The patient’s daily activities — How time is spent during the day and in the evening — Activities that have been performed more often or less often since the onset of pain — Activities that have been modified or eliminated since the onset of pain 3. Relatives or friends that suffer chronic pain or disabilities of a similar nature 4. The degree of affective disturbance — Change in mood or outlook on life — Satisfaction level with friends and family relationships

Slide 38 : Questions to Consider for Screening Assessment What events precede and follow increased episodes of pain? How is time spent during the day and the evening? What activities are performed more often or less often since the onset of pain? What activities have been modified or eliminated since the onset of pain? Do relatives or friends suffer chronic pain or disabilities of a similar nature? Do you characterize yourself as depressed? Do you have changes in sleep pattern, food habits, sexual desire (vegetative signs of depression)? Have there been changes in your relationships with friends, family, co workers? Do you characterize yourself as being anxious or tense? Do you think you have experienced a lot of stressful situations over the past year? What do you think is causing the pain? Do you presently have any diagnosed or undiagnosed pain complaints elsewhere in the body?

Slide 39 : Nerve blocks to diagnose sympathetically maintained pain include local anesthetic block of the sympathetic chain (eg, stellate ganglion), regional guanethedine block (intravenous injection into an arm or leg), and intravenous phentolamine to block the a-adrenoreceptor, preventing the excitation of afferent nociceptors by noradrenaline. The interpretation of these tests has been challenged because of the lack of placebocontrolled procedures and because of a high placebo response, but the weight of evidence supports the hypothesis that the sympathetic nervous system contributes to chronic pain in some circumstances.

Slide 40 : Local anesthetic blocking should be considered in the context of all of the clinical findings. Topical, intraligament, infiltration, and regional block anesthesia may identify a peripheral site that is responsible for pain. A complete resolution of pain after local anesthetic application or injection should prompt an investigation for a local cause. The injection of local anesthesia may produce ambivalent results when patients report a change in symptoms but not necessarily resolution of pain. In these circumstances, one should consider a more central cause of pain.

Slide 41 : Laboratory Tests Laboratory tests have limited value except in special circumstances. Most OFP disorders do not cause abnormalities that can be identified in laboratory specimens. Exceptions include temporal arteritis, in which the erythrocyte sedimentation rate is elevated and temporal artery biopsy is abnormal and collagen vascular diseases that cause detectable immunologic abnormalities.

Slide 42 : Special Circumstances in Assessment of Orofacial Pain Patients OFP DISORDERS POSSIBLY CONFUSED WITH TOOTHACHE 1-Trigeminal neuralgia 2-Trigeminal neuropathy (due to trauma or tumor invasion of nerves) 3-Atypical facial pain and atypical odontalgia 4-Cluster headache 5-Acute and chronic maxillary sinusitis 6-Myofascial pain of masticatory muscles

Slide 43 : OFP SYMPTOMS INDICATING SERIOUS DISEASE 1-Pain at the angle of the mandible, brought on by exertion, relieved by rest Cardiac ischemia 2-New onset; localized progressive headache; superficial temporal artery swelling, tenderness, and lack of pulse; Temporal arteritis 3-New onset of headache in adult life; increasing severe headache, nausea, and vomiting systemic Intracranial tumor 4-Earache, trismus, altered sensation in the mandibular branch distribution Carcinoma of the infratemporal fossa 5-Trigeminal neuralgia in a person less than 50 years of age Multiple sclerosis 6-Pain associated with altered sensation confirmed by physical examination Neurogenic disorder tumor invasion of nerve

Slide 44 : Classification of Pain of Psychological Origin Pain of Psychological Origin Definition Muscle Tension Virtually continuous pain in any part of the body due to sustained muscle contraction and provoked by persistent overuse of particular muscles Delusional or hallucinatory Pain of psychological origin and attributed by the patient to a specific delusional cause Hysterical, conversion, or hypochondriacal Pain specifically attributable to the thought process, emotional state, or personality of the patient in the absence of an organic or delusional cause or tension Associated with depression Pain occurring in the course of a depressive illness usually not preceding the depression and not attributable to any other cause.

Slide 45 : HEADACHE AND OFP SYMPTOMS ASSOCIATED WITH SYSTEMIC DISEASE 1-Paget’s disease 2-Metastatic disease 3-Hyperthyroidism 4-Multiple myeloma 5-Hyperparathyroidism 6-Vitamin B deficiencies 7-Systemic lupus erythematosus 8-Vincristine therapy for cancer 9-Folic acid and iron deficiency anemias

Slide 46 : Classification of Cranial Neuralgias, Nerve Trunk Pain, and De-afferentation Pain IHS Category Specific Disorders or Definition Persistent (in contrast to tic like) pain of cranial origin Compression or distortion of cranial nerves and 2nd or 3rd cervical roots Demyelination of cranial nerves (optic neuritis) Infarction of cranial nerves (diabetic neuritis) Inflammation of cranial nerves (herpes zoster and postherpetic neuralgia) Trigeminal neuralgia (TN) Idiopathic TN Symptomatic TN (caused by demonstrable structural lesion) Glossopharyngeal neuralgia (GN) Idiopathic GN Symptomatic GN (caused by demonstrable structural lesion) Nervus intermedius neuralgia Rare disorder characterized by brief paroxysms of pain felt deeply in the auditory canal Superior laryngeal neuralgia Rare disorder characterized by severe pain in the lateral aspect of the throat, submandibular region, and underneath the ear, precipitated by swallowing, shouting, or turning the head Occipital neuralgia Paroxysmal jabbing pain in the distribution of the greater or lesser occipital nerves, accompanied by diminished sensation or dysesthesia in the affected area; commonly associated with tenderness over the nerve concerned Central causes of head and facial pain other than Anesthesia dolorosa: painful anesthesia or dysesthesia, often related to surgical trauma of the trigeminal ganglion Thalamic pain: unilateral facial pain and dysesthesia, attributed to a lesion of the quintothalamic pathway or thalamus Persistent facial pain that does not have the characteristics of the cranial neuralgias classified (previously used terms: atypical facial pain, atypical odontalgia) above and is n