History

As stated elsewhere in this book, it is sometimes easier for a patient to present with a complaint of ‘physical’ pain rather than ‘emotional’ pain. This is particularly so for people in the armed forces, who may present with tension-type headache when in reality the problem is far more deep seated. For people for whom physical fitness is a prerequisite, it is often considered inappropriate, or even a career hurdle, to present with the complaint of psychological problems. It follows that people with pain, as evidenced by tension-type headaches, need to have psychological issues also explored when taking a history.

The fact that pain may provide the presenting complaint for psychological problems does not negate the fact that the pain is still felt. Pain is a very subjective phenomenon and may follow very specific patterns that go hand-in-glove with specific complaints. The symptom constellation will provide the diagnosis (see Table 13.2).

TABLE 13.2 Pain associated with specific diagnoses

As with all neurology, there are certain questions that need to be asked: When did the pain start? Was there a provocative incident that caused the pain? Where is the pain? Are there precipitating or relieving factors? What is the nature of the pain? Are there associated features with the pain? What is the frequency and duration of the pain? A perfect example of how these questions provide diagnostic answers is found in Chapter 6 on headache. It is these questions that differentiate tension-type headache from migraine.

Certain conditions, such as diabetes with peripheral neuropathy and diabetic amyotrophy, may provoke very severe pain symptoms. Pain is a particular feature of small fibre diabetic sensorimotor neuropathy. From the neurological perspective, pain in the head, neck, back and limbs may be of primary neurological origin. Pain in the thorax or abdomen is almost always a feature of a visceral disorder rather than primary neurological complaint, for instance, spinal or radicular pathology, thus dictating an alternative investigational paradigm to the diagnosis of thoraco or abdominal pain. There are some exceptions, such as herpes zoster infection with shingles (and post-herpetic pain) and diabetic radiculopathy, already identified.

Pain evokes its own set of jargon and possible confounding language, which may lead to confusion. Thankfully much of this jargon has not yet found its way into common daily language and so is largely ignored by patients (see Table 13.3).

TABLE 13.3 Glossary of pain jargon

This does not negate the need to be critical of the term ‘pain’ and to seek clarification as to what type, quality, nature and intrusion the pain causes. A dull ache is quite different to a lancinating, stabbing, throbbing pain. A ‘hot poker’ or ‘stabbing’ pain may be vastly different to ‘feeling as if my head was going to explode!’. Often the word ‘numb’ may enter the patient’s description, even of pain, and the word ‘numb’ demands clarification as it may mean different things to different people.

The concept of paraesthesia (see Table 13.3) may be short-lived with no real consequence (as in ‘my foot went to sleep with pins and needles’). It may reflect altered blood supply to a target region. This produces neurological symptoms but should not dictate neurological consultation. A perfect example of this is the symptom attached to carpal tunnel syndrome with paresthesia in the fingers. This responds favourably to night splinting to obviate palmar–flexion of the wrist, which compromises blood supply to the median nerve (see Ch 11). Where paresthesia persists, it is a warning of abnormality somewhere within the sensory pathway and may dictate additional investigations, such as nerve conduction studies or sensory evoked potential studies and hence referral to a specialist.

To delve further into the understanding of pain, some specific pain complexes or syndromes will be explored.

Reflex sympathetic dystrophy or complex regional pain syndrome

Reflex sympathetic dystrophy (RSD) or complex regional pain syndrome (CRPS) is a refractory pain syndrome in which the term RSD is being replaced with CRPS, as it is neither a true ‘reflex’ nor a ‘dystrophy’. It is a type of limb pain characterised by: disproportional pain (both in character and distribution); allodynia (see Table 13.3); altered limb function (accompanied by antalgic movements); oedema; discolouration (often cyanotic); altered temperature; possible sweating; and maybe dystonia or spasms; or altered anatomy (with nail changes, hair loss, skin thinning or bone demineralisation).

Other terms often also included within the CRPS spectrum include: causalgia; post-traumatic pain syndrome; Sudeck’s atrophy; reflex neurovascular dystrophy; post-traumatic spreading neuralgia, sympathalgia and shoulder–hand syndrome.⁴ CRPS represents regional pain of uncertain pathophysiology, which usually affects the hand or foot but may also involve or spread to other parts of the body.

Mean age of onset is 35–45 years, with male to female ratio approximating 1 : 3. It can affect children with a 3 : 2 distribution of hand to foot involvement. It usually follows an injury—often a minor injury quite out of proportion to the symptoms. In up to 20% of cases the aetiology is idiopathic. It is a clinical diagnosis without implicit pain mechanism and the response to treatment is variable. It is a condition best referred to a consultant, who may investigate with: radiology to assess periarticular demineralisation; bone scan to show enhanced uptake in the affected limb; autonomic testing; and may consider sympathetic block, adrenergic block or maybe even steroids in the early stages of the disease. Additional approaches that may be adopted in general practice include use of tricyclic antidepressants, such as amitriptyline (Endep®) or imipramine (Tofranil®), starting at a dosage of 25 mg nocte and increasing up to ten times that dosage if needed. One can also consider use of antiepileptic medications, such as gabapentin (Neurontin®) starting at 100 mg t.d.s. and titrating to need or pregabalin (Lyrica®) starting at 75 mg b.d. and increasing as needed. It is important to appreciate that the use of gabapentin reflects use of the medication beyond that intended during development and is outside of the Pharmaceutical Benefits Scheme (PBS). Patients need a private prescription as gabapentin is only PBS listed for epilepsy. Pregabalin is not on the PBS. The approach to CRPS may also incorporate alternative remedies, such as a trial of acupuncture or even hypnosis. It is often a refractory form of pain complaint and usually will require specialist referral.

Spinal pain

As with the classification of pain in general³ there have also been attempts to classify spinal pain,⁵ but again this has relevance to international collaboration and less application to the family physician.

What is of value is to determine where in the spine the pain is generated, the level and extent of injury. It helps to determine if the pain is of neurological (nerve) origin or musculoskeletal (bone and muscle derived). This will have direct implication on both choice of investigation and the consultant most appropriate should referral be required. In some cases, the rheumatologist may be preferred over the neurologist.

Some helpful tips for the general practitioner may include description of pain and its distribution, such as neck pain, which may be limited to the neck but have associated neurological signs, such as pain radiation specific to a given nerve root or complex. Such neurological pain includes: radicular pain with sciatica or specific finger involvement that does not respect either ulnar or median nerve distribution; muscle wasting or weakness referrable to a given nerve root; loss of deep tendon reflexes at the level of the damage and hyperreflexia below the spinal level (see Ch 4); or pain exacerbated by coughing, sneezing or straining.

From the perspective of the general practitioner the real issue with spinal pain, be it neck or lower back pain, the two most common sites, is whether to treat conservatively and offer symptomatic relief or to seek rapid referral to a specialist. Some findings will help. The nature of the pain, rather than the intensity, is important. If the pain is strictly localised without any referral, without exacerbation (either progression of symptoms or increase with coughing or straining) and devoid of associated symptoms, such as meningism, sphincter involvement or abnormal neurological signs, then the family physician can ‘wait and see’. When in doubt, the involvement of a specialist may assist—rather than bypassing the consultant and ordering expensive investigations. CT scanning is relatively inexpensive and may offer considerable reassurance.

If simple analgesia or non-steroidal anti-inflammatory medications fail to provide relief, then tricyclic antidepressants often provide pain relief by generating muscle relaxation in addition to analgesia. They also provide anxiolysis and, within the context of chronic pain, the antidepressant enhances mood, sleep and a new approach to the pain by the patient. Similar doses as those suggested for CRPS apply.

One cannot ignore the need for a proper physical examination to determine the range of spinal movement, be it of the neck or the lower back. The patient is asked to touch their toes from the standing position; to slide down the lateral border of the leg with lateral flexion rather than bending forward; to sit on the couch with hands on knees and hips flexed to 90° while the doctor taps over the spine to identify localised discomfort; and to undergo straight leg raising (see Fig 13.1).

FIGURE 13.1 (i) Testing lower spinal movement—flexing in the AP plane. (ii) Testing lower spinal movement—lateral flexion. (iii) Testing lower spinal movement—hip flexion. (iv) Testing lower spinal movement—straight leg raising. (v) Testing lower spinal movement—modified straight leg raising if in doubt.

Straight leg raising is an alternative test for forward flexion in the AP plane (see Fig 13.1(i)) as is sitting on the bunk with hips at flexed at 90° (see Fig 13.1(iii)) while avoiding the tripod position. This can be administered in various guises, as shown in Figure 13.1(iv) and (v). This tests both the validity of the findings and their reliability, if producing the same results irrespective of the method used. Where the results of various methods of testing the same modality are in conflict, it provides strong evidence of a non-organic basis for the complaint. This should alert the clinician to delve further into the psyche (see Ch 5). It may alert the doctor to question the real reason for presentation, which might be anything from a subconscious call for help to a claim for compensation.

Neck movement is tested in different planes: asking the patient to touch the ear on the ipsilateral shoulder; the chin on the shoulder (both sides); fully flex the neck in the AP plane to touch the anterior chest wall; and then to fully extend the neck. This should be objectively recorded and provides objective evidence of range of neck mobility, which may give an important clue to the origin of the pain.

The examination of the spine, re pain, is not complete without a full peripheral neurological examination (see Ch 4). Completely normal upper limb examination (or even features of lower motor neurone deficit) in the upper limb, with upper motor neurone signs in the lower limb (see Ch 4) localises the lesion to either below, or at, the cervical level and above the lumbar spine. Lower motor neurone features in the lower limb also localise the damage to the lumbar spine.

If the pain does not respond to simple analgesia or even tricyclic antidepressants, then referral to a consultant is warranted. It is not advisable for the general practitioner to initiate narcotics as these are addictive and, if the pain is sufficient to require this level of intervention, further opinion is warranted to ensure a serious condition has not been overlooked. CT scanning should be considered before referral but the role of other testing, such as MRI or neurophysiological testing, remains the domain of the consultant.

Trigeminal neuralgia

Trigeminal neuralgia⁶ (tic douloureux) produces paroxysmal jabbing, unilateral facial pain provoked by innocuous stimuli, such as chewing, brushing teeth, touching the face or a gust of wind on the face. Often the cause is unknown but it may accompany multiple sclerosis, the compressive effect of a tumour or even infection, such as chronic meningitis. Current theory favours pain consequent to an aberrant blood vessel stimulating the branch of the trigeminal nerve within the skull, but this is rarely confirmed on imaging.

Generally the neurological examination of the patient with trigeminal neuralgia is normal, but if there is loss of sensation within the distribution of the nerve then cerebral imaging with MRI and MRA is warranted. Similarly, bilateral symptoms clearly justify imaging. Some would routinely image all patients, but the costs involved raise doubt about its effectiveness.

Treatment is usually provided by anti-epileptic medications (AEM), such as carbamazepine (CBZ), which remains the first-line remedy. Other AEM, such as valproate, oxcarbazepine, gabapentin, pregabalin or even lamotrigine or levetiracetam, may be considered but these are off-license uses and should entail specialist consultation. Similarly, antispasmodics, such as baclofen; tricyclic antidepressants, such as amitriptyline or imipramine; or anti-arrhythmic agents, such as mexitil, may be considered. If the patient has not responded to Tegretol CR® 400 mg 1 b.d. then the general practitioner would be wise to call for help.

The role of microvascular decompression, gamma knife surgery or ablative procedures directed at the trigeminal nerve root are definitely beyond the role of the family physician and will not be further discussed.

Temporomandibular joint dysfunction

This is known as TM joint dysfunction⁷ and includes nocturnal bruxism (so called ‘fang grinders’), TM joint malocclusion, and what some refer to as myofacial syndrome. This must be differentiated from ‘claudication of the jaw’, which may occur in the elderly with temporal arteritis.

Diagnosis depends on a high index of suspicion, and can often be enhanced by palpating over the jaw while asking the patient to perform a mimicry of chewing with large bites. During this procedure, crepitus of the TM joint may be palpated as the cartilage clicks in and out of place. This is best managed by the dentist providing a ‘bite plate’, which is specifically moulded to suit the individual patient and worn overnight.

This approach often obviates the need to involve a neurologist, who would likely follow the same approach as first-line therapy by advocating referral to a dentist. The role of the specialist emerges if this does not provide the answer, raising concerns about the diagnosis. One differential diagnosis is glossopharyngeal neuralgia, which produces a pain not dissimilar to a combination of trigeminal neuralgia and TM joint dysfunction, but often includes a lancinating pain shooting through the ipsilateral ear. Its treatment largely mirrors that of trigeminal neuralgia but the fun, that is medicine, is the academic satisfaction of making the correct diagnosis even if it does not change treatment, especially if it also does not cause further inconvenience or cost.

Atypical facial pain

This is the final common pathway when the above differential diagnoses for pain in the face have failed to define a suitable diagnosis. When encountering this dilemma the general practitioner should involve a consultant as it is imperative to exclude occult lesions. This form of pain is often refractory to commonly used remedies and the involvement of a specialist is, of itself, often therapeutic.

Post-herpetic neuralgia

Shingles is the reactivation of herpes varicella zoster viral infection (chickenpox), which has lain dormant in the nerve root. It results in an irritating painful blistering infection that follows the anatomic path of the nerve root or cranial nerve (the dermatome). The pain generated can be severe and debilitating, but may be obviated by adding steroids to the antiviral treatment when the eruption first occurs.

Post-herpetic neuralgia has been treated with a number of approaches⁸ but the principle to management remains the same. The pain needs to fit the accepted pattern: lasting in excess of three months from the bout of shingles; occurring in the route of the dermatome; possible decreased sensation within the distribution of the dermatome; and hyperaesthesia (see Table 13.3) at the transitional borders of the dermatome. The pain may be both deep and superficial with super-added tic-like lancinating pain.

First-line treatment may include application of topical remedies, such as capsaicin ointment, as a counter irritant, or even a xylocaine ointment or cream. This may be complemented with either tricyclic antidepressants (amitriptyline or imipramine) or AEM, such as CBZ, starting with a dosage of 400 mg of the controlled-release formulation b.d. and increasing the dose to mirror the therapeutic levels accepted for epilepsy treatment (see Ch 7). If first-line treatment fails, it may be worth considering a course of steroids, tapering from 75 mg prednisolone per day to nothing over a two-week period. Off-license use of some of the previously cited agents (see trigeminal neuralgia above) may be of help but would justify referral to a consultant.

Conclusion

Pain is a massive topic to cover in such a brief overview. It reflects the idiosyncratic nature of the individual patient, and the approach to treatment is as variable as the background of the patient and the doctor. This review has not even touched on cultural and educational influences that may impact on the management of pain, or the use of traditional remedies, such as acupuncture or herbal treatments, which may have a place but are outside the scope of this book. Hypnosis may be an effective tool, and personal experience has taught that it is very effective when undergoing dental treatment or managing refractory head pain. If using hypnosis, it is imperative to include a protective post-hypnotic suggestion that if pain is providing a protective warning then the patient will still appreciate that warning, even if the severity of the pain is alleviated.

The principal message is that if pain does not respond to simple intervention with analgesics or non-steroidal agents, then it justifies further investigation and possible involvement of a consultant. Where the root cause for the pain is obscure, the involvement of a consultant may be warranted but the family doctor may be the best placed to recognise non-organic causes for pain. There may be unequivocal signs of non-organic disease (see Ch 5), which should not be overlooked because early intervention enhances prognosis. Pain is a common cause for depression and behaviour problems that may cause altered domestic dynamics, which impact negatively on quality of life. The general practitioner is by far the best placed to recognise these issues and to deal with them. As has been repeatedly stated in this book, the best management of pain syndromes is achieved by a close working relationship between general practitioner and consultant. Where this has proven ineffective in pain management, it may be time to involve a multidisciplinary team,⁹ be that within a rehabilitative framework or a recognised pain clinic. Pain is so intrusive that it is sometimes better to call for help early, rather than to allow the establishment of entrenched pain-provoked behaviour.