Chapter 8

Addressing Key Psychological Factors in Orofacial Pain

It is much more important to know what sort of patient has a disease than what sort of disease a patient has.

Sir William Osler, 1849–1919, Canadian physician

Aim

The aim of this chapter is to provide dental practitioners with guidelines to screen for the key psychological factors of depression, anxiety and somatisation, which can affect accuracy of diagnosis and treatment outcomes in patients with orofacial pain (OFP). The screening instruments described in this chapter will also assist in determining whether a psychological or psychiatric referral is required.

Outcome

After reading this chapter, dental practitioners will have an understanding of:

• the important role that depression, anxiety and somatisation play in the pain experience and treatment outcomes

• useful pain rating and psychological screening instruments.

Case Presentation

• Complaint. A 36-year-old female presented to her dentist in a tearful and dramatic manner, complaining of right-sided facial pain of three years’ duration. The current pain began following root canal treatment of her lower left second premolar subsequent to aching toothache. When the pain failed to resolve, the tooth was extracted; however, the pain continued in the region of the lower left second premolar and spread to the lower left first molar and the lower left first premolar.

• Clinical examination. The patient was asked to rate her pain at this stage and she assessed it as 7 on a 1–10 visual analogue scale (VAS) and described it as a constant deep dull sensation. She also complained of intermittent episodes of sharp-electrical shooting sensations down her right mandible, each lasting seconds to minutes, occurring five to ten times a day. The intensity of the shooting pain was 9 on the VAS. The pain had spread to include her entire right face and neck and she described it as hot, burning and aching. She said that the pain was also increasing in intensity and was now accompanied by migraine headaches several times a week. She also bruxes at night and has not slept well since the onset of her pain and feels exhausted all of the time. The patient has become very limited in terms of functioning and activities of daily living, instead opting to stay in bed as much as she can, and she is restricted to a soft food diet as any chewing, talking, smiling or oral activities may aggravate the pain. The pain can be reduced with alternating ice and warm packs and analgesics also help “take the edge off” her pain. She reported taking six to ten dihydrocodeine tablets (30 mg) each day on an “as required” schedule. Additional medications included diazepam, 10 mg three times a day for muscle spasm and anxiety; alprazolam 0.5 mg as needed for panic attacks one to three times a day; and zolpidem 10 mg each night for sleep. She has been given fluoxetine in order to help her severe depression and occasional suicide ideation. She has seen numerous dentists who have tried various splints, orthodontics and other occlusal adjustment techniques, each one further aggravating her pain. She saw a neurologist who tried gabapentin, but she was unable to tolerate it. He told the patient that her problem was a temporomandibular disorder (TMD).

• Investigations. Imaging reveals some mild arthritic changes in her right temporomandibular joint (TMJ). Cracked tooth tests were negative.

• Treatment. She was being considered for further endodontic treatment on the lower left first molar and first premolar although, aside from her pain, there is no good cause for pursuing these procedures. She describes her pain as excruciating, torturing, overwhelming and fatiguing. She thinks frequently of suicide but has no plan or intent because she has children. She is now totally disabled.

• Discussion. Challenging case isn’t it? Where do you start? The patient is saying that her life is increasingly unbearable and that she is suffering. Boundaries between the amount she is hurting and the amount she is suffering are blurring. She is beginning to feel very depressed, helpless and not listened to, or even believed. She is wondering if life is worth living in her state. Her somatic focus has become so severe that she thinks of little else other than her pain and the dentists who “caused” her anguish. Is she using the analgesics as means of modulating her emotional distress? Is the diazepam use excessive and contributing to her depression, fatigue and disability? Perhaps trying another procedure, occlusal adjustment or medication, may not yield a favourable outcome? While these may help the hurt to some small degree, they will do little to stop the patient’s suffering. The suffering has taken on a life of its own and needs to be addressed if the pain is to resolve.

Introduction

Few problems are more perplexing and frustrating to the dental practitioner than attempting to manage a patient with chronic OFP. As the case above illustrates, such patients may present with confusing and vague complaints that have been unresponsive to, if not worsened by, an array of prior treatments. Chronic pain impacts all aspects of a patient’s quality of life, including occupational status, finances, psychosocial interactions and, most importantly, their family. As a result the patient with chronic OFP is likely to present with a host of psychological issues that may cloud the diagnosis and adversely affect treatment responsiveness, irrespective of objective pathophysiological findings.

The chronic pain literature is replete with research reporting the effects of psychological factors on the pain experience. It is hard to imagine having pain for any length of time without it having at least some emotional consequences. These emotional consequences affect pain perception and functioning. Psychological disorders are common in TMD sufferers, and psychological factors are critical determinants of TMD-related pain levels, disability and treatment outcomes. Moreover, when patients bring in premorbid psychological baggage, their pain problem becomes dramatically more complex. For example, the patient with a premorbid history of depression, with or without anxiety, will likely experience much more severe levels of depression and/or anxiety with pain than the patient with no such history. The patient presenting with a premorbid history of a personality disorder will be far more difficult to manage than the patient without such a history. A remarkable study summarised in Box 8-1 makes this point. This study highlights the importance of premorbid psychological traumas as a predictor of post-operative recovery and the increased risk of developing chronic pain. Much speculation has been offered as to possible mechanisms for this now well-replicated study. It appears, however, that persons who present with major premorbid traumatic events are at far greater risk of coping less effectively with future physical or psychological assaults. This would not appear to have been researched in OFP, but similar results would be anticipated.

Box 8-1 Summary of an investigation of premorbid psychological factors and spinal surgery outcome

Preoperative interviews were carried out with 100 adults with MRI-proven severe lumbar disc herniations for a history of:

• physical abuse

• sexual abuse

• emotional neglect/abandonment

• loss of one or both parents (divorce, death, etc.)

• substance abuse at home (alcohol, prescription drugs, etc.).

Patients were assigned to three different groups (0, 1–2, 3+ risk factors) and surgical outcome assessed.

The results were as follows: outcome was excellent in 95% of those with 0 risk factors, 75% of those with 1–2 risk factors and 15% in those with 3+ risk factors.

From Schofferman et al. (1992).

Psychosocial factors may impact a dentist’s ability to diagnose a pain condition accurately and can certainly adversely affect treatment choices and treatment outcomes. Psychosocial issues can:

• exaggerate, distort or suppress pain complaints

• result in poor discrimination of pain levels

• confuse the distinction between pain (how much one is hurting) and suffering (how much that hurt is bothersome)

• result in poor pain memory, compromising reporting accuracy

• result in side-effects to medications and procedures

• determine the amount of medication use and abuse

• result in poor compliance to treatment

• enhance chances of iatrogenic problems.

Failure to recognise and address psychosocial factors is often the cause of over- or undermedication, excessive diagnostic work-ups and inappropriate treatments, which may lead to iatrogenic complications.

Acute versus Chronic Pain

To better understand chronic OFP, it is helpful to contrast acute and chronic pain. Historically, acute and chronic pain were separated based on time and an estimated period of “normal” healing. This perspective has many limitations, the most obvious being that chronic pain is defined after the syndrome has developed; this limits preventive efforts. Moreover, soon after trauma, pathophysiology is frequently adequate to explain pain and pain behaviours and there is a high correlation between tissue repair and resolution of pain. As time passes, this relationship becomes tenuous at best; there is often a poor correlation between tissue repair and chronic pain and, with time, the extent of initial injury is a relatively weak predictor of chronic pain. Thus, there exists a significant disconnect between the extent of pathophysiology and development of chronic pain.

The Disease Model Versus the Biopsychosocial Model of Pain

A dilemma exists between the complexities inherent in OFP and the disease model that dentists typically receive in training. The disease model views pain as a by-product of a disease process or some form of pathophysiology. Under most circumstances, the pain will resolve once nature has run its course, or the dentist has successfully treated the underlying disease. In this way, dentists are taught to identify the disease or pathophysiological process and then develop a treatment plan to “fix” it. This model, though effective for the majority of dental conditions, lacks substance and effectiveness when it comes to the management of chronic OFP. In fact, the disease model may be the major problem.

By contrast, psychologists have developed and researched the only empirically supported model of pain: the biopsychosocial model. Rather than explaining pain purely in terms of pathophysiological processes, the biopsychosocial model explains pain, suffering and disability as a dynamic interaction among biological, psychological, social, cultural and environmental factors. Thus, the experience of pain is not just a function of biological processes, related pathophysiology and nervous system transmission, but is also a response to psychological factors such as mood, anxiety and personality and the patient’s thoughts and beliefs about their pain. Moreover, the pain experience is influenced by social factors such as economic impact and the response of others, for example family and healthcare providers. The implications of this model for the dentist assessing and treating chronic OFP is apparent: when presented with a patient who has significant psychological factors impacting their pain and disability, resolution of pain is unlikely to occur unless treatments that address the relevant psychological factors are included as an integral part of the treatment plan.

Sensory Transmission and Limbically Augmented Pain

The neural pathways of normal pain transmission involve some basic concepts, a knowledge of which is important in understanding the pathophysiology of chronic OFP. These include the concept of transduction of the first-order peripheral afferent nociceptor (pain transmission) neurons. The nociceptor neurons respond to specific mechanical, chemical and thermal stimuli associated with tissue damage through the activation of receptors and ion channels on their peripheral surface membranes. If sufficient stimulation of the receptor occurs, an action potential is generated that travels along the axon either to second-order neurons in the dorsal horn of the spinal cord or directly to the pontine trigeminal nucleus caudalis of the brainstem, depending on the dermatomal level of injury.

Second-order neurons transmit impulses from the spinal cord to the brain. Most second-order neuron action potentials from nociceptors ascend by the spinothalamic tract to tertiary connections in the thalamus, or branch to other neural structures that are involved in pain modulation. Third-order neurons in the thalamus transmit signals to the cerebral cortex.

Evidence exists that pain modulation occurs in numerous supraspinal control areas, including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system (hippocampus and amygdala), cingulate cortex, the basal ganglia and cerebral cortex. Neurons originating from these areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord or the nucleus caudalis.

Sensory transmission defines the injury. Its response is, in part, spinally mediated in reflex withdrawal. This response pinpoints the site of the injury. Sensory transmission assesses the “here and now” of the pain experience: “Ouch, I pricked my finger on that sharp pin”.

Another group of slower-responding nociceptive signals traverse a similar course to that of the sensory transmission signals but project primarily into the />

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