The trigeminal nerve. Part III: The maxillary division

The maxillary nerve gives sensory innervation to all structures in and around the maxillary bone and the midfacial region including the skin of the midfacial regions, the lower eyelid, side of nose, and upper lip; the mucous membrane of the nasopharynx, maxillary sinus, soft palate, palatine tonsil, roof of the mouth, the maxillary gingivae, and maxillary teeth. This vast and complex division of the trigeminal nerve is intimately associated with many sources of orofacial pain, often mimicking maxillary sinus and/or temporomandibular joint involvement. For those who choose to treat patients suffering with orofacial pain and temporomandibular disorders, knowledge of this nerve must be second nature. Just providing the difficult services of a general dental practice should be stimulus enough to understand this trigeminal division, but if one hopes to correctly diagnose and treat orofacial pain disorders, dedication to understanding this nerve cannot be overstated. In this, the third of a four part series of articles concerning the trigeminal nerve, the second or maxillary division will be described and discussed in detail.     

Chronic orofacial pain

The issues specific to trigeminal pain include the complexity of the region, the problematic impact on daily function and significant psychological impact (J Dent, 43 , 2015, 1203). By nature of the geography of the pain (affecting the face, eyes, scalp, nose, mouth), it may interfere with just about every social function we take for granted and enjoy (J Orofac Pain, 25 , 2011, 333). The trigeminal nerve is the largest sensory nerve in the body, protecting the essential organs that underpin our very existence (brain, eyes, nose, mouth). It is no wonder that pain within the trigeminal system in the face is often overwhelming and inescapable for the affected individual.     

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.     

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.     

Recurrent idiopathic trigeminal sensory neuropathy

Idiopathic trigeminal neuropathy is a rare disorder characterized by transient sensory disturbances in the territory of one or more branches of the trigeminal nerve. Acute and chronic forms of the disease have been recognized, but to our knowledge no recurrent cases have been reported. Two cases of recurrent idiopathic trigeminal sensory neuropathy are reported. The patients presented sensory alterations limited to the territory of the trigeminal nerve in the absence of other clinical features. In both cases sensory disturbances began in the tongue and lips and later spread throughout the face. The whole trigeminal nerve territory was involved in the first patient, but in the second patient only the second and third trigeminal branches were affected. There was no muscle weakness or pain, and the corneal reflex was present in both patients. The first patient recovered completely after 3 months, but the symptoms recurred in a similar fashion 3 years later. In the second patient the symptoms occurred each winter for more than 10 years. The conditions in these two patients could be considered as recurrent idiopathic forms of trigeminal sensory neuropathy.     

Bi-modal radiofrequency treatment for coexisting neuralgia and neuropathy in adjacent divisions of the trigeminal nerve

Trigeminal neuralgia and deafferentation neuropathic pain, or trigeminal neuropathy, are different symptomatologies, rarely reported to present together. The case of a 65-year-old gentleman suffering from trigeminal neuralgia of the maxillary and mandibular division is reported. He first underwent an infraorbital neurectomy that was complicated by deafferentation neuropathic pain, whilst his mandibular neuralgia continued. He was treated successfully for both the neuropathic and neuralgic symptoms in the same session using ultra-extended euthermic pulsed radiofrequency treatment for the maxillary division (V2) and radiofrequency thermocoagulation for the mandibular division (V3). This report is novel in describing the use of dual modalities in the same session for two distinct coexisting clinical entities in two different divisions of the same cranial nerve. The use of ultra-extended pulsed radiofrequency treatment for neuropathic pain in this case is also unique. Nearly 2 years after the procedure, the patient continues to have complete pain relief.     

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.     

Herpes zoster of the trigeminal nerve: a case report and review of the literature

Herpes zoster (shingles) is caused when the varicella zoster virus that has remained latent since an earlier varicella infection (chicken-pox) is reactivated. Herpes Zoster is a less common and endemic disease than varicella: factors causing reactivation are still not well known, but it occurs in older and/or immunocompromised individuals. Following reactivation, centrifugal migration of herpes zoster virus (HZV) occurs along sensory nerves to produce a characteristic painful cutaneous or mucocutaneous vesicular eruption that is generally limited to the single affected dermatome. Herpes zoster may affect any sensory ganglia and its cutaneous nerve: the most common sites affected are thoracic dermatomes (56%), followed by cranial nerves (13%) and lumbar (13%), cervical (11%) and sacral nerves (4%). Among cranial nerves, the trigeminal and facial nerves are the most affected due to reactivation of HZV latent in gasserian and geniculated ganglia. The 1st division of the trigeminal nerve is commonly affected, whereas the 2nd and the 3rd are rarely involved. During the prodromal stage, the only presenting symptom may be odontalgia, which may prove to be a diagnostic challenge for the dentist, since many diseases can cause orofacial pain, and the diagnosis must be established before final treatment. A literature review of herpes zoster of the trigeminal nerve is presented and the clinical presentation, differential diagnosis and treatment modalities are underlined. A case report is presented.     

Cryotherapy in the management of paroxysmal trigeminal neuralgia. Four year follow up of 39 patients

Paroxysmal trigeminal neuralgia still remains a difficult condition to treat. Carbamazepine (Tegretol) has been a first line treatment, failing this surgery becomes necessary. However, many surgical procedures result in permanent sensory loss. Peripheral cryotherapy, along with the recently described Jannetta (1976) and Hakanson (1981) techniques, attempt to preserve sensation. Cryotherapy to 53 branches of the trigeminal nerve in 39 patients, who were followed up for 4 years, resulted in pain relief out-lasting return of sensation. These cases show that cryotherapy applied to the correctly located affected nerve branches can produce results which are unobtainable by other methods of pain control in paroxysmal trigeminal neuralgia.     

Peripheral and Central Mechanisms of Trigeminal Neuropathic and Inflammatory Pain

While physiological pain (nociceptive pain) has a protective role in warning of potential tissue damage in response to a variety of noxious stimuli, pathological pain (neuropathic and inflammatory pain) serves no such meaningful purpose. Injury/inflammation in the peripheral tissue that innervates the trigeminal nerve may also alter the properties of trigeminal somatic sensory pathways, causing behavioral hypersensitivity (e.g., pathological pain) and induce pain abnormality caused by noxious stimulation (hyperalgesia) or normally innocuous stimulation (allodynia). These hypersensitivities to nociception are caused by changes in the excitability of trigeminal ganglion neurons (peripheral sensitization), which alter sensory information processing in spinal trigeminal spinal subnucleus caudalis (SpVc)/upper cervical spinal cord (C_1–2) neurons (central sensitization). More is being learned about the activation of peripheral and central glia that play an important role in creating and maintaining pathological pain. This review therefore focuses on the possible sites for sensitization of nociceptive signaling through pain pathways that contribute to trigeminal pathological pain and also discuss potential therapeutic targets in neuron-glial interactions for preventing trigeminal neuropathic and inflammatory pain.     

Trigeminocardiac reflex: a unique case of recurrent asystole during bilateral trigeminal sensory root rhizotomy.

BACKGROUND: The trigeminocardiac reflex is the sudden-onset of dysrhythmia and hypotension during manipulation of any of the branches of the trigeminal nerve. The trigeminal nerve and cardioinhibitory vagus nerve constitute the afferent and efferent pathways in the reflex arc. The trigeminocardiac reflex has been reported to occur during craniofacial surgery, balloon-compression rhizolysis of the trigeminal ganglion, and tumour resection in the cerebellopontine angle. PATIENT & METHOD: A 2-year-old male patient with haemangioma near the sella turcica underwent rhizotomies of both sides of the dorsal sensory roots, of the trigeminal nerves for palliation of intractable trigeminal pain. RESULTS: In this report, we experienced two unexpected episodes of asystole after transection of the sensory roots of the trigeminal nerves. CONCLUSION: Sectioning of the intracranial dorsal sensory root of the trigeminal nerve provides clear evidence of the central role of the trigeminal nerve as the afferent pathway of the trigeminocardiac reflex arc.     

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.     

Persistent orodental pain, atypical odontalgia, and phantom tooth pain: when are they neuropathic disorders?

Patients with unrelenting pain in the teeth, gingival, palatal or alveolar tissues often see multiple dentists and have multiple irreversible procedures performed and still have their pain. Up to one-third of patients attending a chronic facial pain clinic have undergone prior irreversible dental procedures for their pain without success. In these cases, if no local source of infectious, inflammatory, or other pathology can be found, then the differential diagnosis must include a focal neuropathic pain disorder. The common diagnoses given include the terms atypical odontalgia, persistent orodental pain, or if teeth have been extracted, phantom tooth pain. One possibility is that these pain complaints are due to a neuropathic alteration of the trigeminal nerve. There are several diagnostic procedures that need to be performed in any patient suspected of having a trigeminal neuropathic disorder including (1) cold testing of involved teeth for pulpal nonvitality; (2) a periapical radiograph examining the teeth for apical change; (3) a panoramic radiograph examining for other maxillofacial disease; (4) a thorough head and neck examination also looking for abnormality; (5) a cranial nerve examination including anesthetic testing which documents any increased or decreased nerve trigeminal nerve sensitivity and rules out other neurologic changes outside the trigeminal nerve; and (6) MRI imaging in some cases. Finally, when a nonobvious atypical toothache first presents, direct microscopic examination of the tooth for incomplete tooth fracture is also suggested. The majority of these patients are women over the age 30 with pain in the posterior teeth/alveolar arch. Multiple causes exist for sustained neuropathic pain including direct nerve injury (e.g., associated with fracture or surgical treatment), nerve injection injury, nerve compression injury (e.g., implant, osseous growth, neoplastic invasion) and infection-inflammation damage to the nerve itself. Sustained nerve pain is commonly seen in patients with psychiatric impairment. It may be that the unrelenting nature of the pain itself alters the patient's personality. Treatment includes pharmacologic medications which suppress nerve activity. The common medications used for atypical odontalgia and phantom tooth pain include gabapentin, tricyclics, topical anesthetics, and opioids. A list of these medications is provided in table form. Data suggest that once the patient has failed dental treatment and pain persists, the long-term outcome is less than 25 percent will have complete pain relief with treatment. With earlier treatment, better pain control, and improved nerve activity suppression medications, this should also prevent secondary psychiatric disease from developing and lower the number of inappropriate treatments.     

The utility of clinical neurophysiological and quantitative sensory testing for trigeminal neuropathy

This article reviews the utility of neurophysiological recordings and quantitative sensory testing (QST) in providing sensitive, quantitative, and objective tests for the diagnosis and localization of damage to the trigeminal nerve. Electromyography and recordings of the masseter reflex and compound muscle action potential evoked by transcranial magnetic stimulation or direct electrical stimulation of the masseteric nerve can be of value in evaluating the function of a motor neurons supplying the muscles of mastication. Orthodromic recording of the sensory action potential and trigeminal somatosensory-evoked potential recording with the near-nerve stimulation technique are sensitive tools for the investigation of trigeminal sensory Abeta afferents, whereas recordings of polysynaptic trigeminal brainstem reflexes and tactile QST are less sensitive. At late stages of recovery, the blink reflex and masseter inhibitory reflex are often normal, but at earlier stages, the blink reflex recording has good prognostic value, and the presence of a reflex response may confirm continuity of the nerve trunk after partial laceration. Trigeminal small-fiber function (Adelta and C) can be studied with thermal QST of the cool, warm, heat pain, and cold pain detection thresholds or with laser-evoked potential recording. Thermal QST may remain abnormal years after axonal damage and aids in the diagnosis of late sequelae of trigeminal nerve injury. In a study of the diagnostic value of neurography, blink reflex and thermal QST, and various commonly used clinical sensory tests, neurophysiologic tests and thermal QST had better sensitivity (50% to 88% vs 40% to 59%) and negative predictive values (78% to 100% vs 70% to 74%) compared to clinical examination, whereas the specificity (55% to 100%) and positive predictive values (48% to 73%) were similar. At 1 year after trigeminal nerve injury, the risk of a false negative finding with clinical sensory testing was 94%, whereas the combination of nerve conduction recordings and thermal QST increased the diagnostic yield to 100% in patients with long-standing postsurgical sensory alteration. In conclusion, clinical neurophysiological recordings and QST improve the diagnostic accuracy for trigeminal neuropathy.     

Differential diagnosis of toothache to prevent erroneous and unnecessary dental treatment

Toothache represents the most common example of oro-facial pain. Its origin is mostly odontogenic, but several other conditions may mimic dental pain or present themselves as such. Well-known examples are myofascial pain, trigeminal neuropathies like neuralgia and painful post-traumatic trigeminal neuropathic pain, oro-facial neurovascular pains, cardiac pain and sinus disease. This review first discusses the current knowledge on the underlying pathophysiology of heterotopic tooth pain. Afterwards, several conditions potentially presenting as toothache will be illustrated regarding clinical features, diagnosis and management.     

Clinical characteristics of trigeminal nerve injury referrals to a university centre

The aim of this retrospective study was to determine the aetiology and characteristics of trigeminal nerve injuries referred to a university centre with nerve injury care. Fifty-nine patients with 73 injured trigeminal nerves were referred in 10 months. The most common aetiologies were odontectomy (third molar surgery) (52.1% of nerves), local anaesthetic (LA) injections (12.3%), orthognathic surgery (12.3%) and implant surgery (11.0%). The inferior alveolar nerve (IAN) was most commonly injured nerve (64.4%), followed by the lingual nerve (LN) (28.8%). About a quarter of IAN injuries (27.3%) and half of LN injuries (57.1%) from odontectomy had severe sensory impairment. There were twice as many LN than IAN injuries from local anaesthetic injections, but all had mild or no sensory impairment. Nerve injuries from implant surgery occurred only in IAN injuries; none had severe sensory impairment. Neuropathic pain occurred in 14.9% of IAN injuries and only in those with mild or no sensory impairment. Nerve surgery was offered to 45.8% of patients; a third underwent surgery.     

Combined craniofacial approach for the removal of a large trigeminal schwannoma invading the infratemporal fossa

Background

Trigeminal schwannomas are rare tumours accounting for 0.07?C0.36% of all intracranial tumours and 0.8?C8% of intracranial schwannomas. Symptoms and signs of these lesions depend on the site of the tumour, which may compress the nerve of origin or adjacent nerves.

Case report

We describe a case of a 69-year-old woman with a history of progressively worsening hypoesthesia involving the third division of the trigeminal nerve. A tumour of 5-cm diameter was revealed within the right cranial middle fossa, extending to the lateral wall of the cavernous sinus, the infratemporal fossa and the posterior wall of the maxillary sinus. A combined craniofacial approach was undertaken. A right extended subtemporal craniotomy was performed. The intracranial component of the tumour, originating from the third division of the trigeminal nerve and compressing the cavernous sinus, was removed in total. We proceeded with a Weber?CFerguson approach through which the extracranial component of the tumour was also totally resected. The postoperative computed tomography of the head has shown complete tumour removal. The histopathologic examination revealed a cellular neurinoma. Postoperatively, the patient expressed a transitory palsy of the oculomotor nerve, which resolved within a few weeks. The patient remains free of recurrence with mild hypoesthesia of the third trigeminal branch 5 years after treatment.

Discussion

Surgery of trigeminal schwannomas may be a very challenging task. Various surgical approaches for trigeminal schwannomas excision have been described. With this combined approach, the tumour was freed from the surrounding tissues and was easily and totally removed.     

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.     

Psychophysical assessment of patients with posttraumatic neuropathic trigeminal pain

This article reviews the utility of psychophysical approaches in the assessment of posttraumatic neuropathic trigeminal pain. Methods of quantitative sensory testing are derived from psychophysical principles and provide a widely accepted means for characterizing sensory dysfunction in patients who experience injury to the trigeminal nerve. No published study, however, has sought to compare sensory findings from trigeminal nerve-injured patients who develop neuropathic pain with those from trigeminal nerve-injured patients who remain pain-free. Moreover, sensory testing data from trigeminal nerve-injured patients with pain have been published in only a few reports. As a result, remarkably little is known about sensory factors associated with the development of posttraumatic trigeminal neuralgia. Review of the separate literatures suggests that both trigeminal nerve-injured patients with pain and pain-free trigeminal nerve-injured patients exhibit grossly similar impairments in sensory function. In addition, trigeminal nerve-injured patients with pain may be more likely to report cold allodynia than patients without pain and to exhibit signs of central sensitization such as allodynia to light brushing tactile stimuli and abnormal temporal summation of pain. New studies using state-of-the-art psychophysical methods are needed to search for sensory markers that bear on the development of pain. Moreover, the relationship between psychophysical indices of central sensitization and measures of clinical pain should be addressed to obtain a better understanding of the underlying pathophysiology.