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some reservation; and (3) contra-indication for neurostimulation. None of the patients with a negative advice was implanted, but for these an alternative treatment could be proposed. Of the 27 patients for whom the psychiatrist made some reservation, 16 were implanted (59%) and of the 59 patients with a positive advice 81% were implanted. Six month& after implantation, the therapeutic outcome was evaluated. Whereas 64% of the patients with a positive advice were successes, only 18% of the patients for whom the psychiatrist had formulated some reservation were considered as successes.

THE PSYCHOLOGICAL EVALUATION IN THE POST-IMPLANT PERIOD

REFERENCES *Kupers R, van den Oever R, Van Houdenhove B,

Vanmechelen W, Hepp B, Nuttin B, Gybels JM. Spinal cord stimulation in Belgium: a nation-wide survey on the incidence, indications and therapeutic efficacy by the health insurer. Pain 1994; 56: 21 I-216.

Melzack R, Casey KL. Sensory, motivational and central control determinants of pain: a new conceptual model. In: DR Kenshalo, edition. The skin senses. Springfield, IL; Thomas, 1968: 423443.

Moulin DE, Iezzi A, Amireh R, Sharpe WK, Boyd D, Merskey H. Randomised trial of oral morphine for chronic non-cancer pain. Lam-et 1996; 347: 143-147.

Nelson DV, Kennington M, Novy DM. Psychological selec- tion criteria for implantable spinal cord stimulators. Pain Forum 1996; 5: 93-l 03 (see also the commentaries on this focus article in the same issue, pp. 104-120).

Turner JA, Roman0 JM. Psychologic and psychosocial eval- uation. In Bonica JJ, edition. The management of pain, 2nd edition. Philadelphia: Lea and Febiger, 1990: 595-609.

The contribution of the psychologist or psychia- trist does not stop at the moment the decision for implantation has been taken. Among the further 2. BASIC MECHANISMS OF SPINAL roles to be played belong: selection of the ade- CORD STIMULATION quate moment for implantation, formulation and integration of the neuromodulation procedure B.A. Meyerson

with complementary therapies, assessment of the patient’s improvement in functional status and quality of life, counselling role with respect to the potential occurrence of side-effects, etc.

CONCLUSION

Rather than being considered as stand-alone treat- ments, neuromodulation procedures should usu- ally be supplemented with psychologically- or behaviourally-oriented treatment modalities. A close collaboration between the implanting physi- cian and the members of the multidisciplinary team of the pain clinic, both in the selection of the patient and in the follow-up of the neuromodula- tion procedure, is desirable and is expected to increase positive long-term outcome. Although most physicians seem to acknowledge the necessity of a psychological evaluation, this evaluation is often reduced to a single interview before implan- tation. Only rarely is the psychological evaluation embedded in the broader context of a multidisci-

Karolinska Centre for Pain Research, Department of Clinical Neuroscience, Section of Neurosurgery, Karolinska Hospital, Stockholm, Sweden

Spinal cord stimulation (KS) has been in use for more than two decades, but the physiological and biochemical mechanisms involved in its relieving effects, both in neuropathic pain and angina pec- toris, are still poorly understood. Conversely, our knowledge about its mode of action for ishaemic pain in peripheral vascular disease (PVD) is somewhat less fragmentary.

SCS evolved as a direct clinical application of the gate-control theory of 1965, when it was pos- tulated that noxious inflow originating from the periphery can be inhibited at the first dorsal horn relay by the antidromic activation of large dorsal column fibres projecting onto the same spinal segment. However, the relevance of this theory fdr SCS is questionable because of the fact that SCS neither influences acute or chronic nocicep- tive pain nor experimentally-induced pain.

plinary pain evaluation and rehabilitation pro- Nevertheless, a large number -of experimintal gram. This may be partly explained by the fact that studies with the aim of elucidating the mode of many pain centres in the European Communities action of SCS were performed using acute, nox- lack a psychiatrist or psychologist on their team. ious stimuli (heat, pinch, pressure, etc). These

European Journal of Pain (1999), 3

390 TUTORIAL

studies demonstrated that SCS may have tran- sient inhibitory effects on evoked nociceptive activity in the dorsal horn. In a few studies more long-lasting post-stimulatory inhibitory SCS effects on nociceptive dorsal horn neurons were demonstrated.

In spite of the well-known fact that the pres- ence of paraesthesias in the pain area is a prereq- uisite for pain relief, implying the involvement of the dorsal columns, it has been argued that the effect is instead mediated by the activation of pain inhibiting pathways (dorsolateral funiculus) in the spinal cord. This explanation seems less likely considering that the perception of noxious pain is not attenuated and that the fibres con- tained in these descending pathways are thin and have a high threshold. Furthermore, it is known that the preservation of the spinal lemniscal func- tion is a precondition for obtaining pain relief.

Some experimental studies suggested that the pain releiving effect is at least partly dependent on supraspinal pain- inhibitory mechanisms operating via a negative feed-back loop. It has been claimed that the anterior pretectal nucleus is the relay for this loop since stimulation in that area may produce a powerful inhibition of noci- ceptive dorsal horn neurons. However, the clini- cal relevance of all these experiments is limited, since therapeutic SCS is exclusively effective for neuropathic forms of pain (peripheral vascular disease and angina, see below). Moreover, the observed .effects were generally transient, SCS was applied for short periods of time with con- siderably higher intensity than that used clini- cally, and, more importantly, the experiments were performed on intact, anaesthetized animals.

Therefore, rat models of mononeuropathy, produced by partial lesion of the sciatic nerve, seem appropriate for the study of the mode of action of SCS in neuropathic pain. It has been demonstrated that SCS, applied via an implanted spinal electrode in freely moving nerve-injured rats, may suppress tactile allodynia (in the nerve ligated hind paw), and this effect is of clinical rel- evance, since it is well known that in patients SCS may effectively attenuate also evoked pain due to the presence of allodynia and dysaesthesia. Moreover, in acute experiments performed on nerve injured rats it has been found that SCS may

effectively suppress the hyperexcitability of wide- dynamic-range neurones, manifested both by the presence of abnormal spontaneous discharge and enhanced responsiveness to innocuous peripheral stimuli. This effect appears to be mediated principally via the dorsal columns. On the basis of these findings, it has been assumed as very likely that SCS preferentially influences Al5 fibre-mediated functions.

Data from humans on the biochemical corre- lates to SCS are sparse and contradictory. There is no evidence that the pain relief is dependent on the activation of opioid dependent mechanisms. Data on the role of biogenic amines are inconsis- tent, though a few studies have demonstrated a moderate increase of serotonin release produced by SCS. There is some evidence that substance P may be involved, but otherwise the role of neu- ropeptides remains to be further investigated. Conversely, there is much experimental data sub- stantiating that the SCS effect on neuropathic pain is closely related to GABAergic mecha- nisms. For example, in mononeuropathic rats, the extracellular release of GABA in the dorsal horn is increased by SCS, and the SCS effect on tactile allodynia is attenuated by i.t. administration of a GABA antagonist. There are also indications that adenosine-dependent mechanisms are involved in a similar way.

Both clinical and experimental observations have provided evidence that the beneficial effect of SCS in PVD is secondary to vasodilatation and no data substantiate that the ischaemic pain per se is suppressed. This effect on the peripheral vascula- ture is presumably the result of a sympathetically- mediated decrease of vasoconstrictor tone, but antidromic activation of primary afferent libres may also contribute to the vasodilatatory effect. Recent observations suggest that calcitonin-gene- related-peptide (CRC%) is involved in mediating the peripheral vasodilatation.

There is a continuing debate about the mode of action of the SCS pain-suppressing effect in angina pectoris. However, some data indicate that SCS induces an improved balance between coronary oxygen demand and supply mediated by a local redistribution of blood flow. It has been proposed that these effects may be related to a depression of cardiac sympathetic activity.

European Journal of Pain (1999), 3

NEUROMODULATION OF PAIN

REFERENCES

Jessurun GAJ, DeJongste MJL, Blanksma PK. Current views of neurostimulation in the treatment of cardiac ischaemic syndromes. Pain 1996; 66: 1099116.

*Linderoth B, Meyerson BA. Dorsal column stimulation: modulation of somatosensory and autonomic function. Seminars in The Meurosciences 1995; I: 263-217.

Linderoth B. Spinal cord stimulation in ischaemia and ischaemic pain: possible mechanisms of action. In: Horsch S, Claeys L. editors. Spinal cord stimulation. An innovative method in the treatment of’ PVD and angina. Darmstadt: Steinkopff Verlag. 1995: 19-35.

Meyerson BA. Mechanisms of spinal cord stimulation as pain treatment. In: Campbell JN. editor. Rcfiesher course. Role qf implantable devices. Seattle: TASP Press. 1996: 207-216.

Roberts MHT, Rees H. Physiological basis of spinal cord stimulation Pain Reviews 1994; 1: 184198.

Simpson BA. Spinal cord stimulation. Pain Reviews 1994; 1: 1999230.

3. INDICATIONS FOR SPINAL CORD STIMULATION IN NEUROPATHIC PAIN

G.H. Spincemaille

Academisch Neurochirurgisch Centrum Limburg, Academisch Ziekenhuis Maastricht, The Netherlands

Spinal cord stimulation (SCS) is indicated in patients with chronic neuropathic pain due to peripheral nerve and spinal cord lesions. The fol- lowing conditions are good indications.

(1) Pain caused by peripheral nerve lesions following entrapment, accidental trauma, or trauma secondary to surgical interventions of which stripping and surgery around the ankle (saphenous nerve), knee surgery (infrapatellar nerve) and inguinal surgery (inguinal nerve) are the most common. Stump pain after amputation generally responds better than phantom pain. Post-herpetic neuralgia with sparing of some sensory function, post-radiation plexopathy and polyneuropathies such as diabetic, alcoholic and post-chemotherapeutic are possible indications. Complex regional pain syndromes (CRPS) type II, previously described as reflex dystrophy or major causalgia, is a frequently seen problem sec- ondary to surgical interventions close to nerves. Its mechanism is poorly understood but implica- tion of the sympathetic system is accepted. For those patients where all other therapies failed,

391

SCS can be a valuable alternative. The peripheral nerve can be treated either by peripheral nerve or spinal cord stimulation. In many patients, SCS is favoured due to the easier implantation proce- dure distant from the originally damaged nerve. Local re-interventions are deemed to be mostly unsuccessful. SCS is indicated when local non- surgical therapy fails. There are data available on the effect upon the different symptoms of chronic neuropathic pain such as allodynia, hyperpathia and hyperaesthesia.

(2) Pain due to root lesions secondary to root compression due to a slipped disk and less fre- quently to spondylosis or due to postsurgical complications as scarring or arachnoiditis belongs to the diseases most frequently treated with SCS. Failed back surgery syndrome (FBSS) is a bad description of a condition, which is seen after a long-term compression of a nerve root or secondary to changes around the nerve (scar tissue). One must be aware of the various aetio- logical conditions that are covered by the description. Reports should clearly delme the pathological background of the patients treated and the type of the prevalent pain in order to dif- ferentiate between responders and non-respon- ders. There are several well-documented studies on reduction of neuropathic pain components and enhancement of the quality of life.

Plexus lesions, partial or complete avulsion are indications in which SCS is still worth trying. The more complete and extended the lesion is, the less the chance of success becomes. Pain due to plexus lesions disappears in the majority of the patients either spontaneously or secondary to surgical intervention aiming for a functional restoration in which neurolysis and nerve trans- plantation is performed. A plexus lesion, although an example of overt nerve roots dam- age, is less successful than one would expect. There is a correlation between the number of roots avulsed and the loss of large myelinated fibres in the dorsal horn. In cases where there are almost no myelinated fibres left, the chance of pain relief is low. A trial stimulation however still remains indicated.

(3) Pain due to lesions of the spinal cord fol- lowing injury, vascular accidents or secondary to resection of a spinal cord neoplasm are rare

European Journal of Pain (1999), 3