This chapter focuses on the common and significant causes of orofacial pain excluding those related to dental and periodontal pathology. For many patients, orofacial pain is the stimulus to seek dental care, thus the treatment of patients in pain is, unfortunately, going to form a significant part of your practice. In terms of orofacial pain, the basis of accurate diagnosis and appropriate treatment is the information that is obtained from the patient. Consequently, history-taking skills need to be utilised to their best effect.
• the nature of the pain: encourage the patient to describe the pain in their own words by the use of open questions rather than supplying them with a list of descriptors of pain from which to select; the latter can be useful if a patient is finding it particularly difficult to describe their pain. The use of a 0 to 10 scale can assist patients in expressing the severity of their pain with 0 being pain free and 10 representing the worst pain that the patient has ever experienced
• the site(s) affected: ask the patient to point to the source of the pain and/or outline the area affected by it; does the pain radiate to other areas? Is it confined to the distribution of a particular nerve(s) or does it cross anatomical boundaries, for example the midline?
Much of this information will emerge naturally, in most cases, by simply asking the patient to tell you about their pain. Verbal and non-verbal communication skills should be used to encourage the patient to tell their story in a way that is mutually beneficial. At the end of the consultation, the patient should feel that they have been able to impart information that they believed to be relevant and the dentist should have guided them through this process to yield up the information required to reach a differential diagnosis.
A thorough extraoral (including the temporomandibular joint and muscles of mastication) and intraoral examination (see Chapter 2) is obviously mandatory. Additional components of the examination procedure may be required depending on the differential diagnosis, for example assessment of cranial nerve function in patients presenting with symptoms of trigeminal neuralgia. The differential diagnosis will be based on a combination of the outcome of the examination and history. The special investigations that are carried out (these may not always be necessary) will be aimed at clarifying the differential diagnosis and should be carefully tailored to fulfil this purpose, not used as a general screening procedure.
While this chapter will not be considering those diseases of the teeth and their supporting structures that give rise to orofacial pain, it is important to stress that dentists need to be particularly skilled in excluding such structures as the source of the patient’s pain. The principal causes of pain arising from the teeth and their supporting structures are listed below, with reference to the appropriate sections of this book and its companion volume (Master Dentistry Volume 2, edited by Heasman). You must know the signs of symptoms of these conditions and apply this knowledge when reaching a differential diagnosis in the case of a patient with orofacial pain.
The majority of cases (>85%) of trigeminal neuralgia are of classic type (CTN). Compression of the trigeminal nerve in the region of the dorsal root entry zone (DREZ) by a blood vessel has emerged as the leading cause of CTN. In STN, this compression is the result of a structural lesion such as a tumour or vascular malformation. Demyelination secondary to multiple sclerosis also falls within the definition of STN.
Duration: Usually of seconds duration but may last for up to 2 minutes. Occasionally a dull pain persists in the background after the sharp pain has resolved. In severe cases, the episodes of pain may be so close together that they seem continuous, but this is unusual. Spontaneous remission of symptoms can occur, but both this and their recurrence are unpredictable.
Site: The pain is localised to one or more divisions of the trigeminal nerve, most commonly the second and third division. The patient outlines the distribution of the appropriate division(s) when asked to indicate the area affected by the pain. The pain does not usually cross the midline. Bilateral TN is unusual and suggestive of STN.
Initiating factors: The pain may be induced when a particular area of the skin or mucosa is stimulated, the so-called ‘trigger zone’ but this is not invariably the case. Activities of daily living, for example washing the face, shaving, putting on make-up, eating, speaking and exposure to cold may all induce pain.
Associated signs and symptoms: The absence of associated signs and symptoms of sensory or motor deficit is important. Neurological assessment can play a significant role in differentiating between CTN and STN. Trigeminal sensory deficits may be a feature of the latter. The patient’s medical history may already have revealed the existence of a structural abnormality
Magnetic resonance imaging (MRI) is now considered mandatory. In some cases, it demonstrates the intimate, potentially causative, relationship between the trigeminal root and an adjacent blood vessel. MRI is of particular value in excluding posterior cranial fossa lesions and, to some extent, multiple sclerosis.
The therapy of choice is carbamazepine. Reduction or complete resolution of symptoms following its use is considered to be virtually diagnostic of trigeminal neuralgia. However, it should be prescribed cautiously, starting at a dose of 100 mg twice or three times daily and increasing slowly until the patient’s symptoms are controlled. This is usually achieved at between 200 and 400 mg three times daily. Gradual increase in dosage is important as elderly patients are particularly susceptible to carbamazepine’s many side-effects. Some of these, for example nausea, ataxia and dizziness, make taking carbamazepine completely unacceptable to the patient or significantly limit its dose. Others, including leucopenia, thrombocytopenia and skin reactions, necessitate its withdrawal; patients should be informed of the signs and symptoms of these conditions when the drug is prescribed. Full blood count, liver and renal function tests should ideally be carried out prior to its prescription and at regular intervals during at least the first months of treatment. Individuals of Han Chinese or Thai origin should be tested for HLA-B∗ 1502 allele and, if positive, carbamazepine should not be prescribed as a result of the risk of development of Stevens–Johnson syndrome. If withdrawal of carbamazepine proves to be necessary, oxcarbazepine provides an alternative. Should the dose of carbamazepine be limited, the antiepileptic lamotrigine may be added or used an alternative.
Although the evidence base for surgical interventions is weak, microvascular decompression (MVD) appears to have the best outcome and is emerging as the preferred option in those patients who are fit for open surgery. In this procedure, the offending blood vessel is lifted away from the trigeminal root and permanently repositioned. In comparison to peripheral destructive procedures such as neurectomy or central destructive procedures such as percutaneous radiofrequency thermocoagulation, MVD has a low rate of complications. It is, however, important that MVD is performed sooner rather than later as success declines with duration of trigeminal neuralgia symptoms. This is leading to a change in approach with clinicians raising the awareness of patients to the possibility of surgical intervention much earlier in the medical treatment phase rather than as a last resort. Gamma knife stereotactic surgery provides an alternative to MVD in those patients for whom surgery is contraindicated. Other central procedures include retrogasserian glycerol injection, compression or radiofrequency thermocoagulation. The above procedures have largely replaced peripheral treatment options although local anaesthetic injected into the trigger zone will provide temporary relief of symptoms (bupivacaine has a longer duration of action) and is useful in confirming the diagnosis.
Associated signs and symptoms: The absence of associated signs and symptoms of sensory or motor deficit is important. Neurological assessment is mandatory to ensure that the symptoms of glossopharyngeal neuralgia are not the result of a lesion (neoplastic or non-neoplastic) within the posterior cranial fossa or jugular foramen. The patient’s medical history may already have revealed the existence of such a lesion.
Special investigations do not contribute directly to the diagnosis of glossopharyngeal neuralgia but are important in excluding posterior cranial fossa or jugular foramen lesions. MRI or computed tomography (CT) are both appropriate.
The principles of surgical management are the same as those for trigeminal neuralgia: that is, chemical, thermal or physical damage to the appropriate nerve. However, it is usually not possible to use local injections or cryotherapy. Surgical section of the glossopharyngeal nerve can be effective as can other central surgical techniques but these are not without significant side-effects.
Development of the classic vesicles of herpes zoster (Chapter 11; Fig. 14.1) is, in some cases, preceded by facial pain. This leads to the diagnosis being made retrospectively in many cases.
Fig. 14.1 Vesicles of herpes zoster.
Site: The pain is limited to the distribution of the division(s) of the trigeminal nerve in which the lesions of herpes zoster subsequently develop. It may be localised by the patient to a particular tooth or teeth.
There is evidence that prevention or amelioration of postherpetic neuralgia can be achieved by the use of antiviral drugs such as famciclovir to treat the preceding herpes zoster infection. If postherpetic neuralgia develops, its medical management is difficult. Conventional non-steroidal anti-inflammatory agents are largely ineffective, as is carbamazepine. There is evidence to support the use of tricyclic antidepressants and gabapentin – these along with pregabalin and topical lidocaine have been advised as first-line treatment. Strong opiods and capsaicin may also be of benefit.
Initiating factors: A variety of stimuli may induce the headache, for example certain foodstuffs (e.g. chocolate, bananas), alcohol, stress, hormonal changes during the menstrual cycle, the contraceptive pill or noise.
Analgesics such as paracetamol, ibuprofen or aspirin are effective, particularly when used in combination with an antiemetic such as metoclopramide. If such drugs are ineffective, the use of serotonin 5HT1-receptor agonists, for example sumatriptan, is appropriate. In terms of prevention, useful drugs include beta-blockers, tricyclic antidepressants, gabapentin or sodium valproate.
Duration: Typically, there are intermittent episodes of pain of between 15 and 180 minutes’ duration on a daily basis for several weeks, interspersed with pain-free periods of months rather than days in duration.