This chapter aims to make the clinical pattern of different pain problems more recognisable and highlights the importance of using quality of life as a measure of success.
After reading this chapter you should be able to see the patient behind the pain, to form an appropriate differential diagnosis and treatment plan to obtain the best improvement in quality of life.
This section is concerned with chronic facial pain still present once dental and non-dental pathological conditions have been excluded. Pain appreciation can have many triggers, the simplest of which is central or peripheral nerve damage (neuropathic pain). Similarly, when nerve function is changed by an alteration in neurotransmitter balance, synaptic signal transmission is also altered and thus the appreciation of information by the nervous system changes. Both somatic and autonomic pathways pass information to the brain for consideration. Thus damage or alteration to either or both of these can lead to pain appreciation by the individual. In addition, dysfunction of nerves that have a motor or vasomotor ‘component’ can produce changes in the tissues detected by the patient. This is most commonly seen in the autonomic system, where vasomotor changes accompany pain in many individuals, leading them to report swelling, erythema or sweating in the region affected by the pain.
The idea that pain is a simple stimulus and response system as proposed by Descartes is now rarely voiced. In fact, pain as ‘a sensation’ is in question. There are undoubtedly pathways in the nervous system responsible for the transmission of damage signals from the tissues. It is the appreciation and interpretation of this information within the brain that results in the perception of pain. If pain is considered a ‘state of mind’ rather than a pure sensation it is easier to understand how many of the chronic pain conditions can arise when little or no tissue damage is evident. Alteration of the chemical balance of the brain, be it by damage signals from the tissues, emotional changes or drug therapy can all change perception of pain and the pattern or type of signals into the brain that can be interpreted as pain. Pain is now considered multidimensional. It is defined by the International Association for the Study of Pain as ‘an unpleasant sensory and emotional experience, associated with actual or potential tissue damage, or described in terms of such damage’. This reflects both the patient’s experience that pain is often triggered by tissue damage and the clinician’s, that mood and pain perception are intimately linked.
Tissue damage releases chemical mediators that activate both A delta and C fibres. These mediators also lower the threshold sensitivity of the pain nerves, making further firing possible with a lower level of stimulation. Chronic nerve stimulation can therefore lead to such a lowering of the firing thresholds that innocuous triggers, including normal sensation, can be enough to cause the pain nerves to fire. Injury to sensory nerves also triggers nerve ‘sprouting’. This results in new connections forming in the dorsal horn of the spinal cord from somatic sensory nerves to pain fibres after sensory nerve injury. Stimulation of the sensory nerve then causes the pain pathways in the spinal cord to activate inappropriately. The effect of both changes is to promote chronic pain in previously damaged tissue without any ongoing damage. This is known as allodynia.
Even with activation of the A delta and C fibres, pain transmission to the brain is not guaranteed. The ‘Gate Theory’ proposed by Melzak and Wall suggested that other nerve activity within the spinal column could modulate the passage of the pain signals to the brain. This can either inhibit transmission, as with the battlefield casualty unaware of an injury, or facilitate pain as seen in an anxious patient undergoing operative dental care. The control of pain transmission and appreciation by the higher centres is very important in clinical practice, with the brain having the ability to block or facilitate pain appreciation. The anxious patient can even feel true pulpal pain by activation of pain memories by Pavlovian association before the tooth has been touched.
Phantom limb pain provides a clear example that nerve signals from the body are not necessary for pain to be ‘felt’, demonstrating that pain as well as all other sensations are literally ‘in the mind’ rather than localised to a body part. When looking at methods for controlling chronic pain it is important to consider both central and peripherally acting drugs, psychological and physical treatments. All have a role to play. In many cases of chronic pain there may be more than one ‘pain’ problem acting together, and this may require a combination approach to treatment – partly mood and psychological therapy and in part drug or physical treatments.
This section includes a variety of clinical presentations where it appears that normal nerve function is disrupted, leading to the perception of pain. These conditions are listed in Table 9-1.
Trigeminal neuralgia (TN) is a well-recognised condition affecting predominantly older patients. It is a common condition presenting over the winter months. The exact prevalence is not known, but is thought to be in the order of six per million population, with a slight female predisposition.
It is an extremely debilitating condition for the affected individuals, with sudden-onset, short-duration, high-intensity, lancinating or ‘electric shock-type’ pain. This radiates from a focal point or ‘trigger zone’ in the trigeminal distribution and is severe enough to halt the patient’s activities abruptly. The pain usually passes in seconds, but its severity causes the patient to adopt a variety of strategies to try to prevent the pain returning. Most often trigeminal neuralgia involves the mandibular or maxillary divisions and is unilateral. Variations exist, however, with bilateral pain or a persisting burning pain in the trigger area after the initial sudden burst reported by some patients. It is essential to perform a cranial nerve examination for all patients presenting with TN. There should be no neurological deficit detected, but occasionally problems are found. Common findings include trigeminal sensory loss or marked deafness on the pain side. In these circumstances, or when a patient younger than 50 is suspected of having TN, the clinician should be suspicious about the presence of central nervous system (CNS) disease. An MRI examination is then essential and may identify a focal or diffuse brain lesions, such as an acoustic nerve neuroma or multiple sclerosis.
The trigger and mechanism for the pain in TN remains unclear. There is no evidence to support a peripheral nerve dysfunction. An abnormality of nerve signal-processing within the CNS seems more likely, perhaps due to compression of the nerve root at the trigeminal ganglion.
Treatment of TN is initially medical, and most patients respond well to carbamazepine therapy. This medication does have some disadvantages, however, including causing an allergic rash in some. In the elderly population, who most frequently present with TN, the drug side-effects can be very limiting. Sedation, cerebellar and balance disorders together with alterations to liver drug metabolism can all lead to dose limitations or early termination of treatment and consequently the return of the pain. The use of the modified release preparation of carbamazepine can minimise some of these effects. When an alternative medical treatment is required, gabapentin, baclofen, phenytoin, oxcarbazapine and lamotrigine have all been used with success. Occasionally it is necessary to combine one or more drug treatments to get adequate pain relief. Patients with multiple sclerosis can be particularly resistant to conventional therapy but may respond to high-dose systemic corticosteroids. Surgical care has traditionally been reserved for patients for whom medical treatments had failed. However, early surgical intervention is now thought to be an advantage by eliminating the need for medication or, more commonly, reducing the dose required for adequate pain control. Operative morbidity and mortality may also be reduced by treating patients while they are younger and fitter. However, destructive peripheral nerve surgery, such as an alcohol nerve block of the affected trigeminal branch, should now only be performed as a palliative procedure. These procedures ultimately cause allodynia, making the pain problem worse, and should be reserved for patients both unable to tolerate effective medical therapy and unfit for other CNS surgical procedures. Retrogasserian glycerol injection and radiofrequency thermocoagulation of the trigeminal ganglion are destructive neurosurgical procedures that would be expected to leave the patient with hemifacial anaesthesia on the operated side. Surprisingly, light touch is often preserved, although patients do report altered sensation and they tolerate the procedure remarkably well. Vascular decompression procedures around the trigeminal ganglion have met with a high degree of success but with a higher operative risk. At present they seem the best surgical option for the younger patient.
A cerebrovascular accident or stroke is a brain injury that leads to a permanent loss of motor, sensory or cognitive function. Although the brain itself has no pain awareness, damage to parts of the brain involved in pain appreciation can result in altered perception of pain. This can lead the individual to experience pain without a nociceptive input, and in some patients facial or dental pain can result. The time between the onset of the pain and the stroke is the key to the diagnosis. Treatment strategies outlined below for neuropathic pain are the most helpful in managing this difficult condition, but often a full range of pain strategies needs to be employed.
The term ‘neuropathic’ pain implies damage to nerves that leads to altered transmission of normal signals from the tissues to the CNS. These altered signals are then interpreted as pain. Some nerve injury conditions are well known to predispose a patient to chronic pain. These include damage resulting from Herpes zoster reactivation (shingles), alcohol nerve block (anaesthesia dolorosa) or even damage to the inferior alveolar ner/>