A Physiological Approach to Clinical Neurology

Ltd.

1

Pain and other sensations

Publisher Summary

The nervous system of a normal individual is constantly active in conveying information to the brain about the state of the body and of the world outside it. The perception of any sensation, therefore, depends not only on the appropriate receptor organ in skin, muscle, joint, or viscus and the integrity of the peripheral nerve and spinal cord pathways but also on complex connections within the cerebral cortex that may be influenced by the thoughts and emotions of the subject. Pain is the most consistently unpleasant symptom that the nervous system can provide and may signal a disorder in any part of the body through irritation or distortion of sensory end organs or may arise from the disease of the sensory pathways at any level from end organ to cortex. Pain is often associated with an emotional change so that it may be hard to determine as to which is primary and which is secondary. There are two main types of nociceptor in the skin, mechanical and thermal. Mechanical nociceptors respond to pricking, pinching, or squeezing of the skin; thermal nociceptors respond to high and low temperatures. The viscera are insensitive to touching, cutting, or pinching but give rise to the sensation of pain, given an adequate stimulus such as distention, excessive contraction, or irritation by toxins and chemicals. Visceral pain is transmitted by the afferent fibres in the sympathetic nervous system from the thoracic and abdominal cavities or the sacral parasympathetic nerves from the pelvis.

The nervous system of a normal individual is constantly active in conveying information to the brain about the state of the body and of the world outside it. If all these neuronal messages were received in equal measure, consciousness would become a nightmare of confused and largely irrelevant stimuli, so that a selective response would become impossible. Fortunately, there are various physiological processes which speed the passage of pertinent stimuli and retard awareness of the background activity. We thus become oblivious to the touch of clothes, the pressure of a hard seat and the functioning of contented viscera. The processes involved in this selectivity of sensations are as follows.

(1) Adaptation of sensory end organs, which cease to respond after variable periods of stimulation.

(2) Presynaptic inhibition of adjacent nerve cells by collaterals from an active nerve cell, thus assuring priority for ‘the stimulus of the moment’¹¹. This process probably takes place at all levels of the nervous system, thus repeatedly ‘refining’ the impulses representing a particular sensation, or, in electronic jargon, ensuring ‘a high signal-to-noise ratio’.

(3) Regulation of synaptic transmission in sensory nuclei from the motor cortex by pyramidal tract fibres which send collaterals to the cuneate, gracile and trigeminal nuclei, and to the ventrobasal thalamus⁴³. This provides a mechanism for the voluntary suppression of sensory information or for involuntary suppression during movement.

(4) Alteration in the state of awareness at a cortical or subcortical level. A subject, while fully conscious, may so concentrate his attention on a particular sensation, thought or response as to preclude perception of other sensations.

The perception of any sensation therefore depends not only on the appropriate receptor organ in skin, muscle, joint or viscus, and the integrity of the peripheral nerve and spinal cord pathways, but also on complex connections within the cerebral cortex which may be influenced by the thoughts and emotions of the subject. Thus sensation is subjective and each individual has his own ‘perceptual world’ which is unique to him and can be known to others solely by his description of it. A certain stimulus may be registered by some as pleasant, by others as unpleasant but tolerable, and by others as so uncomfortable that they use the term ‘pain’ to describe it. Each person may therefore be regarded as having a ‘pain threshold’, and if the level of sensory stimulation exceeds this, pain is experienced.

When the normal functioning of the body is disturbed, sensory impulses of unusual quantity, quality or pattern are received by the brain, and the resulting ‘sense data’ are expressed by the subject as ‘symptoms’.

SENSORY SYMPTOMS

Symptoms bring the patient to the doctor. It is part of the art of medicine to record the patient’s symptoms accurately and to interpret them in the light of the patient’s intellectual and educational endowment, his personality and his emotional state.

Symptoms may be negative in that the patient complains of numbness or inability to feel touch, pain, temperature or position of the limbs. Symptoms may also be positive, providing curious abnormal sensory experiences (paraesthesiae).

Ischaemia or irritation of peripheral nerves or the central projection of touch pathways gives rise to pain or to prickling sensation described as ‘pins and needles’ or the arm or leg ‘going to sleep’. For example, compression of the lateral cutaneous nerve of the thigh in the inguinal ligament produces a curious creeping feeling in the outer aspect of the lower thigh which has been likened to the sensation of ants crawling under the skin (formication).

A disturbance within the posterior root entry zone or posterior columns of the spinal cord, or pressure upon them, may be responsible for a girdle sensation around the trunk, described as a tight band, or a feeling of pressure in the limbs as though they were being wrapped by a bandage. Sudden flexion of the neck may induce an electric shock sensation which shoots down the back when there is a cervical lesion irritating the posterior columns. This phenomenon (Lhermitte’s sign) is found most commonly in cervical spondylosis and multiple sclerosis. A lesion in the spinothalamic tracts or thalamus produces an unpleasant burning sensation or pain which spreads diffusely down the opposite side of the body.

Irritation or ischaemia of the sensory cortex evokes paraesthesiae, which may spread rapidly over the contralateral side in epilepsy and transient ischaemic attacks, or advance more slowly when caused by migrainous vasospasm. Disturbance of the sensory association areas in the parietal lobe may give rise to weird illusions of the body image so that parts of the body appear larger or smaller than normal.

Pain is the most consistently unpleasant symptom which the nervous system can provide and may signal a disorder in any part of the body through irritation or distortion of sensory endorgans, or may arise from disease of the sensory pathways at any level from endorgan to cortex.

Pain is often associated with an emotional change so that it may be hard to determine which is primary and which secondary. In spite of all the complexities of the individual reaction to pain, it is usually possible to analyse the description of the pain so as to determine its site of origin and often its cause.

THE PERCEPTION OF DIFFERENT KINDS OF SENSATION

Cutaneous nerves and sensory receptors

Human cutaneous nerves contain myelinated fibres which range in diameter from about 1 to 16 μm, and unmyelinated fibres which are less than 2 μm in diameter. The myelinated fibres are designated A fibres and are subdivided into Aα,β (6–16 μm) and Aγ,δ (2–6 μm) groups. The unmyelinated fibres are C fibres. All the fibres have their cell bodies in the dorsal root ganglia, and they terminate peripherally in skin and subcutaneous structures. The sensory receptors in the skin may be encapsulated endings of nerves such as Pacinian corpuscles and Meissner’s corpuscles; specialized free endings, such as Merkel’s discs; and simple free endings. The encapsulated endings are concentrated in areas of the body which are particularly sensitive-the tips of the fingers, the lips, the areola of the breast, and the genitalia. There now seems little doubt that many cutaneous receptors display stimulus specificity and include slowly and rapidly adapting mechanoreceptors, warm and cold receptors and pain receptors¹⁷,²⁰,²¹.

Pacinian corpuscles are extremely sensitive to displacement and vibration. Some receptors respond to more than one stimulus; for example, some mechanoreceptors are sensitive to change in temperature¹⁶. Some free nerve endings have a high threshold and respond to painful stimuli only, while others have a low threshold and probably play an important role in sensory discrimination². The cornea, for instance, has only free nerve endings but is sensitive to touch, heat and cold as well as to pain³¹. There is no absolute relationship between the sensory modality perceived and the diameter of sensory fibres excited although large diameter fibres are important for conveying sensations of light touch, position and vibration sense and small diameter fibres for conveying pain and temperature. Light touch of the skin and movement of hairs activate unmyelinated and small myelinated fibres as well as the large diameter myelinated fibres²⁰,⁵⁷. Evidence in primates indicates that warm and cold receptors are innervated by slowly conducting myelinated fibres of the A group or by unmyelinated C fibres. It seems to be necessary to activate Aδ and C fibres in order to arouse the sensation of pain⁵,⁷,⁵⁷, although these fibre groups play an important role also in the transmission of other sensory modalities.

Light touch

Clinically, light touch is usually tested with cotton wool but quantitative methods of assessment have also been devised. Large myelinated (Aß) fibres are excited by this stimulus, but Aδ and C fibres are also activated. Experiments on man indicate that tactile sensation may be induced by the excitation of only one or two large myelinated fibres¹⁶. Most of the fibres excited in the periphery by light touch pass centrally in the spinal cord by way of the dorsal columns to the gracile and cuneate nuclei, where they synapse⁴⁵ (Figure 1.1). Second order neurones arise in these posterior column nuclei and cross over to pass upwards as the medial lemniscus to the external component of the ventrobasal complex of the thalamus (nucleus ventralis posterolateralis, VPL). The comparable fibres from the main sensory nucleus of the trigeminal nerve cross to join the lemniscal system and end in the arcuate or medial component of the ventrobasal complex of the thalamus (nucleus ventralis posteromedialis, VPM). Thalamocortical fibres project mainly to the postcentral gyrus in the cerebral cortex. Throughout the posterior columns, lemniscal system, thalamus and cerebral cortex there is a topographical distribution of the sensory fibres. The posterior column/lemniscal system is responsible for the finer forms of tactile sensibility in man which are tested by stereognosis, two-point discrimination, and figure writing on the skin. These functions may be severely impaired by destruction of the dorsal columns although, with unilateral lesions, there may be no permanent sensory impairment which is clinically detectable⁹. The classical views of dorsal column function have been criticized by Wall⁵², who suggests that their role is to initiate exploratory movements and to assist in the analysis of information conveyed through other sensory pathways.

Figure 1.1 Spinal pathways for proprioception and touch‥ Anatomy of the Nervous System. Philadelphia and London: Saunders) (After Ranson, S.W. and Clark, S.L. (1959)

Some tactile sensations must be mediated by the spinothalamic system because touch can still be perceived in man after damage to the posterior columns (Figure 1.1). This touch pathway of crossed second order neurones is known as the anterior or ventral spinothalamic tract, but its exact position in the anterolateral columns is unknown⁴⁵.

Joint position sense

It had been accepted for many years that joint position sense and kinaesthesia are signalled by means of afferent fibres which innervate receptors in the ligaments and capsules of joints⁴⁵,⁵⁰. However, it is now known that muscle afferents contribute to the conscious appreciation of joint position and, in certain positions of the limb, provide the main source of kinaesthetic information³³.

Destruction of the posterior columns causes partial impairment of joint position sense and it may therefore be concluded that some afferent fibres responsible for proprioceptive sensation are situated in this spinal pathway⁵⁵. However, position and vibration sensation may be lost in man after infarction of the dorsal spinocerebellar tract while the appropriate part of the posterior columns remains intact⁴⁶. Conscious proprioception in man may be carried by Morin’s spinocervicothalamic pathway which forms part of the dorsal spinocerebellar tract in the spinal cord. Cortical evoked potentials, elicited from the scalp in man following stimulation of a peripheral nerve, travel in the posterior columns and are present in patients who have lost only pinprick and temperature sensation¹⁴.

Estimation of weight appears to depend upon the sense of effort put into lifting an object rather than feedback of the force or muscle tension actually achieved¹². Weights are considered heavier if lifted by a hemiparetic limb or one which has been weakened by the action of curare on the neuromuscular junction.

Vibration sense

The testing of vibration sense with a tuning fork is probably merely a specialized way of testing tactile and pressure receptors and their pathways. The peripheral pathway consists mainly of large afferent fibres which innervate one or two Pacinian corpuscles¹⁹. The central pathway is by way of the posterior columns/lemniscal system, but not exclusively so, since the lateral columns may also relay vibratory sense⁴,⁵⁵.

Temperature sense

Specific warm and cold receptors exist, and both Aδ and C fibres respond to thermal stimulation. The central pathways are in the lateral spinothalamic tracts, in close association with the pain pathways (Figure 1.2).

Figure 1.2 Spinal pathways for pain

Tickle and itch sensations

These sensations probably depend upon activity in Aδ and C fibres, and are abolished by anterolateral cordotomy⁵⁸.

PAIN

There are two main types of nociceptor in the skin, mechanical and thermal²³. Mechanical nociceptors respond to pricking, pinching or squeezing of the skin; thermal nociceptors respond to high and low temperatures. These pain receptors are slowly adapting and are innervated by small myelinated Aδ fibres that conduct at about 10–20 m/second and by unmyelinated C fibres that conduct more slowly at 1–2m/second. It is probable that the time interval in conduction between the two groups gives rise to the clinical phenomenon of ‘immediate’ and ‘delayed’ pain⁴⁹.

Since the time of Bell and Magendie it has been assumed that all fibres in posterior roots are sensory and those in anterior roots are motor. However, some 30 per cent of the fibres of the ventral roots of L7 and S1 segments in the cat are unmyelinated and arise from posterior root ganglia. Most respond to pain but some to thermal and mechanical stimuli⁶.

Fibres concerned with the transmission of pain sensation synapse in the posterior horn of the grey matter of the spinal cord within a few segments of their level of entry, mainly, but by no means exclusively, in layers I and V of Rexed⁴¹, possibly using substance P as a transmitter. There is convergence onto single cells in the dorsal horn of fibres from low threshold cutaneous mechanoreceptors and from high threshold cutaneous nociceptors. The activity in the fibres from the cutaneous mechanoreceptors may inhibit that in fibres from the nociceptors¹⁵.

Neurones from the posterior horns (mainly laminae I, V, VI, VII)²⁹,⁴¹ send axons to the opposite side of the cord to ascend in the lateral spinothalamic tract, which seems to contain only myelinated fibres, to the ventral posterolateral (VPL) nucleus of the thalamus. It is now apparent that there are other ascending pathways scattered throughout the anterolateral white columns of the cord concerned with transmission of painful sensation, since it is necessary to destroy the greater part of this area before pain perception is abolished. Some of these fibres originate from layers IV and V of Rexed. This is the spinoreticulothalamic system which projects to the lateral reticular nucleus, centromedian and parafascicular nucleus and other regions of the brainstem and thalamus³,⁴¹ (Figure 1.3). Both the spinothalamic and spinoreticulothalamic systems project to the cerebral cortex, mainly to the second somatosensory area⁴⁴.

Figure 1.3 Cerebral termination of pain pathways. Specific afferent projections from body and face (spinothalamic and quintothalamic tracts) are indicated as solid lines on the left of the diagram, relaying in nuclei VPL and VPM, and projecting to the postcentral sensory cortex. The diffuse spinoreticulothalamic pain pathway is displayed as interrupted lines relaying in the midline thalamic nuclei, centrum medianum (CM) and lateral reticular nucleus (LR), and projecting diffusely to the cerebral cortex. (After Bowsher³, by courtesy of the Editor of Brain)

Opiate receptors and enkephalin

It is now clear that opiates act on highly specific receptors on cells of target organs in the brain. Opiate receptors have been defined by autoradiographic techniques and biochemical assays in the periaqueductal grey matter, medial thalamus, substantia gelatinosa of the spinal cord and spinal trigeminal nucleus, solitary nuclei and vagal nerve fibres, area postrema and amygdala. In addition endogenous ligands (substances binding to those receptor sites) have been identified, particularly the pentapeptides methionine-enkephalin and leucine-enkephalin which have opiate properties. By using subcellular fractionation, immunohistochemical mapping and autoradiographic mapping, it has been determined that these enkephalins are present at nerve terminals in the same distribution as the opiate receptors. It has been postulated that enkephalins diminish the release of substance P, and hence the transmission of pain impulses. Other substances known as endorphins have been isolated from pituitary extracts and have been shown to have opiate-like activity. Beta endorphin has about five to ten times the potency of morphine. Beta lipotropin may be a precursor of enkephalins and endorphins¹⁸.

Endogenous pain control mechanisms

Electrical stimulation in the periaqueductal grey matter produces long-lasting analgesia in man and experimental animals. The periaqueductal grey matter is moderately rich in opiate receptors and enkephalin while naloxone, a morphine antagonist, blocks the electrically produced analgesia. It therefore seems probable that opiates activate an efferent brainstem system that suppresses pain at a segmental level. The descending pathway seems to be mainly in the dorsolateral fasciculus of the spinal cord (Figure 1.4) since lesions in this region reduce or abolish analgesia produced by opiates or electrical stimulation of the periaqueductal grey matter. The serotonin-rich midline raphe nuclei of the medulla also appear to be involved in the descending pathway although non-serotoninergic descending pathways through the dorsolateral fasciculus also exist. There is anatomical and physiological evidence to suggest that, in addition to receiving inputs from the opiate-sensitive brainstem structures, the midline raphe nucleus of the medulla also receives major though indirect somatosensory inputs from pain pathways, possibly by way of the reticular formation¹.

Figure 1.4 Schematic diagram of pain pathways

NRM, midline raphe nucleus of medulla

DLF, dorsolateral fasciculus of spinal cord

Aβ, Aδ, myelinated afferent fibres in peripheral nerves

ST, spinothalamic tract

SRT, spinoreticulothalamic tract

PAG, periaqueductal grey matter

GRF, gigantocellular reticular formation

Gate control theory

Melzack and Wall³⁹ proposed a hypothesis concerning the mechanism of pain perception which they called the Gate Control Theory. They suggested that activity in large diameter afferent fibres stimulated cells in the substantia gelatinosa of the spinal cord which in turn inhibited transmission in central pain systems. On the other hand, if a sufficient number of small diameter myelinated and unmyelinated fibres were excited by noxious stimuli the activity of cells in the substantia gelatinosa was inhibited and transmission in central pain systems was allowed to proceed. The cells in the substantia gelatinosa therefore acted as a control barrier. The hypothesis has stimulated a great deal of interest and research into pain mechanisms but, since it lacks experimental confirmation, it has been criticized by other workers²¹,²²,⁴¹,⁴⁷. Wall⁵³ has restated the Gate Control Theory in the light of more recent studies on pain mechanisms. He considers that the role of the substantia gelatinosa at present remains unknown; however, it does seem certain that cells in the spinal cord which transmit information from nociceptors are inhibited by low threshold afferents and by descending inhibitory mechanisms. This modified theory provides an explanation for the relief of chronic pain by electrical stimulation of the dorsal columns with implanted electrodes⁴⁸ and of causalgia by selective stimulation of large diameter fibres in the peripheral nerve⁴⁰ and of pain modification by acupuncture and electroanalgesia.

Sensation of pain from the face is served by fibres of the trigeminal nerve which, on entering the pons, pass down through the medulla as the descending or spinal trigeminal tract which lies alongside the nucleus of that tract. In its course, fibres pass from the tract to the nucleus where they synapse. The second-order neurones cross, then run up through the brainstem close to the midline as the secondary trigeminal or quintothalamic tract and enter the ventroposteromedial (VPM) nucleus of the thalamus. It is probable that there are also projections to the midline reticular formation as in the case of pain fibres from the body.

The spinal tract and nucleus of the trigeminal nerve descend into the upper segments of the spinal cord. Fibres are received from the nervus intermedius, glossopharyngeal and vagus nerves, so that the quintothalamic tract transmits impulses from these nerves as well as the trigeminal nerve. Some sensory fibres from the upper three cervical posterior roots synapse with neurones in the spinal trigeminal nucleus, thus permitting referral of pain from the upper head to the neck and vice versa²⁸.

Pain appreciation requires the participation of the cortex—not only the secondary sensory cortex but also the frontal and temporal lobes of the brain which add emotional interpretation of the sensation of pain.

Visceral pain

The viscera are insensitive to touching, cutting or pinching, but give rise to the sensation of pain, given an adequate stimulus such as distention, excessive contraction or irritation by toxins and chemicals.

True visceral pain must be distinguished from somatic pain caused by the spread of a disease process from the viscus to the surrounding serous membrane or body wall which receive their sensory innervation from somatic nerves.

Visceral pain is transmitted by the afferent fibres in the sympathetic nervous system from the thoracic and abdominal cavities, or the sacral parasympathetic nerves from the pelvis. Certain organic sensations such as hunger, satiety, sense of fullness and nausea appear to be mediated by the vagus nerve, but not the sensation of pain.

Sensory fibres in the gut wall are similar to those in the skin, but are sparser, and smaller in diameter. Free nerve endings in the gut wall are the receptors for pain and small myelinated and unmyelinated fibres pass centrally in the splanchnic nerves, traverse the sympathetic ganglia without synapsing, and then enter the posterior roots by way of the white rami communicantes. They have their cell bodies in the posterior root ganglia and their central processes synapse in the posterior horns, cross over and ascend in the vicinity of the spinothalamic tracts to the VPL nucleus of the thalamus. The large diameter fibres in the splanchnic nerves, some of which innervate Pacinian corpuscles in the mesentery, do not convey painful sensations. They ascend in the posterior columns to reach the VPL nucleus of the thalamus (Figure 1.5).

Figure 1.5 Pathways of sympathetic afferent fibres in central nervous system. The large Aα,β fibres, some of which are connected to Pacinian corpuscles, run in the posterior columns. The small Aγδ fibres, which transmit painful sensations, run in the anterolateral columns. Both pathways terminate in the thalamus. (Reproduced from McLeod³⁵ by courtesy of the Editor of the Ausralian and New Zealand Journal of Surgery)

The heart receives sensory fibres from the cardiac nerves, which are connected centrally with T1–5 cord segments.

The splanchnic nerves supply liver, stomach, duodenum, small intestines and kidneys, and run to T6–12 segments of the cord.

The large intestine receives its sympathetic sensory supply via the hypogastric plexus and impulses pass to the T10–L2 segments of the cord.

The pelvic organs are supplied with parasympathetic sensory nerves which enter the spinal cord through the posterior roots of S2–4.

Referred pain

Pain arising from a viscus may appear as though it is arising in any part of the body innervated by the same segments. Recognition of the common types of referred pain is an essential part of clinical diagnosis.

The probable mechanism of referred pain is convergence of somatic and visceral afferent pathways in the central nervous system. This may occur in the posterior horn of the spinal cord or even as high as the VPL nucleus of the thalamus³⁴ (Figure 1.6). Thus sensations arising from viscera may be roughly localized by the subject (for example, above or below the umbilicus, in the midline, or in the centre of the chest), or they may be interpreted as coming from various somatic areas.

Figure 1.6 Afferent pathways from skin and viscera converge on common neurones in spinal cord and thalamus. (Reproduced from McLeod³⁵ by courtesy of the Editor of the Australian and New Zealand Journal of Surgery)

Kellgren²⁶,²⁷ studied the distribution of pain and hyperalgesia which resulted from the injection of hypertonic saline into muscle or interspinous ligaments in man. He found that the areas of referred pain did not correspond exactly to dermatomes described by Foerster but appeared to be projected to the deep structures innervated by the same spinal segment as the structure stimulated. Similar human experiments were carried out by Inman and Saunders²⁴ who reached the same conclusion as Kellgren and designated the segmental areas of skeletal innervation as ‘sclerotomes’. Each dermatome overlies a limited area of the corresponding sclerotome. This concept is illustrated in Figures 1.7 and 1.8), which are a composite of those contained in the papers mentioned. The clinical application of these studies is particularly useful in dealing with cases of compression of nerve roots, where pain may be referred diffusely to deep structures approximating to the sclerotome, whereas paraesthesiae are referred precisely to the appropriate dermatome. There is some individual variation in areas of pain reference and spread may occur to adjacent segments in a fashion which is not always predictable.

Figure 1.7 Dermatomes and sclerotomes of the upper limb. If one nerve root only is damaged, sensory loss is usually restricted to the dotted areas shown on the left. Paraesthesiae are generally referred to the dermatome and pain to the sclerotome. Dermatomes, after M.R.C. Memorandum No. 7 ‘Aids to the Investigation of Peripheral Nerve Injuries’: sclerotomes, after Kellgren, ²⁶,²⁷, and Inman and Saunders²⁴ (by courtesy of the Editor of Clinical Science); (by courtesy of the publisher of Journal of Nervous and Mental Diseases)

Figure 1.8 Dermatomes and sclerotomes of the lower limb, derived from the same sources as Figure 1.7

Phenomena associated with pain

When a painful stimulus is applied to the foot of an experimental animal, the whole limb flexes and the opposite hindlimb extends. These movements, obviously of benefit for protection of the animal, are brought about by multisynaptic reflexes which involve a number of spinal cord segments—the flexor reflex and the crossed extensor response.

Visceral pain can also cause skeletal muscular contraction, and if the painful stimuli are continued, then muscle contraction is sustained in the form of spasm. This is brought about by polysynaptic reflexes at the segmental level (Figure 1.9). Thus the anterior abdominal muscles may become rigid over an inflamed viscus, or the whole abdominal wall may be ‘board-like’ in conditions of general peritoneal inflammation, e.g. after rupture of a peptic ulcer. When pain is severe, arms and legs may assume an attitude of flexion.

Figure 1.9 Muscular rigidity and vasomotor reflexes in visceral disease are caused by the excitement of polysynaptic reflex arcs at the spinal cord level. (Reproduced from McLeod³⁵ by courtesy of the Editor of the Australian and New Zealand Journal of Surgery)

A similar reflex contraction, this time of extensor muscles of the trunk, may be seen in irritation of the meninges. In extreme cases, a general attitude of extension occurs-neck, trunk and limbs–leading to bowing of the trunk backwards (opisthotonos). More commonly, rigidity of the neck can be felt on attempted flexion, and if the hip is flexed at an angle of 90 degrees to the trunk, the leg cannot be fully extended at the knee (Kernig’s sign).

Reflex muscle spasm is often seen around an inflamed joint or in paravertebral muscles when the spine, the vertebrae or the discs between them are diseased, such contraction having the effect of ‘physiological splinting’.

Another common accompaniment of pain is hyperaesthesia of skin areas sharing the same segmental area as the inflamed viscus (Figure 1.10). This can be abolished by infiltration of the affected area by a local anaesthetic agent, even though pain is still referred to the area. Segmental hyperaesthesia may also occur in disease of the nervous system itself when the nerve roots or posterior root entry zones are affected, for example the root pains of herpes zoster or girdle pains of myelitis.

Figure 1.10 Cutaneous hyperaesthesia in visceral disease occurs because activity in afferent pathways from the diseased viscus lowers the threshold for cutaneous sensory impulses at a common pool of neurones in the central nervous system. (Reproduced from McLeod³⁵ by courtesy of the Editor of the Australian and New Zealand Journal of Surgery)

Severe pain may produce generalized autonomic disturbance—nausea and vomiting, bradycardia, cutaneous vasoconstriction and lowering of blood pressure with faintness and sweating.

COMMON PATTERNS OF PAIN

Inflammation of skin, muscles or joints

Pain is induced by swelling of the tissues with resulting deformity of pain receptors. Vascular dilatation and oedema are commonly present so that pulsation of the capillaries gives a throbbing quality to the pain. Pain is relieved by placing the affected part in the ‘position of rest’, i.e. the position in which ligaments are relaxed and the tension of interstitial fluid is least, and by elevating the part if it is swollen.

Headache

Headache is caused by the following conditions.

(1) Dilatation or displacement of the intracranial vessels, for example by drugs or toxins which cause the arteries to dilate, or by a tumour or abscess which stretches the vessels.

(2) Dilatation or inflammation of the extracranial (scalp) vessels, for example in migraine or temporal arteritis.

(3) Irritation of the meninges, for example meningitis and subarachnoid haemorrhage.

(4) Direct compression of the trigeminal nerve, nervus intermedius (the sensory component of the facial nerve), glossopharyngeal or vagus nerves.

(5) Referred pain from disorders of the eyes, sinuses, teeth or upper cervical spine.

(6) Chronic contraction of the scalp muscles in states of nervous tension.

Cardiac pain

Pain is initiated by ischaemia of cardiac muscle, and is therefore liable to appear when the following circumstances apply.

(1) The filling pressure of the coronary arteries is low (for instance, atheroma of the vessels).

(2) The oxygen-carrying capacity of the blood is diminished (as in severe anaemia).

(3) The heart is doing extra work (for instance, when the patient is walking up a hill).

The pain is characteristically ‘pressing’ or ‘constricting’ in nature, and extends across the chest. It may be referred down either arm, most commonly the left, and usually down the inner side of the arm to the elbow (T1–2 segments). It may occasionally extend up the neck to the jaw or down to the upper abdomen.

Pleuritic pain

Pain from the inflamed pleura is aggravated by respiratory movement and usually can be accurately localized. If the diaphragmatic pleura is involved in its central part, where the innervation is from the phrenic nerve (C3, 4, 5) pain may be referred to the shoulder. If the peripheral part of the diaphragm is affected, where the innervation is from the intercostal nerves, pain is referred to the upper abdomen in the distribution of the nerves.

Gastrointestinal tract pain

PEPTIC ULCER

The pain of peptic ulcer depends on many factors—inflammatory oedema of tissue around the ulcer which compresses nerve endings; contraction of the stomach; the action of hydrochloric acid and other pain-producing substances on the ulcer base²⁵. The pain is related to meals, frequently waking the patient at night or coming on at other times when the stomach is empty. It is eased by the taking of food, alkalis, or drugs which diminish the contraction of the stomach. Pain is usually felt in the