The central pain control centers

In a didactic approach, it is possible to describe three main centers which explain the possible efficacy of auriculotherapy:

A. The spinal cord posterior horn selective gate.

In 1965, Melzack and Wall16 formulated the gate control theory of pain, suggesting that some inhibitory neurons of the substantia gelatinosa connected with AS and C pain fibers could be activated by sensory myelinated Ap fibers closing the door to the spinothalamic tract conveying pain sensation. In fact, the posterior horn is divided into six lamina described by Rexed which contains many inter-neurons allowing connections between AS and C

fibers linked to lamina I, II, III and Aa and Ap large myelinated fibers. The spinothalamic neurons are connected according to three modalities: high threshold (HT) for nociception connected with lamina I; low threshold (LT) for mechanical inputs connected to lamina IV/VI; and wide dynamic range (WDR) being the most numerous with three concentric zones: central, intermediate excitatory and peripheral inhibitory, giving priority to nociceptive stimulus (80% nociceptive neurons type II and type IV). M. Sindou17 from Lyons, France, has done substantial work describing this organization in detail for its application in surgery. Some metameric interconnections are possible through the Lissauer tract. The role of substance P and enkephaline neurotransmitters suggesting local or regional metameric pain control should not be underestimated. Finally we have sufficient evidence to be able to ascribe to the posterior horn a further function than merely that of a selective gate, one more concerned with semi-automatic defense reflexes. It is also important to note that any external stimulation of the dorsal funiculus is very painful (C fibers), which is not the case with the anterolateral funiculus.

B. The brainstem reticular formation. This represents a very complex group of nuclei with an anatomical disposition in three columns all along the brainstem: the median, representing the six raphe nuclei, the central or medial reticular formation represented by five identified types of nucleus reticularis in the medulla, pons and mes-encephalon, and the lateral reticular formation with six nuclei, among which is the medial parabrachial nucleus which, together with the nucleus coer-uleus and subcoeruleus, forms the dorsolateral pontic tegmentum (Fig. 2.14). More than a precise description of all those nuclei, it is important to emphasize the great concentration of neurotransmit-ter secretion centers playing a crucial role within the regulation of spinal cord ascending and descending pathways. They can be classified into: • monoamine centers with first noradrenaline (A1 to A7) with descending and ascending fibers (noradrenergic dorsal pathway from locus coer-uleus A6 stimulating the cortex), second adrenaline and dopamine (A8 to A14) more concerned with the mesolimbic system and nucleus accumbens, third serotonin (5-HT) located only in the brainstem within the raphe nuclei (B1 to B9) with descending fibers (B1 to B3) inhibiting the sympathetic spinal centers and posterior horns for pain control, connected to the locus coeru-leus (B3 to B6) and to the mesolimbic and meso-cortical system (B7 and B8) to septal nucleus, hypothalamus and hippocampus

Fig. 2.14 The reticular formation of the brainstem (from Henri Duvernoy with permission).

medial: raphe nuclei with important neurosecretion mainly serotonin:

1 Nucleus raphe dorsalis

2 Nucleus reticularis centralis superior

3 Nucleus raphe pontis

4 Nucleus raphe magnus

5 Nucleus raphe obscurus (dorsal)

6 Nucleus raphe pallidus (ventral)

II central (or median): in relation with motricity:

7 Nucleus reticularis cuneiformis

8 Nucleus reticularis tegmenti pontis

9 Nucleus reticularis pontis oralis

10 Nucleus reticularis pontis caudalis

11 Nucleus reticularis gigantocellularis

III lateral: in relation with afferences:

12 Nucleus reticularis pedunculopontinus

13 Lateral parabrachial nucleus

14 Medial parabrachial nucleus

15 Nucleus reticularis parvocellularis

16 Nucleus reticularis lateralis (connected with cerebellum)

17 Nucleus reticularis medullae oblongatae centralis

Fig. 2.14 The reticular formation of the brainstem (from Henri Duvernoy with permission).

• acetylcholine centers (ACh) in the basal forebrain (Ch1 to Ch4) and in brainstem (Ch5, 6, 8) with ascending fibers for the intralaminar and reticular nuclei of the thalamus and striatum and descending fibers to the brainstem. Finally, the reticular formation of the brainstem has an important neurotransmitter secretion activity and a double system of connections: first ascending from the spinal cord (spinoreticulothalamic pathway with relay in the raphe nuclei and periaqueductal gray matter) and to the reticular thalamus (reticular nucleus surrounding the thalamus 'like a shield' with thalamocortical and corticothalamic fibers, intralaminar nuclei forming the median center, parafascicular nucleus, paracentral and centro-lateral nuclei), and second descending to the spinal cord for inhibitory pain control. But obviously that is only a small part of the function of the reticular formation which is also related to all the management of visceral activities, servomechanisms and cortical ascending activation or deactivation during sleep.

C. The thalamic selective filter. As pointed out many years ago by Head and Holmes,18 the pain control takes place mainly in the thalamus which is a large mass of gray matter located on the lateral wall of the third ventricle within the dien-cephalon. The classification of nuclei is still controversial, but it is possible to identify three groups of thalamic nuclei: anterior connected with the mamillary body and integrated within the Papez circuit of emotions; medial projecting to the frontal, prefrontal and orbitofrontal cortex and connected with amygdaloid nucleus, ventral pallidum and midbrain reticular formation; ven-trolateral subdivided into ventral anterior (VA), lateral (VL) and posterior (VP) and in lateral dorsal (LD), lateral posterior (LP) and pulvinar. In addition there is the lateral geniculate nucleus as an integrator of the two retinal fiber flows and the medial geniculate nucleus as a relay on the auditory pathway going to the temporal lobe. The thalamus has a widespread reciprocal projection system with the entire cortex and roughly its caudal half is concerned with ascending sensory pathways including occipito-temporo-parietal cortex while the rostral half is foremost in relation to motor and limbic activities.

The VP is also called the ventrobasal complex. The medial lemniscus is projected to the VP lateral anterior (VPLa) for conscious statokinetic sense and to the posterior (VPLp) for tactile epicritic sensitivity. The spinothalamic fibers are also connected with the VPL mainly in its superior, lateral and posterior parts in a manner different to that of the lem-niscal fibers. But the functional interaction of those two types of fibers is still controversial: do they really converge on the same thalamic relay neuron or are they projected in parallel with eventual interaction by interneurons? At any rate, it seems that 70% of the relay neurons of the VPL and VPM receive cutaneous inputs according to three functional modalities: 15-20% of nociceptive specific neurons; 20-30% of low threshold mechanical slow adapting (SA) or rapid adapting (RA) neurons; 50% of convergent WDR type neurons sensitive to noxious and non-noxious stimuli. The recognition by the cortex of the nociceptive nature of the signal in the 3b part of the post-central gyrus is largely dependant on the thalamic relay neurons and inter-neuron activity.

In addition, the importance of the trigeminal lemniscus (trigemino-thalamic pathway), also concerned in this activity and in which many sensory fibers from the auricle are traveling, could be an argument to validate the inhibitory action of a stimulation of the auricle on the pain projection of spinothalamic fibers from different body origin. This active thalamic inhibition of pain (ATIP) is a sort of competition between pain stimuli. Therefore it is plausible to consider the existence of oscillatory pain circuits in the thalamus as well as in the spinal cord in case of prolonged pain, reinforced by cortical actions (cingulate gyrus, limbic system, amygdala), which can be 'broken' by another pain stimulus: pinching, needling or electrostimulation of the skin on identified neurovascular bundles or auricular zones. In the experimental work we carried out in research Unit 103 at INSERM, we demonstrated the thalamic inhibition of painful stimuli on the hind limb of rabbit by recording evoked thalamic potentials within the parafascicu-lar nucleus using a stereotactic frame and anatomical cross-sections for precise localization (Plate ID). Electrostimulation of the analgesic points lasting 20 minutes suppressed the thalamic potentials, but at 2 cm from the points it maintained them. This was also confirmed by G. Farnarier and collea-gues19 in Marseille and Chang Hsiang-Tung20 in Shanghai. However, some hypotheses can be formulated: either the inhibition lies at the thalamic level or at the spinal level, or both.

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