Pathophysiology of pain after Spinal Cord Injury
G.P. Novelli*, S. Aito**,
Abstract for the 2003 European congress of Anesthesiology
*Institute of Anaesthesiology, Intensive Care and Pain Therapy; University of Florence, School of Medicine, Florence, Italy.
** Spinal Cord Center of Florence
“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” is the definition of pain given by the IASP, the Innternational Association for Study of Pain.
Pain is always subjective and each individuals refer different sensations if submitted to the same stimulus in the same conditions. This let us affirm that pain sensation is influenced by several factors and not only by nociceptive stimulus or tissue damage.
The neurophysiological basis of transmission of pain involve the nociceptors, the input of stimuli in the spinal cord, the spino-thalamic neurons and the thalamo-cortical fibers.
It is important to quote the descending system of endogenous pain control whose activity is mediated mostly by catecholamines, serotonin and endogenous/exogenous opioids.
According to its origin, pain can be classified as nociceptive or neuropathic.
Nociceptive pain occurs when peripheral nociceptors are excited. It is conducted through unmyelinated and small myelinated peripheral nerve fibres, to reach the brain through specific pathways (anterolateral funiculus of the spinal cord via reticular formation and thalamus ). It is sensitive to opioids.
Neuropathic pain results from a damage within the nervous system itself and it does not involve the nociceptors.. some of the past SCI pains that seem to be caused by lesions of the somatosensory pathways passing through the ventrocaudal nucleaus of the thalamus and of the spino-thalamic traat belong to the group of neuropathic painful syndromes.
The neurological lesion may be either minimal or with complete sensory and motor block; its onset may be immediate or, more frequently, be delayed, increasing in severity and/or extent with time, so suggesting that the central events are progressive.
However, central pain sometimes can be spontaneously reversible, suggesting that the underlying mechanism is not necessarily structural.
Neuropathic pain is characterised by deficient discrimination of temperature and shiarpness; its responsivity to opioids is poor or absent.
The mechanisms of SCI pain are the same as those for all kinds of neuropathic pain. The most common are: a) denervation, neuronal hypersensitivity; b) presence of spontaneously bursting cells and ectopic generators; c) somatotopographycal reorganisation with opening up of inactive synapses; d) imbalance between excitatory and inhibitory systems; e) sympathetic influences.
Incidence of SCI pain
The most frequent causes of SCI are traumas (in fact patients are mostly young males) but there are also inflammatory, vascular, neoplastic, congenital lesions, etc.
The incidence of pain is different according to various reports, going from a minimum of 6,4% of all SCI quoted by Porter (2) to 94% reported by Botterell (3). The severity and characters of pain frequently hase not been reported. A postal survery performed by finnerup (4) in Denmark on 240 patients indicated that pain occurs in 79% of the patients with a median intensity 46 (VAS) and presence of allodynia in 60% of the patients. Tasker quotes two of his patients who suffered similar pain but one had a SCI with no clinical deficits and the other had a complete transection (5).
The onset may be precocious within one month in 30% of patients but after one year and till 5 years in 15%. A percentage, of course, of SCI patients don’t experience pain. The development of a syrinx may introduce another cause of delayed pain (6).
Phantom limb and phantom pain appear sometimes after spinal cord transection and are not as vivid at those of amputees (7): they are the basis of the theory of neuromatrix by Melzack (8).
In a study on the quality of life in cronic spinal injured people, the 37% of tetraplegic and the 23% of paraplegicreferred the problem of pain to be more important than those linked to the bladder, bowel, sexuality or motility.
Pain may strongly influence spinal cord lesioned persons in reaching accettable ability in activity of daily living ( ADL), and in achieving the reintroduction at work or in the normal social life.
It may be present, in its different forms and expression, in the different stages of a spinal cord lesion.
In the acute stage it is mainly due to trauma occurred to the muscolo-skeletal system, while in the post-acute stage it manifests in a more complex way.
Classification of SCI pain.
In order to better understand the type of pain that afflicts the spinal cord lesioned patients, it is very important to classify it in the right way, so that the correct therapeutic approach can be adopted.
Different types of classifications have been proposed and adopted. These were used for the generic pain or for the pain afflicting specifically spinal cord lesioned people.
The best known of them are those proposed by Kaplan (1962) by Michaelis (1970), by Davis (1975), by Burke and Woodward (1976), by Bedbrook.
Siddall (1997) has very well synthesized all of them, proposing a very easy and complete classification.
He listed 5 categories of past SCI pain:
- Neuropathic pain at the level of lesion (neuropatico I)
- Neuropathic pain under the level of lesion (neuropatico II)
- Other Types (Siringomyelia, Compressive Mononeuropathy, Algodistrophy. Etc. )
1. Muscoloskeletal pain is consequence of tissue damage or overuse syndrome on bones, muscles, ligaments, intervertebral discs, facets joints.
2.Visceral pain is obviously linked to internal organs pathology ( spastic cholitys, urinary stones, etc.), that must be excluded bifore classifying it as neuropathic one.
These two classes may express themselves in different ways, such as dull, aching, worse with activities, eased with rest, cramps like, etc. They are to be considered as nociceptive pain.
3. Neuropathic pain, has been divided by Siddal in two subgroups: type I and type II.
Type I is pain occurring at the level of neurologic lesion and type II is that one under the neurologic level of lesion.
Neuropathic pain type I might be referred within two metameres above or under the neurological lesion and can be further divided according to the source of pain in radicular and central.
Radicular pain is due to the pathology of a single nerve root. It can have the same characteristics of the central pain but is referred along a nerve root and often is monolateral. It might increase with the movements of the spine.
Central type pain is due to an intramedullary cells pathology and normally does not change with the movements of the column.
The characteristics of the neuropahic at the level lesion, both radicular or central, are usually referred as burning, stabbing, shooting, electrical shocks, constricting like a chain.
Neuropathic pain type IIis located under the level of lesion and has all the characteristics of deafferentation pain. It must be referred at least 3 levels under the lesion.
During the acute stage of a SCI usually the pain is muscoloskeletal because due to the trauma and the immobilisation. After the spinal shock and in the cronic stage, pain can be present in all its different classes above mentioned.
Typical above the lesion pain is the shoulder pain in tetraplegic patients, or that due to the incorrect posture or gymnastic activity in patient affected by neurogenic muscolar disharmony.
Pharmacological treatment of neuropathic SCI pain
The appeearance of PSI pain in patients just suffering for their plegic lesion looks like a tragedy superimposing in a previous one.
The pharmacologic approach to pain is the primary one; it’s comprehensive of:
a) anticonvulsants like carbamazepine and gabapentine in the attempt to eliminate spontaneous firing of ectopic foci;
b) tricyclic antidepressant, mostly directed to activate the descending system for endogenous pain control;
c) some antiarrhytmic drug derived from lignocaine might be considered as inhibitors of neuronal overexcitability and spontaneous firing;
d) analgesic drugs are obviously necessary. It must be noted that central pain and SCI pain are well known as poor responders to opioids and good responders to FANS; paracetamol seems to be the most effective one, due to its central action. Tramadol could be considered for patients that obtain relief from opioids with very low or absent potential of tolerance also in view of very long therapies. Patients obtaining relief from opioids might be submitted to spinal morphine through a subcutaneous implanted pump: although the technique is well developed, few SCI pain patients are known to receive it.
Anyway neuropathic pain represents great challenge for the clinicians, due to the difficulties in adopting the right solution that many times is never found.
It might also be negatively influenced by other pathologies such as infections or spasticity or by. Nociceptive pain that can be treated pharmacologically by administering FANS, or physical therapies as lase, ultrasound, TENS, local infiltration of anesthetics and cortison, physiotherapy, massages, acupunctute and relaxation techniques.
Stimulation treatment of neuropathic pain
The central pain after neuropathy appears not to be dependent on transmission in pain pathways it could be argued to be relieved by overstimulating and inducing paresthesias.
Deep brain stimulation has been tried in the periacqueductal gray (PAG) or ventrocaudal (Vc) nucleus (12), inducing pain relief only by stimulating Vc electrodes.
Experience with deep brain stimulation is limited to few patients with rarely good relief and with a lot of complications.
Spinal cord electrostimulation (SCS) is directed to induce paresthesias in the painful area by inserting a special electrode in the peridural space at appropriate level. The mechanism of the action of SCS is not completely clarified but it is to be related to paresthesias: in fact SCS relieves steady pain only if precisely located parasthesias are evoked.
Experiments with intrathecal transplant of adrenal medullary chromaffin cells to secrete catecholamines and opioid peptides directly “in situ”: the presented results seem to be effective in reducing pain (13).
Few reports in the literature are very confounding because sone quote good relief in about 50% of the patients but others (14,9) concluded that SCS was a poor operation for treating neuropathic pain. It is worthy to note the difficulties in correct placement of electrode in a peridural space occupied by adhesions, bone fragments, tutors, etc..
My personal experience with SCS for neuropathic pain is limited to two patients: one with incomplete lesion of the cauda whose 60 – 70% pain relief continues since 1986 and the other one with neuropathy at C7 whose pain relief continues from about 20 months although not complete.
Surgical treatment of neuropathic pain
When neuropathic pain is unbearable, disabling and fails to respond to conservative measures, surgery might be considered.
Rhizotomy, cordotomy, cordectomy and dorsal root entry zone lesions (DREZ) and interruption of pain pathways seem to improve neuralgic pain but not steady pain that is affected mostly by chronic stimulation techniques.
Anyway, looking at surgery as treatment of neuropathic pain the cohexistence of different pain sources must be considered. Destructive stereotactic lesions have been reported but with unconclusive or poor results.
Psycological support plays a very important role in the comprehensive management of neuropathic pain. By observing that pain is mostly present during evening and night time or when patients are not involved in activities let us believe that better results might be achieved by using behavioural techniques.
Although none of the above mentioned treatments is, alone, sufficient to win the challenge of the neuropathic pain in spinal cord lesioned patients, I think that success can be reached only by adopting some of them in association with a multidisciplinary approach.
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