Supraspinal Engrams Relevant In Transition From Acute To Chronic Pain

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Nociceptive afferent signals from damaged peripheral tissue are relayed to the posterior column where they transmit to second order neurons of the spinal cord where they are being modulated. Nociceptive simuli originating in the head or the face are conveyed via the trigeminal nerve to the trigeminal nerve nucleus in the brain stem. There, all afferent signals are being modulated after which they cross to the opposite side, further ascending to the thalamus. From there, fibers ascend rostrally to lemniscal and thalamic structures, before they reach the somatosensory cortex (Figure I-44). Each long-term or even a paroxysmal increase of activity of afferents to the posterior column of the spinal cord or to the trigeminal nerve nucleus also induce an activity-dependent adaptation of the rostrally located thalamic and neocortical structures [86]. In the process of development of chronic pain, besides adaptive peripheral changes, also an alteration at the cortical level is instigated resulting in central sensitization (Table I-4).

For instance, hyperexcitability of cortical neurons was documented in patients with chronic pains, where experimentally pain-related stimulation with sensory-evoked potentials resulted in an augmented response in the primary cortical projection area. Such response could be derived within 80-129 ms after the stimuli. Such increase in excitability of specific cortical areas in pain patients was also reflected in the augmentation to acoustic stimuli. Similar to the process of sensiti-zation at the peripheral site, non-nociceptive stimuli are felt as painful. And simple words or even thoughts can cause pain sensations. This is because during the process

Figure I-44. In chronified pain the touch at the skin induces activation at the corresponding sensory cortical area (cueing of nociception). Because of an elevated basal activity even minor stimuli are able to induce a hyperexcitatory state resulting in allodynia 1 = AS- and C-fibers; 2 = spinothalamic tract; 3 = intrathalmic pain-related nuclei; 4 = sensory cortex

Figure I-44. In chronified pain the touch at the skin induces activation at the corresponding sensory cortical area (cueing of nociception). Because of an elevated basal activity even minor stimuli are able to induce a hyperexcitatory state resulting in allodynia 1 = AS- and C-fibers; 2 = spinothalamic tract; 3 = intrathalmic pain-related nuclei; 4 = sensory cortex

Sequence of Resulting in Neuropathic Pain Table I-4. The changes within the supraspinal system, resulting in central sensitization

1. Reduction of threshold to incoming excitatory stimuli

2. Expansion of receptive fields within the corresponding sensory cortical area

3. Lowering of threshold of cortical cells for excitability followed by hyperalgesia

4. Synaptic long-term potentiation of cells in the hippocampal area with prolonged memorization of nociceptive propagation, within cortical structures, a localized recollection of pain impulses is set-off, which can be activated without peripheral stimulation. Excitatory amino acids (e.g. glutamate, tachykinins) seem to play a significant role in such situation, because painful reactions can be induced experimentally following microinjection into different mesencephalic and diencephalic parts involved in pain transmission [87].

Therefore pain without any doubt, is also a subjective experience where the first level of consciousness is due to a connection between the intralaminary nuclei to the pallidum and the second level of consciousness, the cerebral cortex. It is here where the activity of sensory organs will be translated into pain, while at the same time resulting in an individual complexion of painful afferences. In chronified pain conditions, aside from neurochemical changes within the first transmission site in the spinal cord in the spinal cord, as demonstrated by Beechy and McKenzie [88] also a learning effect at the ventral area of the hippocampus. This is because the hippocampus is an area where traces of memory are being consolidated permanently into so-called engrams. They result in an attitude of expectations in the chronic pain patient. On the other hand during nociceptive processing, the pallidum is responsible for the affective component of pain. It is therefore not too surprising, that aside from the striatum and the nucleus coeruleus, the pallidum is rich in opioid receptor sites and a place where endogenous opioids bind [89, 90]. Opioids given for the suppression of pain exert their primary site of action in the pallidum by blocking the negative and agonizing character of pain. Such agents are also of value when the neuronal stored information on a previous pain experience is to be deleted. On the other hand, it also becomes clear why unsolved conflicts, aggressions, fear, resignation and passiveness, contempt, and psychological imbalance reinforce pain sensations. On the other hand psychic balance, satisfaction, joy, enforcement strategies, all result in a reduction of pain intensity. Consequently, pain experience is not comparable with one another. It is an extremely individual feeling, subjectively colored, emotionally tuned and assessed differently by each person. According to the individual experience and its sequences pain is difficult to measure and can hardly be classified as such. Lastly, such considerations underline the theory of Melzack [21], in that pain is an individual sensory feeling, which incorporates the neuronal networks of the entire body, being affected by cultural, genetic, socio-economic as well as individual experiences in the past.

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