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GR (1998) The role of IGF-I in the regulation of skeletal muscle adaptation. In: Holloszy JR (Hrsg) Exercise and sport science reviews, Bd. 26. Williams & Wilkins, Baltimore, S 31–60\nAdamsGR, McCue SA (1998) Localized infusion of IGF-I results in skeletal muscle hypertrophy in rats. J Appl Physiol 84:1716–1722\nBaldwin KM, Haddad F (2002) Skeletal muscle plasticity: cellular and molecular responses tp altered physical activity paradigms. Am J Phys Med Rehabil 81:S40–S51\nBengtson CP, Dick O, Bading H (2008) A quantitative method to assess extrasynaptic NMDA receptor function in the protective effect of synaptic activity against neurotoxicity. BMC Neurosci 24:9–11\nBickel CS, Slade JM, Haddad F et al (2003) Acute molecular responses of skeletal muscle to resistance exercise in able-bodied and spinal cord-injured subjects. J Appl Physiol 94:2255–2262\nBinder DK, Scharfman HE (2004) Brain-derived neurotrophic factor. Growth Factors 22:123–131\nBondy CA, Lee WH (1993) Patterns of insulin-like growth factor and IGF receptor gene expression in the brain. Functional implications. Ann N Y Acad Sci 692:33–43\nBorg G (1961) Perceived exertion in relation to physical work load and puls-rate. Kungliga Fysiografisca Sallskapets I Lund Forhandlingar 31:105–115\nBorg G (1961) Interindividual scaling and perception of muscular force. Kungliga Fysiografisca Sallskapets I Lund Forhandlingar 31:117–125\nBorg GA (1982) Psychophysical bases of perceived exertion. Med Sci Sports Exerc 14:377–381\nCadore EL, Lhullier FL, Brentano MA et al (2008) Hormonal responses to resistance exercise in long-term trained and untrained middle-aged men. J Strength Cond Res 22:1617–2624\nChang HC, Yang YR, Wang PS et al (2011) IGF-I signaling for brain recovery and exercise ability in brain ischemic rats. Med Sci Sports Exerc 20 (im Druck)\nCoelho FM, Pereira DS, Lustosa LP et al (2011) Physical therapy intervention (PTI) increases plasma brain-derived neurotrophic factor (BDNF) levels in non-frail and pre-frail elderly women. Arch Gerontol Geriatr 16. (im Druck)\nCarro E, Spuch C, Trejo JL et al (2005) Choroid plexus megalinm is involved in neuroprotection by serum insulin-like growth factor I. J Neurosci 25:10884–10893\nCarro E, Trejo JL, Gomez-Isla T et al (2000) Serum insulin-like growth factor I regulates brain amyloid-beta levels. Nat Med 8:1390–1397\nDunn SE (2000) Insulin-like growth factor I stimulates angiogenesis and production of vascular endothelial growth factor. Growth Horm IGF Res 10(Suppl A):4–42\nFernandez AM, Gonzales de la Vega AG, Planas B, Torres-Aleman I (1999) Neuroprotective actions of peripherally administered insulin-like growth factor I in the injured olivo-cerebellar pathway. Eur J Neurosci 11:2019–2030\nGarcía-Mesa Y, López-Ramos JC, Giménez-Llort L et al (2011) Physical exercise protects against Alzheimer’s disease in 3xTg-AD mice. J Alzheimers Dis 24:421–454\nGoldspink G (2003) Gene expression in muscle in response to exercise. J Muscle Res Cell Motil 24:121–126\nHaddad F, Adams GR (2002) Selected contribution: acute cellular and molecular responses to resistance exercise. J Appl Physiol 93:394–403\nHaddad F, Adams GR (2006) Aging-sensitive cellular and molecular mechanisms associated with skeletal muscle hypertrophy. J Appl Physiol 100:1188–1203\nHameed M, Orrell RW, Cobbold M et al (2003) Expression of IGF-I splice variants in young and old human skeletal muscle after high resistance exercise. J Physiol 547:247–254\nHeinemeier KM, Olesen JL, Schjerling P et al (2007) Short-term strength training and the expression of myostatin and IGF-I isoforms in rat muscle and tendon: differential effects of specific contraction types. J Appl Physiol 102:573–581\nHill M, Goldspink G (2003) Expression and splicing of the insulin-like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. J Physiol 549:409–418\nIde K, Secher NH (2000) Cerebral blood flow and metabolism during exercise. Prog Neurobiol 61:397–414\nJones SW, Hill RJ, Krasney PA et al (2004) Disuse atrophy and exercise rehabilitation in humans profoundly affects the expression of genes associated with the regulation of skeletal muscle mass. FASEB J 18:1025–1027\nKavey RE, Daniels SR, Lauer RM et al (2003) American Heart Association guidelines for primary prevention of atherosclerotic cardiovascular disease beginning in childhood. American Heart Association. J Pediatr 142:368–372\nKinni H, Guo M, Ding JY et al (2011) Cerebral metabolism after forced or voluntary physical exercise. Brain Res 146:48–55\nKünstlinger U (2004) Bewegungsmangel bei Kindern – Fakt oder Fiktion? 3. Konferenz des Clubs of Cologne, 4. 12. 2003 in Köln. Dtsch Z Sportmed 55:29–30\nKunz T (1993) Weniger Unfälle durch Bewegung: Mit Bewegungsspielen gegen Unfälle und Gesundheitsschäden bei Kindergartenkindern. Hofmann, Schorndorf\nKraemer WJ, Ratamess NA (2005) Hormonal responses and adaptations to resistance exercise and training. Sports Med 35:339–361\nLaube W (1990) Zur Rückführung des vegetativ-chronotropen Tonus, der Erholung im neuromuskulären System und den Wechselbeziehungen zwischen beiden Funktionssystemen nach Auslösung einer identischen anaeroben Stoffwechselsituation durch verschiedene Belastungsarten. Dissertation B (Dr. med. sc.), Humboldt-Universität zu Berlin, Bereich Medizin Charité, Physiologisches Institut\nLaube W (Hrsg) (2009) Sensomotorisches System. Thieme, Stuttgart\nLaube W (2009) Physiologie der Hauptbeanspruchungen des sensomotorischen Systems. In: Laube W (Hrsg) Sensomotorisches System. Thieme, Stuttgart, New York, S 165–227\nLaube W (2009) Diagnostik der Leistungen des Sensomotorischen Systems: Koordination – Ausdauer – Kraft. In: Laube W (Hrsg) Sensomotorisches System. Thieme, Stuttgart, S 228–274\nLaube W (2009) Deadaptationsprozesse durch Inaktivität und Immobilisation. In: Laube W (Hrsg) Sensomotorisches System. Thieme, Stuttgart, S 370–374\nLaube W (2009) Physiologie des Zyklus Belastung – Beanspruchung – Ermüdung – Erholung – Adapatation. In: Laube W (Hrsg) Sensomotorisches System. Thieme, Stuttgart, S 499–555\nLaube W (2009) Training der Sensomotorischen Hauptbeanspruchungsformen Koordination, Ausdauer und Kraft. In: Laube W (Hrsg) Sensomotorisches System. Thieme, Stuttgart, S 556–600 und 617–637\nLefaucheur J-P, Drouot X, Cunin P et al (2009) Motor cortex stimulation for the treatment of refractory peripheral neuropathic pain. Brain 132:1463–1417\nLeite RD, Prestes J, Rosa C et al (2011) Acute effect of resistance training volume on hormonal responses in trained men. J Sports Med Phys Fitness 51:322–328\nLopez-Lopez C, LeRoith D, Torres-Aleman I (2004) Insulin-like growth factor I is required for vessel remodeling in the adult brain. Proc Natl Acad Sci U S A 101:9833–9838\nMaihöfner C, Handwerker HO, Neundörfer B, Birklein F (2003) Cortical reorganization during recovery from complex regional pain syndrome. Neurology 63:693–701\nMatsakas A, Friedel A, Hertrampf T, Diel P (2005) Short-term endurance training results in a muscle-specific decrease of myostatin mRNA content in the rat. Acta Physiol Scand 183:299–307\nMatsakas A, Diel P (2005) The growth factor myostatin, a key regulator in skeletal muscle growth and homöostasis. Int J Sports Med 26:83–89\nNoble BJ, Robertson RJ (1996) The borg scale: development, administration, and experimental use. In: Noble BJ, Robertson RJ (Hrsg) Perceived exertion. Human Kinetics, Champaign, IL, S 59–92\nPeyron R, Garcìa-Larrea L, Grègoire MC et al (1999) Haemodynamic brain responses to acute pain in humans. Brain 122:1765–1779\nPoehlman ET, Copeland KC (1990) Influence of physical activity on insulin-like growth factor-1 in healthy younger and older men. J Clin Endocrinol Metab 71:1468–1473\nPritzlaff CJ, Wideman L, Weltman JY et al (1999) Impact of acute exercise intensity on pulsatile growth hormone release in men. J Appl Physiol 87:498–504\nRadaka Z, Kanekob T, Taharab S et al (2001) Regular exercise improves cognitive function and decreases oxidative damage in rat brain. Neurochem Int 38:17–23\nRaue U, Slivka D, Jemiolo B et al (2006) Myogenic gene expression at rest and following a bout of resistance exercise in young (18–30 Yr) and old (80–89 Yr) women. J Appl Physiol 101:53–59\nRojas-Piloni G, Martínez-Lorenzana G, Condés-Lara M, Rodríguez-Jiménez J (2010) Direct sensorimotor corticospinal modulation of dorsal horn neuronal C-fiber responses in the rat. Brain Res 1351:104–114\nSonntag WE, Lynch CD, Cooney PT, Hutchins PM (1997) Decreases in cerebral microvasculature with age are associated with the decline in growth hormone and insulin-like growth factor-I. Endocrinology 138:3515–3520\nTorres-Aleman I (2001) Serum neurotrophic factors and neuroprotective surveillance: focus on IGF-I. Mol Neurobiol 21:153–160\nTrejo JL, Carro E, Torres-Aleman I (2001) Circulating insulin like growth factor I mediates exercise-induced increases in the number of new neurons in the adult hippocampus. J Neurosci 21:1628–1634\nPraag H van, Kempermann G, Gage FH (1999) Running increases cell proliferation and neurogenesisin the adult mouse dentate gyrus. Nat Neurosci 2:266–270\nPraag H van, Christie BR, Sejnowski TJ, Gage FH (1999) Running enhances neurogenesis, learning, and long-term potentiation in mice. Proc Natl Acad Sci U S A 96:13427–13431\nWalsh NP, Gleeson M, Shephard RJ et al (2011) Position statement. Part one: Immune function and exercise. Exerc Immunol Rev 17:6–63\nZhang SJ, Buchthal B, Lau D et al (2011) A signaling cascade of nuclear calcium-CREB-ATF3 activated by synaptic NMDA receptors defines a gene repression module that protects against extrasynaptic NMDA receptor-induced neuronal cell death and ischemic brain damage. J Neurosci 31:4978–4990",{"EN":547},"Der Organismus benötigt Belastung, um die Organe und ihr Zusammenspiel strukturell und funktionell zu entwickeln, zu erhalten und die Alterungsprozesse zu beeinflussen. Zum Vollzug der Leistungsvorgabe, der Belastung, realisiert der Organismus einen biologischen Aufwand, die Beanspruchung, und es entsteht eine beanspruchungsspezifische Ermüdung. Essenziell für alle Erholungsprozesse (Restitution, Reparatur, Adaptation) sind die Beanspruchungen der anabolen hormonellen, parakrinen und autokrinen Systeme. Sie vermitteln alle strukturellen Vorgänge in der Erholung. Herausragend ist die Achse Wachstumshormon – insulinähnlicher Wachstumsfaktor der Leber, aber auch der Körperzellen und die Testosteronproduktion. Die Hormone sichern zunächst die restitutiven und reparativen Prozesse. Diese gehen fließend in die anabolen Vorgänge über. Sie repräsentieren das Ergebnis der Beanspruchung, zu erkennen an der Funktions- und Leistungsfähigkeit. Inaktivität führt zu einem negativen Zyklus, wodurch es zu Atrophie und Funktionsverlust bis hin zur Degeneration kommt. Der Zyklus ist auch in die Prävention und Therapie von Schmerzen involviert. Zum einen haben während der Bewegungsausführung sowohl die zentralen motorischen Efferenzen als auch die propriorezeptiven Afferenzen einen hemmenden Einfluss auf die schmerzrelevanten Neuronenpopulationen im Hinterhorn. 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I (2016) Editorial: knowledge, understanding, and application of function-related insights – more important than ever before. J Craniomand Func 8(2):95–97\nGangloff P, Louis JP, Perrin PP (2000) Dental occlusion modifies gaze and posture stabilization in human subjects. Neurosci Lett 293:203–206\nSolow B, Sonnesen L (1998) Head posture and malocclusions. Eur J Orthod 20:685–693\nSonnesen L (2010) Associations between the Cervical Vertebral Column and Craniofacial Morphology. Int J Dent 2010:295728. doi:10.1155\u002F2010\u002F295728\nSonnesen L, Bakke M, Solow B (2001) Temporomandibular disorders in relation to craniofacial dimensions, head posture and bite force in children selected for orthodontic treatment. Eur J Orthod 23(2):179–192\nNebel R (2016) Iatrogene Zahnlängenänderungen – ursächlich für sogenannte „CMD“? Dent Barom 3:22–26\nSchadwinkel A (2009) http:\u002F\u002Fwww.zeit.de\u002Fwissen\u002F2009-10\u002Fzugvoegel-orientierung. website [Internet]. Available from: http:\u002F\u002Fwww.zeit.de\u002Fwissen\u002F2009-10\u002Fzugvoegel-orientierung. Zugegriffen: 3.3.2017\nMorningstar MW, Pettibon BR, Schlappi H, Schlappi M, Ireland TV (2005) Reflex control of the spine and posture: a review of the literature from a chiropractic perspective. Chiropr Osteopat 13:16\nIvanenko YP, Grasso R, Lacquaniti F (2000) Influence of leg muscle vibration on human walking. J Neurophysiol 84(4):1737–1747\nMaurer C, Mergner T, Bolha B, Hlavacka F (2000) Vestibular, visual, and somatosensory contributions to human control of upright stance. Neurosci Lett 281(2–3):99–102\nPersch M, Hans C, Getto R (2008) Normale Bewegungsmuster der oberen Extremität. Prax Ergother 21(21):298–301\nMaeda N, Sakaguchi K, Mehta NR, Abdallah EF, Forgione AG, Yokoyama A (2011) Effects of experimental leg length discrepancies on body posture and dental occlusion. Cranio 29(3):194–203\nEl Gourari M, Ohlendorf D, Kopp S (2013) Effekte eines Aufbissbehelfs auf die Oberkörperstatik bei Patienten mit kraniomandibulären Beschwerden. Man Med 51(6):484–492. doi:10.1007\u002Fs00337-013-1070-4\nKopp S, Friedrichs a, Pfaff G, Langbein U (2003) Beeinflussung des funktionellen Bewegungsraumes von Hals-, Brust- und Lendenwirbelsäule durch Aufbissbehelfe. Man Med 41(1):39–51. doi:10.1007\u002Fs00337-002-0200-1\nOhlendorf D, Seebach K, Hoerzer S, Nigg S, Kopp S (2014) The effects of a temporarily manipulated dental occlusion on the position of the spine: a comparison during standing and walking. Spine J 14(10):1–8\nMiles TS (2007) Postural control of the human mandible. Arch Oral Biol 52(4):347–352\nChapman RJ, Maness WL, Osorio J (2014) Occlusal contact variation with changes in head position. Int J Prosthodont 4(4):377–381\nMakofsky HW, Sexton TR, Diamond DZ, Sexton MT (1991) The effect of head posture on muscle contact position using the T‑Scan system of occlusal analysis. Cranio 9(4):316–321\nUrbanowicz M (1991) Alteration of vertical dimension and its effect on head and neck posture. Cranio 9:174–179\nWühr E (2006) Kieferanomalien und Körperfehlhaltungen – Die Morphogenese des Kraniomandibulären Systems aus osteopathischer und systemischer Sicht Inhaltsverzeichnis. Zentrum für interdisziplinäre Zahnmedizin der Donau-Universität, Krems\nNebel R (2017) A critical view on occlusion and registration. Dent Oral Craniofac Res 3(2):1–4\nArmijo-Olivo S, Rappoport K, Fuentes J, Gadotti IC, Major PW, Warren S et al (2011) Head and cervical posture in patients with temporomandibular disorders. J Orofac Pain 25:199–209\nAraki NG, Araki CT (1987) Head angulation and variations in the maxillomandibular relationship. Part II: the effects on facial contour and lip support. J Prosthet Dent 58(2):218–221\nObert M, Ohlendorf D, Kopp S (2012) Okklusionsstörungen und Auswirkungen auf den funktionellen Bewegungsraum der Lendenwirbelsäule. Man Med 50(50):124–131\nPassero PL, Wyman BS, Bell JW, Hirschey SA, Schlosser WS (1985) Temporomandibular joint dysfunction syndrome. A clinical report. Phys Ther 65(8):1203–1207\nSchupp W, Oraki A, Haubrich J, Freesmeyer WB, Kopsahilis N (2009) Okklusionsveränderungen und deren Auswirkungen auf den Halte- und Stützapparat. Untersuchung durch manualmedizinische Testverfahren. Man Med 47:107–111\nAzato FK, Castillo DB et al (2013) Influence of temporomandibular disorders management on pain and global posture. Rev Dor Sao Paolo 14(4):280–283. doi:10.1590\u002FS1806-00132013000400009\nMarini I, Gatto MR, Bartolucci ML, Bortolotti F, Alessandri Bonetti G (2013) Michelotti a. Effects of experimental occlusal interference on body posture: an optoelectronic stereophotogrammetric analysis. J Oral Rehabil 40(7):509–518\nHuggare J (1991) Association between morphology of the first cervical vertebra, head posture, and craniofacial structures. Eur J Orthod 13(6):435–440\nSonnesen L, Pedersen CE, Kjaer I (2007) Cervical column morphology related to head posture, cranial base angle, and condylar malformation. Eur J Orthod 29(4):398–403",{"EN":664},"Nach dentaler prothetischer Versorgung sind häufig Diskrepanzen zu beobachten. So stimmt ein neuer Zahnersatz nach den Kriterien der Okklusion, passt aber im Alltag des Patienten nicht. Entsprechend können bei Behandlung der kraniomandibulären Dysfunktion (CMD) nach Herstellung einer guten Okklusion die Beschwerden des Patienten sich wenig beeinflusst zeigen. Diese Diskrepanz scheint zwischen der Okklusion im zahnärztlichen Behandlungsstuhl und der Bewegung des Patienten in seiner Umwelt zu entstehen. Es wird die Hypothese aufgestellt, dass die Beschwerden keine Folge des gnathologischen Parameters Okklusion, sondern der Änderung der Zahnlänge sind – was ein posturaler Parameter ist. Es wird weiter hypothetisiert, dass das Kiefersystem neben seiner Funktion im Kausystem zusätzlich eine Funktion im posturalen System innehat. Dentale Längenänderungen am Oberkiefer verändern die Lage der Oberkieferkauebene zum Schädel. Es wird die Hypothese aufgestellt, dass die Oberkieferkauebene eine posturale Orientierungsebene ist. Sie wird als einzige somatische Struktur bei der Fortbewegung nicht nach Körper-, sondern nach den Ebenen des äußeren Raums ausgerichtet. Genau dies ist der springende Punkt, an dem Pathologien entstehen können: Steht die Oberkieferkauebene nach Zahnlängenänderungen schräg im Schädel, wird mit dem Ziel ihrer „echten“ horizontalen Raumausrichtung der ganze Körper in permanenten Neigungen und Rotationen fehlgehalten, was posturale Funktionen sind. Dies kann nach Jahren zu schweren Schmerzen aufgrund von Scherkräften im ganzen Körper führen. 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Thomas",{"DE":734},"Ziel der manuellen Medizin ist es, die Patienten von ihren Beschwerden zu befreien. Allerdings gibt es Schmerzen, die sich mit der manuellen Medizin nicht behandeln lassen. Daher werden im vorliegenden Beitrag nichtmanuelle Behandlungsverfahren und ihre Wirkungsweise dargestellt. Dabei ist zwischen nozizeptivem und neuropathischem Schmerz zu unterscheiden. Bei den Verfahren handelt es sich einerseits um pharmakologische Ansätze, die auf Empfehlungen der WHO und aktuellen Behandlungsrichtlinien basieren, andererseits um invasive Therapien, wie z. B. die Neuromodulation. Somit kann eine Brücke über beide schmerzmedizinische Herangehensweisen zum Wohle der Patienten geschlagen werden.",{"DE":736},"Nichtmanuelle Schmerztherapie der Lenden-Becken-Hüft-Region",{"VOID":738},"10.1007\u002Fs00337-017-0357-2","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00337-017-0357-2","https:\u002F\u002Flink.springer.com\u002Fcontent\u002Fpdf\u002F10.1007\u002Fs00337-017-0357-2.pdf",[742],{"id":743,"sortIndex":21,"researcher":20,"roles":744,"affiliations":745,"properties":754},"6b984ff4-d1ad-449f-9097-643c6a32d43f",[216],[746],{"id":20,"sortIndex":21,"affiliation":747,"properties":20},{"id":748,"createTime":749,"updateTime":749,"relativeEntities":750,"slug":20,"properties":751,"entityType":57,"verifyStatus":19,"verifyTime":20,"verifyNote":20,"syncStatus":19,"languages":20,"translateLanguages":20,"viewCount":21},"6cc76161-be3a-45e6-b70b-8fed7b5a97ea","2023-12-13T09:45:30.693+00:00",[],{"title":752},{"VI":753},"Universitätsklinik für Neurochirurgie, Medizinische Universität Innsbruck, Innsbruck, Deutschland",{"title":755},{"VI":756},"Eisner, 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WJ, Schloemer P, Timm J, Muehlbauer B (2013) Spinal high-velocity low amplitude manipulation in acute non-specific low back pain. 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Nat Methods 4:331–336\nTaguchi T, Hoheisel U, Mense S (2008) Dorsal horn neurons having input from low back structures in rats. Pain 138:119–129\nMense S, Hoheisl U, Taguchi T (2008) Neuroanatomische und elektrophysiologische Untersuchungen zur Neurobiologie des Rückenschmerzes: tierexperimentelle Studien an der Ratte. Abschlussbericht zum Kooperationsvertrag mit ÄMM, MWE und SAMM\nTsuji T, Hamada T (1981) Age-related changes in human dermal elastic fibres. Br J Dermatol 105:57–63\nJärvinen TA, Józsa L, Kannus P, Järvinen TL, Järvinen M (2002) Organization and distribution of intramuscular connective tissue in normal and immobilized skeletal muscles. An immunohistochemical, polarization and scanning electron microscopic study. J Muscle Res Cell Motil 23:245–254\nStecco C (2015) Functional atlas of the human fascial system. Churchill Livingstone\u002FElsevier, Edinburgh\nTesarz J, Hoheisel U, Wiedenhöfer B, Mense S (2011) Sensory innervation of the thoracolumbar fascia in rats and humans. Neuroscience 194:302–308\nHoheisel U, Rosner J, Mense S (2015) Innervation changes induced by inflammation of the rat thoracolumbar fascia. Neuroscience 300:351–359\nHandschin C, Spiegelman BM (2008) The role of exercise and PGC1alpha in inflammation and chronic disease. Nature 454:463–469\nMeeusen R (2014) Exercise, nutrition and the brain. Sports Med 44(Suppl 1):47–56\nBöhni M, Locher H, Böhni U, von Heymann W (2012) Die körpereigene Schmerzhemmung – Ständig vorhanden, aber klinisch immer noch zu wenig beachtet. Man Med 50:175–182\nvon Heymann W (2013) Vergleich chirotherapeutischer Manipulation mit Diclofenac- und Placebobehandlung bei akuter, nichtspezifischer Lumbalgie – Prospektiv-randomisierte Doppelblindstudie der MWE. Man Med 51:307–312\nvon Heymann W, Locher H, Böhni U, Habring M (2012) Neuroanatomie - Teil 2: Fakten und Hypothesen zu Faszien, Dura und Hirnstamm. Man Medizin 50:6–15",{"EN":864},"Der akute Schmerz bei segmentaler Dysfunktion ist die ideale Indikation für manuelle Therapie, insbesondere für eine Manipulation, sofern keine Kontraindikationen vorliegen. Dieser körperprotektive Schmerz wird damit sehr rasch verschwinden. Chronischer Schmerz ist aber nicht einfach die zeitliche Fortsetzung des akuten Schmerzes, sondern stellt eine Änderung des Verhaltens der Nervenzellen ab dem 2. Neuron dar (sog. Neuroplastizität). Es gibt kein Medikament gegen den chronischen Schmerz. 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