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Australische Manipulative Physiotherapie

Eine Klinische, Neurophysiologische und Biomechanische Richtung in der Dosierung der Behandlung von Wirbelsaeule - Schulter Dysfunktion.

Martin Krause 1996

Einfuehrung

Schulter Dysfunktion kann verschiedene Urspruenge haben. Biomechanische Urspruenge der Dysfunktion deuten eine Instabilitaet an. Oefters wird der Subscapularis Muskel als Hauptfaktor in der Rehabilitation ange deutet. Nicht nur helfen solche einfachen Behandlungen nur wenigen Patienten, sondern es kann auch ein stoerender Faktor in dem Gedankenprozess des Therapeuten sein. Klinische Behandlungen und Neurophysiologische Erklaerungen von Schulter Dysfunktion gebrauchen vielfaeltige Dimensionen von Schmerz, Entzuendungsprozessen, und Kontrolle der Motorik um umfassende Erklaerungen zu bringen. Leider koennen solche vielfaeltigen Gedankensprozesse auch als Stoerfaktor wirken wenn die Organisationsstruktur des Wissens des Therapeuten nicht klar ist. Dieser Artikel wird von den organisierten Konzepten Geoffery Maitland's (1991) (Abb 1) und vom 'Klinisches Denken' (clinical reasoning) (Abb 2)  ausgehen um die Bedeutung der  Biomechanik (Abb 2-4) und Neurophysiologie (Abb.5) in dem Krankheitsbild zu erklaeren.

 

German1

Abb 1 : Klinisches Denken und Kognitive Strukturierung des Maitlands Konzept

Neurogenische und Biomekanische Stabilitaet

Im Gegensatz zur Huefte kann die Schulter wenig Stabilitaet von den Ligumentaeren und vonder Knochenorientierung bekommen (Paavolainen et al 1984; Sarrafian 1983). Statt- dessen hat man postuliert dass es die Koordination der Muskulatur und des Bandapparates ist dass diese Stabilitaet erzeugt. Risse der Manschettenmuskulatur der Schulter hat man in drei kinematischen Dysfunktionen unterteilt. In dieser Unterteilung sind

'Stable Fulcrum Kinematics' verbunden mit Rissen des Supraspinatus Muskels (und Teile des Infraspinatus),

'Unstable Fulcrum Kinematics' verbunden mit grossen Rissen der oberen und hinteren Manschettenmuskulatur.

'Captured Fulkrum Kinematics' ist mit grossen Rissen der hinteren and voderen Manschettenmuskulatur verbunden und wirkt sich wie ein 'awning effect' unter den Akromion aus (Burkhart 1992).

Diese Studie deutet an dass wenn irgend ein Teil der Manschetten gerissen ist, dass es dann mindestens zu einem Schmerzhaftsbogen waehrend der Abduktion fuehren kann.  Zum beispiel, kontraktion des Delta's erzeugt eine vertikale 'Shaerkraft' ohne Depression und Kompression der Manschettenmuskulatur (Baleman 1977). Es ist wahrscheinlich, dass wenn ein Komponent der Manschettenmuskulatur 'kompromiert' ist, dass dieses eine Auswirkung auf die restliche Manschettenmuskulatur, welches dass sich dann in 'Shaer' und Kompression der Blutgefaesse auswirkt, was zu einem Sauerstoffmangel fuehren kann (Poppen et al 1976; Post et al 1983).

Ein Schmerzhaftsbogen ist auch impliziert worden mit

' Verkuerzung der hinteren Kapsul und Schwaeche der Aussenrotatoren des Glenohumeralengelenkes

'Schwaeche der Innenrotatoren mit excessiver Aussenrotation des Glenohumeralengelenkes (Warner et al 1990).

Auch die lange Bicepsehne ist ein Teil der voderen Manschette und sollte in der Annamnesse betrachtet werden.

Fuer Abduktion braucht man unter anderem Aussenrotation des Humerus unterhalb des Akromions (Cailliet 1980; Sarrafian 1983; Schenkman und de Cartaya 1987). Weiterhin braucht man Rotation des Skapulas um eine effiziente Kontraktion ('line of pull') der Manschetten und Deltamuskulatur gewaehrleisten zu koennen (sehe Abb. 2) (Cailliet 1977). Ausserhalb der Klavikulabaender wird die Schulter von Muskeln des Skapulas 'aufgehaengt' (Baleman 1977) (sehe Abb.3). Die oberen Teile des Trapezius ziehen den Skapula hoch und nach innen um die Axen des Sternoklavikular und Akromioklavikulargelenkes (Cailliet 1980). Die mittleren Teile des Trapezius stabilisieren den Skapula und den unteren Teile ziehen den medialen Rand des Skapulas nach unten und dadurch erzeugen sie eine Rotation des Glenoideus nach oben. Durch diese Abduktion wechselt der Rotationsaxe von dem Glenohumeralengelenk, zum Sternoklavikularen- und Akromioklavikularengelenk. Um diese Stabilitaetsanderungen zu optimisieren braucht man auch die Kokontraktion des Serratus Anteriors, eine ekzentrische Kontraktion der Levator Skapulae, Rhomboidein, Pectoralis Minor, und Teres Major Muskulatur. Auch der Korakobrachialas und die Kurze-Biceps Muskel spielen eine Rolle waehrend der Abduktion. Dies bedeutet, dass die Muskulatur nicht als Agonist-Antagonist betrachtet werden sollte, sondern als eine koordinierte Mannschette (sehe Abb.2) (Kugler et al 1980; Schenkman et al 1987; Turvey et al 1978a, 1978b; 1981).

Abb. 2 : Koordinierte Synergistische Stabilitaet durch Kontraktion des Schulterblatts und der Schultermuskulatur

Abb. 3: Dynamische Stabilitaet des Schulterblatts

Abb. 4 : Unkoordinierte Schulterblatt Synergie

Auch das Zwerchfel ist von Bedeutung zur Schulter Problemen wobei die Luft im unteren Lungenbereich die Schulterblaettern hebt.

Objekt-Orientierte Kontrolle der Muskulatur

Eine Hypotese dieser koordinierten Stabilitaet ist, dass das Nervensystem wie ein 'Federungssystem' wirkt wo dynamische Stabilitaet durch 'Periodische Oscillierung' der gesamten elektrischen Aktivitaet der sensorisch-motorischen Neuronen darstellt (siehe Abb.5) (Kugler et al 1980; Segundo et al 1995; Jefferys et al 1996). Dies bedeutet, dass die Ausgangsphase jeder Bewegung der Schulter kritisch ist und dass diese in der funktionellen Behandlung von Schulterschmerzen betrachtet werden sollte. Was sich unterscheidet zwischen Bewegungen  ist die Bedeutung dieser Bewegung zu der Funktion die erreicht werden moechte (Bernstein 1967; Glencross 1980; Kelso et al 1983; Turvey et al 1978; Reed 1982; Whiting 1980). Es ist wichtig zu verstehen, dass in diesem Konzept die Parameter 'Steifheit' und 'Grundlaenge' mit der gesamten elektrischen Aktivitaet im Nervensystem zusammen haengen (Kelso 1982).

Abb. 5 : 'Federungssytem' fuer dynamische Stabilitaet des Nervensystems.

sehe : www.bodyblade.com

Klinisches Denken : Afferente-Efferente Imbalanz wegen Schmerzen und Entzuendungen

Die Bedeutung eines Kommandos von hoeheren Zentren des Nervensystems wird vom Grundstatus der elektrischen Aktivitaet in den Rueckenmarkneuronen beeinflusst. Der Grundstatus der elektrischen Aktivitaet wird von Afferenz und Efferenz gesteuert. Diese Afferenz kann durch Schmerzen erhoeht sein. Eine Reaktion einer erhoehten Afferenz resultiert in einer erhoehte Efferenz was eine erhoehte Spannung in der Muskulatur erzeugen kann (Gracely et al 1983; Woolf et al 1994; Woolf & Swett 1984). Das Maitland Konzept gebraucht Schmerz als Mittelpunkt der Behandlung von muskuloskeletischen Dysfunktionen (Abb.6). Um dieses Konzept zu verstehen sollte man 'klinisches Denken' und die Neurophysilogie der Biomechanik und der Schmerz in Betracht ziehen.  Da der Organismus ueber das Nervensystem seine Existenz steuert, die richtigen Fragen stellen und Erklaerungen geben, koennten den Patienten seinen Kognitive Prozesse so steuern um die Optimale Erhohlung zu erreichen.

Abb 6: Klinisches Demken

Moderne medizinische und paramedizinische Behandlung hat versucht die Krankheiten in Griff zu bekommen durch Diagnostizieren verschiedener Pathologien mit Benennungen wie z.B. Periarticulare Artrose, Omoartrose, usw. (Cohen & Quintner 1993; Quintner & Cohen 1994; Cohen 1995)

Fuer die Verbesserung der Geschicklichkeit der klinischen Begruendung koennte es fuer den Therapeuten wichtig sein die Pathophysiologie (die der Phenomenologie zugrunde liegt) besser zu verstehen.

Entzuendung

Die Reaktion des Gewebes nach einer Verletzung nennt man Entzuendung. Eine Entzuendung schliesst eine Serie von Vorgaengen in den Zellen (Enwemeka & Spielholz 1992; Schmidt et al 1994; Tillman & Cummings 1992). Eine Entzuendung kann der Grund fuer ein Oedem sein das als ?Irritant? auf Nervenrezeptoren, Nerven und deren Blutgefaesse wirken kann (Holthusen & Arndt 1996). Dieses kann Auswirkungen haben wo

  • die Leitgeschwindichkeit der Nerven vermindert werden kann.
  • erhoehte elektrische Aktivitaet der Nervenrezeptoren zu einer neurochemischen Reaktion im Rueckenmark fuehren kann.

Weiterhin das heisst, dass Nerven mit gleicher Innervation wie das verletzte Gewebe entweder verminderte oder erhoehte motorische Aktivitaet haben koennte. Wenn es zu einer Verletzung der Wirbelsaeulestruktur kommt, dann koennte es zu einer Verspannung oder Entspannung von Muskeltonus in der Peripherie kommen wobei eine Instabilitaet und Bewegungsdysfunktion entsteht (z.B. Schmerzhaftsbogen). Ein Grund fuer verminderte Leitgeschwindichkeit kann durch einer Nervenkompromierung eines Oedems oder durch veraenderte neuronale Prozesse im Rueckenmark entstehen. Eine Kompromierung der Nerven kann nicht nur in der Wirbelsaeule entstehen (Abb.7), sondern auch in der Peripherie; z.B. koennte der Nervus Radialis zwischen Teres Major und Teres Minor kompromiert werden, der Nervus Supraskapularis kann im Fossa Supraskapularis kompromiert werden, das Plexus Brachialis kann unterhalb des Prozesus Korakoideus und des Pectoralis Minors kompromiert werden. Kompromierung unterschiedlicher Nerven koennte das 'Federungssytem' und somit die mechanische Stabilitaet des Glenohumeralengelenkes vermindern.

Abb.7: Somatischer - Neurogenischer Innervations Bereiche

Klinische Begruendung einer solchen Hipotese entstehte wenn durch korrelation subjektiver und objektiver Untersuchungen ein Zusammenhang zwischen Wirbelsaule und Schulter gezeigt werden kann (Abb 1). Durch Behandlung der betroffenen Struktur sollte man eine Normalisierung der Anzeichen und Symptome zeigen koennen. Die Erwartung einer Behandlungsmethode sollte dann 'dem Stadium'(stage), 'der (Klinische und Neurophysiologischen [K&N]) Stabilitaet' (stability), 'der Heftigkeit' (severity) und 'der Reizbarkeit' (irritability) der Dysfunktion entsprechen (Maitland 1991) (Abb 8). Oefters kann man erwarten, dass z.B. neurologische Veraenderungen sich gleichzeitig normalisieren wenn eine Behandlungsmethode angewendet wird. Man kann auch eine Veaenderung des Schmerzhaftsbogen erwarten, wenn die richtige Behandlungsmethode fuer 'das Stadium'(stage), 'die (K&N) Stabilitaet'(stability), 'die Heftigkeit'(severity) und 'die Reizbahrkeit'(irritability) der Dysfunktion angewendet wird. Im Gegensatz kann man auch einer Verschlechterung der Anzeichen und Symptome erwarten wenn die Behandlungsmethode nicht dem klinischen Krankheitsbild entspricht. Das heisst auch, dass nicht nur die Behandlungsmethode genau sein muss sondern dass auch die Dosierung genau sein muss. Dosierung kann man mit Kraft, Richtung, Wiederholungen, Amplitude und Frequenz unterzeichnen : je mehr je hoeher die Dosierung. Man muss sich auch im Klaren sein, ob man das verletzte Gewebe mit erhoehtem mechanischem Reiz behandlen sollte oder ob man den mechanischen Reiz vermindern sollte; z.B. bei konstanten Schmerzen, grosser 'Heftigkeit' oder bei neurologischem Defizit in einem klinschen Bild einer Radikulopathie moechte man eher den mechanischen Reiz vermindern (Abb.9). Im Gegensatz, bei einem intermittierender Schmerz, kleiner 'Heftigkeit' moechte man eher den Schmerz provozieren um die Schwelle der Mechanorezeptoren zu erhoehen oder um die Modulierung der elektrischen Aktivitaet im Rueckenmark zu verbessern (Abb 10). Im diesem Konzept braucht eine minimale Dosierung um das Maximale verbesserung zu bekommen.

Abb. 8: Wichtige Aspekte des Klinisches Denkens

Click on pic to view enlarged image

 

Abb. 9: Verminderte Aktivierungsschwelle von Nervenrezptoren

 

Abb. 10: Kortikale Elektrische Einflusse

Neurophysiologische Modulierung von Schmerzen und Entzuendungen

Neurophysiologische Erklaerung der Wirkung von Tape (Klebverband) (wie bei McConnell), Nervenmobilisationen von Butler (1991), Gelenkmobilisationen von Maitland (1986;1991); Aktiv-Passiv Mobilisationen '(Mobilisation with Movement [MWM])' von Mulligan; 'Muskelenergie' von Babara Hungerford; Stabilisationsuebungen von Jull und 'posturelle Integrierung' von Shirley Sahrman haben eine aehnlichen Erklaerung. Diese Erklaerung entspricht das, dann wenn ein Organismus ueberleben moechte wird es versuchen die elektrische Aktivitaet im Nervensystem zu verringern wo es nicht erwuenscht ist, und zu optimieren wo es erwuenscht ist. Das bedeutet, dass dann wenn eine Entzuendung entsteht das Nervensystem versuchen wird diese konsequente elektrische Aktivitaet der Entzuendung zu verringern durch

  • Modulierung der Entzuendung durch das peripherale, symapthische und somatische Nervensystem (Abb.11),
  • Modulierung der Nervenrezeptoren ueber das peripherale sympatische Nervensystem (SNS) (Abb.12),
  • Auto-Modulierung der Neuronen im Rueckenmark (Abb.13),
  • deszendierende Modulierung der Rueckenmarkneuronen (Abb.14),
  • deszendierende Modulierung des Schutzspasmus gewisser Muskulatur (Abb.14),
  • Modulierung der Gehirn- und Rueckenmarkneuronen ueber dem Locus Coeruleus (Abb.15).

Abb.11 : Modulierung der Entzuendung durch das peripherale, sympathische und somatische Nervensystem

 

Abb. 12 : Modulierung der Nervenrezeptoren ueber das peripherale sympatische Nervensystem (SNS)

(adaptiert von : Groenblad et al 1991, p617; Jaenig 1985; Lotz et al 1988; Handwerker et al 1991; Levine et al 1986; Taiwo & Levine 1989).

Abb. 13 : Auto-Modulierung der Neuronen im Rueckenmark (NS = Schmerzvermittelnd Neurone; WDR Breitbandvermittelnde Dynamische Neurone)

 

Abb. 14 : Deszendierende Modulierung des Muskelschutzspasmus

Abb.15 : Viele Kortikale Bereiche sind in das Modulierung des Schmerzens betaetigt (Hsieh, J-C., Stahle-Backdahl, M., Hagermark, O., Stone-Elander, S., Rosenquist, G., Ingvar, M., {1995}. Traumatic nociceptive pain activates the hypothalamus and the periaqueductal gray: a positron emission tomography study.)

Eine neurogenische Entzuendung ist der Vorgang wobei freigelassene Neuropeptide der somatischen C-Fasern und sympatischen C-Fasern vaskulaere Membranveraenderungen bewirken welche zum Durchsickern von Proteinen des Gefaessystems in die umgebenden Gewebe fuehren (Ahmed et al 1991; Blottner & Baumgartner 1994; Donnerer et al 1991; Heller et al 1994; Kobayashi et al 1993; LaMotte et al 1991; Levine et al 1986; Markowitz et al 1989; Suval et al 1987; Zochodne 1993). Wenn die Entzuendung mechanischen Ursprung ist, dann erhoehen C-Fasern Rezeptoren ihre neurogenische Entzuendungsreaktion und erhoehen somit ihre Entladungsfrequenz mit Stimulation der sympatischen Nerventerminale (Levine et al 1986). Empfindlichkeitsfaehigkeit der peripheralen Nervenenden durch neurogenische und nicht-neurogenische Entzuendung koennte die Mechanorezeptorenschwelle verringern und dabei zum Schmerz leiten (siehe Abb.9).

Eine Reaktion auf Schmerzen ist eine erhoehte elektrische Aktivitaet in der Muskulatur die man im Tierexperiment auf den Versuch des Organismus zur Entlastung der elektrischen Aktivitaet der Mechanorezeptoren und Rueckenmarkneuronen zurueckfuehren kann (Abb.14) (Ferrell et al 1988; Woolf 1983; Woolf 1984; Woolf & McMahon 1985; Woolf & Wall 1986; Woolf et al 1994). Klinischer Beweis fuer Schutzspasmus kommt von Versuchen in Patienten mit cervikaler Radikulopathie wobei die Untersuchung eine erhoehte elektrische Aktivitaet in der innervierten Muskulatur gezeigt hat (Hall & Quintner 1996). Weiterhin wurde verminderte Beweglichkeit des Nervus Radialis im Epicondylitis des Ellenbogens auf Schmerzen und neurophysiologische Veraenderungen im Rueckenmark zurueckgefuehrt (Vicenzino, Collins, Wright 1996). Es ist wichtig zu wissen, dass man demonstrieren konnte, dass Manipulative Physiotherapie* der HWS diese Schmerzen im Ellenbogen vermindern konnte mit einer konsequenten Vermehrung der Beweglichkeit des Nervus Radialis (Vicenzino et al 1996).

- Manipulative Physiotherapie : das ganze Konzept der Manuellen Therapie gelehrt in Australien und nicht unbedingt eine Manipulation (Mobilisation mit Impulsen).

Extrapolation dieser Daten wuerde andeuten dass es Schutzspasmus verschiedenen Grades und in verschiedenen Gebieten gibt. Weil die Muskultur der Schulter und des Schulterblatt verschiedene Nerveninnervationen haben, ist es moeglich dass eine Dysfunktion der Wirbelsaulenstruktur zu einer Inkoordination von Schulter-Schulterblatt Muskulatur fuehren koennte (Abb.4). Eine Folge einer solchen Incoordination waere zu mindestens ein Schmerzhaftsbogen. Weiterhin, irgendeine konsequente Entzuendung der Schulterstrukturen koennte die Modulation der elektrischen Aktivitaet im Rueckenmark vermindern durch die (trophische) Einfluesse des innervierten Gewebes auf die Neuronen (Blottner & Baumgartner 1994). Dadurch koennte eine Hexenkreis zwischen Wirbelsaule und Schulter entstehen wobei beide Gebiete behandelt werden muessen.

Neurophysiologischer Beweis der Modulierung der entzuendeten Mechanorezeptoren und folglichem Heilungsprozess kommt von Studien des peripheralen sympatischen Nervensystems (Abb.11 und Abb.12). Die sympatischen postganglionischen Nerven entladen Entzuendungsvermittler, die die Plasmaextravasation, einschliesslich der Prostaglandine, erhoeht (Coderre et al 1989; Gonzales et al 1989; 1991; Green et al 1991). Ausserdem hat man gefunden, dass im Anwesen sympatischer postganglionischer neuronaler Modulierung, Plasmaextravasation durch Bradykinin erhoeht wurde (Green et al 1992). Die sympatischen, postganglionischen Neuronen geben auch Vermittler ab, die Plasmaextravasation verringern (Green et al 1991;1992). Ausser der Modulierung der Plasmaextravasation koennen diese Substanzen auch mit dem endothelialen Entspannungsfaktor (Greenberg et al 1991) und dem Blutplaettchenaktivierungsfaktor (Heller et al 1994) in den Blutgefaessen aufeinander einwirken. Der Mechanismus, wobei die symaptischen Nervenenden die Gewebeverletzung verringen, ist nicht geklaert. Es kann jedoch eine erhoehte Plasmaextravastion erwartet werden, wenn die Konzentration der Entzuendungssubstanzen durch die Facilitierung Lymph- und Venendraenage bewirkt wurde. Dadurch wird dann die Heilung beschleunigt (Heller et al 1994). Untersuchungen deuten an, das der Oedem dieses Entzuendungsprozesses nur im Zusammenhang mit Schmerzen entstehen kann (Holthusen & Arndt 1996). Wie beim Maitland Konzept ist eine Verringern der Schmerzen mit einer Resolution der Dysfunktion verbunden. Es ist wichtig zu verstehen dass bei intermittierenden (nicht-reizbaren) Schmerzen die Reproduzierung der Symptome manchmal wichtig ist um die Heilungsprozesse und die Normalisierung von Anzeichen und Symptomen zu beschleunigen (Maitland 1991).

Auto-Modulation elektrischer Aktivitaet der Rueckenmarkneuronen kann durch ein Oedem verringert werden (Abb.13). Eine Entzuendung kann der Grund fuer ein Oedem und Wirbel-Schulter Schmerzen sein (Barker et al 1991; Gallin et al 1992; Groenblad et al 1991; 1994b; Kawakami et al 1994a; 1994b; McKenzie & Saunder 1990; Rothwell & Hopkins 1995; Rydevik et al 1989; Williams & Hellewell 1992). Waehrend sich das Oedem vergroessert, koennen Kompression der intraneuralen Blutgefaesse und Nervengewebe vorzugsweise die Leitungsgeschwindigkeit der myelinischen Empfindungsnerven und der motorischen Nerven verringern und dabei wahrscheinlich die Leitungsgeschwindigkeit entlang der nicht-myelinischen Nervengewebe groesstenteils unbeeinflusst lassen (Cornefjord et al 1992; Kobayashi et al 1993; Matsui et al 1992; Olmarker et al 1989; Rydevik et al 1984; Takahashi et al 1993). Die verringerte Leitung entlang myelinischen Nervengewebe mit grossem Durchmesser entspricht einer konsequent verringerten Auto-Modulation der schmerzleitenden Neuronen im Rueckenmark (Dickenson & Sullivan 1987; Ochoa & Yarnitsky 1993; Price et al 1994). Als Resultat der Entzuendung ist zusaetzlich eine erhoehte elektrische Aktivitaet in den nicht-myelinischen Nerven zu erwarten. (Bennet & Xie 1988; Dubner 1991; Sugimoto et al 1990). Durch dosierte Manipulative Therapie wie z.B. Traktion, Rotation, Taping, oder spezifische Uebungen ist es moeglich die Leitgeschwindigkeit zu verbessern. Dieser wird bewirkt durch

  • verbesserte Durchblutung (Selander, et al 1985).
  • vermindertem Schutzspasmus (Abb.14)
  • vermindertem Reiz auf Mechanorezeptoren
  • verbesserte postganglionische, sympathische Modulierung der Mechanorezeptoren (Abb.11 und Abb.12)
  • verbesserte postganglionische, sympathische Modulierung der Irrigation/Durchblutung

Leitung elektrischer Aktivitaet der Rueckenmarkneuronen als Folge eines Schmerzes kann auch von hoeheren Zentren stammen. Das zentrale, sympatische Nervensystem und spezifisch das Periaqueductale Grau spielt wahrsheinlich eine Rolle in Deszendierender Modulation der Schmerzleitung . Mindestens zwei moegliche Arten deszendierender Neuromodulation koennten angewendet werden (Bandler & Shipley 1994). Beide Arten deszendierender Modulation betrifft pontile, noradrenergische Projektion auf ventrale, dorsale und intermediolaterale (IML) Rueckenmarkneuronen (Proudfit 1992; Jaenig 1985; Morgan et al 1989; Nakagawa et al 1990; Post et al 1986; Ren et al 1990) Deszendierende Modulation wird als opiat- un abhaengige Analgesieart angegeben (Proudfit 1992) aber es gibt auch einen Beweis der die Meinung bestaetigt, dass m -opiat und a -2 noradrenalin Rezeptoren funktionell mit Schmerzmodulation verbunden sind (Kalso et al 1993). Die andere Art deszendierender Modulation wird als opiat-abhaengig angesehen (Bandler & Shipley 1994). Man glaubt, dass das noradrenalin System willkuehrlich motorische Aktivitaet vermehrt, wobei das opiat-abhaengige System Entspannung bewirkt (Bandler & Shipley 1994; Lovick 1991).

Klinische Untersuchungen haben beide diese Systeme als Grund gefunden fuer die Schnelle und andauernde Wirkung spezifischer Manipulativer Physiotherapie auf die Halswirbelsaeule (Wright & Vicenzino 1995). Eine Ueberpruefung der Akupunkturliteratur weisst darauf hin, dass der anfaengliche sympathoexcitatorische Effekt innerhalb 15 Sekunden von einer Sympathohemmung 20-45 Minuten spaeter gefolgt wird (Wright & Vicenzino 1995). Dieser Effekt konnte fuer 2 bis 40 Stunden andauern. Diese Anfangsergebnisse sind deshalb interessant weil es sehr wenige aufschlussreiche Studien gibt, die die neurophysiologischen und analgesischen Effekte der Manipulativen Physiotherapie untersuchen.

Abb. 16: Somatosensorische, Motorische und Limbische Bereiche werden bei der Untersuchung und Behandlung und Weideruntersuchung einbezogen

Ausser den obengenannten deszendierenden Systemen der Schmerzmodulation werden noch andere Quellen in Betracht gezogen die von sensorimotorkortikalen Regionen stammen und mit Eingabe auf Rueckenmark- und den Hirnstammregionen zu tun haben (Wall 1995). Wall (1995) beschreibt dieses System als eine 'sensible Haltung' wobei Motoreingabe (Efferenz) eine starke Kontrolle ueber Sensorische (Afferente) Rueckenmarkvorgaenge ausuebt 'die sich mehr auf Aktion als auf Perzeption konzentriert'(p35; Galea & Darian-Smith 1995). Wall (1995) gebraucht Positive Emissions Tomograghie (PET) in Studien in Pateienten mit chronischen Schmerzen fuer den Beweis seiner Theorie, wohingegen Galea & Darian-Smith (1995) PET und anatomische Sektion von Primaten angewendet haben. Weiterer Beweis fuer deszendierende Modulation kommt von Gogas et al (1991) die fanden, dass supraspinale Opiate die Schmerzempfindung durch eine 64% Reduktion in oberflaechlicher Lamina-Hinterhornaktivitaet blockierten (gewoehnlich verbunden mit einer Ueberwiegenheit schmerzvermittelnder spezifischer Neuronen (NS) (Lima et al 1994)) und eine 85% Reduktion in Voderhornaktivitaet (gewoehnlich in Zusammenhang mit Motoraktivitaet) (Abb.14 und Abb.15) (Schomburg & Steffens 1991). Untersuchungen bestaetigten das Ergebnis, dass hoehere Zentren in einer anti-Schmerz vermittelnder Weise wirken koennen wo eine Ueberwiegenheit an Hemmung bei den NS Neuronen auftritt, wo aber Anregung und Hemmung mit gleicher Frequenz bei Breitenband Dynamischen Neuronen (WDR) auftritt (Sandkuehler et al 1995). Dies scheint eine besondere Denkweise zu sein wobei der kortikale Einfluss primaer zu einem sekuendaer ansteigenden schmerzvermittelenden Reiz ist. Es wird vorgeschlagen, dass das Nervensystem sehr spezifisch diskriminiert und dadurch auch die subjektive und physikalische Untersuchung, sowie die Dosierung der Behandlung sehr spezifisch sein muss fuer das 'Stadium', 'die (K&N) Stabilitaet', 'die Heftigkeit' und 'die Reizbarkeit' der Dysfunktion um die beste Normalisierung von Anzeichen und Symptomen zu erreichen (Abb.17).

Abb.17 : Korrelation zwischen Neurophysiologie (Theorie) und Klinischem Denken

Auch die subjektive und physikalische Untersuchung kann ein wichtiger Teil der neurophysiologischen Modulierung der Schmerzen sein. Der Locus Coeruleus (LC) ist auch der Grund fuer Analgesia in Tieren und wahrscheinlich auch in Menschen (Fillenz 1990). Den LC hat man in der Modulierung von neuronaler Aktivitaet nicht nur im Rueckenmark sondern auch im kortikalem Bereich gefunden (Jefferys et al 1996; Fillenz 1991). Das LC braucht visuelle, akustische, und proprioceptorische Information um die Bedeutung der Stimulation der Behandlung und Untersuchung zu bewerten. Das bedeutet, dass eine Hypothese gemacht werden kann wobei eine Bewertung der Funktionsstoerungen und Behandlung LC's wird entscheiden wo es eine Dysfunktion gibt und ob die Behandlung diese elektrische Stoerung wieder normalisieren kann. Nicht nur der Therapeut/in muss wissen ob eine Bewegungsstoerung vorliegt, sondern der Patient muss es auch wissen (Abb. 18). Weiter muesste sowohl der Therapeut/in als auch der Patient eine klare Vorstellung haben wo die Ziele der Behandlung liegen. Es ist nicht genug zu glauben, dass die Schulterschmerzen von der Wirbelsaule kommen, oder dass Wirbelsaeulenschmerzen von der Schulter kommen, sondern man muss es auch zeigen koennen waehrend der Annamnese und waehrend der Behandlung. Wenn man genau weiss wo die Ziele liegen dann wird man auch wissen wann eine Behandlung wegen mangelder Fortschritte geaendert werden muss. Glauben ist nicht Wissen.

 

Abb. 18:  Deszendierende Modulation ueber den Thalamus und Hirnstamm

 

Durch eine Bewertung des 'Stadiums' und 'der Reizbarkeit' (Maitland 1991) der Dysfunktion sollte man feststellen koennen wie weit man mit der physikalische Untersuchung gehen moechte. Als Folge dieser beiden Untersuchungen kann man versuchen die genaue Dosierung der Behandlung der Dysfunktion anzupassen (Maitland 1991). Somit ist das Risiko verringert, dass sich die Symptome des Patienten durch die Behandlung verschlechtern. Faktoren die man in der Dosierung von Uebungen und Mobilisation in Betracht ziehen sollte sind :

  • Konstant oder Intermittierend
  • Belasten oder Entlasten
  • Frequenz der Wiederholungen
  • Wie viele Wiederholungen
  • Dauer der Wiederholungen
  • Kraftanwendung
  • Kombinierte Bewegungen zum Belasten oder Entlasten
  • Richtung der Anwendung
  • Eine oder mehrere Strukturen belasten

Als facet; wenn bei einer Dysfunktion neurologische Veraendurungen in einer klaren radikularen Distribution vorliegen, und/oder wenn es in einem akuten oder verschlimmernten 'Stadium' ist, und/oder 'Reizbar' ist, dann gebraucht man eher Entlastungsmethoden die konstant (nicht-intermittierend) sind, mit wenig Kraft, wenigen Wiederhohlungen, wenig Dauer, kombinierte Bewegungen um zu Entlasten, tape (Klebverband) zum entlasten, Waerme/Kaelte und Elektroterapie. Wenn eine Dysfunktion im Heilungsstadium ist wobei es nicht 'Reizbar' ist, kann man die Dosierung vermehren um die Belastbahrkeit der Struktur bis zu 100% der zu erwarteten Resolution der Dysfunktion zu erhoehen. Man muss sich klar sein, ob man eine Struktur entlasten oder belasten moechte und die Antwort dieser Frage sollte im Zusammenhang mit Biomechanik, Neurophysiologie und klinischer Annamnese stehen.

Abb 19: Eventuel kann eine gute und fruehe Behandlung der "Sensitisierte Suppe" mechanischen allodynia und chronischer Schmerz vermeiden?

Sehe :  Uebungen in Klinisches Denken (Deutsch)

Lendenwirbel Dysfunktion und Klinisches Denken

Kursen fuer Deutschland

Geschrieben von Martin Krause hauptsaechtlich in 1996 und in 1986.

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Last update : 20 April 2008


 

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  • Sun 15 Oct 2017

    Neuroplasticity in Tendon Dysfunction

    Neuroplasticity in Tendinopathy by Martin Krause A multitude of contributing factors to altered motor control must be addressed when treating tendon dysfunction. What we have failed to consider in the past when dealing with chronic or recurrent tendon issues are motor control problems encompassing corticospinal control of excitation and inhibition as well as belief systems about pain and contextual factors related to imaging.  Research by Ebonie Rio et al (2015) (BJSM Sept 25, 10.1136/bjsports-2015-095215) suggest that the pain state sets up an adaptive pathway whereby the ipsilateral kinetic chain is directly inhibited by reflexogenic pathways, as well as being inhibited by contralateral hemispheric activity. Simultaneously excitation is enhanced in the opposite limb as well as in antagonists...at least in the case of enhanced excitation of the hamstrings in quadricep tendinopathy. If this is true, then so much for training the contralateral limb for 'cross training' purposes! This may also explain why a lot of people seem to have "all their injuries on the same side" (of the body). Furthermore, they recommend enhancing corticospinal drive through the use of 30-60 second isometric holds at 70-80% MVC to load the muscle whilst using isokinetics to load the tendon. Moreover, they recommend the use of a metronome at 60bpm (stages 1 and 2) with a count of 3 up, 2 down for quads, and 2 up, 3 down for calf isokinetics to optimally engage corticospinal drive through the visual and auditory stimuli (also shown by Kohei et al 2012 for motor imagery and M1 stimulation) .....read more Cortical mapping of infraspinatus muscle in chronic shoulder pain demonstrating higher motor thresholds (aMT= activation MT) and hence reduced excitability on the affected side (39 vs 35) (Ngomo et al 2015 Clinical Neurophysiol, 126, 2, 365-371) Cortical mapping of pain and fear. Lots of overlap suggesting that taking away the fear from the pain with clear clinical explanations and a focused goal directed program using specific functional outcomes is important.  Individuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)  Uploaded : 18 October 2017 Read More
  • Mon 09 Oct 2017

    Imaging

    Do I need a scan? "a picture tells a thousand words" - not really! by Martin Krause A scan, in it's self, will not improve anyone's condition. The purpose of a scan is to gain more information about the pathology. Sometimes this information may be irrelevant to the management of a patient's condition. For example, if you knocked your elbow on a door frame and suffered a bruise, which was already beginning to resolve, an ultrasound scan may show some minor soft tissue damage, but that was already obvious by the fact of the bruise, and the information gained from the scan has not helped nor changed the management of the bruise. Therefore, the main reason for getting a scan would be because there is concern that the presence of certain pathologies may lead to a change in the medical management. For example, sometimes a rolled ankle can be more than sprained ligaments, and may require surgey or immobilisation in a boot. If the therapists suspects this might be the case, then they will recommend or refer for a scan (probably an X-Ray) to check the integrity of the bones (especially the fibular and talar dome), because if there is no bony damage then the patient can be managed conservatively with taping, exercises, ultrasound, massage, joint mobilisations etc. However, if there is boney damage, for example, then it might be necessary for the ankle to be immobilised in a boot for three - six weeks, for example. This dramatically different medical management depends on the results of a scan, and it is therefore worth doing. However, scans have no predictive value to the presence or severity of pain. Thirty-three articles reporting imaging findings, in the low back, for 3110 asymptomatic individuals were investigated for pathology. The prevalence of disk degeneration in asymptomatic individuals increased from 37% of 20-year-old individuals to 96% of 80-year-old individuals. Disk bulge prevalence increased from 30% of those 20 years of age to 84% of those 80 years of age. Disk protrusion prevalence increased from 29% of those 20 years of age to 43% of those 80 years of age. The prevalence of annular fissure increased from 19% of those 20 years of age to 29% of those 80 years of age. (Brinjikji, W et al Spine Published November 27, 2014 as 10.3174/ajnr.A4173). Hence, the results of imaging need to be assessed within the context of the entire clinical picture. Frequently too much emphasis is placed on the imaging not only by the clinician but also by the patient. Some people react to pathology seen on scanning as an affirmation of their problem and can either use it to gain clarity and become better or conversely become worse. Moreover, some people find imaging with inconclusive results as a 'panic moment' - "no one knows what is wrong". Similarly, ultrasound imaging of the tendond has good predictive diagnostic and aids in clinical reasoning when it comes to full tears. However, with partial tears it is a totally different 'ball game'. Ultrasound is highly user dependent, with specifically trained musculoskeletal radiologists able to produce high-quality images that may provide more clinically relevant information than those produced by clinicians with less experience in imaging. Sean Docking, a leading tendon researcher at Monash University, cited 7 authors who found pathological tendon chnages in 59% of asymptomatic individuals, whereas he found that 52% of asymptomatic elite AFL sportsmen had tendon pathology on imaging! Furthermore, symptomatic individuals who improved clinically to the point of resuming play, weren't shown to have improvements on imaging. Again, the clinical context and the clinical reasoning can in many instances prove to be the 'gold standard' not the imaging itself, when considering management options. Shoulder supraspintatus tendon pathology, in the abscence of trauma, is known, in many instances, to be a disorder of immune-metabolic compromise of the tendon and bursa. Imaging may show some changes in signal intensity but, unless it's a complete tear, it can reveal neither the intensity nor the severity of pain when taken outside of the clinical context. A thorough physical and subjective examination integrating all the clinical dimensions of the problem will have far greater value than any one single imaging modality. Yet, imaging still should be used in instances of progressive rapid deterioration and suspected serious pathology which may require surgery and/or immediate medical intervention. In summary, sometimes it is worthwhile getting a scan, because the information gained from that scan will determined the type of medical management that is employed. However, at other times, the scan may be unneccessary, because the information may be irrelevant or lead to an incorrect change in medical management, due to over-reporting of 'false positives'. You will be able to make this decision on the advice of your health care professional. On occasions it can actually be detrimental to have a scan, because some patients can become overly obsessed with the medical terms used to describe their scan results, which then can become the major focus for the clinician and the patient, rather than the more prefereable focus on their symptoms and functional abilities. For example, many people have lumbar buldging discs yet have no symptoms, yet sometimes when these patients have an MRI or CT scan, they can develop symptoms because they think they should have pain if the scan says so! Conversely, for some people the results of imaging can have a positive and reassuring affect. Therefore, it is very important to assess a clients attitude to scans before prescibing them so that the patient's expectations are managed appropriately, and not burdened by the additional, sometimes confusing, information supplied by a scan. Uploaded : 10 October 2017 Read More
  • Thu 14 Sep 2017

    Cervical Spine implications in concussion

    Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS) by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia  A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer. Confounding Variables : end of season injury and hence no follow up from the academy suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9. suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues. had just gone through a growth spurt (190cm) Imaging : Brain MRI normal Medical Examination : Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range. History : School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.  Current History : September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.  Literature Review : Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"  Further complications of PCS also appear to be an increased risk of musculoskeletal injury Nordstrom et al (2014, BMJ Sports Med, 48, 19, http://bjsm.bmj.com/content/48/19/1447) Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154). Unlike the 'good old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill.  http://www.dysautonomiainternational.org/pdf/CHOP_Modified_Dallas_POTS_Exercise_Program.pdf Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain. Ongoing Symptoms : The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions. Physiotherapy Assessment : One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously. Physical Examination : cervical and thoracic spine Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. In particular, the right C1/2 regions demonstrated most marked restrictions in movement. Eye - Neck proprioceptive assessment using blind folds and laser pointer also  revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.  Occulomotor assessment and training Upper Cervical Spine : The upper cervical spine (atlas and axis) represents approximately 50% of the available rotation. An investigation into the environmental and physiological factors affecting football head impct biomechanics found that rotational acceleration was one of the few factors approaching significance and concluded that more research should be undertaken to evaluate this (Mihalik et al 2017 Med Sc Sp Ex, 49, 10, 2093-2101). Headache : Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed. Cervicogenic Headaches Further Interventions : Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet. Diet :  In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults. See Nutritional Section of this Site Conclusion  Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48,  12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.    Uploaded : 17 November 2017 Read More
  • Thu 24 Aug 2017

    Pain in the Brain - neural plasticity

    Pain in the Brain and Neural Plasticity by Martin Krause There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state.  Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.  further reading Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex. ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)   AKP = anterior knee pain The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation. Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'. Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include motor map topography reflecting the capacity for skilled movement reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483). Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement. Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb. However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.   Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state. One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together. Uploaded : 18 October 2017 Read More
  • Thu 03 Aug 2017

    Sickle Cell Trait and Acute Low Back Pain

    Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Acute_Lumbar_Paraspinal_Myonecrosis_in_Football.1.aspx Read More
  • Thu 03 Aug 2017

    Ibuprofen, Resistance Training, Bone Density

    Taking Ibuprofen immediately after resistance training has a deleterious effect on bone mineral content at the distal radius, whereas taking Ibuprofen or undertaking resistance training individually prevented bone mineral loss. http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Effects_of_Ibuprofen_and_Resistance_Training_on.2.aspx Read More
  • Tue 11 Jul 2017

    Mitochondrial Health and Sarcopenia

    The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living. Published 11 July 2017 Read More
  • Thu 22 Dec 2016

    Ehlers Danlos Syndrome

    Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help. Joint Hypermobility Syndrome (JHS) by Martin Krause When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations. Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping.  I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head).  What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid.  I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex).  Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters.  Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks.  After that, her discolcations improved a lot.  It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa" Surgery : The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.  Voluntary Posterior Shoulder Subluxation : Clinical Presentation A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups.  https://youtu.be/4rj-4TWogFU In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm Headaches Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613). People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary. An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site. Temperomandibular Joint (TMJ) Disorders The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors). Updated 17 October 2017  Read More
  • Fri 09 Dec 2016

    Physiotherapy with Sharna Hinchliff

    Physiotherapy with Sharna Hinchliff    Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017.  Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University. read more Read More

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Updated : 10 May 2014

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Copyright Martin Krause 1999 - material is presented as a free educational resource however all intellectual property rights should be acknowledged and respected