229 NEUROPATHIC Aspects Spine Surgery: Current Minimally Invasive COMPONENT OF LOW BACK PAIN 36 Simin Hepguler MD month study period, it was estimated that direct re- Introduction source cost was 96 million $ for patients with CLBP and neuropathic component of CLBP accounted for ow back pain is a frequent problem of mus- 96% of the total cost. Cost of care is 160% higher for culo-skeletal system. Life-long prevalence is patients with CLBP associated with NP than patient 60-85% and the incidence is 15% (12-30%) in with CLBP not associated with NP. CLBP with NP L26 adults. Although underlying cause is not known component is found in 4% of German adult popula- in most cases, compression fracture was found in tion. Care cost of neuropathic low back pain is 67% 4% of all low back pain cases, while spondylolisthe- higher than care cost of nociceptive pain. Of the to- sis, tumor or metastasis, ankylosing spondylitis and tal care cost of low back pain, 16% is reserved for infection were determined in 3%, 0.07%, 0.3% and neuropathic component.39 0.01%, respectively. It was also found that remain- ing cases were secondary to mechanical spraining of structures forming the lumbar region.26 Definition This is the most common and most expensive Low back pain is felt in a region ranging from in- reason of occupation-related disability in subjects ferior margin of rib cage to waistline; the pain can who are aged <45 years. The estimated direct cost be localized in lumbar region, but it may also radi- of the condition was 1.6 billion £ and the total cost ate to the leg. Following a pain-free period of six was 6.6-12.3 billion £ in U.K. in 1998. Moreover, di- weeks, sudden-onset pain lasting <6 weeks is re- rect cost is 12.2-90.6 billion $ in USA study was con- ferred as acute low back pain, while the term will ducted with 30.074 subjects suffering low back pain be subacute if it lasts 6 to 12 weeks or chronic if it in 1998 and the study found that the condition leads lasts longer than 12 weeks.14 Most low back pain to 140 million lost workdays per year and the fig- attacks disappear within one week and 90% of pa- ure is 101, 8 million lost workdays for occupation- tients return to work within 2 months. However, related low back pain.14 the longer pain lasts, the rate of return to work de- Pathophysiology of low back pain is complex creases, and 50% of patients, who have been suffer- and the mechanisms leading to both nociceptive and ing pain for 6 months, may return to work, while neuropathic pain (NP) are involved. Rate of neuro- the chance is very low if the patient has been suf- pathic component ranges between 17 and 54 per- fering the pain for 2 years.26 cent in patients with chronic low back pain (CLBP), When low back pain occurs, most common un- depending on the study method.29 In a U.S. Study, derlying reasons should be taken into consider- Mehra M et al.29 found the NP component in 90.4% ation and one should pay attention to “red flags” of 39.425 patients with CLBP. At the end of the 12- which imply very serious conditions.16 (Table 1). Red Simin Hepguler MD 230 flags require physicians order further examinations and tests and make the final diagnosis, since they Neuropathic Pain Mechanism involve conditions requiring emergency interven- Peripheral changes tions or very important conditions such as infection and malignancy.16 Under normal conditions, pain impulses are transmitted by afferent nociceptive fibers to the spi- In addition, psychosocial state of the patient nal cord. Those afferent fibers are comprised of my- should be taken into consideration, since it may elinated Aδ with high conduction velocity and non- prolong sick period and adversely affect prognosis. myelinated C fibers with low conduction velocity. Those conditions are referred as yellow flags and they Both fibers end on laminate I and II of dorsal horn. include behavior, belief, occupational history and af- Under pathological condition, A β fibers play role fective conditions, which should be taken into con- in conduction of pain signal.42 sideration by physicians.14 (Table 2) Immune cells are activated and they accumu- Acute low back pain is usually nociceptive and it late at damage site after peripheral nerve is injured. is caused by tissue damage or a signal indicative of Intracellular substances secreted by such cells in- tissue damage potential. In general, there is no neu- creases sensitivity of nociceptors for the sake of ropathic component. Only disc disorders have neu- Minimally Invasive Spine Surgery: Current Aspects Spine Surgery: Current Minimally Invasive more stimulation. Activation of inflammatory cells ropathic component. Chronic pain persists although lead to vasodilatation and extravasation of plasma underlying mechanism of pain is eliminated. Pathol- proteins including serotonin, bradykinin, Substance ogy of nervous system results with persistent pain. P and histamine and plasma cyclo-oxygenase and A lesion or disease of somatosensorial system will lipo-oxygenase of arachidonic acid metabolism. As result with occurrence of the neuropathic pain com- a consequence, high-threshold nociceptors are sen- ponent. Characteristics of NP are as follows; sitized and they become permeable to low-density 1. Pain and abnormal sensorial symptoms persist pain stimulations. All those events result with in- following normal recovery process creased response to thermal and mechanical sig- 2. Presence of sensorial neurological findings (hy- nals; “peripheral sensitization”, primary hyperal- 42 poaesthesia, hyperalgesia) at various grades gesia and allodynia. (Figure 1) Final events lead to intense stimulation on dorsal horn of medulla spina- 3. Other neurological findings including motor lis. Demyelination is secondary to nerve injury and and autonomic dysfunction (various grades) it causes ectopic discharge along the entire nerve fi- 4. Presence of neuropathic pain does not rule out ber. It is believed that the ectopic signals play role other type of pain, which is referred as noci- in occurrence and persistence of neurogenic pain.42 ceptive pain, and pain mechanisms.6 Neuromas develop at injury site, resulting with ag- Neuropathic component of chronic pain is not gravation of ectopic signal formation. Cell content fully understood. Nociceptive and neuropathic com- is transported from nerve cell to the periphery with ponents are found in combination in chronic low back antegrade axoplasmic transportation; the content ac- pain and therefore, they are regarded as mixed pain cumulates in neuroma and increases number of re- syndrome. Sensorial disorders, motor weakness and ceptors and chemical mediators. Excessive Na ion particularly pain indicate that more than one mech- channels and α-adrenoreceptors accumulate at this anism is involved in spinal axis. Reasons of chronic location and they make contribution to the devel- low back pain are as follows; opment of ectopic activity. Potassium channels also make contributions. Following nerve injury, concen- 1. Mechanical nerve root compression (mechan- tration of several receptor proteins [including tran- ical neuropathic root pain) sient receptor potential vanilloid 1 (TRPV-1)] increases. 2. Lesion of nociceptive sprouts in degenerated TRPV-1 is activated by noxious hot stimulant; after disc (local neuropathic pain) nerve lesion occurs, concentration of TRPV-1 in- 3. Inflammatory effect resulting from chemokin creases in non-injured nerve fibers, while the concen- and cytokines which are released from de- tration decreases in injured ones. Pathological con- generated disc (inflammatory neuropathic dition results with heat hyperalgesia.5 In addition, root pain).20 α-adrenoreceptors form around dorsal root ganglions Neuropathic Component of Low Back Pain 231 Minimally Invasive Spine Surgery: Current Aspects Spine Surgery: Current Minimally Invasive Figure 1: Peripheral modification of high-threshold nociceptor sensitivity by various factors and sympathetic efferent terminals of the ganglion enlargement of area is referred as “wind-up”. This innerve them. Secretion of noradrenalin from dor- event further sensitizes neurons for permeability to sal root ganglions triggers nociceptive signal conver- other stimulations. 42 sion in central nervous system (CNS). Neurotransmitters such as substance P, glu- tamate, calcitonin gene-related peptide (CGRP), Central Changes γ-aminobutiric acid (GABA) and neurokinin A, Primary hyperalgesia develops at tissue damage site, are significant substances for dysinhibition and in- while “secondary hyperalgesia” develop in intact ducing central sensitization.31 Α-amino-3-hidroxy- tissue, which surrounds the damage site. Second- 5-methyl-4-isoxasolepropionic acid (AMPA) and ary hyperalgesia is dependent on both peripheral N-Methyl-D-aspartate (NMDA) activation is con- and central changes. Excessive sensorial stimula- stant.42 Glutamate exerts effects on AMPA recep- tion following the peripheral nerve injury is trans- tor and Substance P exerts effects on neurokinin re- mitted to CNS, resulting with neuroplastic re-or- ceptor. Calcium (Ca+2) is secreted into intracellular ganization and changes on dorsal horn of spinal space when substance P is binds to neurokinin re- column. Receiver area of CNS enlarges, while re- ceptor. During steady state, ion channel of NMDA sponse to the stimulation is amplified and thresh- receptor is blocked by magnesium (Mg+2). Discharge old of stimulation decreases.31 Pain-free mechanical of NMDA receptor removes (Mg+2) block and Cal- stimulation activate neurons, which conduct nocice- cium (Ca+2) enters into cell. The results include in- ptive information. Hyperexcitability of neuron and creased cellular excitability, oncogen induction and Simin Hepguler MD 232 synthesis of nitric oxide (NO). Ca+2 ion influx main- small part of those conditions leads to chronic de- tains central sensitization. It also results with activa- generative disc disease. Secretion of inflammatory tion of protein kinase C, phospholipase C and NO mediators from damages disc to epidural space and synthase and early gene expression.
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