The trigeminal nerve. Part II: the ophthalmic division

The ophthalmic, or first division (V1) of the trigeminal nerve, is the smallest of the three divisions and is purely sensory or afferent in function. It supplies sensory branches to the ciliary body, the cornea, and the iris; to the lacrimal gland and conjunctiva; to portions of the mucous membrane of the nasal cavity, sphenoidal sinus, and frontal sinus; to the skin of the eyebrow, eyelids, forehead, and nose; and to the tentorium cerebelli, dura mater, and the posterior area of the falx cerebri. At first glance, one might not expect one interested in the diagnosis and treatment of orofacial pain and temporomandibular joint disorders to have a need to be concerned with the ophthalmic division. Although much of this division's influence is dedicated to structures within the orbit, nose, and cranium, still, the ophthalmic division may be afflicted with a lesion or structural disorder which can cause all sorts of orofacial pain. Ignorance of this or any portion of the trigeminal nerve will lead to diagnostic and therapeutic failures. In this, the second of four (4) articles concerning the trigeminal nerve, the first division of this vast cranial nerve will be described in detail.     

The trigeminal nerve. Part I: An over-view

The trigeminal nerve is the largest and most complex of twelve cranial nerves. Its vast size and influence are greatly appreciated when one attempts to diagnose and treat patients suffering from orofacial pain and temporomandibular joint disorders. Without a thorough knowledge of the trigeminal nerve, the efficacy of diagnostic and therapeutic procedures will be very disappointing. This is the first of a four-part series of articles about the trigeminal nerve, a basic over-view of both the gross and neuroanatomical structures is presented.     

Idiopathic maxillary painPrevalence of maxillary sinus hyperreactivity in relation to allergy, chronic mucosal inflammation, and eosinophilia

OBJECTIVE: In patients with chronic orofacial pain, an underlying sinus hyperreactivity may contribute to the clinical symptoms of a diagnosis of atypical odontalgia, trigeminal neuralgia, or temporomandibular disorders. The purpose of this study was to assess the prevalence of histamine-related maxillary sinus hyperreactivity in patients manifesting signs and symptoms of idiopathic maxillary pain and to correlate the respective findings with the presence or absence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. STUDY DESIGN: Fifty patients who had been assigned a diagnosis of idiopathic maxillary pain underwent skin allergy tests, maxillary sinus histamine provocation tests, and maxillary sinus mucosa biopsy. Histamine challenge to a selected area was performed during transoral sinuscopy of the maxillary sinus; a positive test result was defined as the development of a significant local mucosa response such as reddening and swelling. RESULTS: Comparison of the data showed most patients (38%) to have an absence of chronic maxillary sinusitis-related diagnoses, whereas the most common multiple diagnosis was found to be chronic mucosal inflammation in combination with eosinophilia (22%). Regarding the prevalence rates of positive histamine provocation test outcomes, a significant difference was found between the diagnostic subgroup "absence of chronic maxillary sinusitis-related diagnoses" (36.9%) and the diagnostic subgroups "chronic mucosal inflammation" (20%; P< .05), "chronic mucosal inflammation in combination with eosinophilia" (18.2%; P< .05), and "chronic mucosal inflammation in combination with eosinophilia and allergy" (14.3%; P < .01). An analysis of the distribution of chronic maxillary sinusitis-related diagnoses revealed absence of chronic mucosal inflammation-related diagnoses to be significantly more frequently associated with positive histamine provocation test outcomes than with negative histamine provocation test outcomes (41.2% vs 19.7%; P< .01), whereas chronic maxillary sinusitis (41.0% vs 29.4%), eosinophilia (26.2% vs 17.6%), and allergy (13.1% vs 11.8%) were found to be more prevalent in patients with negative histamine provocation test outcomes. CONCLUSIONS: The findings of this study suggest patients with idiopathic maxillary pain to be associated with a low rate of sinus hyperreactivity, whereas a positive test outcome with histamine provocation may not be linked to the presence of chronic maxillary sinusitis-related diagnoses such as allergy, chronic mucosal inflammation, and eosinophilia. Further investigations using a larger sample size of patients with idiopathic maxillary pain and nonidiopathic maxillary pain are necessary to demonstrate the presence or absence of an idiopathic maxillary pain-specific prevalence of maxillary sinus hyperreactivity.     

The prevalence of trigeminal neuritis with TMD

Subjects with temporomandibular joint disorder (TMD) occasionally present with additional orofacial pain complaints. These can arise from dysfunction in teeth, bones, ligaments, tendons, nerves, and other structures. In this retrospective study, a group of 501 consecutive subjects with TMD complaints were evaluated for the presence of trigeminal neuritis. Very little information on the prevalence of this condition concomitant with TMDs exists in the literature. The existence of trigeminal neuritis was determined by the presence of pain when palpating trigeminal peripheral nerve branches exiting the supraorbital, infraorbital, and mental foramina in addition to the supratrochlear nerve. Each subject in this study had the involved nerves blocked with local anesthesia injections or lidocaine iontophoresis to assist in confirming the source of pain. Sixty subjects with TMD were found to have trigeminal neuritis. Early recognition of this disorder is important because treatment is usually more successful in the acute peripheral state.     

Orofacial Sensory Changes and Temporomandibular Dysfunction

Orofacial sensory changes are uncommon complaints that can coexist with temporomandibular dysfunction (TMD). The location, character, and intensity vary greatly with each individual and symptom fluctuation is not unusual for any patient. The etiology of orofacial sensory changes may be related to either local or systemic factors. Several investigators have reported that muscle entrapment of branches of the third division of the trigeminal nerve may result in orofacial sensory disruption. Different theories have been suggested to illustrate how TMD and trauma might be associated with these neurological changes. Additionally, several mechanisms exist to explain how muscle spasms may be responsible for nerve compression in individuals with normal anatomy and in those with anatomical variations. In this study, thirty subjects from a group of 282 TMD patients were found to have coexisting orofacial sensory disturbances and TMD. Subjects presenting with any neurological complaints should alert the clinician to the possibility that these symptoms may be the early clinical signs of serious disease.     

Orofacial sensory changes and temporomandibular dysfunction

Orofacial sensory changes are uncommon complaints that can coexist with temporomandibular dysfunction (TMD). The location, character, and intensity vary greatly with each individual and symptom fluctuation is not unusual for any patient. The etiology of orofacial sensory changes may be related to either local or systemic factors. Several investigators have reported that muscle entrapment of branches of the third division of the trigeminal nerve may result in orofacial sensory disruption. Different theories have been suggested to illustrate how TMD and trauma might be associated with these neurological changes. Additionally, several mechanisms exist to explain how muscle spasms may be responsible for nerve compression in individuals with normal anatomy and in those with anatomical variations. In this study, thirty subjects from a group of 282 TMD patients were found to have coexisting orofacial sensory disturbances and TMD. Subjects presenting with any neurological complaints should alert the clinician to the possibility that these symptoms may be the early clinical signs of serious disease.     

Diagnosis and management of non-dental orofacial pain

Careful history-taking improves diagnosis of non-dental orofacial pain, a not uncommon group of conditions. Accurate diagnosis of conditions such as chronic idiopathic facial pain, temporomandibular disorders, burning mouth syndrome and trigeminal neuralgia is essential if inappropriate dental treatment is to be avoided. There are few investigations to help in the diagnostic process and many of these patients have other forms of chronic pain. All the conditions are best treated using a holistic approach. Drugs, such as tricyclic antidepressants and anticonvulsants, are often effective and surgery can be highly successfully in trigeminal neuralgia. Patient education is paramount. CLINICAL RELEVANCE: Although the majority of pain seen in general dental practice is dental in origin, chronic non-dental orofacial pain must be recognized as its management is entirely different.     

Chronic paroxysmal hemicrania: a case report and review of the literature

Chronic paroxysmal hemicrania (CPH) is a rare type of headache that is characterized by daily, multiple, short-lasting attacks of severe pain and associated autonomic symptoms. The pain is strictly unilateral and presents most commonly in the ocular, temporal, maxillary, and frontal areas. The excruciating, throbbing pain of CPH can be misdiagnosed as pain associated with dental pathology, especially when located in the maxillary area. Moreover, pain manifesting in the maxillary and temporal areas can be confused with temporomandibular disorders. CPH patients occasionally seek treatment in dental offices or orofacial pain centers. Accordingly, dentists should be familiar with CPH in order to avoid unnecessary, irreversible dental treatment. A case is presented to highlight many of the features of CPH.     

Toothache with a multifactorial etiology: a case report

Abstract A case report of orofacial pain originating from both dental and nondental conditions is presented. The spontaneous throbbing pain initiated from the left maxillary second premolar and spread throughout the entire upper part of the lace to the frontoparietal area. Root canal treatment of the maxillary second premolar did not resolve the chief complaint. Magnetic resonance imaging examination revealed hypertrophy of the left inferior turbinate and soft tissue haziness in the left maxillary sinus floor. After antrostomy, submucosal turbinectomy; and endodontic treatment, the patient was free from pain. The final diagnosis of this case, in addition to pulpitis, was maxillary sinusitis with chronic rhinitis. The multiple factors associated with the etiology made the diagnosis difficult. The mechanism of referred pain from the maxillary sinus and paranasal nuicosa to the maxillary teeth and face is discussed.     

Plastic changes in nociceptive pathways contributing to persistent orofacial pain

BackgroundPain is a warning signal for the body defense mechanisms and is a critical sensation for supporting life. However, there are still many unclear points about the pathophysiological mechanism of orofacial pain. This situation makes it difficult for many clinicians to treat orofacial pain hypersensitivity.HighlightNoxious information on the orofacial region received by trigeminal ganglion neurons is recognized as “orofacial pain” by being transmitted to the somatosensory cortex and limbic system via the spinal trigeminal nucleus and the thalamic sensory nuclei. Orofacial inflammation or trigeminal nerve injury causes neuropathic changes in various nociceptive signaling pathways, resulting in persistent orofacial pain. It is also considered that persistent orofacial pain is triggered by plastic changes in nociceptive signaling pathways involving various cells such as satellite glial cells, astrocytes, microglia, and macrophages, as well as nociceptive neurons.ConclusionRecent studies have shown that hyperexcitability of nociceptive neurons in the nociceptive signaling pathways of the orofacial region caused by a variety of factors causes persistent orofacial pain. This review outlines the pathophysiology of orofacial pain along with the results of our study.     

Malignant lymphoma of the maxillary sinus manifesting as a persistent toothache.

Many teeth have been mistakenly extracted or endodontically treated because of an incorrect diagnosis of orofacial pain, including toothache. A case of persistent toothache originating from a malignant lymphoma of the left maxillary sinus is presented. Root canal therapy and extraction of the upper left quadrant teeth from the canine to the second molar did not resolve the chief complaint. The patient was referred to a neurologist and received a diagnosis of a malignant lymphoma, a rare lesion of the maxillary sinus. This case stresses the importance of considering malignant neoplasm of the maxillary sinus as a potential etiologic factor in the differential diagnosis of orofacial pain.     

The Trigeminal Nerve. Part IV: The Mandibular Division

The mandibular or third division of the trigeminal nerve is the largest of the three divisions. It is considered a mixed nerve. That is, like the ophthalmic and maxillary divisions, the mandibular conveys afferent fibers. But unlike the former two divisions, the mandibular also contains motor or efferent fibers to the muscles of mastication, the mylohyoid and anterior digastric muscles, and the tensor veli palatini and tensor tympani muscles. So intimately associated with dentistry, the mandibular nerve has also been termed the dental nerve by anatomists in the past. This extensive and complicated division of the trigeminal nerve can cause confusion to both patient and doctor. Pain is often referred within its branches and even into other trigeminal divisions, chiefly the maxillary. This fourth and last article about the trigeminal nerve will present in detail the mandibular division.     

经上颌窦神经撕脱术治疗三叉神经痛Ⅱ支

目的:评价经上颌窦神经撕脱术治疗三叉神经痛Ⅱ支的疗效。方法:选择1994-08—2009-05期间我科收治的60例经上颌窦神经撕脱术治疗三叉神经痛Ⅱ支的患者进行疗效观察。结果:60例患者手术后均无疼痛,随访1～3年,术后2年疼痛复发6例,术后3年疼痛复发4例,复发率为16.67%。但复发后疼痛均较术前明显减轻,患者能够忍受。所有患者术后除患支区皮肤和黏膜有麻木感外均无其他并发症,麻木感在0.6～1年后逐渐减轻。结论:经上颌窦神经撕脱术治疗三叉神经痛Ⅱ支,效果较好,复发率低,并发症少,是安全有效的治疗方法。     

Chronic orofacial pain: a clinical challenge

Most orofacial pain originates in the oral cavity and the surrounding structures. However, advances in the understanding of pain neurophysiology have shown that convergent afferent nociceptive transmissions from non-trigeminal, extraoral sources can enter the trigeminal system. This may confuse the diagnosis by presenting as (or contributing to) dental, sinus, temporomandibular and other head and neck pains. Incorrect diagnoses may lead to inappropriate and/or invasive procedures, creating further problems. Professor Richard Kroening (former Director of the UCLA Pain Management Center) repeatedly emphasised the maxim that "without correct diagnosis, there can be no prognosis". My own areas of special interest have included acute pain management (anaesthesia and conscious sedation) and chronic orofacial pain. I have seen many dental patients who have been referred to multidisciplinary pain management clinics, often after years of failed treatment attempts. More recent experience as a member of a hospital team evaluating long term ACC patients with many types of persistent pain problems again confirms the premise that accurate diagnosis is critical if management is to be successful.     

The trigeminal nerve. Part IV: the mandibular division

The mandibular or third division of the trigeminal nerve is the largest of the three divisions. It is considered a mixed nerve. That is, like the ophthalmic and maxillary divisions, the mandibular conveys afferent fibers. But unlike the former two divisions, the mandibular also contains motor or efferent fibers to the muscles of mastication, the mylohyoid and anterior digastric muscles, and the tensor veli palatini and tensor tympani muscles. So intimately associated with dentistry, the mandibular nerve has also been termed the dental nerve by anatomists in the past. This extensive and complicated division of the trigeminal nerve can cause confusion to both patient and doctor. Pain is often referred within its branches and even into other trigeminal divisions, chiefly the maxillary. This fourth and last article about the trigeminal nerve will present in detail the mandibular division.     

Clinical neurophysiology and quantitative sensory testing in the investigation of orofacial pain and sensory function

Chronic orofacial pain represents a diagnostic and treatment challenge for the clinician. Some conditions, such as atypical facial pain, still lack proper diagnostic criteria, and their etiology is not known. The recent development of neurophysiological methods and quantitative sensory testing for the examination of the trigeminal somatosensory system offers several tools for diagnostic and etiological investigation of orofacial pain. This review presents some of these techniques and the results of their application in studies on orofacial pain and sensory dysfunction. Clinical neurophysiological investigation has greater diagnostic accuracy and sensitivity than clinical examination in the detection of the neurogenic abnormalities of either peripheral or central origin that may underlie symptoms of orofacial pain and sensory dysfunction. Neurophysiological testing may also reveal trigeminal pathology when magnetic resonance imaging has failed to detect it, so these methods should be considered complementary to each other in the investigation of orofacial pain patients. The blink reflex, corneal reflex, jaw jerk, sensory neurography of the inferior alveolar nerve, and the recording of trigeminal somatosensory-evoked potentials with near-nerve stimulation have all proved to be sensitive and reliable in the detection of dysfunction of the myelinated sensory fibers of the trigeminal nerve or its central connections within the brainstem. With appropriately small thermodes, thermal quantitative sensory testing is useful for the detection of trigeminal small-fiber dysfunction (Adelta and C). In neuropathic conditions, it is most sensitive to lesions causing axonal injury. By combining different techniques for investigation of the trigeminal system, an accurate topographical diagnosis and profile of sensory fiber pathology can be determined. Neurophysiological and quantitative sensory tests have already highlighted some similarities among various orofacial pain conditions and have shown heterogeneity within clinical diagnostic categories. With the aid of neurophysiological recordings and quantitative sensory testing, it is possible to approach a mechanism-based classification of orofacial pain.     

Physiotherapy as an adjuvant therapy for treatment of TMJ disorders

Physiotherapy has long been used to cure joint and muscle diseases. It has also been used to treat various diseases without inflicting mental trauma or the pain of surgery. This adjunctive therapeutic modality is widely used for patients with orofacial disorders, especially in the prevention or treatment of temporomandibular joint (TMJ) disorder, hypomobility, or ankylosis. Physiotherapy has a particular importance in the treatment of TMJ disorders such as myofascial pain and internal derangement. This review article highlights the importance of physiotherapy as an emerging adjuvant therapy in the treatment of TMJ disorders.     

A case of zoster sine herpete of the trigeminal nerve

Varicella-zoster virus reactivation causes zoster (shingles), a syndrome characterized by severe pain and a vesicular rash. The present report details a case of varicella-zoster virus reactivation of the maxillary and mandibular division of the right trigeminal nerve without evidence of vesicular rash (zoster sine herpete). It is difficult to identify owing to no typical clinical signs such as vesicular eruption. Zoster sine herpete of the trigeminal nerve, in particular, is rarely reported. In this case, the diagnosis was based on clinical findings and was supported by the demonstration of an immunoglobulin G antibody. Zoster sine herpete of the trigeminal nerve, in particular, should be considered in patients with severe facial pain over specific dermatomes, if they do not demonstrate appreciable findings of traumatic neuropathy, tumor or herpes zoster.     

Meningioma as a cause of chronic orofacial pain: case reports

We describe two middle-aged men whose chronic orofacial pain was caused by underlying meningiomas. In both cases treatment was delayed because evolving dentoalveolar and possible chronic idiopathic facial pain had been investigated before presentation. Subsequent disturbances of the ipsilateral VII (and later VIII) nerves prompted magnetic resonance imaging (MRI) of one patient, while the possibility of a central lesion was recognised at presentation in the second, whose atypical focus of trigeminal neuralgia was labile within the ipsilateral distribution of the trigeminal nerve. Both cases highlight the importance of considering proximal intracranial lesions as a possible cause of atypical or refractory chronic orofacial pain so unnecessary delay in the diagnosis of otherwise operable tumours can be avoided.     

Clinical implications of the innervation of the temporomandibular joint

The successful management of temporomandibular joint (TMJ) pain remains elusive. Often, the initial relief of pain is complicated by recurrence of the symptoms. This time frame suggests that the pain may be related to neuromas of the nerves that innervate the TMJ. The current study attempted to define the innervation pattern of the TMJ as identified in 16 embalmed and 8 fresh-frozen specimens. In each specimen, the auriculotemporal nerve, a branch of the mandibular portion (V3) of the trigeminal nerve, was found to innervate the lateral capsule of the TMJ. In 75% of the specimens, the masseteric nerve, a branch of the maxillary portion (V2) of the trigeminal nerve, was found to innervate the anteromedial capsule of the TMJ. In 33% of the specimens, there was a branch coming through the mandibular notch to innervate the anteromedial capsule that was not from the masseteric nerve; this nerve is believed to have passed through the lateral pterygoid muscle after leaving V2. These consistent patterns of innervation of the TMJ suggest that diagnostic nerve blocks can be done to determine the pain pathway in these patients. It is suggested that if the nerve blocks are successful, TMJ denervation may be a future method of pain relief in patients with recalcitrant or recurrent TMJ pain.