Zespół bólu mięśniowo-powięziowego
Patofizjologia i mechanizm
Zespół bólu mięśniowo-powięziowego (MPS) charakteryzuje się obecnością punktów spustowych – bolesnych, napiętych guzków w mięśniach szkieletowych, które wywołują ból lokalny i promieniujący. Patofizjologia MPS obejmuje kryzys energetyczny włókien mięśniowych, prowadzący do hipoksji, niedokrwienia i zaburzeń funkcji pomp wapniowych, co skutkuje utrzymującym się skurczem mięśni i uwalnianiem mediatorów zapalnych (bradykinina, substancja P, serotonina). W środowisku punktów spustowych pH może spaść nawet do 4,3, a stężenia prozapalnych cytokin i neuropeptydów (CGRP, TNF-α, IL-1β) są znacznie podwyższone. Dodatkowo, mechanizmy stresu oksydacyjnego i aktywacja szlaku X-ROS nasilają uwalnianie jonów Ca2+, co potęguje skurcz mięśni. Przewlekły bodziec nocyceptywny prowadzi do centralnej sensytyzacji w rogu grzbietowym rdzenia kręgowego i wyższych ośrodkach OUN, co utrwala ból i może rozszerzać jego zasięg (ból odniesiony). MPS często współistnieje z fibromialgią i może przechodzić w ból nociplastyczny, mimo że pierwotnie jest klasyfikowany jako ból nocyceptywny.
- Zespół bólu mięśniowo-powięziowego – Patogeneza
- Charakterystyka punktów spustowych
- Główne hipotezy patofizjologiczne
- Związek z innymi zaburzeniami bólowymi
- Czynniki ryzyka i wyzwalające
- Molekularne aspekty patogenezy
- Zmiany biochemiczne w punktach spustowych
- Zmiany w mikrokrążeniu
- Rola komórek glejowych i zapalenia neurogennego
- Zmiany w powięziach
- Mechanizmy bólu odnoszonego
- Konwergencja neuronów rdzeniowomózgowych
- Koncepcja połączeniowości powięziowej i tensegracji
- Rola miofibroblastów w utrzymywaniu napięcia powięziowego
- Podsumowanie mechanizmów patogenezy
Zespół bólu mięśniowo-powięziowego – Patogeneza
Zespół bólu mięśniowo-powięziowego (ang. Myofascial Pain Syndrome, MPS) to powszechne zaburzenie układu mięśniowo-szkieletowego charakteryzujące się regionalnym bólem zlokalizowanym w mięśniach, powięziach lub otaczających tkankach miękkich. Schorzenie to dotyka około 85% populacji ogólnej w ciągu życia, przy czym całkowita częstość występowania szacowana jest na około 46%12. Pomimo rozpowszechnienia i znaczącego wpływu na zdrowie publiczne, dokładne mechanizmy patofizjologiczne stojące za rozwojem zespołu bólu mięśniowo-powięziowego nie zostały jeszcze w pełni wyjaśnione3.
Charakterystyka punktów spustowych
Podstawową cechą charakterystyczną zespołu bólu mięśniowo-powięziowego jest obecność punktów spustowych (ang. trigger points). Są to zlokalizowane, bolesne węzły w napiętych pasmach włókien mięśniowych szkieletowych4. Punkty spustowe definiuje się jako nadwrażliwe obszary w wyczuwalnym, napiętym paśmie mięśnia5. Podczas badania palpacyjnego można wyczuć sztywne, tkliwe guzki, które powodują zarówno ból lokalny, jak i promieniujący do innych części ciała (ból odniesiony)6.
Wyróżnia się dwa główne rodzaje punktów spustowych7:
- Aktywne punkty spustowe – powodują spontaniczny ból bez manipulacji i są obszarami skrajnej tkliwości, zazwyczaj zlokalizowanymi w mięśniu szkieletowym, związanymi z bólem lokalnym lub regionalnym89.
- Latentne punkty spustowe – są uśpionymi (nieaktywnymi) obszarami, które mogą funkcjonować jak punkty spustowe, ograniczające ruch lub powodujące osłabienie mięśni, ale wymagają ucisku, aby wywołać ból1011.
Główne hipotezy patofizjologiczne
Mimo że dokładna patofizjologia zespołu bólu mięśniowo-powięziowego pozostaje niewyjaśniona, istnieje kilka akceptowanych teorii wyjaśniających mechanizm powstawania punktów spustowych i związanych z nimi objawów12:
Hipoteza kryzysu energetycznego
Jedna z najbardziej akceptowanych teorii dotyczy kryzysu energetycznego włókien mięśniowych. Powtarzająca się lub przedłużająca się aktywność może przeciążyć włókna mięśniowe, prowadząc do hipoksji i niedokrwienia mięśni1314. Wyczerpanie energii powoduje dysfunkcję pomp wapniowych, prowadząc do zwiększonego stężenia wapnia wewnątrzkomórkowego i utrzymującego się skurczu mięśni, odpowiedzialnego za rozwój napiętych pasm15. Ten trwały skurcz dodatkowo nasila zapotrzebowanie na tlen i niedokrwienne uszkodzenie mięśni16.
Lokalne niedokrwienie ogranicza przepływ krwi, powodując niewystarczającą syntezę ATP niezbędnego do odzyskania energii. Zwiększone zapotrzebowanie i zmniejszona podaż ATP tworzą kryzys energetyczny i sprzyjają uwalnianiu substancji neuroreaktywnych i produktów metabolicznych (jak bradykinina, substancja P, serotonina)17, które powodują, że obwodowe nocyceptory stają się wrażliwe18.
Hipoteza zintegrowana
Hipoteza zintegrowana to sześcioczęściowy łańcuch, który rozpoczyna się od (1) nieprawidłowego uwalniania acetylocholiny. To wywołuje (2) zwiększone napięcie włókien mięśniowych, widoczne jako napięte pasmo występujące w punkcie spustowym1920. Lokalny trwały skurcz w punkcie spustowym może prowadzić do ograniczenia lokalnego krążenia, co może powodować miejscowe niedokrwienie/hipoksję i obserwowane zmiany, takie jak zwiększone gromadzenie się kwasu, skutkujące obniżeniem pH21.
Według tej teorii nadmierne uwalnianie acetylocholiny z płytek motorycznych prowadzi do zwiększonego napięcia włókien i miejscowego niedokrwienia. Zlokalizowane niedokrwienie ogranicza przepływ krwi i niewystarczającą syntezę ATP22. Kwaśne środowisko hamuje rozkład acetylocholiny, prowadząc do zwiększonego stężenia acetylocholiny w szczelinie synaptycznej i zwiększonej częstotliwości miniaturowych potencjałów płytki końcowej23.
Rola procesów zapalnych i stresu oksydacyjnego
Nocyceptory i chemoreceptory uwalniają prostaglandyny i cytokiny w odpowiedzi na niedokrwienie i hipoksję. Te substancje aktywują pobliskie zakończenia nerwowe, inicjując sygnały i szlaki bólowe2425. W konsekwencji uwalniane są neurotransmitery, takie jak serotonina i noradrenalina, które modulują transmisję bólu i przyczyniają się do cyklu utrzymującego się skurczu mięśni i bólu2627.
Stres oksydacyjny, czyli dysproporcja reaktywnych form tlenu (ROS) i zdolności systemów biologicznych do detoksykacji niebezpiecznych reaktywnych pośredników, odgrywa również rolę w patofizjologii bólu mięśniowo-powięziowego. Warunki stresu oksydacyjnego zwiększają poziom wolnych jonów wapnia i żelaza w komórkach, co powoduje uszkodzenie komórek, a nawet śmierć komórki28.
Kaskada sygnalizacji X-ROS (produkcja ROS aktywowana rozciąganiem) zmienia kształt mikrotubul, aktywując oksydazę NADPH (NOX2) do produkcji ROS, które utleniają receptory rianodynowe (RyRs) i zwiększają uwalnianie jonów Ca2+ z siateczki sarkoplazmatycznej. Ten mechanizm pokazuje, że nadmierny skurcz jest związany ze stresem, który angażuje mikrotubule cytoszkieletowe do aktywacji oksydazy NADPH w celu wytworzenia ROS29.
Rola centralnej sensytyzacji
Długotrwały bodziec nocyceptywny z punktu spustowego może powodować centralne zmiany neuroplastyczne. Przewlekły dopływ nocyceptywny z obwodu prowadzi do sensytyzacji (zwiększonej pobudliwości) neuronów w rogu grzbietowym rdzenia kręgowego, a także struktur wyższych pięter ośrodkowego układu nerwowego, takich jak wzgórze, kora mózgowa, ciało migdałowate i istota szara okołowodociągowa30.
Ciągły szkodliwy bodziec docierający do rogu grzbietowego, nazywany bombardowaniem aferentnym, powoduje wspólne uwalnianie L-glutaminianu i substancji P. Uwalnianie tych dwóch substancji może obniżyć progi aktywacji synaptycznej i otworzyć wcześniej nieefektywne połączenia synaptyczne w neuronach szerokiego zakresu dynamicznego (WDR), prowadząc do centralnej sensytyzacji3132.
Sensytyzacja zwiększa ekspresję kanałów jonowych i receptorów oraz zwiększa liczbę tych białek błonowych na nocyceptorach i neuronach rogu grzbietowego3334. Zjawisko to znane jako segmentalna sensytyzacja rdzeniowa (SSS) jest hiperreaktywnym stanem rogu grzbietowego spowodowanym bombardowaniem impulsami nocyceptywnymi z uwrażliwionych tkanek3536.
Związek z innymi zaburzeniami bólowymi
Zespół bólu mięśniowo-powięziowego może współistnieć z innymi zaburzeniami bólowymi lub przejść w nie, szczególnie fibromialgię. Niektóre badania sugerują, że zespół bólu mięśniowo-powięziowego może prowadzić do fibromialgi u niektórych osób37. Fibromialgię charakteryzuje uogólniony przewlekły ból i uważa się, że mózgi osób z fibromialgią silniej reagują na sygnały bólowe w miarę upływu czasu. Niektórzy eksperci uważają, że zespół bólu mięśniowo-powięziowego może zapoczątkować ten proces38.
Chociaż zespół bólu mięśniowo-powięziowego często klasyfikuje się jako ból nocyceptywny, coraz więcej dowodów potwierdza, że stan ten może występować u pacjentów z dominującym bólem nociplastycznym, szczególnie gdy jest związany z podstawowym stanem medycznym39. Prosty zespół bólu mięśniowo-powięziowego spowodowany przez punkty spustowe jest przede wszystkim stanem nocyceptywnym i raczej nie zostanie sklasyfikowany jako neuropatyczny lub nociplastyczny, ale może występować u pacjentów jako współistniejący stan wraz z dominującym bólem neuropatycznym lub nociplastycznym40.
Czynniki ryzyka i wyzwalające
Rozwój lub aktywacja punktów spustowych może wynikać z różnych czynników wpływających na tkankę mięśniową41. Do najczęstszych przyczyn i czynników ryzyka zespołu bólu mięśniowo-powięziowego należą:
- Przeciążenie mięśni – powtarzające się ruchy, przewlekłe napięcie, niewłaściwa postawa lub trauma mogą prowadzić do przeciążenia mięśni4243.
- Urazy mięśni – bezpośredni uraz mięśnia lub powtarzające się mikrourazy mogą prowadzić do rozwoju punktów spustowych44.
- Stres i lęk – osoby często odczuwające stres i niepokój mogą być bardziej podatne na rozwój punktów spustowych w mięśniach. Jedna z teorii sugeruje, że takie osoby mogą być bardziej skłonne do zaciskania mięśni4546.
- Zaburzenia hormonalne – zaburzenia hormonalne, przewlekłe infekcje, niedobory żywieniowe, zła postawa i stres psychologiczny mogą odgrywać rolę w powstawaniu zespołu bólu mięśniowo-powięziowego47.
- Brak aktywności fizycznej – unieruchomienie lub brak aktywności fizycznej może przyczyniać się do rozwoju punktów spustowych48.
Molekularne aspekty patogenezy
Na poziomie molekularnym w patogenezie zespołu bólu mięśniowo-powięziowego uczestniczy szereg mechanizmów biochemicznych i komórkowych, które przyczyniają się do powstawania i utrzymywania się punktów spustowych oraz związanego z nimi bólu.
Zmiany biochemiczne w punktach spustowych
Analiza środowiska punktów spustowych wykazała, że pH wokół aktywnych punktów spustowych spada nawet do 4,349. Ponadto, w odróżnieniu od zdrowego mięśnia, środowisko punktów spustowych zawiera cytokiny zapalne i peptyd związany z genem kalcytoniny (CGRP). Stężenia protonów (H+), bradykininy, CGRP, substancji P, czynnika martwicy nowotworu-α, interleukiny 1-β, serotoniny i norepinefryny okazały się znacznie wyższe w grupie aktywnych punktów spustowych niż w grupach z latentnymi punktami spustowymi lub bez punktów spustowych50.
Uszkodzenie mięśni powoduje uwalnianie neuropeptydów, cytokin i substancji zapalnych, takich jak potas, bradykinina, cytokiny, czynnik martwicy nowotworu, interleukina 1, norepinefryna, protony, prostaglandyny, ATP i substancja P, które mogą stymulować nocyceptory w mięśniach, uwalniając CGRP. Uwalnianie TNF-α wywołuje produkcję norepinefryny51.
Badania wykazały wzrost zarówno serotoniny, jak i norepinefryny u pacjentów z aktywnymi punktami spustowymi. Hipotezy wyrażone przez Simonsa i wyjaśnione przez Gerwina i współpracowników stwierdzają, że CGRP hamowałby acetylocholinoesterazę. Zwiększenie liczby receptorów acetylocholiny i zwiększenie uwalniania acetylocholiny (wyciek acetylocholiny) prowadzi do długotrwałego skurczu lokalnych włókien mięśniowych, znanych jako punkty spustowe52.
Zmiany w mikrokrążeniu
Małe tętnice (lub powiększone tętniczki) w pobliżu aktywnych punktów spustowych wykazywały wsteczny przepływ w rozkurczu, wskazując na bardzo oporowe łożysko naczyniowe53. Skurcz naczyń, spowodowany podwyższonym poziomem wapnia, powoduje niedokrwienie i produkcję wolnych rodników tlenowych, które uszkadzają śródbłonek i powodują dalsze niedokrwienie, co odgrywa rolę w patofizjologii bólu mięśniowo-powięziowego54.
Obniżenie pH (poniżej 5,0), które występuje z powodu miejscowego niedokrwienia w punkcie spustowym, jest więcej niż wystarczające, aby wywołać pobudzenie nocyceptorów mięśniowych, w tym nocyceptorów kanałów ASIC3 (kanały jonowe wykrywające kwasy) i TRPV1 (receptory potencjału przejściowego), które są znane jako receptory kapsaicyny na nerwach bólowych55.
Rola komórek glejowych i zapalenia neurogennego
Przedłużony bodziec nocyceptywny może powodować nieprawidłowe zmiany w ośrodkowym układzie nerwowym. Przedłużony aferentny bodziec nocyceptywny z punktu spustowego aktywuje i uwrażliwia neurony w rogu grzbietowym, które są przenoszone przez drogę rdzeniowo-wzgórzową do wyższych ośrodków mózgowych56.
Czynniki prozapalne, takie jak cytokiny, stres oksydacyjny i wolne rodniki, które występują u pacjentów z bólem mięśniowo-powięziowym, inicjują reaktywne astrocyty. Ta inicjacja reaktywnych astrocytów następuje poprzez szlak czynnika jądrowego kappa-B (NFκB). Aktywacja astrocytów i uwalnianie IL-1 biorą udział w mechanizmie hiperalgezji57.
Hipoteza, że sensytyzacja centralna odgrywa rolę w patogenezie bólu mięśniowo-powięziowego, jest poparta odkryciem opóźnionych i skróconych okresów ciszy skórnej w kończynach ochotników i pacjentów z bólem mięśniowo-powięziowym, co wskazuje na dysfunkcję w mechanizmie hamującym szlaków bólu rdzeniowego/nadrdzeniowego58.
Zmiany w powięziach
Alternatywnie, Stecco i współpracownicy zasugerowali, że powięź mięśniowa, forma tkanki łącznej, może ulegać zmianom patologicznym pod wpływem przeciążenia i uszkodzenia, prowadząc do zmiany biomechanicznej mięśni, a ostatecznie do zmniejszenia siły skurczu i elastyczności mięśni59.
W warunkach przeciążenia lub urazu warstwy ślizgające zaczynają wytwarzać ogromne ilości kwasu hialuronowego (HA), który następnie tworzy struktury supermolekularne, zmieniając zarówno swoją konfigurację, lepkosprężystość, jak i lepkość. Ze względu na zwiększoną lepkość, HA nie może już funkcjonować jako skuteczny środek smarujący, co zwiększa opór w warstwach ślizgających i prowadzi do zagęszczenia powięzi lub nieprawidłowego ślizgania się włókien mięśniowych60.
Zmiany zapalne wymienione powyżej mogą zaostrzać zmiany patologiczne, prowadząc do bólu lub nasilając ból. Zmiany patologiczne powięzi mięśniowej mogą być związane z nieprawidłowymi zmianami w miofibrylach, fibroblastach i macierzy pozakomórkowej61.
Mechanizmy bólu odnoszonego
Ból odniesiony, czyli ból odczuwany w obszarze oddalonym od pierwotnego źródła bólu, jest istotną cechą zespołu bólu mięśniowo-powięziowego. Mechanizmy leżące u podstaw tego zjawiska są złożone i nie w pełni wyjaśnione.
Konwergencja neuronów rdzeniowomózgowych
Ból odniesiony, główny objaw punktów spustowych, jest zjawiskiem centralnym napędzanym przez bodźce obwodowe62. Pojedynczy punkt spustowy może postępować do wielu punktów, utrzymując się i powodując zmiany neuroplastyczne na poziomie rogu grzbietowego, co prowadzi do wzmocnienia odczucia bólu (tzn. centralnej sensytyzacji) i rozszerzenia bólu poza jego pierwotne granice63.
Dystrybucja nocyceptorów w obrębie mięśni szkieletowych jest ograniczona do powięzi między włóknami mięśniowymi, przy czym największe stężenie nocyceptorów znajduje się w pobliżu regionu płytki końcowej mięśnia, gdzie zwykle znajdują się punkty spustowe64. Zaproponowano, że w regionie punktu spustowego istnieje wiele wrażliwych loci, a każde locus zawiera jedno lub więcej uwrażliwionych zakończeń nerwowych nocyceptywnych65.
Koncepcja połączeniowości powięziowej i tensegracji
Fakt, że powięź może przenosić napięcie na odległość, jest podstawą koncepcji bio-tensegracji66. Kiedy napięcie powięzi wzrasta, tkanka łączna może rozprowadzać siły na otaczających obszarach, rozprzestrzeniając się wzdłuż systemu mięśniowo-powięziowego67.
Wzajemne połączenie powięzi i jej zdolność do przenoszenia siły są podstawą jej funkcji6869. Koncepcja ta tłumaczy, dlaczego napięcie w jednym obszarze ciała może wpływać na odległe obszary i przyczyniać się do występowania bólu odnoszonego.
Rola miofibroblastów w utrzymywaniu napięcia powięziowego
Miofibroblasty odgrywają rolę w utrzymywaniu napięcia mięśniowo-powięziowego, które może się rozprzestrzeniać i stanowi podstawę dla struktury tensegracyjnej70. Miofibroblasty mogą przenosić znaczne siły7172.
Miofibroblasty są obecne w niektórych rozwijających się lub normalnych tkankach dorosłych, zmieniając napięcie tkanek7374. Miofibroblasty mogą bezpośrednio łączyć swoją aktywność z innymi komórkami, takimi jak miocyty, za pośrednictwem połączeń szczelinowych i działać jako jednostka75.
Chroniczne napięcie jest zaostrzane wraz z większym napięciem generowanym przez skurcze włókien aktyny mięśni gładkich miofibroblastów76. Napięcie jest przekształcane w agregację kwasu hialuronowego i entropię, o ile kompensacja wzdłuż krzywej relaksacji naprężeń może na to pozwolić77.
Podsumowanie mechanizmów patogenezy
Zespół bólu mięśniowo-powięziowego można postrzegać jako patologiczny stan nierównowagi w naturalnym procesie, manifestujący się z właściwości właściwych powięzi, wyzwolony przez zaburzoną interakcję biomechaniczną7879. Procesy prowadzące do rozwoju i utrzymywania się punktów spustowych oraz związanego z nimi bólu mięśniowo-powięziowego obejmują:
- Inicjację – przeciążenie mięśni, uraz, stres lub inne czynniki prowadzą do zwiększonego uwalniania acetylocholiny w płytce motorycznej80.
- Skurcz mięśni – nadmierne uwalnianie acetylocholiny prowadzi do lokalnego skurczu włókien mięśniowych, tworząc napięte pasma81.
- Niedokrwienie i hipoksję – utrzymujący się skurcz powoduje kompresję naczyń krwionośnych, prowadząc do miejscowego niedokrwienia i niedotlenienia82.
- Kryzys energetyczny – zarówno niedokrwienie wywołujące niedobór energii, jak i zwiększone zużycie energii niezbędne do aktywacji pompy wapniowej potrzebnej do rozdzielenia aktyny i miozyny, mogą przyczyniać się do rozwoju lokalnego kryzysu energetycznego83.
- Uwalnianie mediatorów zapalnych – niedokrwienie i hipoksja prowadzą do uwolnienia substancji prozapalnych i algeogennych84.
- Sensytyzację obwodową – mediatory zapalne uwrażliwiają obwodowe nocyceptory, zwiększając transmisję sygnałów bólowych85.
- Sensytyzację centralną – długotrwały bodziec nocyceptywny z obwodu prowadzi do nadpobudliwości neuronów w ośrodkowym układzie nerwowym86.
- Zmiany w powięziach – przewlekłe przeciążenie lub uraz prowadzi do zmian w strukturze i funkcji powięzi, co dodatkowo przyczynia się do dysfunkcji mięśniowej i bólu87.
Dokładne mechanizmy inicjujące powstawanie punktów spustowych pozostają niejasne i są przedmiotem badań. Złożoność patofizjologii zespołu bólu mięśniowo-powięziowego sugeruje, że skuteczne leczenie tego stanu wymaga kompleksowego podejścia uwzględniającego zarówno mechanizmy obwodowe, jak i centralne88.
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Materiały źródłowe
- #1 Mechanisms of Myofascial Pain – ProQuesthttps://www.proquest.com/scholarly-journals/mechanisms-myofascial-pain/docview/1760293960/se-2
Myofascial pain syndrome is a significant health problem affecting as much as 85% of the general population sometime in their lifetime while the estimated overall prevalence is ~46%. Myofascial pain syndrome is a collection of the sensory, motor, and autonomic symptoms that include local and referred pain, decreased range of motion, and weakness. […] While myofascial pain syndrome is complex in its presentation, the onset and persistence of myofascial pain syndrome are known to be caused by myofascial trigger points. […] Despite the causal association of myofascial trigger points with the underlying physiology of myofascial pain syndrome, the mechanisms that induce the onset and maintenance of myofascial trigger points are unknown. Hence, a mechanistic understanding of myofascial trigger points is critical to developing treatments for myofascial pain syndrome.
- #2 Mechanisms of Myofascial Pain – Southeast Pain & Spine Carehttps://www.sepainandspinecare.com/mechanisms-of-myofascial-pain/
Myofascial pain, also known as chronic soft tissue, is a significant health problem. The difficulty in understanding the underlying mechanism is exacerbated by the fact that it is highly prevalent among many people. Great research details that myofascial pain remarkably affects about 85% of the general population during their lifetime, while the overall prevalence stands at 46%. […] This is a condition that typically occurs when pressure is applied on sensitive parts in your muscles(trigger points), resulting in pain in the muscles and other parts of your body. […] Repetitive muscle contraction due to repetitive motions while at work or due to stress-related muscle tension leads to pain in the muscles. In such cases, the sensitive areas known as trigger points develop in your muscles after injuries or due to muscle tightness. As a result, the muscles trigger points cause you to experience pain and strain throughout the muscle. […] Trigger points are highly likely to develop in the muscles of people experiencing stress. This argument is supported by the theory that most people who experience stress tend to clench their fists, therefore applying pressure on their muscles, which leads to the development of trigger points.
- #3 Mechanisms of Myofascial Painhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4285362/
Myofascial pain syndrome is an important health problem. It affects a majority of the general population, impairs mobility, causes pain, and reduces the overall sense of well-being. Underlying this syndrome is the existence of painful taut bands of muscle that contain discrete, hypersensitive foci called myofascial trigger points. In spite of the significant impact on public health, a clear mechanistic understanding of the disorder does not exist. This is likely due to the complex nature of the disorder which involves the integration of cellular signaling, excitation-contraction coupling, neuromuscular inputs, local circulation, and energy metabolism. […] The mechanisms that induce the onset and maintenance of myofascial trigger points are unknown. Hence, a mechanistic understanding of myofascial trigger points is critical to developing treatments for myofascial pain syndrome.
- #4 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Myofascial pain syndrome is a musculoskeletal condition characterized by regional pain within the muscle, fascia, or surrounding soft tissue. This condition often presents with localized or referred pain, typically associated with hyperirritable trigger points within taut bands of skeletal muscle. […] The exact cause remains unclear, although muscle overload due to overuse or disuse is a key factor. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #5 Cervical Myofascial Pain: Practice Essentials, Etiology, Epidemiologyhttps://emedicine.medscape.com/article/305937-overview
Pain attributed to muscle and its surrounding fascia is termed myofascial pain, with cervical myofascial pain thought to occur following either overuse of or trauma to the muscles that support the shoulders and neck. It can also result from compensation for an underlying spinal problem such as facet joint arthropathy or an annular tear in one of the discs. In the cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae, rhomboids, supraspinatus, and infraspinatus. […] Myofascial pain in any location is characterized on examination by the presence of trigger points located in skeletal muscle. A trigger point is defined as a hyperirritable area located in a palpable, taut band of muscle fibers. […] The primary concern for patients with cervical myofascial pain is chronicity. Recurrence of myofascial pain is a common scenario.
- #6 Mechanisms of Myofascial Painhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4285362/
Myofascial pain syndrome arises from the muscle and is composed of symptoms from the sensory, motor, and autonomic systems. Myofascial pain syndrome is caused by myofascial trigger points which are identified by palpation as discrete foci of hypercontracted areas within a muscle. […] In all cases, myofascial trigger points are associated with areas in muscle that have stiff, tender nodules under palpation. It is believed that this stiffness might arise from hypercontracture of the sarcomere in this area. […] Sustained contractile activity leading to increased metabolic stress and reduced blood flow is likely the foci for secondary changes that contribute to the persistence of the myofascial trigger point. […] The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process.
- #7 Myofascial Pain: Treatment, Symptoms, Causes, and Morehttps://www.healthline.com/health/myofascial-pain
There are several different types of myofascial trigger points that your doctor may find, including: active trigger points, latent trigger points, secondary trigger point, satellite myofascial point. […] Myofascial pain syndrome requires a multipronged treatment plan. Many people combine medications with other therapies that relieve muscle stiffness and pain. […] There are several medications that can ease the symptoms of MPS, including: nonsteroidal anti-inflammatory drugs (NSAIDs), analgesics, muscle relaxants, anticonvulsants, tricyclic antidepressants, Botox injections. […] Dry needling is one of the quickest ways to inactivate myofascial trigger points. […] Trigger point injections are like dry needling, but only a solution is injected into the tissue. […] Ultrasound machines transmit sound waves into tissue through a sound-conducting gel applied to the skin.
- #8 Myofascial Pain Syndrome (Chronic Soft Tissue Pain)https://www.webmd.com/pain-management/myofascial-pain-syndrome
Myofascial pain syndrome (MPS) is a chronic pain disorder that affects the fascia (the connective tissue that covers the muscles) and causes inflammation. MPS may affect a single muscle or a muscle group. In some cases, the area where a person has the pain may not be where the myofascial pain generator is located. Experts believe that the actual site of the injury or the strain prompts the development of a trigger point that, in turn, causes pain in other areas. This is known as referred pain. […] Myofascial pain (MFP) may come from a muscle injury or from heavy strain on a particular muscle or muscle group, ligament, or tendon. Other causes include: Injury to muscle fibers, Repetitive motions, Lack of activity (such as having a broken arm in a sling). […] Trigger points can be identified by pain that results when pressure is applied to a specific area of a person’s body. In the diagnosis of myofascial pain syndrome, two types of trigger points can be distinguished: An active trigger point is an area of extreme tenderness that usually lies within the skeletal muscle and which is linked to local or regional pain. A latent trigger point is a dormant (inactive) area that has the potential to act like a trigger point. It may restrict movement or cause muscle weakness.
- #9 Myofascial Pain Syndrome Symptoms & Treatment | Cleveland Clinic Abu Dhabihttps://www.clevelandclinicabudhabi.ae/en/health-hub/health-resource/diseases-and-conditions/myofascial-pain-syndrome
The recognition of this syndrome requires a precise understanding of the body’s trigger points. Trigger points can be identified by pain that results when pressure is applied to an area of the patient’s body. […] In the diagnosis of myofascial pain syndrome, four types of trigger points can be distinguished: An active trigger point is an area of extreme tenderness that usually lies within the skeletal muscle and which is associated with a local or regional pain. […] Physical therapy methods are considered the best treatments for myofascial pain syndrome. Other treatments include a stretch and spray technique, in which the muscle with the trigger point is sprayed along its length with a coolant, then slowly stretched. […] In some chronic cases of myofascial pain, combinations of physical therapy, trigger point injections, and massage are needed.
- #10 Mechanisms of Myofascial Painhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4285362/
The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. […] The essence of this question is what positive feedback mechanisms exist that can sustain a myofascial trigger point once initiated. […] X-ROS signaling is a newly characterized mechanoactivated ROS-dependent signaling cascade in cardiac and skeletal muscle. […] The above mechanism purports that excessive contraction dependent stress acts through the microtubule cytoskeletal elements to activate NADPH oxidase to produce ROS. […] Myofascial trigger points yield pain upon palpation. If they are only painful upon palpation, they are called latent. If they are painful without manipulation they are considered to be active. […] In summary, it appears that myofascial pain is likely due to a combined activation of several ligand gated ion channels in the pain sensing neuron.
- #11 Myofascial Pain Syndrome (Chronic Soft Tissue Pain)https://www.webmd.com/pain-management/myofascial-pain-syndrome
Myofascial pain syndrome (MPS) is a chronic pain disorder that affects the fascia (the connective tissue that covers the muscles) and causes inflammation. MPS may affect a single muscle or a muscle group. In some cases, the area where a person has the pain may not be where the myofascial pain generator is located. Experts believe that the actual site of the injury or the strain prompts the development of a trigger point that, in turn, causes pain in other areas. This is known as referred pain. […] Myofascial pain (MFP) may come from a muscle injury or from heavy strain on a particular muscle or muscle group, ligament, or tendon. Other causes include: Injury to muscle fibers, Repetitive motions, Lack of activity (such as having a broken arm in a sling). […] Trigger points can be identified by pain that results when pressure is applied to a specific area of a person’s body. In the diagnosis of myofascial pain syndrome, two types of trigger points can be distinguished: An active trigger point is an area of extreme tenderness that usually lies within the skeletal muscle and which is linked to local or regional pain. A latent trigger point is a dormant (inactive) area that has the potential to act like a trigger point. It may restrict movement or cause muscle weakness.
- #12 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Myofascial pain syndrome is a musculoskeletal condition characterized by regional pain within the muscle, fascia, or surrounding soft tissue. This condition often presents with localized or referred pain, typically associated with hyperirritable trigger points within taut bands of skeletal muscle. […] The exact cause remains unclear, although muscle overload due to overuse or disuse is a key factor. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #13 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Myofascial pain syndrome is a musculoskeletal condition characterized by regional pain within the muscle, fascia, or surrounding soft tissue. This condition often presents with localized or referred pain, typically associated with hyperirritable trigger points within taut bands of skeletal muscle. […] The exact cause remains unclear, although muscle overload due to overuse or disuse is a key factor. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #14 Myofascial Pain Syndrome | Treatment & Management | Point of Carehttps://www.statpearls.com/point-of-care/25476
The etiology of myofascial pain syndrome is not yet fully understood, although muscle overload is thought to be a cause as a consequence of overuse or disuse. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #15 Myofascial Pain Syndrome | Treatment & Management | Point of Carehttps://www.statpearls.com/point-of-care/25476
The etiology of myofascial pain syndrome is not yet fully understood, although muscle overload is thought to be a cause as a consequence of overuse or disuse. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #16 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Myofascial pain syndrome is a musculoskeletal condition characterized by regional pain within the muscle, fascia, or surrounding soft tissue. This condition often presents with localized or referred pain, typically associated with hyperirritable trigger points within taut bands of skeletal muscle. […] The exact cause remains unclear, although muscle overload due to overuse or disuse is a key factor. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #17https://www.leagravetherapy.co.uk/post-title2
An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. […] A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. […] The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive. […] Localized areas containing „contraction knots” are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension.
- #18https://www.leagravetherapy.co.uk/post-title2
An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. […] A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. […] The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive. […] Localized areas containing „contraction knots” are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension.
- #19 Mechanisms of Myofascial Painhttps://pmc.ncbi.nlm.nih.gov/articles/PMC4285362/
The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. […] The essence of this question is what positive feedback mechanisms exist that can sustain a myofascial trigger point once initiated. […] X-ROS signaling is a newly characterized mechanoactivated ROS-dependent signaling cascade in cardiac and skeletal muscle. […] The above mechanism purports that excessive contraction dependent stress acts through the microtubule cytoskeletal elements to activate NADPH oxidase to produce ROS. […] Myofascial trigger points yield pain upon palpation. If they are only painful upon palpation, they are called latent. If they are painful without manipulation they are considered to be active. […] In summary, it appears that myofascial pain is likely due to a combined activation of several ligand gated ion channels in the pain sensing neuron.
- #20 Mechanisms of Myofascial Pain – ProQuesthttps://www.proquest.com/scholarly-journals/mechanisms-myofascial-pain/docview/1760293960/se-2
The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. […] The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. […] The local sustained contraction in a myofascial trigger point can result in restriction of local circulation which can cause the local ischemia/hypoxia and the observed changes caused by it such as increased acid accumulation resulting in a decrease in pH. […] Myofascial trigger points yield pain upon palpation. If they are only painful upon palpation, they are called latent. If they are painful without manipulation they are considered to be active.
- #21 Mechanisms of Myofascial Pain – ProQuesthttps://www.proquest.com/scholarly-journals/mechanisms-myofascial-pain/docview/1760293960/se-2
The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. […] The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. […] The local sustained contraction in a myofascial trigger point can result in restriction of local circulation which can cause the local ischemia/hypoxia and the observed changes caused by it such as increased acid accumulation resulting in a decrease in pH. […] Myofascial trigger points yield pain upon palpation. If they are only painful upon palpation, they are called latent. If they are painful without manipulation they are considered to be active.
- #22https://www.leagravetherapy.co.uk/post-title2
An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. […] A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. […] The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive. […] Localized areas containing „contraction knots” are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension.
- #23 Myofascial Pain | PM&R KnowledgeNowhttps://now.aapmr.org/myofascial-pain/
Myofascial pain syndrome (MPS) is a regional muscle pain syndrome caused by myofascial trigger points (TrPs). A TrP is defined as a hyperirritable spot in a palpable taut band of skeletal muscle. MPS is characterized by pain, both local and referred, muscle stiffness, and sensory changes. […] Chronic muscle stretch and overload are thought to play a key role in the development of TrPs, with direct and indirect trauma as possible but less likely causes. […] The most accepted theory of trigger point formation is Travell and Simons Integrated Trigger Point Hypothesis. According to this hypothesis, the initiating event is muscle overload and/or injury. This leads to local capillary constriction and ischemia, an increase in sympathetic nervous system adrenergic activity, formation of an acidic hydrogen ion concentration within the muscle tissue, and the release of sensitizing substances (substance P, calcitonin gene-related peptide [CGRP], protons, serotonin, norepinephrine, prostaglandins, bradykinins, tumor necrosis factor, interleukin (IL)-6, IL-8 and IL-1). In addition, a reduction of locally available adenosine triphosphate (ATP) to muscle tissue results in inhibition of return of calcium to the sarcoplasmic reticulum, causing a sustained contraction of the sarcomere. The acidic environment inhibits the breakdown of acetylcholine, resulting in increased acetylcholine within the synaptic cleft and increased frequency of miniature end plate potentials (EPPs). Together, the sustained sarcomere contraction and increased EPPs promote formation of a taut band of muscle tissue. The biochemicals released account for the peripheral sensitization of nociceptors, which contribute to the pain associated with active trigger points, allodynia, and hyperalgesia. Available evidence supports the hypothesis that TrPs are a persistent peripheral source of nociception, contributing to pain propagation and widespread, referred pain elsewhere.
- #24 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Myofascial pain syndrome is a musculoskeletal condition characterized by regional pain within the muscle, fascia, or surrounding soft tissue. This condition often presents with localized or referred pain, typically associated with hyperirritable trigger points within taut bands of skeletal muscle. […] The exact cause remains unclear, although muscle overload due to overuse or disuse is a key factor. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #25 Myofascial Pain Syndrome | Treatment & Management | Point of Carehttps://www.statpearls.com/point-of-care/25476
The etiology of myofascial pain syndrome is not yet fully understood, although muscle overload is thought to be a cause as a consequence of overuse or disuse. […] Despite extensive research and formulation of various hypotheses, the exact pathophysiology of myofascial pain syndrome is still unknown. One of the most accepted theories is the energy crisis of muscle fibers. Repetitive or prolonged activity can overload muscle fibers, leading to muscle hypoxia and ischemia. Energy depletion causes calcium pumps to become dysfunctional, leading to increased intracellular calcium and sustained muscle contraction responsible for taut band development. This persistent contraction further exacerbates the oxygen demand and hypoxic injury to the muscles. Nociceptors and chemoreceptors release prostaglandins and cytokines in response to ischemia and hypoxia. These substances activate nearby nerve endings, initiating pain signals and pathways.
- #26 Myofascial Pain Syndrome – StatPearls – NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK499882/
Consequently, neurotransmitters such as serotonin and norepinephrine are released, modulating pain transmission and contributing to a cycle of sustained muscle contraction and pain. This process reinforces the release of these neurotransmitters, further influencing pain transmission and perpetuating the cycle of muscle contraction and discomfort. […] In addition to this hypothesis, several other theories, including neurogenic inflammation, sensitization, and limbic dysfunction, have been proposed as contributing factors to myofascial pain syndrome.
- #27 Myofascial Pain Syndrome | Treatment & Management | Point of Carehttps://www.statpearls.com/point-of-care/25476
Consequently, neurotransmitters such as serotonin and norepinephrine are released, modulating pain transmission and contributing to a cycle of sustained muscle contraction and pain. This process reinforces the release of these neurotransmitters, further influencing pain transmission and perpetuating the cycle of muscle contraction and discomfort. […] In addition to this hypothesis, several other theories, including neurogenic inflammation, sensitization, and limbic dysfunction, have been proposed as contributing factors to myofascial pain syndrome.
- #28 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Oxidative stress is a disproportion of reactive oxygen species (ROS) and the capability of biological systems to detoxify dangerous reactive intermediates. Conditions of oxidative stress will increase levels of free calcium and iron ions in cells that cause cell damage and even cell death. Activities that cause ongoing muscle contraction can cause an increase in metabolic stress and decreased blood flow resulting in persistence of the myofascial trigger point. Vasoconstriction, due to the increased calcium levels, causes ischemia and produces free oxygen radicals that damage endothelial and cause further ischemia, which plays a role in the pathophysiology of myofascial pain. Cascade of X-ROS signaling (stretch-activated ROS production) will change the shape of microtubules to activate NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (NOX2) to produce ROS which will be oxidized to RyRs (ryanodine receptors) and increase the sarcoplasmic reticulum to release Ca2+ ions. This mechanism shows that excessive contraction is associated with stress that involves cytoskeletal microtubules to activate NADPH oxidase to produce ROS. Calcium release can stimulate contractions to form a myofascial trigger point. In this condition, there will be a decrease in glutathione levels and an increase in glutathione disulfide levels, which is oxidized glutathione. The main function of glutathione as an anti-oxidant is to detoxify free radicals and reactive oxygen (ROS) in cells.
- #29 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Oxidative stress is a disproportion of reactive oxygen species (ROS) and the capability of biological systems to detoxify dangerous reactive intermediates. Conditions of oxidative stress will increase levels of free calcium and iron ions in cells that cause cell damage and even cell death. Activities that cause ongoing muscle contraction can cause an increase in metabolic stress and decreased blood flow resulting in persistence of the myofascial trigger point. Vasoconstriction, due to the increased calcium levels, causes ischemia and produces free oxygen radicals that damage endothelial and cause further ischemia, which plays a role in the pathophysiology of myofascial pain. Cascade of X-ROS signaling (stretch-activated ROS production) will change the shape of microtubules to activate NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (NOX2) to produce ROS which will be oxidized to RyRs (ryanodine receptors) and increase the sarcoplasmic reticulum to release Ca2+ ions. This mechanism shows that excessive contraction is associated with stress that involves cytoskeletal microtubules to activate NADPH oxidase to produce ROS. Calcium release can stimulate contractions to form a myofascial trigger point. In this condition, there will be a decrease in glutathione levels and an increase in glutathione disulfide levels, which is oxidized glutathione. The main function of glutathione as an anti-oxidant is to detoxify free radicals and reactive oxygen (ROS) in cells.
- #30 Myofascial pain syndrome and sensitizationhttps://oatext.com/Myofascial-pain-syndrome-and-sensitization.php
The mechanism consists of the nociceptive stimuli generated in the sensitized areas bombarding the dorsal horn of the spinal cord. This causes central nervous system sensitization with resultant hyperalgesia of the dermatome and sclerotome and spreads from the sensory component of the spinal segment to the anterior horn cells, which control the myotome within the territory of the SSS. The development or amplified activity of MTrPs is one of the clinical manifestations of SSS. […] Myofascial pain syndrome induced profound altering neuronal excitability and architecture in structures of the pain matrix structures as the spinal cord, thalamic nuclei, cortical areas, amygdala and periaqueductal gray area. This dynamic process can alter pain threshold, pain intensity and emotional affect. […] A continuous noxious input into the dorsal horn called afferent bombardment results in the co-release of L-glutamate and substance P (SP). The releasing of these two substances can lower thresholds for synaptic activation and open previously ineffective synaptic connections in wide dynamic range (WDR) neurons, leading to central sensitization.
- #31 Myofascial pain syndrome and sensitizationhttps://oatext.com/Myofascial-pain-syndrome-and-sensitization.php
The mechanism consists of the nociceptive stimuli generated in the sensitized areas bombarding the dorsal horn of the spinal cord. This causes central nervous system sensitization with resultant hyperalgesia of the dermatome and sclerotome and spreads from the sensory component of the spinal segment to the anterior horn cells, which control the myotome within the territory of the SSS. The development or amplified activity of MTrPs is one of the clinical manifestations of SSS. […] Myofascial pain syndrome induced profound altering neuronal excitability and architecture in structures of the pain matrix structures as the spinal cord, thalamic nuclei, cortical areas, amygdala and periaqueductal gray area. This dynamic process can alter pain threshold, pain intensity and emotional affect. […] A continuous noxious input into the dorsal horn called afferent bombardment results in the co-release of L-glutamate and substance P (SP). The releasing of these two substances can lower thresholds for synaptic activation and open previously ineffective synaptic connections in wide dynamic range (WDR) neurons, leading to central sensitization.
- #32 Myofascial pain syndrome and sensitizationhttps://www.oatext.com/Myofascial-pain-syndrome-and-sensitization.php
The development or amplified activity of MTrPs is one of the clinical manifestations of SSS. […] Myofascial pain syndrome induced profound altering neuronal excitability and architecture in structures of the pain matrix structures as the spinal cord, thalamic nuclei, cortical areas, amygdala and periaqueductal gray area. […] A continuous noxious input into the dorsal horn called afferent bombardment results in the co-release of L-glutamate and substance P (SP). […] The releasing of these two substances can lower thresholds for synaptic activation and open previously ineffective synaptic connections in wide dynamic range (WDR) neurons, leading to central sensitization. […] Sensitization up-regulates ion channel and receptor expression and increases the number of these membrane proteins on nociceptors and dorsal horn neurons.
- #33 Myofascial pain syndrome and sensitizationhttps://oatext.com/Myofascial-pain-syndrome-and-sensitization.php
Sensitization up-regulates ion channel and receptor expression and increases the number of these membrane proteins on nociceptors and dorsal horn neurons. […] Spinal segmental sensitization (SSS) is a hyperactive state of the dorsal horn caused by bombardment of nociceptive impulses from sensitized tissues (such as active MTrPs or visceral structures such as the renal calculi). Clinical manifestations of the sensitized spinal segment include MTrPs, dermatomal allodynia (pain by non-painful stimulus) and hyperalgesia (increased pain by painful stimulus) in addition to sclerotome tenderness within the involved myotomes. […] Segmental sensitization occurs throughout neuron hypertrophy as well as upregulation of excitatory neurons, prohyperalgesic peptides, and neurotransmitters at the dorsal horn.
- #34 Myofascial pain syndrome and sensitizationhttps://www.oatext.com/Myofascial-pain-syndrome-and-sensitization.php
The development or amplified activity of MTrPs is one of the clinical manifestations of SSS. […] Myofascial pain syndrome induced profound altering neuronal excitability and architecture in structures of the pain matrix structures as the spinal cord, thalamic nuclei, cortical areas, amygdala and periaqueductal gray area. […] A continuous noxious input into the dorsal horn called afferent bombardment results in the co-release of L-glutamate and substance P (SP). […] The releasing of these two substances can lower thresholds for synaptic activation and open previously ineffective synaptic connections in wide dynamic range (WDR) neurons, leading to central sensitization. […] Sensitization up-regulates ion channel and receptor expression and increases the number of these membrane proteins on nociceptors and dorsal horn neurons.
- #35 Myofascial pain syndrome and sensitizationhttps://oatext.com/Myofascial-pain-syndrome-and-sensitization.php
Sensitization up-regulates ion channel and receptor expression and increases the number of these membrane proteins on nociceptors and dorsal horn neurons. […] Spinal segmental sensitization (SSS) is a hyperactive state of the dorsal horn caused by bombardment of nociceptive impulses from sensitized tissues (such as active MTrPs or visceral structures such as the renal calculi). Clinical manifestations of the sensitized spinal segment include MTrPs, dermatomal allodynia (pain by non-painful stimulus) and hyperalgesia (increased pain by painful stimulus) in addition to sclerotome tenderness within the involved myotomes. […] Segmental sensitization occurs throughout neuron hypertrophy as well as upregulation of excitatory neurons, prohyperalgesic peptides, and neurotransmitters at the dorsal horn.
- #36 Myofascial pain syndrome and sensitizationhttps://www.oatext.com/Myofascial-pain-syndrome-and-sensitization.php
Spinal segmental sensitization (SSS) is a hyperactive state of the dorsal horn caused by bombardment of nociceptive impulses from sensitized tissues (such as active MTrPs or visceral structures such as the renal calculi). […] Clinical manifestations of the sensitized spinal segment include MTrPs, dermatomal allodynia (pain by non-painful stimulus) and hyperalgesia (increased pain by painful stimulus) in addition to sclerotome tenderness within the involved myotomes. […] Segmental sensitization occurs throughout neuron hypertrophy as well as upregulation of excitatory neurons, prohyperalgesic peptides, and neurotransmitters at the dorsal horn. […] Modalities and manual therapies are often clinically effective for eradication of active MTrPs and desensitization sensitized spinal segments.
- #37 Myofascial pain syndrome – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/myofascial-pain-syndrome/symptoms-causes/syc-20375444
Stress and anxiety. People who often feel stressed and anxious may be more likely to get trigger points in their muscles. One theory is that these people may be more likely to clench their muscles. Clenching is a form of repeated strain that leaves muscles open to trigger points. […] Some research suggests that myofascial pain syndrome may lead to fibromyalgia in some people. Fibromyalgia is a long-term condition of widespread pain. It’s believed that the brains of people with fibromyalgia respond more to pain signals over time. Some experts believe myofascial pain syndrome might help start this process.
- #38 Myofascial pain syndrome – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/myofascial-pain-syndrome/symptoms-causes/syc-20375444
Stress and anxiety. People who often feel stressed and anxious may be more likely to get trigger points in their muscles. One theory is that these people may be more likely to clench their muscles. Clenching is a form of repeated strain that leaves muscles open to trigger points. […] Some research suggests that myofascial pain syndrome may lead to fibromyalgia in some people. Fibromyalgia is a long-term condition of widespread pain. It’s believed that the brains of people with fibromyalgia respond more to pain signals over time. Some experts believe myofascial pain syndrome might help start this process.
- #39 Myofascial Pain Syndrome: A Nociceptive Condition Comorbid with Neuropathic or Nociplastic Painhttps://www.mdpi.com/2075-1729/13/3/694
Myofascial pain syndrome is featured by the presence of myofascial trigger points (TrPs). Whether TrPs are primary or secondary phenomena or if they relate to central or peripheral nervous system disorders is controversial. Referred pain, a cardinal sign of TrPs, is a central phenomenon driven by peripheral input. […] Myofascial TrP pain has been traditionally categorized as a nociceptive phenotype; however, increasing evidence supports that this condition could be present in patients with predominantly nociplastic pain, particularly when it is associated with an underlying medical condition. […] The clinical response of some therapeutic approaches for managing TrPs remains unclear. […] It is concluded that myofascial pain caused by TrPs is primarily a nociceptive pain condition, is unlikely to be classified as neuropathic or nociplastic, but can be present in patients with predominantly neuropathic or nociplastic pain.
- #40 Myofascial Pain Syndrome: A Nociceptive Condition Comorbid with Neuropathic or Nociplastic Painhttps://www.mdpi.com/2075-1729/13/3/694
Myofascial pain has been traditionally classified as nociceptive pain. The current paper summarizes data supporting the subgrouping of patients with myofascial TrP pain into nociceptive, nociplastic, or mixed-type phenotype. Simple myofascial pain syndrome caused by TrPs is primarily a nociceptive condition, is unlikely to be classified as neuropathic or nociplastic, but can be present in patients as a comorbid condition along with predominantly neuropathic or nociplastic pain syndromes. […] The presence of underlying painful nociplastic comorbidities may lower the threshold for pain by increasing the central nervous system gain, leading to sensitization, and hence TrPs may become a painful generator of pain.
- #41 Myofascial Pain Syndrome: A Nociceptive Condition Comorbid with Neuropathic or Nociplastic Painhttps://www.mdpi.com/2075-1729/13/3/694
The development or activation of TrPs can result from a variety of factors affecting the muscle tissue, e.g., repetitive muscle overuse, acute muscle overload, or repetitive minor muscle trauma. […] The integrated hypothesis postulates that TrPs represent a primary dysfunction of the motor endplate that results in sensitized peripheral nerve endings (nociceptive pain phenotype). […] As such, TrPs, particularly active TrPs, can act as sources of persistent or long-lasting peripheral nociceptive input, independent of tissue damage. […] The presence of multiple TrPs (spatial summation) or the presence of TrPs for long-lasting periods (temporal summation) sensitize spinal cord neurons and supra-spinal structures because they are effective peripheral nociceptors whose afferent input can produce an afferent nociceptive barrage into the central nervous system.
- #42 Myofascial pain syndrome – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/myofascial-pain-syndrome/symptoms-causes/syc-20375444
Myofascial pain syndrome is a long-term pain condition. It involves some muscles and the thin cover of tissue that holds muscles in place, called fascia. Pressure on these areas, called trigger points, causes pain. […] The exact cause of myofascial pain syndrome is not known. Areas of tight muscle fibers, called trigger points, form in muscles. Too much use of the muscles, most often with poor form, injury to the muscle and mental stress likely help cause trigger points. […] In myofascial pain syndrome, something such as muscle tightness sets off trigger points in the muscles. Factors that may increase the risk of muscle trigger points include: Muscle injury. A muscle injury or ongoing muscle stress may lead to the forming of trigger points. For instance, a spot in or near a strained muscle may become a trigger point. Repeat motions and poor posture also can increase the risk.
- #43 Cervical Myofascial Pain: Practice Essentials, Etiology, Epidemiologyhttps://emedicine.medscape.com/article/305937-overview
Cervical myofascial pain is thought to occur following either overuse of or trauma to the muscles that support the shoulders and neck. It can also occur as a reaction to an underlying spinal pathology such as facet joint arthropathy or an annular tear in one of the cervical discs. […] Other issues that may play a role in the clinical picture of cervical myofascial pain include endocrine dysfunction, chronic infections, nutritional deficiencies, poor posture, and psychological stress. […] When the patient with cervical myofascial pain undergoes appropriate treatment (eg, physical therapy, massage therapy, stretch and spray, trigger point injections, identification and elimination of an underlying, triggering pathology), the prognosis is generally good. However, recurrence can be a common scenario. […] Increased mortality is not associated with cervical myofascial pain.
- #44https://link.springer.com/article/10.1007/s11916-012-0289-4
Myofascial pain syndrome (MPS) is described as the sensory, motor, and autonomic symptoms caused by myofascial trigger points (TrPs). […] There is general agreement that muscle overuse or direct trauma to the muscle can lead to the development of TrPs. Muscle overload is hypothesized to be the result of sustained or repetitive low-level muscle contractions, eccentric muscle contractions, and maximal or submaximal concentric muscle contractions. […] Knowing the potential causes of TrPs is important to prevent their development and recurrence, but also to inactivate and eliminate existing TrPs. […] Although muscle damage is not required for the development of TrP, there may be a disruption of the cell membrane, damage to the sarcoplasmic reticulum with a subsequent release of high amounts of calcium-ions, and disruption of cytoskeletal proteins, such as desmin, titin, and dystrophin.
- #45 Myofascial pain syndrome – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/myofascial-pain-syndrome/symptoms-causes/syc-20375444
Stress and anxiety. People who often feel stressed and anxious may be more likely to get trigger points in their muscles. One theory is that these people may be more likely to clench their muscles. Clenching is a form of repeated strain that leaves muscles open to trigger points. […] Some research suggests that myofascial pain syndrome may lead to fibromyalgia in some people. Fibromyalgia is a long-term condition of widespread pain. It’s believed that the brains of people with fibromyalgia respond more to pain signals over time. Some experts believe myofascial pain syndrome might help start this process.
- #46 Mechanisms of Myofascial Pain Syndrome – Texas Pain Expertshttps://texaspainexperts.com/mechanisms-of-myofascial-pain-syndrome/
Trigger points are highly likely to develop in the muscles of people experiencing stress. This argument is supported by the theory that most people who experience stress tend to clench their fists, therefore applying pressure on their muscles, which leads to the development of trigger points. […] There are some effective treatments for myofascial pain which are meant to reduce the pain and also prevent the development of trigger points on the muscles.
- #47 Cervical Myofascial Pain: Practice Essentials, Etiology, Epidemiologyhttps://emedicine.medscape.com/article/305937-overview
Cervical myofascial pain is thought to occur following either overuse of or trauma to the muscles that support the shoulders and neck. It can also occur as a reaction to an underlying spinal pathology such as facet joint arthropathy or an annular tear in one of the cervical discs. […] Other issues that may play a role in the clinical picture of cervical myofascial pain include endocrine dysfunction, chronic infections, nutritional deficiencies, poor posture, and psychological stress. […] When the patient with cervical myofascial pain undergoes appropriate treatment (eg, physical therapy, massage therapy, stretch and spray, trigger point injections, identification and elimination of an underlying, triggering pathology), the prognosis is generally good. However, recurrence can be a common scenario. […] Increased mortality is not associated with cervical myofascial pain.
- #48 Myofascial Trigger Points: Understanding, Diagnosis, Management and Treatment. Pelvic pain symptoms. | Actual Gynecology And Obstetricshttps://www.actualgyn.com/en/article/2024/296
It describes an excessive release of ACh in the synaptic cleft, triggering high-frequency miniature endplate potentials and thus permanent depolarization. […] The main reasons for persistent contractures and nociceptor activity are local hypoxia and ischaemia. […] The contraction of knots leads to the compression of vascular capillaries, resulting in local ischaemia. […] Both ischaemia-induced energy deficiency and increased energy consumption for Ca-pump activation necessary for actin-myosin separation can contribute to developing a local energy crisis. […] Increased levels of sensitizing substances are found near trigger points. […] Individuals who engage in minimal physical activity daily but experience occasional intense physical exertion are likelier to have trigger points. […] The self-healing capability of affected muscles is minimal. […] The process often requires repeated approaches to prevent redirection and transformation in the spinal cord.
- #49 Myofascial trigger point – Wikipediahttps://en.wikipedia.org/wiki/Myofascial_trigger_point
An analysis of the environment of trigger points found the pH around active trigger points going down to pH 4.3. Furthermore, the environment of trigger points (unlike healthy muscle) contained inflammatory cytokines and CGRP. Concentrations of protons (H+), bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-, interleukin 1-, serotonin, and norepinephrine were found to be significantly higher in the active trigger point group than either of the other two groups (latent trigger points and no trigger points).
- #50 Myofascial trigger point – Wikipediahttps://en.wikipedia.org/wiki/Myofascial_trigger_point
An analysis of the environment of trigger points found the pH around active trigger points going down to pH 4.3. Furthermore, the environment of trigger points (unlike healthy muscle) contained inflammatory cytokines and CGRP. Concentrations of protons (H+), bradykinin, calcitonin gene-related peptide, substance P, tumor necrosis factor-, interleukin 1-, serotonin, and norepinephrine were found to be significantly higher in the active trigger point group than either of the other two groups (latent trigger points and no trigger points).
- #51 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Prolonged muscle contraction, ischemia/hypoxia, metabolic disorders, and cell stress also lead to increased release of neurotransmitters, inflammatory cytokines, and myokines, which necessary in the pathophysiology of myofascial pain. Damage to these muscles cause the release of neuropeptides, cytokines, and inflammatory substances such as potassium, bradykinin, cytokines, tumor necrosis factor, interleukin 1, norepinephrine, protons, prostaglandins, ATP and substances P that can stimulate nociceptors in the muscle thereby releasing CGRP (calcitonin gene-related peptide). The release of TNF- will trigger norepinephrine production. Studies found an increase in both serotonin and norepinephrine in patients with active myofascial trigger points. Hypotheses expressed by Simons and further explained by Gerwin et al. stated that CGRP would inhibit acetylcholinesterase. Increase of the acetylcholine receptors and increase of acetylcholine release (acetylcholine leakage) will lead to prolonged contraction of local muscle fibers, known as myofascial trigger points. Continuous input at myofascial trigger point will cause apoptosis of inhibitory neurons at the segmental level and will sensitize neurons at dorsal horn causing hyperalgesia, allodynia, and prolonged pain.
- #52 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Prolonged muscle contraction, ischemia/hypoxia, metabolic disorders, and cell stress also lead to increased release of neurotransmitters, inflammatory cytokines, and myokines, which necessary in the pathophysiology of myofascial pain. Damage to these muscles cause the release of neuropeptides, cytokines, and inflammatory substances such as potassium, bradykinin, cytokines, tumor necrosis factor, interleukin 1, norepinephrine, protons, prostaglandins, ATP and substances P that can stimulate nociceptors in the muscle thereby releasing CGRP (calcitonin gene-related peptide). The release of TNF- will trigger norepinephrine production. Studies found an increase in both serotonin and norepinephrine in patients with active myofascial trigger points. Hypotheses expressed by Simons and further explained by Gerwin et al. stated that CGRP would inhibit acetylcholinesterase. Increase of the acetylcholine receptors and increase of acetylcholine release (acetylcholine leakage) will lead to prolonged contraction of local muscle fibers, known as myofascial trigger points. Continuous input at myofascial trigger point will cause apoptosis of inhibitory neurons at the segmental level and will sensitize neurons at dorsal horn causing hyperalgesia, allodynia, and prolonged pain.
- #53 Myofascial pain syndrome | MedLink Neurologyhttps://www.medlink.com/articles/myofascial-pain-syndrome
Dysfunction of intracellular calcium pumps due to energy depletion of muscles leads to increase of intracellular calcium, which induces sustained muscle contraction resulting in the development of taut bands. […] Moreover, inflammatory mediators caused by muscle injury contribute to pain and tenderness of the affected muscles. […] Small arteries (or enlarged arterioles) near active myofascial trigger points showed retrograde flow in diastole, indicating a highly resistive vascular bed. […] Myofascial pain syndromes occur in muscles that have been overused as well as underused. […] Other factors such as faulty positioning, malalignment of forces, and underlying joint dysfunction provide important external influences. […] Myofascial perpetuating factors are those mechanical, systemic, and psychological conditions that facilitate either injury of the affected muscle group or provocation of the neuromuscular feedback group theorized to result in chronic myofascial trigger point manifestations.
- #54 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Oxidative stress is a disproportion of reactive oxygen species (ROS) and the capability of biological systems to detoxify dangerous reactive intermediates. Conditions of oxidative stress will increase levels of free calcium and iron ions in cells that cause cell damage and even cell death. Activities that cause ongoing muscle contraction can cause an increase in metabolic stress and decreased blood flow resulting in persistence of the myofascial trigger point. Vasoconstriction, due to the increased calcium levels, causes ischemia and produces free oxygen radicals that damage endothelial and cause further ischemia, which plays a role in the pathophysiology of myofascial pain. Cascade of X-ROS signaling (stretch-activated ROS production) will change the shape of microtubules to activate NADPH (nicotinamide adenine dinucleotide phosphate) oxidase (NOX2) to produce ROS which will be oxidized to RyRs (ryanodine receptors) and increase the sarcoplasmic reticulum to release Ca2+ ions. This mechanism shows that excessive contraction is associated with stress that involves cytoskeletal microtubules to activate NADPH oxidase to produce ROS. Calcium release can stimulate contractions to form a myofascial trigger point. In this condition, there will be a decrease in glutathione levels and an increase in glutathione disulfide levels, which is oxidized glutathione. The main function of glutathione as an anti-oxidant is to detoxify free radicals and reactive oxygen (ROS) in cells.
- #55 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Myofascial pain is one of the health problems that attract the attention of clinicians and has also caused confusion and errors in recent decades. Myofascial pain consists of autonomic, motoric, and sensory symptoms that involve both the muscles and surrounding connective tissue (fascia). Myofascial pain is caused by myofascial trigger points, which are located on the taut muscle band. The shortening of the contracted taut muscle band results in movement restriction and pain. Continuous peripheral nociceptive input activates dorsal horns through the release of substance P. This process causes neuroplastic changes (increased excitability) in the central nervous system and causes central sensitization, which results in allodynia and hyperalgesia from stimulation of activity in the region of the brain to process sensory discrimination. According to Travell and Simon, vasoconstriction will cause the local hypoxia/ischemia. This vasoconstriction occurs due to increased calcium in tissues when the sarcoplasmic reticulum rupture occurs. Decreased oxygen will disrupt mitochondrial metabolism. In this situation, the reduction of ATP will cause an energy crisis and distress in the tissue. Therefore anaerobic metabolism will occur that produces lactic acid, reducing the intramuscular pH. Two mechanisms that cause pain at the myofascial trigger point, such as the involvement of ASIC3 nociceptors (acid-sensing ion channels) and TRPV1 (transient receptor potential) channels, which are known as capsaicin receptors on pain nerves. The decrease in pH (below 5.0) that occurs due to local ischemia at the myofascial trigger point is more than sufficient to cause excitation of muscle nociceptors, including the ASIC3 and TRPV1 canal nociceptors.
- #56 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Prolonged nociceptive input can cause maladaptive changes in the central nervous system. Prolonged afferent nociceptive input from the myofascial trigger point activates and sensitizes the neurons in the dorsal horn, which carried by the spinothalamic tract to higher brain centers. Muscle afferent input activates not only the thalamus but also the limbic system, which plays an important role in pain modulation and emotions. The pro-inflammatory factors such as cytokines, oxidative stress, and free radicals found in patients with myofascial pain will initiate the reactive astrocytes. This initiation of reactive astrocytes occurs through the nuclear factor kappa-B (NFB) pathway. Astrocyte activation and release of IL-1 take part in the mechanism of hyperalgesia. These cytokines and chemokines act in the induction and persistence of pain. The activation of astrocytes has been investigated in relation to the pathogenesis of pain through the release of pro-inflammatory and pro-algesic mediators such as TNF-, IL-1, and IL-6.
- #57 The role of oxidative stress, inflammation and glial cell in pathophysiology of myofascial painhttps://www.termedia.pl/The-role-of-oxidative-stress-inflammation-and-glial-cell-in-pathophysiology-of-myofascial-pain,116,42111,1,1.html
Prolonged nociceptive input can cause maladaptive changes in the central nervous system. Prolonged afferent nociceptive input from the myofascial trigger point activates and sensitizes the neurons in the dorsal horn, which carried by the spinothalamic tract to higher brain centers. Muscle afferent input activates not only the thalamus but also the limbic system, which plays an important role in pain modulation and emotions. The pro-inflammatory factors such as cytokines, oxidative stress, and free radicals found in patients with myofascial pain will initiate the reactive astrocytes. This initiation of reactive astrocytes occurs through the nuclear factor kappa-B (NFB) pathway. Astrocyte activation and release of IL-1 take part in the mechanism of hyperalgesia. These cytokines and chemokines act in the induction and persistence of pain. The activation of astrocytes has been investigated in relation to the pathogenesis of pain through the release of pro-inflammatory and pro-algesic mediators such as TNF-, IL-1, and IL-6.
- #58 Myofascial pain syndrome | MedLink Neurologyhttps://www.medlink.com/articles/myofascial-pain-syndrome
The concept that the myofascial trigger point represents a transient state of neuromuscular dysfunction is a recent introduction. […] The hypothesis that central sensitization plays a role in the pathogenesis of myofascial pain is supported by the finding of delayed and shortened cutaneous silence periods in limbs of volunteers and patients with myofascial pain, which indicates dysfunction in the inhibitory mechanism of the spinal/supraspinal pain pathways. […] The distribution of nociceptors within skeletal muscle is confined to the fascia between muscle fibers, with the highest concentration of nociceptors near the muscle endplate region where myofascial trigger points are usually found. […] It has been proposed that multiple sensitive loci exist in a trigger point region, and that each locus contains one or more sensitized nociceptive nerve endings.
- #59 Expert consensus on the diagnosis and treatment of myofascial pain syndromehttps://www.wjgnet.com/2307-8960/full/v9/i9/2077.htm
The consistent muscle contraction in turn increases local energy consumption and local ischemia. The changes may induce pain or pain hypersensitivity by enhancing the local release of nociceptive substances, including substance P, calcitonin gene-related peptide and proinflammatory cytokines. […] The central pain sensitization can increase the excitability of neurons and the expansion of the neuronal receptive fields causing refractory referred pain. […] Alternatively, Stecco et al suggested that muscular fascia, a form of connective tissue, may undergo pathological change under overload and damage leading to the biomechanical change of muscles and eventually to the reduction of contraction force and flexibility of muscles. […] The inflammatory changes mentioned above may exacerbate the pathological change, leading to pain or enhancing pain. The pathological change of muscular fascia may be related to the abnormal changes in myofibrils, fibroblasts and extracellular matrix.
- #60https://www.leagravetherapy.co.uk/post-title2
Until this positive-feedback loop is interrupted, the muscle sarcomeres at the TrP remain in a shortened state, resulting in a local energy crisis. […] There is no explanation or description for the initiating event that causes the excessive release of ACh to occur in the first place. […] This theory also assumes that the motor endplates are the focus of attention for trigger point development. […] Muscle overuse or traumatic injury, the sliding layers start to produce immense amounts of HA which then aggregate into supermolecular structures changing both its configuration, viscoelasticity and viscosity. […] Due to its increased viscosity, HA can no longer function as an effective lubricant which increases resistance in the sliding layers and leads to densification of fascia or abnormal sliding in muscle fibers.
- #61 Expert consensus on the diagnosis and treatment of myofascial pain syndromehttps://www.wjgnet.com/2307-8960/full/v9/i9/2077.htm
The consistent muscle contraction in turn increases local energy consumption and local ischemia. The changes may induce pain or pain hypersensitivity by enhancing the local release of nociceptive substances, including substance P, calcitonin gene-related peptide and proinflammatory cytokines. […] The central pain sensitization can increase the excitability of neurons and the expansion of the neuronal receptive fields causing refractory referred pain. […] Alternatively, Stecco et al suggested that muscular fascia, a form of connective tissue, may undergo pathological change under overload and damage leading to the biomechanical change of muscles and eventually to the reduction of contraction force and flexibility of muscles. […] The inflammatory changes mentioned above may exacerbate the pathological change, leading to pain or enhancing pain. The pathological change of muscular fascia may be related to the abnormal changes in myofibrils, fibroblasts and extracellular matrix.
- #62 Myofascial Pain Syndrome: A Nociceptive Condition Comorbid with Neuropathic or Nociplastic Painhttps://www.mdpi.com/2075-1729/13/3/694
Myofascial pain syndrome is featured by the presence of myofascial trigger points (TrPs). Whether TrPs are primary or secondary phenomena or if they relate to central or peripheral nervous system disorders is controversial. Referred pain, a cardinal sign of TrPs, is a central phenomenon driven by peripheral input. […] Myofascial TrP pain has been traditionally categorized as a nociceptive phenotype; however, increasing evidence supports that this condition could be present in patients with predominantly nociplastic pain, particularly when it is associated with an underlying medical condition. […] The clinical response of some therapeutic approaches for managing TrPs remains unclear. […] It is concluded that myofascial pain caused by TrPs is primarily a nociceptive pain condition, is unlikely to be classified as neuropathic or nociplastic, but can be present in patients with predominantly neuropathic or nociplastic pain.
- #63 Myofascial Pain Syndrome and Trigger Point Injections – OpenAnesthesiahttps://www.openanesthesia.org/keywords/myofascial-pain-syndrome-and-trigger-point-injections/
Myofascial pain syndrome is a pain disorder characterized by chronic pain originating from myofascial trigger points and fascial constrictions. […] The mechanism of action of trigger points remains unknown and systematic reviews have shown neither benefit or ineffectiveness. […] A single trigger point may progress to multiple points by persisting and causing neuroplastic changes at the level of the dorsal horn, which results in the amplification of the pain sensation (i.e., central sensitization) and expansion of pain beyond its original boundaries. […] The mechanism of action of trigger point injections in treating trigger points found in myofascial pain syndrome is still unknown. […] A systematic review assessing the effectiveness of trigger point injections for chronic nonmalignant chronic pain found no clear evidence in the medical literature of either benefit or ineffectiveness.
- #64 Myofascial pain syndrome | MedLink Neurologyhttps://www.medlink.com/articles/myofascial-pain-syndrome
The concept that the myofascial trigger point represents a transient state of neuromuscular dysfunction is a recent introduction. […] The hypothesis that central sensitization plays a role in the pathogenesis of myofascial pain is supported by the finding of delayed and shortened cutaneous silence periods in limbs of volunteers and patients with myofascial pain, which indicates dysfunction in the inhibitory mechanism of the spinal/supraspinal pain pathways. […] The distribution of nociceptors within skeletal muscle is confined to the fascia between muscle fibers, with the highest concentration of nociceptors near the muscle endplate region where myofascial trigger points are usually found. […] It has been proposed that multiple sensitive loci exist in a trigger point region, and that each locus contains one or more sensitized nociceptive nerve endings.
- #65 Myofascial pain syndrome | MedLink Neurologyhttps://www.medlink.com/articles/myofascial-pain-syndrome
The concept that the myofascial trigger point represents a transient state of neuromuscular dysfunction is a recent introduction. […] The hypothesis that central sensitization plays a role in the pathogenesis of myofascial pain is supported by the finding of delayed and shortened cutaneous silence periods in limbs of volunteers and patients with myofascial pain, which indicates dysfunction in the inhibitory mechanism of the spinal/supraspinal pain pathways. […] The distribution of nociceptors within skeletal muscle is confined to the fascia between muscle fibers, with the highest concentration of nociceptors near the muscle endplate region where myofascial trigger points are usually found. […] It has been proposed that multiple sensitive loci exist in a trigger point region, and that each locus contains one or more sensitized nociceptive nerve endings.
- #66 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
Myofibroblasts might transmit considerably high forces. […] A systematic search was held for multiple combinations of keywords in multiple databases. […] The findings are presented with the purpose of understanding the elements relevant to MPS and fascia, in order to assemble them and discuss a suggested mechanism of MPS and fibromyalgia. […] The fact that fascia can transmit tension to a distance is a basis for a bio-tensegrity framework. […] When the tension of fascia increases, the connective tissue can distribute the forces throughout the surrounding areas, propagating along the myofascial system. […] The interconnectedness of fascia and its ability to transmit force are at the basis of its functions.
- #67 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
Myofibroblasts might transmit considerably high forces. […] A systematic search was held for multiple combinations of keywords in multiple databases. […] The findings are presented with the purpose of understanding the elements relevant to MPS and fascia, in order to assemble them and discuss a suggested mechanism of MPS and fibromyalgia. […] The fact that fascia can transmit tension to a distance is a basis for a bio-tensegrity framework. […] When the tension of fascia increases, the connective tissue can distribute the forces throughout the surrounding areas, propagating along the myofascial system. […] The interconnectedness of fascia and its ability to transmit force are at the basis of its functions.
- #68 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
Myofibroblasts might transmit considerably high forces. […] A systematic search was held for multiple combinations of keywords in multiple databases. […] The findings are presented with the purpose of understanding the elements relevant to MPS and fascia, in order to assemble them and discuss a suggested mechanism of MPS and fibromyalgia. […] The fact that fascia can transmit tension to a distance is a basis for a bio-tensegrity framework. […] When the tension of fascia increases, the connective tissue can distribute the forces throughout the surrounding areas, propagating along the myofascial system. […] The interconnectedness of fascia and its ability to transmit force are at the basis of its functions.
- #69 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Myofibroblasts are present in some developing or normal adult tissues, altering tissue tension. […] Myofibroblasts can couple their activity directly to other cells like myocytes via gap junctions and act as a unite. […] The interconnectedness of fascia and its ability to transmit force are at the base of its functions.
- #70 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Myofascial Pain Syndrome (MPS) is a common overlooked and underdiagnosed condition. […] MPS can evolve into fibromyalgia, and many studies focus on central mechanisms. […] Review suggests fascia can adapt to various states by reversibly changing biomechanical and physical properties. […] Trigger points, tension, and pain are a hallmark of MPS. […] Myofibroblasts play a role in sustained fascial tension which can propagate and is a bases for a tensegrity framework. […] MPS can be seen as a pathological state of imbalance in a natural process; manifesting from inherent properties of the fascia, triggered by a disrupted biomechanical interplay. […] MPS might evolve into fibromyalgia through deranged myofibroblasts in connective tissue, or fascial armoring, which may explain pain distribution, decreased pressure/pain thresholds, occasional resolution after surgery, etc.
- #71 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Various hypotheses have been suggested to explain the mechanism of MPS, among them are trigger points, non-muscular sensitization of the nervi nervorum, central nervous system, and several other theories. […] Chronic tension is exacerbated with more tension generated by myofibroblast smooth muscle actin fiber contractions. […] Tension is converted to HA aggregation and entropy so long as compensation along the stress relaxation curve can allow for it. […] If the values of tension reached at the stress relaxation curve plateau tend to be above the value of the threshold for myofibroblast differentiation, it will be a major driver for MPS. […] Myofibroblasts might transmit considerably high forces. […] The visible appearance of continuous tension in pathological contractures is the consequence of contraction and remodeling.
- #72 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
The mechanism of needling is suggested to be more mechanical than currently thought. A global percutaneous needle fasciotomy that respects tensegrity principles may treat MPS/fibromyalgia more effectively. […] Myofibroblasts play a role in sustained myofascial tension. […] Theories of the origin of TrPs emphasize the chronic contraction associated with them or their tendency of appearing at the muscle spindle. […] Various hypotheses have been suggested to explain the mechanism of MPS, among them are trigger points, non-muscular sensitization of the nervi nervorum, central nervous system, and several other theories. […] Myofibroblasts are present in some developing or normal adult tissues, altering tissue tension. […] Myofibroblasts generate the mechanical conditions that enhance their contractility in a detrimental loop.
- #73 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Myofibroblasts are present in some developing or normal adult tissues, altering tissue tension. […] Myofibroblasts can couple their activity directly to other cells like myocytes via gap junctions and act as a unite. […] The interconnectedness of fascia and its ability to transmit force are at the base of its functions.
- #74 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
The mechanism of needling is suggested to be more mechanical than currently thought. A global percutaneous needle fasciotomy that respects tensegrity principles may treat MPS/fibromyalgia more effectively. […] Myofibroblasts play a role in sustained myofascial tension. […] Theories of the origin of TrPs emphasize the chronic contraction associated with them or their tendency of appearing at the muscle spindle. […] Various hypotheses have been suggested to explain the mechanism of MPS, among them are trigger points, non-muscular sensitization of the nervi nervorum, central nervous system, and several other theories. […] Myofibroblasts are present in some developing or normal adult tissues, altering tissue tension. […] Myofibroblasts generate the mechanical conditions that enhance their contractility in a detrimental loop.
- #75 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Myofibroblasts are present in some developing or normal adult tissues, altering tissue tension. […] Myofibroblasts can couple their activity directly to other cells like myocytes via gap junctions and act as a unite. […] The interconnectedness of fascia and its ability to transmit force are at the base of its functions.
- #76 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Various hypotheses have been suggested to explain the mechanism of MPS, among them are trigger points, non-muscular sensitization of the nervi nervorum, central nervous system, and several other theories. […] Chronic tension is exacerbated with more tension generated by myofibroblast smooth muscle actin fiber contractions. […] Tension is converted to HA aggregation and entropy so long as compensation along the stress relaxation curve can allow for it. […] If the values of tension reached at the stress relaxation curve plateau tend to be above the value of the threshold for myofibroblast differentiation, it will be a major driver for MPS. […] Myofibroblasts might transmit considerably high forces. […] The visible appearance of continuous tension in pathological contractures is the consequence of contraction and remodeling.
- #77 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Various hypotheses have been suggested to explain the mechanism of MPS, among them are trigger points, non-muscular sensitization of the nervi nervorum, central nervous system, and several other theories. […] Chronic tension is exacerbated with more tension generated by myofibroblast smooth muscle actin fiber contractions. […] Tension is converted to HA aggregation and entropy so long as compensation along the stress relaxation curve can allow for it. […] If the values of tension reached at the stress relaxation curve plateau tend to be above the value of the threshold for myofibroblast differentiation, it will be a major driver for MPS. […] Myofibroblasts might transmit considerably high forces. […] The visible appearance of continuous tension in pathological contractures is the consequence of contraction and remodeling.
- #78 Scoping Review and Interpretation of Myofascial Pain/Fibromyalgia Syndrome: An Attempt to Assemble a Medical Puzzle | medRxivhttps://www.medrxiv.org/content/10.1101/2021.07.06.21260111v2.full-text
Myofascial Pain Syndrome (MPS) is a common overlooked and underdiagnosed condition. […] MPS can evolve into fibromyalgia, and many studies focus on central mechanisms. […] Review suggests fascia can adapt to various states by reversibly changing biomechanical and physical properties. […] Trigger points, tension, and pain are a hallmark of MPS. […] Myofibroblasts play a role in sustained fascial tension which can propagate and is a bases for a tensegrity framework. […] MPS can be seen as a pathological state of imbalance in a natural process; manifesting from inherent properties of the fascia, triggered by a disrupted biomechanical interplay. […] MPS might evolve into fibromyalgia through deranged myofibroblasts in connective tissue, or fascial armoring, which may explain pain distribution, decreased pressure/pain thresholds, occasional resolution after surgery, etc.
- #79 Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle | PLOS Onehttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0263087
Myofascial Pain Syndrome (MPS) is a common, overlooked, and underdiagnosed condition and has significant burden. MPS can evolve into fibromyalgia, however, effective treatments for both are lacking due to absence of a clear mechanism. Many studies focus on central sensitization. […] The purpose of this paper is to systematically search the empirical studies and components of MPS in an effort to assemble them into a suggested organic mechanism, explaining its pathophysiology and how it may evolve into fibromyalgia. […] MPS can be seen as a pathological state of imbalance in a natural process; manifesting from the inherent properties of the fascia, triggered by a disrupted biomechanical interplay. MPS might evolve into fibromyalgia through deranged myofibroblasts in connective tissue (fascial armoring).
- #80https://www.leagravetherapy.co.uk/post-title2
An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. […] A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. […] The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive. […] Localized areas containing „contraction knots” are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension.
- #81https://www.leagravetherapy.co.uk/post-title2
An MTrP is a common physical finding and often overlooked of non-articular musculoskeletal pain as its pathophysiology (explanation) is not fully understood. […] A more widely accepted hypothesis is that trigger points develop because some initiating event causes an excessive release of acetylocholine (ACh) from the motor endplates resulting in increased fiber tension and localized ischemia. […] The localized ischemia restricts the blood flow and insufficient ATP synthesis which is needed to restore energy. The increased demand and reduced supply of ATP forms the energy crisis and encourages the release of neuroreactive substances and metabolic byproducts (i.e., bradykinin (BK), substance P (SP), serotonin (5-HT)) which causes the peripheral nociceptors to become sensitive. […] Localized areas containing „contraction knots” are believed to release sensitizing agents and additional acetylcholine (ACh) that cycles back to cause increased fiber tension.
- #82 Myofascial Trigger Points: Understanding, Diagnosis, Management and Treatment. Pelvic pain symptoms. | Actual Gynecology And Obstetricshttps://www.actualgyn.com/en/article/2024/296
It describes an excessive release of ACh in the synaptic cleft, triggering high-frequency miniature endplate potentials and thus permanent depolarization. […] The main reasons for persistent contractures and nociceptor activity are local hypoxia and ischaemia. […] The contraction of knots leads to the compression of vascular capillaries, resulting in local ischaemia. […] Both ischaemia-induced energy deficiency and increased energy consumption for Ca-pump activation necessary for actin-myosin separation can contribute to developing a local energy crisis. […] Increased levels of sensitizing substances are found near trigger points. […] Individuals who engage in minimal physical activity daily but experience occasional intense physical exertion are likelier to have trigger points. […] The self-healing capability of affected muscles is minimal. […] The process often requires repeated approaches to prevent redirection and transformation in the spinal cord.
- #83 Myofascial Trigger Points: Understanding, Diagnosis, Management and Treatment. Pelvic pain symptoms. | Actual Gynecology And Obstetricshttps://www.actualgyn.com/en/article/2024/296
It describes an excessive release of ACh in the synaptic cleft, triggering high-frequency miniature endplate potentials and thus permanent depolarization. […] The main reasons for persistent contractures and nociceptor activity are local hypoxia and ischaemia. […] The contraction of knots leads to the compression of vascular capillaries, resulting in local ischaemia. […] Both ischaemia-induced energy deficiency and increased energy consumption for Ca-pump activation necessary for actin-myosin separation can contribute to developing a local energy crisis. […] Increased levels of sensitizing substances are found near trigger points. […] Individuals who engage in minimal physical activity daily but experience occasional intense physical exertion are likelier to have trigger points. […] The self-healing capability of affected muscles is minimal. […] The process often requires repeated approaches to prevent redirection and transformation in the spinal cord.
- #84https://grantome.com/grant/NIH/R01-AR057348-01A1
Chronic soft-tissue (or myofascial) pain is a significant public health problem. Despite its high prevalence, the underlying mechanisms are poorly understood. In particular, very little is known about the pathophysiology and soft tissue environment of a myofascial trigger point (MTrP). MTrPs are palpable, localized painful nodules in a taut band of skeletal muscle that are a characteristic finding in myofascial pain syndrome (MPS). […] Our working hypothesis is that MTrPs are sites of muscle injury where local biochemical changes lead to sustained muscle contracture, compression of blood vessels and a local energy crisis that causes tissue hypoxia. This condition perpetuates the release of inflammatory cytokines and nociceptive (pain-inducing) substances. […] Demonstrating which tissues are involved (e.g., muscle, fascia, vessels), and which biochemicals are abnormal in MTrPs, will help develop appropriate preventive and therapeutic strategies, establish diagnostic criteria and potential outcome measures that can be used in treatment trials.
- #85 Expert consensus on the diagnosis and treatment of myofascial pain syndromehttps://www.wjgnet.com/2307-8960/full/v9/i9/2077.htm
The consistent muscle contraction in turn increases local energy consumption and local ischemia. The changes may induce pain or pain hypersensitivity by enhancing the local release of nociceptive substances, including substance P, calcitonin gene-related peptide and proinflammatory cytokines. […] The central pain sensitization can increase the excitability of neurons and the expansion of the neuronal receptive fields causing refractory referred pain. […] Alternatively, Stecco et al suggested that muscular fascia, a form of connective tissue, may undergo pathological change under overload and damage leading to the biomechanical change of muscles and eventually to the reduction of contraction force and flexibility of muscles. […] The inflammatory changes mentioned above may exacerbate the pathological change, leading to pain or enhancing pain. The pathological change of muscular fascia may be related to the abnormal changes in myofibrils, fibroblasts and extracellular matrix.
- #86 Myofascial pain syndrome and sensitizationhttps://oatext.com/Myofascial-pain-syndrome-and-sensitization.php
The mechanism consists of the nociceptive stimuli generated in the sensitized areas bombarding the dorsal horn of the spinal cord. This causes central nervous system sensitization with resultant hyperalgesia of the dermatome and sclerotome and spreads from the sensory component of the spinal segment to the anterior horn cells, which control the myotome within the territory of the SSS. The development or amplified activity of MTrPs is one of the clinical manifestations of SSS. […] Myofascial pain syndrome induced profound altering neuronal excitability and architecture in structures of the pain matrix structures as the spinal cord, thalamic nuclei, cortical areas, amygdala and periaqueductal gray area. This dynamic process can alter pain threshold, pain intensity and emotional affect. […] A continuous noxious input into the dorsal horn called afferent bombardment results in the co-release of L-glutamate and substance P (SP). The releasing of these two substances can lower thresholds for synaptic activation and open previously ineffective synaptic connections in wide dynamic range (WDR) neurons, leading to central sensitization.
- #87 Expert consensus on the diagnosis and treatment of myofascial pain syndromehttps://www.wjgnet.com/2307-8960/full/v9/i9/2077.htm
The consistent muscle contraction in turn increases local energy consumption and local ischemia. The changes may induce pain or pain hypersensitivity by enhancing the local release of nociceptive substances, including substance P, calcitonin gene-related peptide and proinflammatory cytokines. […] The central pain sensitization can increase the excitability of neurons and the expansion of the neuronal receptive fields causing refractory referred pain. […] Alternatively, Stecco et al suggested that muscular fascia, a form of connective tissue, may undergo pathological change under overload and damage leading to the biomechanical change of muscles and eventually to the reduction of contraction force and flexibility of muscles. […] The inflammatory changes mentioned above may exacerbate the pathological change, leading to pain or enhancing pain. The pathological change of muscular fascia may be related to the abnormal changes in myofibrils, fibroblasts and extracellular matrix.
- #88 Myofascial pain syndrome and sensitizationhttps://www.oatext.com/Myofascial-pain-syndrome-and-sensitization.php
However, if pain relief is only partial or pain persists despite several treatments using such various modalities, then needling and injection techniques should be considered, particularly in chronic cases in which the physical examination reveals severe and persistent allodynia and hyperalgesia, suggesting dense dermatomal, myotome and sclerotome manifestations of SSS. […] MPS, a common pain syndrome consists of local pathology and SSS. Hence therapeutic approaches require varieties of techniques for eradiation of trigger point and desensitization of the whole related spinal segment.