ELEMENTE DE FIZIOPATOLOGIE

DURERII

Ce este durerea??

Durerea nu poate fi considerat nici ca o "senzaie neplcut" nici ca o emoie opus uneia plcute i nici ca o senzaie particular asociat sau generat de stimuli nociceptivi. Indiferent de calitile i aspectele ei cantitative, durerea nu este o simpl senzaie, ci un fenomen psihofiziologic complex, declanat uneori de aciunea diverilor stimuli nociceptivi (mecanici, chimici, termici) asupra terminaiilor nervoase libere - inclusiv asupra celor specializate; alteori, durerea poate fi generat de diverse circumstane psiho-patologice psihalgii.

n prima categorie, potenialele electrice declanate de aciunea stimulilor nociceptivi sunt vehiculate - sub denumirea de impuls nervos - spre sistemele neuronale ascendente (specifice i nespecifice) spre structurile neuronale talamocorticale de analiz i sintez, a cror funcionalitate contureaz caracterul elementar al durerii arhaice.

Modelarea durerii elementare somatice, nceput nc din etapele iniiale ale cilor ascendente extranevraxiale, este definitivat la nivel talamocortical i transformat n durere psihic. Multiple implicaii de ordin motivaional, psihopatologic i social, modeleaz caracterul individual al durerii psihice.

La animale, durerea arhaic poate fi studiat prin fenomenele care o nsoesc concomitens- multiple i proteiforme, n general necuantificabile. Este vorba de o serie de reflexe segmentare medulare i suprasegmentare bulbopontine, la care se adaug tulburrile de comportament talamocorticale.

Reflexele medulare sunt de aprare, de ndeprtare a agentului vtmtor - R. de flexie sau de reducere a suferinei - poziie antalgic.
Ex. reflexul de extensie incrucisata

Aceste reflexe, imperative prin caracterul lor i predominante prin capacitatea de a diminua suferina, inhib prin inducie negativ celelalte reflexe mai puin urgente pentru momentul dat. Ele se pot nsoi de reflexe vegetative cu caracter local, ex. vasodilataie.

Reflexele bulbopontine intereseaz: frecvena cardiac, respiratorie, tonusul vascular i presiunea arterial care crete n durerea cutanat i scade n durerea muscular, arterial sau visceral. n plus, se asociaz ca urmare, pe de o parte, a creterii tonusului simpatic: midriaza i secreia sudoral rece etc., iar pe de alt parte, modificri de comportament (agresivitate, fuga, lupta etc.). n ansamblu, toate acestea sunt fenomene care nsoesc durerea arhaic, dar nu reprezint durerea propriu-zis.

La om ns, n cursul dezvoltrii ontogenetice, se contureaz un adevrat model cerebral, mult mai complex al durerii, capabil s genereze suferin.
Dei durerea poate genera suferin, cale dou noiuni nu se suprapun. Suferina nu implic ntotdeauna durere, iar durerea nu necesit intervenii antialgice, dect atunci cnd genereaz suferin. n prima cicumstan, durerea, ca noiune biologic, este un semnal imperativ de protecie, iar comunicarea lui un apel; n cea de a doua circumstan, ca rspuns afectivemoional fa de durere, suferina este o manifestare a bolii.

Exist precizri care ncearc s stabileasc relaiile dintre durere, suferin i boal. Durerea este semnalul, iar suferina este manifestarea ei. Deci, n sens biologic, durerea este, n primul rnd, purttoare a unei informaii. Ea semnaleaz un atentat mpotriva integritii corporale. La figurat, durerea apare ca un ru necesar, capabil s declaneze reacii ce concur la nlturarea pericolului sau s impun msuri pentru tratarea urmrilor acestuia.

Dovada: pierderea reactivitii la stimuli algogeni prin boal sau accidente ale sistemului nervos are repercusiuni grave asupra integritii corporale. Un exemplu elocvent l reprezint bolnavii cu analgie congenital la care, lipsii de sistemul de alarm i de protecie, respectiv de durere, agresiunile evitabile la omul sntos, produc grave leziuni cutanate, mucoase etc.

Congenital Analgesia
A well-known case of congenital insensitivity to pain is a girl referred to as 'miss C' who was a student at McGill university in Montreal in the 1950s. She was normal in every way, except that she could not feel pain. When she was a child she had bitten off the tip of her tongue and had suffered third-degree burns by kneeling on a radiator.

Congenital Analgesia
When she was examined by a psychologist (Charles Murray) in 1950 she did not feel any pain when she was given strong electric shocks or when exposed to very hot and very cold water. When these stimuli were presented to her she showed no change in heart rate, blood pressure or respiration. She did not remember ever having coughed or sneezed, and did not show a blinking reflex. She died at the age of 29 as a result of her condition.

Congenital Analgesia
Although during a post-mortem there were no obvious signs of what had caused the analgesia in the first place, she had damaged her knees, hips and spine. This damage was due to the fact that she did not shift her weight when standing or sitting, did not turn over in bed and did not avoid what would normally be considered to be uncomfortable postures. This caused severe inflammation in her joints.

n cea de a doua categorie sunt incluse psihalgiile, dureri generate de anumite circumstane psihopatologice, mecanismul lor, mai puin sau deloc cunoscut, este totdeauna generat de tulburri ale activitii psihice. De ex. psihalgia poate reflecta o nereuit n viaa personal, un eec sentimental etc. n acest sens, practica demonstreaz c muli dintre cei care i plng durerea pe la uile cabinetelor de consultaii medicale sunt ratai, anxioi, nenelei etc. Raiunea existenei lor s-a prbuit dup un eec sentimental, profesional etc. Eecul le-a generat durerea, care le servete ca mijloc de comunicaie. Statisticile arat c peste 30% din bolnavii suferind de boli interne acuz dureri psihice i peste 50% dintre bolnavii psihici acuz dureri organice (cenestopatii).

Exist dureri psihotice i nevrotice, dup cum exist psihoze i nevroze generate de boli somatice. Depresia endogen poate genera halucinaii de durere. Durerea e prezent frecvent la bolnavii cu depresie nevrotic sau reacional complicat cu anxietate sau isterie. 75% din bolnavii cu psihalgii sufer de nevroze de alt gen dect isteria de conversie pur prin conflict de situaie. Anxietatea provoac rareori halucinaii de durere net identificabile; durerea care nsoete anxietatea este atribuit tensiunii musculare. Se consider c anxietatea antreneaz creterea tonusului muscular, care la rndul lui provoac durere; aceasta continu cercul vicios i adncind anxietatea, accentueaz durerea. La aproximativ 50% din anxioi durerea cedeaz prin terapie relaxant. Schizofrenicii prezint numai ocazional halucinaii de durere. Un ultim aspect: durerea genernd NU suferin, ci contrariul ei, devine o manifestare a bolii psihice - ex. masochismul.

PSIHOFIZIOLOGIA DURERII
Durerea apare rudimentar pe o anumit treapt a evoluiei filogenetice i se manifest sub forma unei reacii instinctive de aprare, care poate fi numit durere arhaic. Pe fondul ei, la om, n primele etape de dezvoltare ontogenetic, sub influena aciunii directe a stimulilor nespecifici (tactili, termici, chimici) din ambian se contureaz schema somatognozic.

Faptul c dup natere schema somatognozic nu este complet conturat explic de ce la nou nscut toate agresiunile exo- sau endogene genereaz disconfort (probabil durere arhaic), care n absena unor leziuni vizibile, este localizat invariabil n regiunea periombilical. Ea este nsoit de plns, micri dezordonate etc., care n fond nu reprezint dect un semnal de alarm, un apel. Este vorba probabil de aceleai instincte, poate ceva mai complexe, pe care nou nscutul le-a motenit.

Ulterior, pe msura mielinizrii cilor de conducere i sub influena aciunii directe a acelorai factori nociceptivi din mediu, la care se adaug probabil rudimente de influen social, schema somatognozic se definitiveaz treptat i paralel cu vrsta. Copilul, cptnd o anumit experien individual, ncepe (chiar n absena unor leziuni corporale vizibile) s localizeze disconfortul n funcie de condiiile concrete ale declanrii lui. n aceast etap de dezvoltare ontogenetic, experiena individual elementar i legat de ea, aa-numita senzaie de disconfort evolueaz treptat (pe fondul durerii arhaice instinctuale), transformndu-se n senzaie de durere elementar (somatic).

Ne aflm n faza senzorial, adic n faza n care transformarea durerii instinctuale n durere elementar somatic se bazeaz pe procesul de nvare..

n aceast etap, nvarea are la baz elaborarea unor legturi temporare la nivelul etajelor superioare ale SNC (deja mielinizat), respectiv elaborarea unor reflexe necondiionate de diferite grade. n contextul experienei personale, individuale, analiza durerii elementare capt valoare de simbol al unui anumit tip de relaii (vtmtoare) cu ambiana. Prin legturi intercentrale, simbolul durere se asociaz la nivel talamocortical cu componente afectiv emoionale i motivaionale. Aceste componente, integrndu-se durerii elementare, i modific, cantitativ i calitativ, caracterul: modificrile cantitative se refer la intensitatea durerii, durat, prag de excitabilitate, iar cele calitative modeleaz durerea i nuannd-o, o individualizeaz.

n acest fel se modific att capacitatea algogen a stimulilor nociceptivi din ambian (cretere sau scdere), ct i comportamentul fat de durere (exist boli cu leziuni ntinse, care nu acuz durere sau acuz dureri care nu necesit medicaie analgetic, dup cum exist boli care acuz dureri dramatice n prezena unor leziuni minore). Aadar, nvarea conduce la memorizare, care presupune participare cortical. Aceasta, conferind durerii elementare elemente afectiv emoionale, o transform n durere psihic. n continuare urmeaz faza de abstractizare, apoi cea operaional (colarul va utiliza noiunea de durere n formularea de judeci, raionamente etc.). n evoluia fenomenelor descrise se contureaz dou etape: perceptiv (obiectiv) i psihic (subiectiv).

Etapa perceptiv
Durerea elementar (somatic) se elaboreaz pe fondul durerii instinctuale, nnscute (arhaice), n timpul etapelor senzorial i perceptiv de dezvoltare ontogenetic. Esena mesajului dolorigen este impulsul nervos iar esena acestuia sarcinile electrice vehiculate de aferenele periferice i declanate de stimulii algogeni. Aspectul fiziologic obiectiv al senzaiei subiective de durere rezid n urmtoarea secven de fenomene: Elaborarea de sarcini electrice, declanat de aciunea direct a stimulilor nociceptivi. Transmiterea impulsului nervos prin ci aferente rapide (sau lente) la etajele superioare ale S. N. C. Elaborarea durerii prin decodificarea i modelarea impulsurilor nervoase. ACESTEA, SEMNALIZND AGRESIUNEA, DECLANEAZ REACII DE APRARE I REACII DE NSOIRE.

Etapa psihic
Aceast etap ncepe aproximativ n faza noional a dezvoltrii ontogenetice. Este rezultatul memorizrii i abstractizrii durerii elementare, devenit simbol al unui anumit tip de experien trit de fiecare individ, n anumite condiii de mediu, pe care-l numim dolorigen. Analiza acestei experiene, memorizarea i abstractizarea ei, la care se adaug elementele afectiv emoionale, moduleaz durerea psihic, diferit calitativ de cea elementar. Durerea psihic are repercusiuni asupra comportamentului, ce variaz n raport cu vrsta, sexul, nivelul intelectual etc.

Se poate vorbi de un comportament caracteristic, n funcie de particularitile reactive individuale i pe de alt parte de caracterul agresiunilor care genereaz durerea. Sub aceste aspecte se poate vorbi de comportamentul celor cu dureri neoplazice radiculare, trigeminale etc. La rndul su, comportamentul este influenat de: motivaie, tendine, necesiti, aspiraii etc.

Precizri:
Durerile psihice prezint unele caractere comune diurne, localizare preferenial la extremitatea cefalic, nu tulbur somnul nocturn; durerea care trezete bolnavul din somn nu este de origine psihic. Factorul emotiv agraveaz durerea. 30% din bolnavii cu dureri psihice beneficiaz de placebo. Asociaia Internaional pentru Studiul Durerii d urmtoarea definiie: Noiunea de durere se refer la experiena senzorial i emoional (psihic) dezagreabil, asociat cu leziuni tisulare prezente sau numai descrise n termenii unei anumite leziuni (somatic). Aceast definiie nglobeaz durerile de origine organic (somatic) i pe cele psihice. ntre cele dou noiuni nu exist opoziie.

Durerea cronic (cea malign) altereaz n mod cert i grav personalitatea. Durerea nu poate fi nici neleas, nici bine tratat dac e asimilat unei senzaii obinuite (tactil, termic etc.). Este un fenomen complex, cu baze morfofiziologice (relativ) proprii, care o mediaz, o moduleaz i include profunde implicaii psihologice, sociale, motivaionale i de ordin psihopatologic. Se consider c toate componentele afectiv emoionale, care dau coloratur durerii psihice, constituie n realitate, elemente de supramodulare, realizat la nivelul scoarei emisferelor cerebrale (Arseni i Oprescu, 1982). Devierile de la normal ale semnificaiei durerii sunt dobndite (ex. artropatia tabetic, siringomielia) i nnscute (asimbolia la durere; insensibilitatea la durere).

Modularea durerii
Se realizeaz prin intermediul a dou sisteme: Unul ascendent care topografic ncepe la nivelul terminaiilor nervoase senzitive, receptoare i se termin n F. R. a trunchiului (n nucleii reticulari ai rafeului); Unul descendent ncepe la diferite nivele din trunchi i complexul diencefalo hipofizar i se termin n scoar. Funcional ele exercit influene inhibitorii asupra sistemelor neuronale din cordoanele posterioare (substana gelatinoas Rolando). Se consider c n modularea durerii este implicat i sistemul de substane endogene opioide (n special encefalinele). Mai exact, sistemul opioid descendent fiind permanent hiperreactiv ar augmenta inhibiia, respectiv activitatea neuronilor de origine ai tractului spinotalamic.

Suportul morfofuncional al sistemului algic

n limbaj cibernetic se poate considera c, n general, conceptul de durere include cel puin trei componente: -detecia de ctre organism a unor stimuli (algogeni) i semnalizarea evenimentelor nociceptive recepia aa-numit nociceptiv (etapa de intrare); -percepia contient sau recunoaterea sistemului nociceptiv durerea (etapa de integrare); -rspunsul afectiv - comportamental sau emoional fa de durere suferina (etapa de ieire). n acest cadru, evenimentele nociceptive devin algogene prin intensitate i durata aciunii lor sau prin leziunile care le produc la nivelul aparatului de recepie. Aici ele sunt detectate i de aici sunt generate sarcinile electrice, care vehiculate, analizate i modelate intra i extranevraxial capt caracterul de semnal al unei senzaii neplcute de disconfort, numit convenional durere. Este vorba de percepia contient a durerii, respectiv de recunoatere a stimulului nociceptiv devenit durere. Urmeaz corolarul ei suferina. Recunoaterea i corolarul ei nu sunt posibile n absena structurilor neuronale centrale.

Etapa de intrare
Stimulii algogeni Se consider c durerea este declanat de o stimulare multinodal, care include n combinaii diferite, factori de natur fizic (mecanici, termici, chimici). n raport cu intensitatea, stimularea genereaz somestezia (modul de informare al organismului asupra propriei condiii i asupra raporturilor sale cu mediul exterior). Stimulii mecanici: distensia organelor cavitare, a capsulei unor organe, a periostului, ligamentelor, durei mater, traciuni i distorsiuni vasculare etc.

Stimulii termici: temperatura radiant care atinge 450 C. Pentru a genera durere e necesar o cantitate de energie de aproximativ 2000 de ori mai mare dect cea necesar producerii senzaiei termice. ntre atingerea pragului dureros i intensitatea maxim exist o diferen de 210C. Unitatea de msur este dolul, care echivaleaz cu diferena abia perceptibil ntre dou grade.

Clinic, durerea determinat de stimuli termici este indus de arsuri. Stimulii chimici par a fi cei ce produc propriu-zis durerea. n producerea ei, rolul factorilor chimici este limitat la eliberarea de substane chimice declanatoare ale durerii. Grupul aminelor mai ales histamina (durere de scurt durat), acetilcolina (dac e potenat de histamin), serotonina. Grupul peptidelor: bradikinine, substana P. Alte substane: prostaglandinele (Pg. E) etc. n concluzie, nu exist stimuli algogeni specifici. Dup locul de aciune, stimularea dolorigen este: -exteroceptiv (durere superficial, tegumentar, epicritic); -interoceptiv (durere profund, visceral, protopatic).

Pragul de percepie al stimulilor nociceptivi

Pragul la durere este aproximativ acelai la toi indivizii; el este sczut prin inflamaie i crescut prin anestezie. Stimulul nociceptiv lezeaz esuturile, dup care aciunea lui nceteaz; esutul lezat elibereaz P.P.S. (pain productive substances), responsabile de iniierea activitii electrice n terminaiile algoreceptoare. Intercalarea mediatorilor chimici a fost demonstrat (salicilaii, fenilbutazona blocheaz mai ales bradikinina i inhib sinteza PG., avnd efect antiinflamator i analgezic).

Recepia periferic nociceptiv

Exist o teorie temporospaial a nespecificitii receptorilor periferici. Aceasta neag existena de dispozitive periferice algoreceptoare specifice i consider c exist numai terminaii nervoase mielinice i puine amielinice, plexiforme, rspndite difuz n tegumente, seroase, fascii etc. Ele reprezint de fapt terminaiile prelungirilor periferice ale protoneuronilor receptori din ganglionii spinali sau omologii lor cranieni i recepioneaz stimuli tactili, termici i chimici. Pentru a declana durere, intensitatea stimulilor trebuie s fie foarte intens. Diferitele formaiuni receptoare (Golgi, Meisner etc.) specializate particip la declanarea durerii numai dac aciunea stimulilor respectivi depete anumite limite de intensitate. Densitatea terminaiilor algoreceptoare nespecifice e mai mare la nivel visceral durerea visceral este surd, difuz. Durerea tegumentar este net, localizat. O particularitate a lor este adaptabilitatea lent.

Nociceptorii sunt conectai la dou tipuri de fibre nervoase periferice: Fibre subiri mielinice de tip A delta (6 ) care conduc cu o vitez de circa 10 m/s; Fibre nemielinizate de tip C (2) care conduc cu circa 0,5m/s; Aceste fibre sunt dendritele neuronilor receptori ai cii sensibilitii dureroase din ganglionii rdcinii posterioare. Existena a dou ci de conducere explic fenomenul de dubl durere. Un stimul nociceptiv declaneaz o durere primar intens, ascuit, bine localizat, senzaia fiind mediat de fibrele de tip A delta cu vitez mare de conducere. Transmiterea aceluiai stimul prin fibre lente de tip C declaneaz o durere tardiv de tip arsur, slab localizat, numit durere secundar (delayed pain)-durerea protopatic . Fibrele A delta mediaz sensibilitatea tactil, termic i dureroas intrnd intranevraxial n constituia tractului spinotalamic (tractul durerii).

Fibrele aferente algoconductoare

Cile ascendente ale sensibilitii dureroase

Axonii protoneuronilor receptori ai cii sensibilitii dureroase intr n mduva spinrii prin rdcinile posterioare, urc sau coboar 12 segmente medulare i intr n coarnele posterioare. Coarnele posterioare prezint 6 straturi de substan cenuie (lamine). Fibrele sensibilitii dureroase se termin mai ales n lamina 1 i 5, unde fac sinaps cu deutoneuronii cii sensibilitii dureroase (neuronii T).

1.) Tractul neospinotalamic deservete percepia intensitii i localizrii durerii. Axonii tractului neospinotalamic din deutoneuronii cii sensibilitii dureroase din lamina 1 i 5 a coarnelor posterioare, se ncrucieaz n comisura anterioar, dup care urc n poriunea antero-lateral a mduvei spinrii. Aceti axoni se termin n nucleii complexului ventro-bazal al talamusului, unde fac sinaps cu al 3lea neuron din calea sensibilitii dureroase. Axonii celui de-al 3-lea neuron se proiecteaz pe aria I somato-senzorial. Leziunile cii neospinotalamice (la nivel talamic sau cortical) nu nltur durerea, dimpotriv leziunile la nivel talamic determin durerea cronic talamic.

2.) Tractul paleospinotalamic deservete componenta de alert i emoional a durerii. i are originea n neuronii coarnelor posterioare care primesc aferene prin fibrele de tip C. Axonii acestor neuroni se ncrucieaz n comisura anterior i urc n nucleii centrali, laterali i intralaminari ai talamusului, unde fac sinaps cu al 3-lea neuron. Pe traiectul lor, aceste fibre dau colaterale pentru formaiunea reticulat din trunchiul cerebral. Axonii celui de-al 3-lea neuron se proiecteaz pe aria II somatosenzorial (cortexul frontal).

REPREZENTAREA SCHEMATIC A APARATULUI SENZORIAL PENTRU DURERE. TRACT CS=TRACTUL CORTICOSPINAL.TRACT RS=TRACT RETICULO-SPINAL

3.) Calea spinoreticulat (arhispinolemniscal). i are originea n neuronii din coarnele posterioare, urc multisinaptic i se termin n formaiunea reticulat a trunchiului cerebral. De aici pornesc proiecii talamice. Dei aceast cale nu intervine n percepia contient a durerii, importana ei deriv din faptul c: stimularea electric la acest nivel produce analgezie i reprezint locul de aciune al narcoticelor.

Cile descendente ale sensibilitii dureroase

Sunt formate din: a.) fibre care provin din cortexul orbital i frontal, realiznd tractul corticospinal i b.) fibre care provin din formaiunea reticulat a mezencefalului, care prin ci multisinaptice coboar ctre coarnele posterioare ale mduvei realiznd tractul reticulo-spinal. Cile descendente se termin mai ales n lamina 5 a coarnelor posterioare unde prin contacte pre- sau postsinaptice joac un rol facilitator sau inhibitor n transmiterea aferenelor dureroase.

Controlul transmiterii aferenelor de durere este explicat prin teoria porii(gate teory), reprezentat n figura nr. IV.2. Conform acestei teorii, neuronii mici (interneuronii) din substana gelatinoas a mduvei spinrii moduleaz (controleaz) transmiterea aferenelor dureroase prin fibrele A delta i C, nainte ca acestea s activeze deutoneuronii (celulele T) din coarnele posterioare ale mduvei. Din schem rezult c descrcrile interneuronilor substanei gelatinoase exercit un efect de inhibiie presinaptic asupra transmiterii aferenelor ctre neuronii T. Fibrele A delta i C fac sinaps att cu celulele T, ct i cu interneuronii substanei gelatinoase. Se observ c aferenele prin fibrele C scad frecvena de descrcare (efect negativ) a interneuronilor substanei gelatinoase, diminund efectul lor inhibitor i astfel in deschis poarta, facilitnd astfel transmiterea aferenelor de durere ctre neuronii T.

Controlul transmiterii aferenelor de durere

Aferenele prin fibrele A delta cresc frecvena de descrcare a interneuronilor substanei gelatinoase (efect pozitiv), accentueaz inhibiia presinaptic i nchid poarta. Efecte similare au i cile descendente (tractul corticospinal: C-S i tractul reticulospinal: R-S) care moduleaz transmiterea aferenelor dureroase la nivelul coarnelor posterioare. Pe baza acestei teorii hiperalgezia poate fi explicat printr-o stimulare continu i excesiv a fibrelor C care deschid poarta sau prin pierderea selectiv a fibrelor A delta, cu reducerea inhibiiei presinaptice, efect care de asemenea deschide poarta. Efectul de reducere al durerii prin stimularea electric, mecanic sau chimic a fibrelor A delta din zonele receptoare cutanate poate fi i el explicat pe baza acestei teorii.

First Order Neurons

Stimulated by sensory receptors End in the dorsal horn of the spinal cord Types A-alpha non-pain impulses

NCV - 70-120m/sec NCV 36-72m/sec Large diameter, myelinated, NCV 4-30m/sec Short duration, sharp, prickling, localized Small diameter, unmyelinated, NCV - .5-2m/sec Delayed onset, diffuse, aching, throbbing

A-beta non-pain impulses

A-delta pain impulses due to mechanical pressure

C pain impulses due to chemicals or mechanical

Neurotransmitters
Chemical substances that allow nerve impulses to move from one neuron to another Found in synapses

Norepinephrine Substance P Acetylcholine Enkephalins Endorphins Serotonin

Can be either excitatory or inhibitory

Descending Neurons
Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina)

Periaquaductal gray area (PAG) release enkephalins Nucleus Raphe Magnus (NRM) release serotonin The release of these neurotransmitters inhibit ascending neurons

Assessment of pain
Visual analogue scale

Picture Part I: is used to localize the pain and identify whether the perceived source of the pain is superficial (external), internal, or both. Part II: incorporates the visual analogue scale. Part III: is the pain rating index, a collection of 76 words grouped into 20 categories. Patients are to underline or circle the words in each group that describes the sensation of pain being experienced.

McGill pain questionnaire

Groups 1-10= somatic in nature Groups 11-15= affective Group 16= evaluative Group 17-20= miscellaneous words that are used in the scoring process.

Pain Scales
Visual Analog Scale
None 0 Severe 10

Locate area of pain on a picture McGill pain questionnaire

Evaluate sensory, evaluative, & affective components of pain

20 subcategories, 78 words

Scoring
Add up the total number of words chosen, up to the maximum of 20 words (one for each category)

The level of intensity of pain is determined by the value assigned to each word.

1st word = 1 point 2nd word = 2 point And so on

Pt could have a high score of 20, but have a lowintensity score by selecting the 1st word in each category.

Submaximal Effort Tourniquet Test

In 1966, Smith et al described a method of matching a patients pain using a SETT. The SETT is performed by inflating a BP cuff to above systolic pressure on the pt elevated arm. Once the cuff is inflated, the pt is instructed to open and close the hand or fist rhythmically.

A handgrip dynamometer and a metronome can be used for standardization.

The pt should continue opening and closing the hand or fist until the cramping sensation that he or she feels matches the pain from the original pathology. The amount of time that elapses from onset to fruition of matched pain is the recorded objective measure. The SETT can be repeated at every tx session to gauge tx progress and is effective in matching all types of pain

Pain Threshold level of noxious stimulus required to alert an individual of a potential threat to tissue
Pain Tolerance amount of pain a person is willing or able to tolerate

Pain Control Theories

Where have we been?
Where are we now?

Where have we been?

Specificity theory

4 types of sensory receptors heat, cold, touch, pain A nerve responded to only one type Nerve was continuous from the periphery to the brain
A single nerve responded to each type of sensation by creating a code (i.E. Different telephone rings) Melzack & wall, 1965 the basis for theories today Non-painful stimulus can block the transmission of a painful stimulus

Pattern theory

Gate control theory

Pain
Of all the components of the injury response, none is less consistent or less understood than an individuals response to pain The sensation of pain is a diffuse entity inherent to the nervous system and basic to all people It is a personal experience that all humans endure Acute pain is the primary reason why people seek medical attention and the major complaint that they describe on initial evaluation.

Chronic pain may be more debilitating than the trauma itself and, in many instances, is so emotionally and physically debilitating that it is a leading cause of suicide. Pain serves as one of the bodys defense mechanisms by warning the brain that its tissues may be in jeopardy, yet pain may be triggered without any physical damage to tissues. The pain response itself is a complex phenomenon involving sensory, behavioral (motor), emotional, and cultural components.

Once the painful impulse has been initiated and received by the brain, the interpretation of pain itself is based on interrelated biological, psychological, and social factors. What are the nerve fibers that stimulate pain?

Nociceptors.

Once these are stimulated, pain impulses are sent to the brain as a warning that the bodys integrity is at risk. The emotional response may be expressed by screaming, crying, fainting, or just thinking #@%&, that hurts!

When the pain is intense or unexpected, an immediate reflex loop activates the behavioral response by sending instructions to motor nerves to remove the body part from the stimulus.
Sticking your finger with a needle Placing your hand on a hot stove

These stimulis activate specialized nerve fibers to send signals through a peripheral nerve network

Routing the impulses up the spinal cord to the brain

When the afferent impulse reach the spinal cord, a reflex loop is formed within the tract to activate the muscles necessary to remove your hand or finger from the stimulus. The remaining impulses of the reflex continue on to the brain, where they are translated as pain, and you respond by saying ouch! or other choice words. If an individual has knowledge about a potentially painful stimulus, such as receiving an injection, cognitive mechanisms can inhibit the reflex loop and block portions of the behavioral response. As a the painful stimulus increases, so does the conscious effort required to keep from trying to escape from the stimulus.

The emotional component may still be in place as you grimace, make a fist, or think what the @%^$ is this jerk doing to me. The cultural components of pain are almost too complex to define.

However, pain perception has been linked to ethnicity and socioeconomic status.

Example

Italian patents are less inhibited in the expression of pain than are the Irish or Anglo-Saxon patients

Ultimately, cultural components can be viewed as any variable that relates to the environment in which a person was raised and how that environment deals with pain and responses to pain.

Pain Process
Noxious input or nociceptive stimulus causes the activation of pain fibers. The painful impulse is triggered by the initial mechanical force of the injury (whether sudden or gradual onset) and is continued by chemical irritation resulting from the inflammatory process In subacute and chronic conditions, pain may be continued by reflex muscle spasm in a positive feedback loop or through the continued presence of chemical irritation

The pain response is initiated by stimulation of nociceptors

Nociceptors- specialized nerve endings that respond to painful stimuli

Mechanical stress or damage to the tissues excite mechanosensitive nociceptors Chemosensitive nociceptors are excited by various chemical substances released during the inflammatory response Chemical irritation of nerve endings may produce a severe pain response without true tissue destruction

Unlike other types of nerve receptors, nociceptors display a sensitization to repeated or prolonged stimulation During the inflammatory process, the threshold required to initiate an action potential is lowered, and the continued stimulation of the chemosensitive receptors perpetuates the cycle

Modulation of Pain
Acute pain response begins with a noxious stimulus.

IE. A burn or cut externally or internally a muscle strain or ligament sprain

After trauma chemicals are released in and around the surrounding tissues. Immediately after the trauma, primary hyperalgesia occurs

Lowers the nerves threshold to noxious stimuli and magnifying the pain response

Pain fibers
A-delta fibers- a type of nerve that transmits painful information that is often interpreted by the brain as burning or stinging pain
C-fibers- a type of nerve that transmits painful information that is often interpreted by the brain as throbbing or aching

After an injury, A-delta and C fibers carry noxious stimuli from the periphery to the spinal cord. The noxious stimuli activates 10-20% of the Adelta fibers and 50-80% of the C-fibers. Triggered by strong mechanical pressure or intense heat, A-delta fibers produce a fast, bright, localized pain sensation. C-fibers are triggered by thermal, mechanical, and chemical stimuli and generate a more diffuse, nagging sensation

After an injury, such as a sprained ankle, an athlete feels

Sharp, well-localized, stinging or burning sensation coming from which fibers??

A-delta fibers

This initial reaction allows an individual to realise that trauma has occurred and to recognize the response as pain

Very quickly, the stinging or burning sensation becomes an aching or throbbing sensation, which indicates activation of which fiber

C-fibers

A third type of peripheral afferent nerve fiber warrants mention. A-beta fibers, respond to light touch and low intensity mechanical information.

Rubbing and injured area These interrupt nociception to the dorsal horn

The brains limbic system aids in integrating higher brain function with motivational and emotional reactions.

Contains afferent nerves from the hypothalamus and the brain stem. Receives descending influence from the cortex. This communication is responsible for the emotional response to painful experiences.

When an injury occurs, the neural communication between the limbic system, thalamus, RF, and cortex produces reactions such as fear, anxiety, or crying. In short , the limbic system is responsible for the bodys affective qualities of reward, punishment, aversive drives, and fear reactions to pain AKA: motivational-affective system.

The integration of the cortex is an important component in both the ascending and descending aspects of pain modulation. Via axons, ascending pain stimuli are transmitted from the thalamus to the central sulcus in the parietal lobe (somatosensory cortex), where the pain is discriminated and localized. Because of the proliferation of nerve cells and the cortexs functions

Consciousness Speech Hearing Memory Thought

It is unlikely that the afferent synapses that occur during noxious stimulation affect only one efferent neuron. Thus, many areas of the cortex can be stimulated during a painful experience.

The notion of central control and descending inhibition of pain is based on the bodys ability to use and produce various forms of endogenous opiates.

Each having a distinct function and a specific receptor affinity.

The enkephalins are found throughout the central nervous system, but particularly in the dorsal horn. Thus, the aggregation of noxious stimuli may cause both presynaptic and postsynaptic control of nociception in the dorsal horn via enkephalin release

Much decision making in the tx of pain can be based on the understanding of the physiological and chemical interaction that occurs after trauma. In simple terms, pain transmission appears to be fairly straightforward.

Review of the process of Pain Transmission

The acute pain response is initiated when substances are released form injured tissues, causing a noxious stimulus to be transmitted via A-delta and C fiber to the dorsal horn

Pain Theory: Historical Perspectives

Theories regarding the cause, nature, and purpose of pain have been debated since the dawn of humankind. Most early theories were based on the assumptions that pain was related to a form of punishment. The word pain is derived from the Latin word poena meaning fine, penalty, or punishment.

The ancient Greek believed that pain was associated with pleasure because the relief of pain was both pleasurable and emotional. Aristotle reassessed the theory of pain and declared that the soul was the center of the sensory processes and that the pain system was located in the heart

The Romans, coming closer to contemporary thought, viewed pain as something that accompanied inflammation. In the 2nd century, Galen offered the Romans his works on the concepts of the nervous system.

However, the views of Aristotle weathered the winds of time.

In the 4th century, successors of Aristotle discovered anatomic proof that the brain was connected to nervous system

Despite this, Aristotles belief prevailed until the 19th century, when German scientist provided irrefutable evidence that the brain is involved with sensory and motor function

Specificity Theory of Pain Modulation

Modern concepts of pain theory continue to advance from the ideas of Aristotle.

However, controversy still exists as to which theories are correct.

The theories accepted at the turn of the century were the specificity theory and the pattern theory, two completely different and seemingly contradictory views

The specificity theory suggests that there is a direct pathway from peripheral pain receptors to the brain.

The pain receptors are located in the skin and are purported to carry pain impulses via a continuous fiber directly to the brains pain center The pathway includes the peripheral nerves, the lateral STT (spinothalamic tract) in the spinal cord and the hypothalamus (the brains pain center) This theory was examined and refuted using clinical, psychological, and physiological evidence by Melzack and Wall in 1965.

They discussed clinical evidence describing pain sensations in severe burn patients, amputee patients, and patients with degenerative nerve disease.

These syndromes do not occur in a fixed, direct linear system Rather in the quality and quantity of the perceived pain are directly related to a psychological variable and sensory input. This theory had been previously addressed by Pavlov, who inflicted dogs with a painful stimulus, then immediately gave them food. The dogs eventually responded to the stimulus as a signal for food and showed no responses to the pain

The psychological aspect of pain perception was later addressed by Beecher, who studied 215 soldiers seriously wounded in the Battle of Anzio, finding that only 27% requested pain-relieving medication (Morphine). When the soldiers were asked if they were experiencing pain, almost 60% indicated that they suffered no pain or only slight pain, and only 24% rated the pain as bad. This was most surprising because 48% of the soldiers had received penetrating abdominal wounds. Beecher also noted that none of the men were suffering from shock or were insensitive to pain because inept intravenous insertions resulted in complaints of acute pain.

The conclusion was drawn that the pain experienced by these men was blocked by emotional factors. The physical injuries that these men had received was an escape from the life-threatening environment of battle to the safety of a hospital, or even release form the war. This relationship suggests that it is possible for the central nervous system to intervene between the stimulus and the sensation in the presence of certain psychological variables. No physiological evidence has been found to suggest that certain nerve cells are more important for pain perception and response than others; therefore, the specificity theory can be discounted.

Contemporary Pain Control Theories

Although both the specificity and pattern theories of pain transmission were eventually refuted, they did provide some lasting principles that are still present in contemporary pain modulation theories

The strengths of these 2 theories, plus findings obtained through additional research, were factored together to for the basis of the current perspective regarding pain transmission and pain modulation.

Still, there is much to be learned and studied before the exact mechanisms of pain transmission and perception are understood.

Pattern Theory of Pain

States that there are no specialized receptors in the skin. Rather, a single generic nerve responds differently to each type of sensation by creating a uniquely coded impulse formed by a spatiotemporal pattern involving the frequency and pattern of nerve transmission.

An analysis of the words elements

Spatio- the distance between the nerves impluses temporal- the frequency of the transmission

An example of this type of coding can be found with most institutional phone systems.

A call from inside a university has a different ring from an outside call.

Although this theory was closer to being neurological correct there were still shortcomings Melzack and Wall refuted this theory as well, based on the physical evidence of physiological specialization of receptor-fiber units.

Plus this theory failed to account for the brains role in pain perception.

Gate Control Theory

Implies a non-painful stimulus can block the transmission of a noxious stimulus. Is based on the premise that the gate, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses.

The SG (substantia gelatinosa) acts as a modulating gate or a control system between the peripheral nerve fibers and central cells that permits only one type of nerve impulse (pain or no pain) to pass through. Serving in a capacity similar to that of a switch operator in a railroad yard, the SG monitors the amount of activity occurring on both incoming tracts in a convergent system Opening and closing the gate to allow the appropriate information to be passed along to the T cell. Impulses traveling on the fast, non-pain fibers activity in the SG. Impulses on the slower pain fibers exert an inhibitory influence. When the SG is active, the gate is in its closed position and a non-painful stimulus is allowed to pass on to the T cell.

Example:

Bumping the head

The initial trauma activates the A-delta and, eventually, C fibers Rubbing the traumatized area stimulates the Abeta fibers, which activate the SG to close the spinal gate Thus inhibiting transmission of the painful stimulus

Placebo Effect
Placebo stems from the Latin word for I shall please
Used to describe pain reduction obtained from a mechanism other than those related to the physiological effects of the tx. Linked to psychological mechanisms

All Treatments have some degree of placebo effect

Most studies involving TM involving the use of a sham TM (ultrasound set at the intensity of 0) and an actual treatment have shown levels of pain in each group.

Two main categories of pain

1. Acute - is a relatively brief sensation, usually less than six months duration usually a response to a specific trauma - forms the basis for danger warnings and subsequent learning.

Two main categories of pain

2. Chronic - lasts more than six months exists beyond the time for normal organic healing The pain begins to impair other functions Patients may begin to experience learned helplessness and hopelessness this leads to the classic signs of depression (lethargy, sleep disturbance, weight loss) May quit work and adopt a self imposed invalid existence.

Chronic Pain
Characteristics of
Symptoms last longer than 6 months Few objective medical findings Medication abuse Difficulty sleeping Depression Manipulative behavior Somatic preoccupation

Categories of Chronic Pain

*Chronic recurrent pain -- benign condition consisting of intense pain alternating with pain-free periods. eg, migraine, tension headaches, endometriosis. * Chronic intractable-benign pain -- benign condition where pain is persistent with no pain free periods, although the pain may vary in intensity eg low back pain.

Categories of Chronic Pain

* Chronic progressive pain --malignant condition where pain is continuous and increases in intensity as the organic condition (disease) worsens eg. Cancer and rheumatoid arthritis.

Congenital Analgesia
A well-known case of congenital insensitivity to pain is a girl referred to as 'miss C' who was a student at McGill university in Montreal in the 1950s. She was normal in every way, except that she could not feel pain. When she was a child she had bitten off the tip of her tongue and had suffered third-degree burns by kneeling on a radiator.

Congenital Analgesia
When she was examined by a psychologist (Charles Murray) in 1950 she did not feel any pain when she was given strong electric shocks or when exposed to very hot and very cold water. When these stimuli were presented to her she showed no change in heart rate, blood pressure or respiration. She did not remember ever having coughed or sneezed, and did not show a blinking reflex. She died at the age of 29 as a result of her condition.

Congenital Analgesia
Although during a post-mortem there were no obvious signs of what had caused the analgesia in the first place, she had damaged her knees, hips and spine. This damage was due to the fact that she did not shift her weight when standing or sitting, did not turn over in bed and did not avoid what would normally be considered to be uncomfortable postures. This caused severe inflammation in her joints.

Congenital Analgesia
Although there is some evidence that this condition may be inherited, there are other causes such as neurological damage. However, some cases cannot be explained in this way. Most people with this condition learn to avoid causing themselves too much harm but, as in the case of 'Miss C, may die as a result of the problems caused by the analgesia.

Episodic Analgesia
Serious injury (e.g. loss of limb) - little pain felt. 6 characteristics (Melzack and Wall 1988). 1. The condition has no relationship to the severity or the location of the injury. 2. No simple relationship to circumstances occurs in battle or at home. 3. Victim fully aware of injury but feels no pain 4. Analgesia is instantaneous 5. Analgesia lasts for a limited time

Episodic Analgesia
6 Analgesia is localised, pain can be felt in other parts of the body (arm blown off is not felt, but injection is!)

Episodic Analgesia
Carlen et al (1978) - Israeli soldiers Yom Kippur War. Loss of arm - 'bang', 'thump' or 'blow'. Melzack, Wall and Ty (1982) - 37% of accident victims reported the experience of episodic analgesia.

Fibromyalgia: Pain Without Injury

The occurrence of body-wide pain in the absence of tissue damage, as in fibromyalgia, interferes with all aspects of a person's life and undermines their credibility. The problem is that normal activities can be exhausting, sleep is disturbed, the ability to concentrate is impaired, gastrointestinal function is often abnormal, persistent headaches are common, and the unrelenting pain that no one can see is often detrimental to their personal and professional lives--as it creates a "credibility gap."

Pain - Injury
Neuralgia - sharp pain along a nerve pathway. Causalgia - burning pain Both develop after wound or disease has ended. Triggered by a simple stimulus e.g. breeze or vibration. Physiological cause of headaches not known. Melzack and Wall (1988) report that migraine causes dilation of blood vessels, not the other way around! Pain out of proportion to the injury Some cancers produce little pain until they are advanced. (Serious illness, little pain). Kidney stones are not serious, but produce excruciating pain.

Purpose of pain
1. Prevents serious damage. If you touch something hot, you are forced to withdraw your hand before it gets seriously burnt. 2. Teaches one what to avoid 3. If pain is in joints, pain limits the activity, so no permanent damage can occur. but pain can become the problem, and cause people to want to die.

Phantom limb pain

1. 2.

3.

4.

Melzack (1992) 7 features Phantom limb feels real. Sometimes amputees try to walk on their phantom limb. Phantom arm hangs down at the side when resting. Appears to swing in time with other arm, when walking. Sometimes gets stuck in awkward position. If behind the patients back, then patient feels obliged to sleep on stomach. Artificial limb appears to fit like a glove. See artificial limb as part of their body.

Phantom limb pain

5 Phantom limbs give impression of pressure and pain 6 Even if phantom limb is experienced as spatially detached from the body, it is still felt to belong to the patient. 7 Paraplegic people experience phantom limbs. They can even experience continually cycling legs.

Phantom limb pain

Not just the cut nerve endings (neuromas) sending messages to the brain, because cuts made along the neural pathways only produce a temporary relief from pain.

Phantom limb pain

Melzack believes - brain contains a neuromatrix of the body image neurosignature - like a hologram.

Phantom limb pain

Connections to this neuromatrix - sensory systems, emotional and motivational systems. It is the emotional and motivational systems that cause the phantom limb experience.

Phantom limb pain

Neuromatrix pre-wired - young amputees experience phantom limb pain. People born without limbs also experience phantom limb pain.

Gate Control Theory

Proposed by Melzack and Wall in the 1960's

Gate opened or closed by 3 factors

1. Activity in the pain fibres - opens the

gate 2. Activity in other sensory nerves - closes the gate 3. Messages from the brain concentrating on the pain or trying not to think about it

Conditions that open or close the gate

Conditions that open the gate Physical conditions Extent of the injury Inappropriate activity level Conditions that close the gate Medication Counterstimulation, eg massage Positive emotions Relaxation Rest Intense concentration or distraction Involvement and interest in life activities

Emotional Conditions

Anxiety or worry Tension Depression

Mental conditions

Focusing on the pain

Boredom

Three variables control this gate

A-Delta fibres (sharp pain) 2. C fibres (dull pain) 3. A-Beta fibres that carry messages of light touch
1.

Pain Gate Theory

Special neurons located in the grey matter of the spinal cord make up the gate This gate has the ability to block the signals from the a-delta and c-delta fibres preventing them from reaching the brain.

Pain Gate Theory

The special neurons in the spinal cord are inhibitory ie they keep the gate closed. These special neurons make a pain blocking agent called enkephalin. This is an opiate substance similar to heroin which can block Substance P the neurotransmitter from the C fibres and the A-delta fibres and this keeps the gate closed.

Pain Gate Theory

C-Fibres and A-Delta fibres obstruct (inhibitory) the special gate neurons and tend to open the gate. A-beta fibres are irritable (excitatory) to the special gate neurons and tend to keep the gate closed.

Pain Gate Theory

If impulses in the C and A-Delta Fibres are stronger than the A-beta Fibres the gate opens. A-delta fibres are always stronger.

Pain Gate Theory

Specialised nerve impulses arise in the brain itself and travel down the spinal cord to influence the gate. This is called the central control trigger and it can send both obstructive and irritable messages to the gate sensitising it to either C or Abeta fibres.