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Inicio Gaceta Médica de Bilbao La Sensibilización Central en la fisiopatología del dolor
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Vol. 104. Núm. 4.
Páginas 136-140 (enero 2007)
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Vol. 104. Núm. 4.
Páginas 136-140 (enero 2007)
Acceso a texto completo
La Sensibilización Central en la fisiopatología del dolor
Central Sensitization in the pathophysiology of pain
Erdiko sentiberatzea minaren patofisiologian
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50093
Jon Jatsu Azkue,1, Vicente Ortiz2, Fernando Torre3, Luciano Aguilera2
1 Departamento de Neurociencias, Facultad de Medicina y Odontología, UPV / EHU. Leioa. Bizkaia. España UE.
2 Servicio de Anestesiología y Reanimación, y Unidad de Tratamiento del Dolor, Hospital de Basurto. Bilbao. Bizkaia. España UE.
3 Servicio de Anestesiología y Reanimación, y Unidad de Tratamiento del Dolor, Hospital de Galdakao-Usansolo. Galdakao. Bizkaia. España UE.
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Resumen

Pruebas clínicas y experimentales han demostrado que un trauma tisular provoca en el Sistema Nervioso Central (SNC) un incremento de la excitabilidad neuronal, conocido como Sensibilización Central (SC), caracterizado por la presencia de dolor espontáneo o persistente, expansión de las áreas afectadas por el dolor, y trastornos sensoriales cualitativos que incluyen alodinia e hiperalgesia. La SC resulta de una serie de alteraciones funcionales y anatómicas en el SNC, algunas de ellas potencialmente irreversibles, las cuales pueden ser responsables, al menos en parte, de la persistencia del dolor tras la resolución de la lesión tisular desencadenante. Un factor clave en todos ellos parece ser la severidad del propio dolor en la fase aguda, con o sin neuropatía concomitante. Más allá del ámbito puramente experimental, la SC constituye un mecanismo relevante en la fisiopatología del dolor en una variedad de situaciones clínicas comunes.

Palabras clave:
dolor neuropático
nocicepción
plasticidad
Summary

Experimental and clinical evidence has shown that tissue injury may lead to Central Sensitization (CS), i.e. a reversible increase in the excitability of central nervous system (CNS) neurones which is characterised by spontaneous or persistent pain, expansion of painful areas, and qualitative sensory disturbances including allodynia and hyperalgesia. CS results from a series of functional and anatomical changes, some of which may be potentially irreversible, that may be at least partially responsible for the persistence of pain once the triggering tissue injury has healed. The severity of acute pain appears to be a key factor therein, irrespective of accompanying neuropathy. Beyond the experimental setting, CS arises as a clinically relevant mechanism in the pathophysiology of pain in a variety of common clinical conditions.

Key words:
neuropathic pain
nociception
plasticity
Laburpena

Esperimentu-arloko eta klinikako froga ugarik jakinarazi dute gorputzeko zauri edo kalte batek Erdiko Sentiberatze (ES) izena hartzen duen kitzikagarritasun-areagotze egoera leheneragarri bat sortzen duela Erdiko Nerbio Sistemako (ENS) neuronetan. Egoera honen ezaugarriak zerak dira, berezko mina edo min iraunkorra, eskualde mingarrien hedapena, eta minaren kalitate-ezaugarrien aldaketak, barne besteak beste alodinia eta hiperalgesia. ENSko neuronetan leheneraezinak ere izan daitezkeen zenbait fisiologi eta anatomi aldaketen ondorioz bilakatzen da ES, eta aldaketok omen dira, zati batez bahintzat, gorputzean hartutako kaltea sendatzearen ondoren minak oraindik ere irautea eragiten dutenak. Egoera hauetan guztietan, minak berak egoera akutuan duen larritasuna omen da gakoetako bat, duela ala ez aldi bereko neuropatia. Esperimentu-arlotik kanpo ere, ES minaren patofisiologiaren mekanismo aipagarri bat da klinikako hainbat egoera arruntetan ere.

Gako hitzak:
min neuropatikoa
nozizepzioa
plastikotasuna
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References
[1.]
Davies S.N., Lodge D..
Evidence for involvement of N-methylaspartate receptors in ‘wind-up’ of class 2 neurones in the dorsal horn of the rat.
Brain Res., 424 (1987), pp. 402-406
[2.]
Azkue J.J., Liu X.G., Zimmermann M., Sandkühler J..
Induction of long-term potentiation of C fibre-evoked spinal field potentials requires recruitment of group I, but not group II/III metabotropic glutamate receptors.
Pain, 106 (2003), pp. 373-379
[3.]
Liu X.G., Sandkuhler J..
Long-term potentiation of C-fiber-evoked potentials in the rat spinal dorsal horn is prevented by spinal N-methyl-D-aspartic acid receptor blockage.
Neurosci Lett., 191 (1995), pp. 43-46
[4.]
Zimmermann M..
Pathobiology of neuropathic pain.
Eur J Pharmacol, 429 (2001), pp. 23-37
[5.]
Sandkuhler J., Liu X..
Induction of long-term potentiation at spinal synapses by noxious stimulation or nerve injury.
Eur J Neurosci., 10 (1998), pp. 2476-2480
[6.]
Zimmermann M., Herdegen T..
Plasticity of the nervous system at the systemic, cellular and molecular levels: a mechanism of chronic pain and hyperalgesia.
Towards the Neurobiology of Chronic Pain, Progress in Brain Research 110, pp. 233-259
[7.]
Noguchi K., Kawai Y., Fukuoka T., Senba E., Miki K..
Substance P induced by peripheral nerve injury in primary afferent sensory neurons and its effect on dorsal column nucleus neurons.
J Neurosci., 15 (1995), pp. 7633-7643
[8.]
Zhang X., Xu Z.O., Shi T.J., Landry M., Holmberg K., Ju G., et al.
Regulation of expression of galanin and galanin receptors in dorsal root ganglia and spinal cord after axotomy and inflammation.
Ann N Y Acad Sci., 863 (2001), pp. 402-413
[9.]
Castro-Lopes J.M., Malcangio M., Pan B.H., Bowery N.G..
Complex changes of GABAA and GABAB receptor binding in the spinal cord dorsal horn following peripheral inflammation or neurectomy.
Brain Res., 679 (1995), pp. 289-297
[10.]
Azkue J.J., Zimmermann M., Hsieh T.F., Herdegen T..
Peripheral nerve insult induces NMDA receptor-mediated, delayed degeneration in spinal neurons.
Eur J Neurosci., 10 (1998), pp. 2204-2206
[11.]
Moore K.A., Kohno T., Karchewski L.A., Scholz J., Baba H., Woolf C.J..
Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord.
J Neurosci., 22 (2002), pp. 6724-6731
[12.]
Woolf C.J., Shortland P., Coggeshall R.E..
Peripheral nerve injury triggers central sprouting of myelinated afferents.
Nature, 355 (1992), pp. 75-78
[13.]
Woolf C.J., Salter M.W..
Neuronal plasticity: increasing the gain in pain.
Science, 288 (2000), pp. 1765-1769
[14.]
Gautron M., Guilbaud G..
Somatic responses of ventrobasal thalamic neurones in polyarthritic rats.
Brain Res., 237 (1982), pp. 459-471
[15.]
Guilbaud G., Benoist J.M., Levante A., Gautron M., Willer J.C..
Primary somatosensory cortex in rats with pain-related behaviours due to a peripheral mononeuropathy after moderate ligation of one sciatic nerve: neuronal responsivity to somatic stimulation.
Exp Brain Res., 92 (1992), pp. 227-245
[16.]
Lamour Y., Guilbaud G., Willer J.C..
Altered properties and laminar distribution of neuronal responses to peripheral stimulation in the SmI cortex of the arthritic rat.
Brain Res., 273 (1983), pp. 183-187
[17.]
Maihofner C., Handwerker H.O., Neundorfer B., Birklein F..
Cortical reorganization during recovery from complex regional pain syndrome.
Neurology, 63 (2004), pp. 693-701
[18.]
Pleger B., Tegenthoff M., Ragert P., Forster A.F., Dinse H.R., Schwenkreis P., et al.
Sensorimotor retuning in complex regional pain syndrome parallels pain reduction.
Ann Neurol., 57 (2005), pp. 425-429
[19.]
Flor H., Elbert T., Knecht S., Wienbruch C., Pantev C., Birbaumer N., et al.
Phantom-limb pain as a perceptual correlate of cortical reorganization following arm amputation.
Nature, 375 (1995), pp. 482-484
[20.]
Pleger B., Tegenthoff M., Schwenkreis P., Janssen F., Ragert P., Dinse H.R., et al.
Mean sustained pain levels are linked to hemispherical side-to-side differences of primary somatosensory cortex in the complex regional pain syndrome I.
Exp Brain Res., 155 (2004), pp. 115-119
[21.]
Maihofner C., Forster C., Birklein F., Neundorfer B., Handwerker H.O..
Brain processing during mechanical hyperalgesia in complex regional pain syndrome: a functional MRI study.
[22.]
Willoch F., Rosen G., Tolle T.R., Oye I., Wester H.J., Berner N., et al.
Phantom limb pain in the human brain: unraveling neural circuitries of phantom limb sensations using positron emission tomography.
Ann Neurol., 48 (2000), pp. 842-849
[23.]
Willoch F., Schindler F., Wester H.J., Empl M., Straube A., Schwaiger M., et al.
Central poststroke pain and reduced opioid receptor binding within pain processing circuitries: a [11C]diprenorphine PET study.
[24.]
Baron R., Baron Y., Disbrow E., Roberts T.P..
Brain processing of capsaicin induced secondary hyperalgesia: a functional MRI study.
Neurology, 53 (1999), pp. 548-557
[25.]
Baron R., Baron Y., Disbrow E., Roberts T.P..
Activation of the somatosensory cortex during A -fiber mediated hyperalgesia: a MSI study.
Brain Res., 871 (2000), pp. 75-82
[26.]
Jensen T.S., Krebs B., Nielsen J., Rasmussen P..
Immediate and long-term phantom limb pain in amputees: incidence, clinical characteristics and relationship to pre-amputation limb pain.
Pain, 21 (1985), pp. 267-278
[27.]
Jensen T.S., Krebs B., Nielsen J., Rasmussen P..
Phantom limb, phantom pain and stump pain in amputees during the first 6 months following limb amputation.
Pain, 17 (1983), pp. 243-256
[28.]
Bloomquist T..
Amputation and phantom limb pain: a pain-prevention model.
AANA J., 69 (2001), pp. 211-217
[29.]
Nikolajsen L., Ilkjaer S., Corner K., Christensen J.H., Jensen T.S..
The influence of preamputation pain on postamputation stump and phantom pain.
Pain, 72 (1997), pp. 393-405
[30.]
Schley M., Topfner S., Wiech K., Schaller H.E., Konrad C.J., Schmelz M., et al.
Continuous brachial plexus blockade in combination with the NMDA receptor antagonist memantine prevents phantom pain in acute traumatic upper limb amputees.
Eur J Pain, (2006),
[31.]
Bach S., Noreng M.F., Tjellden N.U..
Phantom limb pain in amputees during the first 12 months following limb amputation, after preoperative lumbar epidural blockade.
Pain, 33 (1988), pp. 297-301
[32.]
Jahangiri M., Jayatunga A.P., Bradley J.W., Dark C.H..
Prevention of phantom pain after major lower limb amputation by epidural infusion of diamorphine, clonidine and bupivacaine.
Ann R Coll Surg Engl., 76 (1994), pp. 324-326
[33.]
Reisner H..
Phantom sensations (phantom arm) in plexus paralysis.
Phantom and Stump Pain, pp. 62-65
[34.]
Jensen T.S., Rasmussen P..
Phantom pain and related phenomena after amputation.
Textbook of Pain, 2ª, pp. 508-521
[35.]
Conomy J.P..
Disorders of body image after spinal cord injury.
Neurology, 23 (1973), pp. 842-850
[36.]
Berger M., Gerstenbrand F..
Phantom illusions in spinal cord lesions.
Phantom and Stump Pain, pp. 66-73
[37.]
Kroner K., Krebs B., Skov J., Jorgensen H.S..
Immediate and long-term phantom breast syndrome after mastectomy: incidence, clinical characteristics and relationship to pre-mastectomy breast pain.
Pain, 36 (1989), pp. 327-334
[38.]
Reynolds O.E., Hutchins H.C..
Reduction of central hyper-irritability following block anesthesia of peripheral nerve.
Am J Physiol., 152 (1948), pp. 658-662
[39.]
Hutchins H.C., Reynolds O.E..
Experimental investigation of the referred pain of aerodontalgia.
J Dent Res., 26 (1947), pp. 3-8
[40.]
Szasz T.S..
Psychiatric aspects of vagotomy: IV.
Phantom ulcer pain. Arch. Neurol. Psychiat, 62 (1949), pp. 728-733
[41.]
Gloyne H.F..
Psychosomatic aspects of pain.
Psychoanal Rev., 41 (1954), pp. 135-159
[42.]
Dorpat T.L..
Phantom sensation of internal organs.
Compr Psychiatry, 12 (1971), pp. 27-35
[43.]
Ovesen P., Kroner K., Ornsholt J., Bach K..
Phantom-related phenomena after rectal amputation: prevalence and clinical characteristics.
Pain, 44 (1991), pp. 289-291
[44.]
Brena S.F., Sammons E.E..
Phantom urinary bladder pain-case report.
Pain, 7 (1979), pp. 197-201
[45.]
Minski L..
Psychological reactions to injury.
Rehabilitation of the War Injured, pp. 115-122
[46.]
Jung B.F., Johnson R.W., Griffin D.R., Dworkin R.H..
Risk factors for postherpetic neuralgia in patients with herpes zoster.
Neurology, 62 (2004), pp. 1545-1551
[47.]
Buchgreitz L., Lyngberg A.C., Bendtsen L., Jensen R..
Frequency of headache is related to sensitization: a population study.
[48.]
Burstein R., Cutrer M.F., Yarnitsky D..
The development of cutaneous allodynia during a migraine attack clinical evidence for the sequential recruitment of spinal and supraspinal nociceptive neurons in migraine.
Brain, 123 (2000), pp. 1703-1709
[49.]
Bouin M., Meunier P., Riberdy-Poitras M., Poitras P..
Pain hypersensitivity in patients with functional gastrointestinal disorders: a gastrointestinal-specific defect or a general systemic condition?.
Dig Dis Sci., 46 (2001), pp. 2542-2548
[50.]
Verne G.N., Robinson M.E., Price D.D..
Hypersensitivity to visceral and cutaneous pain in the irritable bowel syndrome.
Pain, 93 (2001), pp. 7-14
[51.]
Verne G.N., Himes N.C., Robinson M.E., Gopinath K.S., Briggs R.W., Crosson B., et al.
Central representation of visceral and cutaneous hypersensitivity in the irritable bowel syndrome.
Pain, 105 (2003), pp. 17-25
[52.]
Curatolo M., Petersen-Felix S., Arendt-Nielsen L., Giani C., Zbinden A., Radanov B..
Central hypersensitivity in chronic pain after whiplash injury.
Clin J Pain, 17 (2001), pp. 306-315
[53.]
Johansen M., Graven-Nielsen T., Schou Olesen A., Arendt-Nielsen L..
Generalised muscular hyperalgesia in chronic whiplash syndrome.
Pain, 83 (1999), pp. 229-234
[54.]
Sórensen J., Graven-Nielsen T., Henriksson K.G., Bengtsson M., Arendt-Nielsen L..
Hyperexcitability in fibromyalgia.
J Rheumatol, 25 (1998), pp. 152-155
[55.]
Berglund B., Harju E., Kosek E., Lindblom U..
Quantitative and qualitative perceptual analysis of cold dysesthesia and hyperalgesia in fibromyalgia.
Pain, 96 (2002), pp. 177-187
[56.]
Desmeules J., Cedraschi C., Rapiti E., Baumgartner E., Finckh A., Cohen P., et al.
Neurophysiologic evidence for a central sensitization in patients with fibromyalgia.
Arthritis Rheum, 48 (2003), pp. 1420-1429
[57.]
Kosek E., Ekholm J., Hansson P..
Increased pressure pain sensibility in fibromyalgia patients is located deep to the skin but not restricted to muscle tissue.
Pain, 63 (1995), pp. 335-339
[58.]
Kosek E., Ekholm J., Hansson P..
Sensory dysfunction in fibromyalgia patients with implications for pathogenic mechanisms.
Pain, 68 (1996), pp. 375-383
[59.]
Staud R., Vierck C., Cannon R., Mauderli A., Price D..
Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome.
Pain, 91 (2001), pp. 165-175
[60.]
Bajaj P., Graven-Nielsen T., Arendt-Nielsen L..
Osteoarthritis and its association with muscle hyperalgesia: an experimental controlled study.
Pain, 93 (2001), pp. 107-114
[61.]
Sarlani E., Greenspan J..
Evidence for generalized hyperalgesia in temporomandibular disorders patients.
Pain, 102 (2003), pp. 221-226
[62.]
Bajaj P., Bajaj P., Madsen H., Arendt-Nielsen L..
Endometriosis is associated with central sensitization: a controlled study.
J Pain, 4 (2003), pp. 372-380
[63.]
Clauw D., Williams D., Lauerman W., Dahlman M., Aslami A., Nachemson A.L., et al.
Pain sensitivity as a correlate of clinical status in individuals with chronic low back pain.
Spine, 24 (1999), pp. 2035-2041
[64.]
Giesecke T., Gracely R., Grant M., Nachemson A., Petzke F., Williams D.A., et al.
Evidence of augmented central pain processing in idiopathic chronic low back pain.
Arthritis Rheum, 50 (2004), pp. 613-623
[65.]
Kosek E., Ordeberg G..
Abnormalities of somatosensory perception in patients with painful osteoarthritis normalize following successful treatment.
Eur J Pain, 4 (2000), pp. 229-238
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