Presented overview literature,concerning neuropathic pain one of the actual problems in modern world. One of the reason injury peripheral nerves connect. Psychogenic pathological conditions with chronic pain syndromes well described enough in literature. Foreign researchers have paid great attention to psychogenic factors formation and saving pain. But other factors not enough studied and first turn illuminated from point of view participation in the process of development peripheral neuropathy. It maybe the some mechanisms included at the core long-term preservation pain syndrome in case of damage peripheral nerves,that requires further research [1,2]. Keywords: neuropathic pain, epidemiology, peripheral nerves.
Neuropathic pain is an urgent problem in the modern world.According to the definition of H.Merskey and N.Bogdua 1994, it is pain that is caused by primary injury or disease of the somatosensory system .
According to an epidemiological study conducted in Europe in 2005,the frequency of neuropathic pain in different countries ranges from 6-7.7%. For example in France it was 6.4%, in Germany 6%, in the U.K -7.5% and in Spain- 7.7%. In 2008, a multicenter clinical and epidemiological study of neuropathic pain was completed in Russia [4,5].
The incidence of any pain among patients who has consulted a neurologist was 39%, and neuropathic pain or its component was 18% of all outpatients.
Neuropathic pain most often occurs with tuner syndromes, mono and polyneuropathies, compression of nerves to nuts, trigeminal neurologia, syringomyelia, multiple scelerosis, vitamin B12 dificiency, myelopathy, brain and spinal cord tumors, acute cerebrovascular accidents, surgical operations arteriovenous aneurysms, craniocerebral injuries and injuries of peripheral nerves [6,7].
According to statistics the nerves of the upper extremities are radial ulnar and median less often the nerves of the lower extremities the sciatic and peroneal which is due to the anatomical relationship with the surrounding tissues.
As evidenced by the Literature data, the frequency of damage to the brachial plexus trunks and peripheral nerves remains stably high and amounts to 3-10% of all injuries of the musculoskeletal system.
All the same time, the frequency of postoperative neuropathies, according to various sources ranges from 7.5 to 16% with the ulnar nerve being most often affected (33-85% of all postoperative neuropathies) .
According to the classification of H.J Seddon (1943) and S.Sunderland(1951), nerve injuries, depending on the severity of damage, are divided into neuropraxia (temporary disturbance of innervations compression of the nerve without any structural damage), axonotmesis ( the degree of damage to the nerve fiber in peripherial lesions), of the nerves, morphologically characterized by a violation of the integrity/rupture of the axon with the structural elements of the sheath in tact) and neurotmesis, complete violation of its integrity with total degeneration of the never section distal to the injury [9,10].
N.N. Yaichno (2005) presented this classification as follows:
Type I injuries a treatment transient conduction blocked due to ischemia (mild sensory disturbances and paresis, for example, due to the leg to leg posture) with a quick and complete recovery.Cases of demyelination of the radial nerve with gradual within a week complete recovery belong to the same type.
Type II injuries violation of the integrity of the axon with intact connective tissue sheath and nerve skeleton, arising from its compression; Wallerian degeneration is observed distal to the site of the lesions; sensory, motor and autonomic defects are found. Recovery is very slow. The more distal the lesion, the better the prognosis. Surgical treatment is not indicated.
Type III injury destruction of the axon and connective tissue membrane. A complete nerve rupture is usuallycaused by penetrating and traction injuries. Clinical syndrome complete loss of sensory, motor and autonomic functions. The prognosis is poor; surgery usually gives insignificance improvement [11,12,13].
According to same studies, the risk of neuropathic pain in nerve injuries is high and amounts to 71-95%, while according to others, it is less than ½ 134%). P.Ciaramitaro et al (2010) examined 158 patients with peripheral nerve injuries and found that pain syndrome was present in 66% and neuropathic pain was present in 50% of all patients. Moreover in 79% of patients with neuropathic pain, its intensity was moderate or severe.
International experts led by R.DTreeds (2008) suggested using the criteria for grading the probability of a diagnosis of neuropathic pain. Diagnosis using this algorithm is based on 4 criteria: (1) Localization of pain in the neuroanatomical area; (2) history of lesion or disease of the peripheral of central somatosensory nervous system; (3) identification of positive and negative sensory symptoms in the neuroanatomical zone; (4) objective confirmation of the lesion of somatosensory nervous system [14,15].
If the patient has all 4 of the above criteria, the diagnosis above criteria the diagnosis of neuropathic pain is considered reliable. The diagnosis of neuropathic pain is highly. Likely when criteria 1 and 2 are combined on of the other two, 3 or 4. Neuropathic pain is considered possible if only criteria 1 and 2 are combined. According to the proposed algorithm, the diagnosis of neuropathic pain should be considered fully confirmed only when it is reliable and highly probable. At the same time, instrumental pain (electroneuromyography, registration of evolved potentials, computed and magnetic resonance imaging, microneurography, study of reflexes and biopsy) do not reveal strictly specific changes, but can be informative in the study of the mechanisms of pain and the effect of drugs .
To facilitate the diagnosis of neuropathic pain, several questioned have been developed world wide. It should be noted that question varies can only be used as a convenient auxillary diagnostic method (as well as instrumental research methods) and differential diagnosis of pain syndromes, only complementing the patient’s examination.
In addition to neuropathic pain, there are neuroceptive pain occurs with any tissue damage that causes excitation of peripheral pain receptors and specific somatic or visceral afferent fibers. Primarily in patients with nerve injuries, the myogenic, asteo and arthrogenic, components of neuroceptive pain predominate. However chronic of neuroceptive pain occurs less frequently than neuropathic pain [17,18].
One should not forget about chronic psychogenic pain, often discussed as neuropathic and/or neuroceptive pain which can occur regardless of somatic visceral or neuronal damage and is largely determined by psychological and social factors. It remains debatable whether psychogenic pain exists in its purest form. To identify psychogenic pain, the DSM-IV classification is used in which two main and three additional criteria are distinguished. The main criteria include: 1-prevalence of multiple and prolonged pain: 2- the absence of an organic cause of pain or in the presence of any organic pathology, the patient’s complaints are much lighter than those that are possible with those changes. Additional criteria include: 1- the existence of a temporary connection between a psychological problem and the development or growth of pain syndrome; 2- pain allows the patient to avoid unwanted activities: 3- gives the patient the right to achieve certain social support that cannot be achieved in any other way. In this case, psychogenic pain often manifests itself not in isolation, but is superimposed on neuropthic and nociceptive pain, intersifying the symtomatology .
Chronic pain and the causes of this formation. Despite the fact that in the past 30 years there has been an increased interest in the study of pain,most Russian scientists have covered the issues of determining the mechanisms of formation and chronicity of pain without touching into account additional factors that affect the body as a whole and are not directly related to pain syndrome. The central mechanisms of pathological pain were formulated which led to the creation of the concept of pathological pain which made it possible to explain the persistence of pain after the completion of the healing process [20,21].
The International Association for the study of pain defines chronic pain as continuing beyond the normal healing period and lasting more than 3 months (IASP, 2004). Based on this definition, it can be concluded that chronic pain is always pathological .
The central modification of the incoming sensory impulse is considered to be the main theory for the occurrence of chronic pain syndrome. This theory assumes the presence of several synapses along the path of sensory stimulus to the cerebral cortex, the most important of which are the posterior horns of the spinal cord, stem structures, thalamus and the cortex itself. According to the theory of gate control, at each of the above levels, the impulses is stimulated or inhibitory from the side of collateral axons, as well as the ascending or descending pathways of the nociceptive and antinociceptive systems .
The most important neurotransmitters that act at the level of the dorsal horns of the spinal cord are substance producing pain impulse and endogenous opioids such as methenuephalin ( inhibiting pain impulses). Possible inhibitory effect from the corticospinal tract due to the neurotransmitter glycine. At the level of the brain stem, the inhibitory effect is serotonergic and noradrenergic structures. Moderate short term deficiency of serotonergic structures leads to the development of anxiety and pain, with long-term serotonin deficiency depression can develop. The next synaptic level includes the thalamus the limbic system, and the adjacent subcortical and cortical structures of the brain. this is where the subjective assessemt of pain occurs. Neurotransmitters that inhibit the transmission of nociceptive information form subcortical structures to the cortex are poorly understood, one of them is beta-aminobutyric acid. Chronic pain develops when the last cortical synaptic level is sensitized by afferent sensory influx .
If we consider separately the alleged pathogenesis of various sensory symptoms, we get the following: prolonged burning pain is associated with impaired central inhibitory control, central sensitization and ectopic discharges; shooting piercing pain with ectopic discharges; paresthesia or dysesthesia ectopic discharges and central sensitization; hyperalgesia with central sensitization caused by increased nociceptive atterentation; mechanical allodynia is associated with disorders of central sensitization, sensitization of nociceptors .
However, the chronicity of pain is not an autonomus process. It can be influenced by external and internal factors of the body that requires more detailed consideration.
Psychological factors contributing to the persistence of pain syndrome.
Foreign researches pay more attention to the psychological and socio cultural and persistence of pain. It has been shown that patients with chronic pain in, contrast to patients with acute pain, develop specific psychological problems associated with persistent pain. These problems can, in turn, pressure the progression of the pain syndrome and nullify all efforts to restore the patients ability to work [26,27].
Psychological changes are most likely associated with constant discomfort, hopelessness and excessive attention to pain, which becomes dominant in the lives of these patients as well as their inability to solve ordinary family, professional and Leisure- related tasks [ Danilev A.B Golubev V.L 2009]. Physicians often underestimate the importance of psychological factor in the development of chronic pain and do not give them due attention when planning treatment. These issue were first developed and generalized in the work at R.J Catchel (1996), who proposed a concept that describes the very process of the transition from acute pain to chronic pain mainly from a psychological and sociocultural point of view. This model suggests three stages at acute to chronic pain transition. The first stage is associated with such emotional reactions as team, anxiety. They are the result of the perception of pain during the acute phase and are a natural emotional response to a potential threat of the body .
If the pain continue to persist after an appropriate period of time (2-4 months), then this already reflects the transition to the second stage which is manifested by a wide range at such behavioral and psychological reactions as “learned helpless- depression stress- irritability and somatization” : all they are considered to be characteristic attribute of already chronic pain. It is assumed that some patients have certain permeable personality/ psychological characteristics that distinguish them from others and may be exacerbated by the stress associated with trying to adapt to chronic pain. If the overlaying of behavioral problems continues, this leads to a transition to the patients trial acceptance of the patient’s role, when these psychological disorders are fixed in behavior and the patient begins to gravitate towards a decrease or release from his usual duties and social obligation. The letter circumstances can be a potential incentive in order not to strive for recovery. In this phase, physical and psychological disability is consolidated, which turns into pathological pain behavior .
Depression is a common comorbid diagnosis in patients with neuropathic pain/average57%. Depression is a mental disorder characterized by a depressive period: decreased mood, loss at the ability to experience joy ( anhedonia), impaired thinking (negative judgments, pessimistic outflow on what is happening, etc) and motor rebardation with depression self esteem is reduced, there is a loss of interest in life and habitual activities.
According to other data, the frequency of depression among patients with pain syndrome in psychiatric clinics was 35%, in pain clinics-38% in rheumatology clinics-52%, in dental clinics-78%. This combination was called by some authors the syndrome of depression-pain or the emphasizing that the conditions after co-exist, respond to similar treatment factors, reinforce each other, share common biological pathways and neurotransmitters in (for examples both of these states arte models of defectiveness serotonergic systems of the brain). In addition, the difficulty of assessing depression in patients with pain is associated with the similarity of some of the symptoms of these pathological conditions leg, anxiety, sleep disturbance).
The most researched painful condition is pain in the lower back. Several studies have linked depression to poor treatment outcomes and poor prognosis in these patients. Patients with pain syndrome and depression complained more and experienced more instance pain, were more inclined to exaggerate and persist for a long time. In patients with a combination of these two processes, the pain syndrome often persisted for a long time or did not recover.
Post-traumatic stress disorder (PTSD) is a complex of reactions when a traumatic event is persistently experienced over and over again, and this can occur in various forms: (a) repetitive and violently breaking through taking root in the consciousness of memories of the event; (b) repetitive nightmares about the event; (c) actions or feelings that corresponds to those experienced during the trauma; (d) intense negative experience when faced with something that resembles(symbolizes) a traumatic event; (e) physiological reactivity, if something resembles or symbolizes a traumatic event- stomach cramps, headache. Clinical experience with PTSD, however shows that there are individual differences in the ability to cope with catastrophic stress, due to which some people who have experienced traumatic events do not developed PTSD, while others have a pronounced syndrome. Such observations force us to admit that trauma, like pain, is not an external phenomenon fully accessible to objectification. Like pain, traumatic experiences are filtered through cognitive and emotional processes before they can be assessed as extreme threats. Due to individual differences in this assessment process, people have different thresholds of trauma- some are more protected, while others are more vulnerable to the onset of clinical symptoms after being in a stressful situation .
- Epidemiology of neuropathic pain. Danilova A.B. OC Davidson pain 2007 №4 (17) P 12-16.
- Diagnostic scale for appraisals neuropathic pain. Danilova A.B.davidav O.C 2007 №3(16) P 11-1
- Kukushicin M.L.Etiopathogenic principles treatment chronic pain 2007 T 15, №10 P 827.
- Iahno n. n. Illness nervous system : management for doctor medicine 2005\
- Nerve injury associated with anesthesia / D.A.Kroll, R.A. Caplan, K.posner et al.//Anesthesiology 1990;73:202-7
- Вarinov A.N. Complex treatment of pain. №4 P215-219.
- Fridman M.G. Post-traumatic stressful disorder 2005,P 991-994.
- Italian Network for traumatic Neuropathies. Traumatic peripheral nerve injuries: epidemiological findings, neuropathic pain and quality of life in 158 patients /P.Ciaramitaro, M.Mondelli, F.Logullo et al. // J.peripher Nerv Syst.2010. Jun .15(2): 120-127.
- Smith H.S.The evolving nature of neuropathic pain: individualizing treatment / H.s.Smith, C.N.Sang //European journal of pain .2002.V.6, suppl. B, P.13-18.
- Depression and pain comorbidity: a literature review / M.J.bair, R.L. Robinson, W.Med 2003;163:2433- 2445Katon, K.Kroenke // Arch Int Med.2003; 163: 2433-2445.
- https://www.brainandspine.org.uk/information-and-support/living-with-a-neurological-problem/neuropathic- pain/