Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:
Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6012_Библиотеки_им_академика_М_И_Перельмана.pdf
Скачиваний:
0
Добавлен:
29.08.2026
Размер:
93 Мб
Скачать
Chapter 2 Applied Anatomy of the Spine 53
3. Grunhagen T, Shirazi-Adl A, Fairbank JC, Urban JP. Intervertebral
disk nutrition: a review of factors inuencing concentrations of nutrients and metabolites. Orthop Clin North Am. 2011;42(4):465-477, vii.
4.
Ibrahim DA, Myung KS, Skaggs DL. Ten percent of patients with
adolescent idiopathic scoliosis have variations in the number of thoracic or lumbar vertebrae. J Bone Joint Surg Am. 2013;95(9):828-833.
5.
Lehman RA Jr, Kang DG, Lenke LG, Gaume RE, Paik H. The
ventral lamina and superior facet rule: a morphometric analysis for an ideal thoracic pedicle screw starting point. Spine J. 2014;14(1):137-144.
6.
Magro E, Gentric JC, Talagas M, et al. Venous organization in
the transverse foramen: dissection, histology, and magnetic resonance imaging. J Neurosurg. 2015;123(1):118-125.
7.
Osmotherly PG, Rivett DA, Mercer SR. Revisiting the clinical
anatomy of the alar ligaments. Eur Spine J. 2013;22(1):60-64.
8.
Trimba R, Spivak JM, Bendo JA. Conjoined nerve roots of the
lumbar spine. Spine J. 2012;12(6):515-524.
9.
Tubbs RS, Wellons JC 3rd, Banks J, Blount JP, Oakes WJ.
Quantitative anatomy of the transverse ligament tubercles. J Neurosurg. 2002;97(3 suppl):343-345.
10.
Zhong W, Driscoll SJ, Wu M, et al. In vivo morphological
features of human lumbar discs. Medicine (Baltimore). 2014;93(28):e333.

REFERENCES

1. Francis WR, Fielding JW. Traumatic spondylolisthesis of the axis. Orthop Clin North Am. 1978;9:1011-1027.
2. McCulloch JA, Transfeldt EE. Macnab’s Backache. Baltimore: Williams & Wilkins; 1997.
3. Weiner BK, Walker M, Wiley W, et al. e lateral buttress: an anatomic feature of the lumbar pars interarticularis. Spine. 2002;27:E385-E387.
4. Bajwa NS, Toy JO, Ahn NU. L5 pedicle length is increased in subjects with spondylolysis: an anatomic study of 1072 cadavers. Clin Orthop Relat Res. 2012;470(11):3202-3206.
5. Ibrahim DA, Myung KS, Skaggs DL. Ten percent of patients with adolescent idiopathic scoliosis have variations in the number of thoracic or lumbar vertebrae. J Bone Joint Surg Am. 2013;95(9):828-833.
6. An HS, Wise JJ, Xu R. Anatomy of the cervicothoracic junction: a study of cadaveric dissection, cryomicrotomy and magnetic resonance imaging. J Spinal Disord. 1999;12:519-525.
7. Ebraheim NA, Xu R, Knight T, et al. Morphometric evaluation of lower cervical pedicle and its projection. Spine. 1997;22:1-6.
8. Pait TG, McAllister PV, Kaufman HH. Quadrant anatomy of the articular pillars (lateral cervical mass) of the cervical spine. J Neurosurg. 1995;82:1011-1014.
9. Xu R, Burgar A, Ebraheim NA, et al. e quantitative anatomy of the laminas of the spine. Spine. 1999;24:107-113.
10. Goldstein RY, Sunde CD, Assaad P, et al. Location of the vertebral artery at C1 in children: how far out laterally can one safely dissect? J Bone Joint Surg Am. 2014;96(18):1552-1556.
11. Magro E, Gentric JC, Talagas M, et al. Venous organization in the transverse foramen: dissection, histology, and magnetic resonance imaging. J Neurosurg. 2015;123(1):118-125.
12. Tubbs RS, Wellons JC 3rd, Banks J, Blount JP, Oakes WJ. Quantitative anatomy of the transverse ligament tubercles. J Neurosurg. 2002;97(3 suppl):343-345.
13. Osmotherly PG, Rivett DA, Mercer SR. Revisiting the clinical
anatomy of the alar ligaments. Eur Spine J. 2013;22(1):60-64.
14. Chaynes P, Sol JC, Vaysse P, et al. Vertebral pedicle anatomy
in relation to pedicle screw xation: a cadaver study. Spine.
2001;23:85-90.
15. Cinotti G, Gumina S, Ripani M, et al. Pedicle instrumentation in the thoracic spine: a morphometric and cadaveric study for placement of screws. Spine. 1999;24:114-119.
16. Scoles PV, Linton AE, Latimer B, et al. Vertebral body and posterior element morphology: the normal spine in middle life. Spine. 1988;13:1082-1086.
17. Lehman RA Jr, Kang DG, Lenke LG, Gaume RE, Paik H. e ventral lamina and superior facet rule: a morphometric analysis for an ideal thoracic pedicle screw starting point. Spine J. 2014;14(1):137-144.
18. Olszewski AD, Yaszemski MJ, White AA. e anatomy of the human lumbar ligamentum avum: new observations and their surgical implications. Spine. 1996;21:2307-2312.
19. von Luschka H. Die Halbgelenke des Menschlichen Korpers. Berlin: Karpess; 1858.
20. Beadle OA. e Intervertebral Discs. Special Report No. 160. London: Medical Research Council; 1931:6-9.
21. Bradford DL, Spurling RG. e Intervertebral Disc. Springeld, IL: Charles C omas; 1945.
22. Humzah MD, Soames RW. Human intervertebral disc: structure and function. Anat Rec. 1988;229:337-356.
23. Bick EM. e osteohistology of the normal human vertebra. J Mt Sinai Hosp N Y. 1952;19:490-527.
24. Aeby C. Die Alterverschiedenheiten der menschlichen Wirbelsaule. Arch Anat Physiol (Anat Abst). 1879;10:77.
25. Zhong W, Driscoll SJ, Wu M, et al. In vivo morphological features of human lumbar discs. Medicine (Baltimore). 2014;93(28):e333.
26. Dommissee G. Morphological aspects of the lumbar spine and lumbosacral regions. Orthop Clin North Am. 1975;6:163-175.
27. Wiltse LL. Anatomy of the extradural compartments of the lumbar spinal canal: peridural membrane and circumneural sheath. Radiol Clin North Am. 2000;38:1177-1206.
28. Ugur HC, Attar A, Uz A, et al. Surgical anatomic evaluation of the cervical pedicle and adjacent neural structures. Neurosurgery. 2000;47:1162-1168.
29. Ugur HC, Attar A, Uz A, et al. oracic pedicle: surgical anatomic evaluation and relations. J Spinal Disord. 2001;14:39-45.
30. Ebraheim NA, Xu R, Darwich M, et al. Anatomic relations between the lumbar pedicle and the adjacent neural structures. Spine. 1997;15:2338-2341.
31. Hogan Q, Toth J. Anatomy of the so tissues of the spinal canal. Reg Anesth Pain Med. 1999;24:303-310.
32. Kobrine AI, Doyle DF, Rizzoli HV. Spinal cord blood ow as aected by changes in systemic arterial blood pressure. J Neurosurg. 1976;44:12-15.
33. Golub GS, Silverman B. Transforaminal ligaments of the lumbar spine. J Bone Joint Surg Am. 1969;51:947-956.
34. Park HK, Rudrappa S, Dujovny M, et al. Intervertebral foraminal ligaments of the lumbar spine: anatomy and biomechanics. Childs Nerv Syst. 2001;4-5:275-282.
35. Grimes PF, Massie JB, Garn SR. Anatomic and biomechanical analysis of the lower lumbar foraminal ligaments. Spine. 2000;25:2009-2014.
36. Alleyne CH, Cawley CM, Barrow DL, et al. Microsurgical anatomy of the dorsal cervical nerve roots and the cervical dorsal root ganglion/ventral root complexes. Surg Neurol. 1998;50:213-218.
SECTION
I
54 BASIC SCIENCE
37. Kadish LJ, Simmons EH. Anomalies of the lumbosacral nerve roots. J Bone Joint Surg Br. 1984;66:411-416.
38. Trimba R, Spivak JM, Bendo JA. Conjoined nerve roots of the lumbar spine. Spine J. 2012;12(6):515-524.
39. Kikuchi S, Hasue M. Anatomic features of the furcal nerve and its clinical signicance. Spine. 1986;11:1002-1007.
40. Piacsecka-Kacperska A, Gladykowska-Rzeczycka J. e sacral plexus in primates. Folia Morphol (Warsz). 1972;31:21-31.
41. Parke WW, Watanabe R. Lumbosacral intersegmental epispinal axons and ectopic ventral nerve rootlets. J Neurosurg. 1987;67:269-277.
42. Hasue M, Kunogi J, Konno S, et al. Classication by position of dorsal root ganglia in the lumbosacral region. Spine. 1989;14:1261-1264.
43. Kikuchi S, Hasue M. Combined contrast studies in lumbar spine diseases. Spine. 1988;13:1327-1331.
44. Bogduk N, Tynan W, Wilson AS. e nerve supply to the human lumbar intervertebral disc. J Anat. 1981;132:39-56.
45. Bogduk N, Windsor M, Inglis A. e innervation of the cervical intervertebral discs. Spine. 1988;13:2-8.
46. Hirsch C. Studies on mechanism of low back pain. Acta Orthop Scand. 1953;22:184-231.
47. Jung A, Brunschwig A. Recherches histologiques sur l’innervation des articulations et des corps vertebreaux. Presse Med. 1932;40:316-317.
48. Larmon AW. An anatomic study of the lumbosacral region in relation to low back pain and sciatica. Ann Surg. 1944;119:892.
49. Malinsky J. e ontogenetic development of nerve terminations in the intervertebral discs of man. Acta Anat (Basel). 1959;38:96-113.
50. Nade S, Bell S, Wyke BD. e innervation of the lumbar spine joints and its signicance. J Bone Joint Surg Br. 1980;62:225-261.
51. Wiberg G. Back pain in relation to nerve supply of intervertebral disc. Acta Orthop Scand. 1949;19:211-221.
52. Parke WW. Applied anatomy of the spine. In: Rothman RH, Simeone FA, eds. e Spine. Philadelphia: WB Saunders; 1982:18-51.
53. Groen GJ, Baljet B, Drukker J. e nerves and nerve plexuses of the human vertebral column. Am J Anat. 1990;188:282-296.
54. Pedersen HE, Blunck CFJ, Gardner E. e anatomy of the lumbosacral posterior rami and meningeal branches of spinal nerves (sinuvertebral nerves). J Bone Joint Surg Am. 1956;38:377-391.
55. Hirsch C, Inglemark B, Miller M. e anatomical basis for low back pain. Acta Orthop Scand. 1963;33:1-17.
56. McCouch GP, During ID, Ling TH. Location of receptors for tonic reexes. J Neurophysiol. 1951;14:191-195.
57. Stilwell DL. e nerve supply of the vertebral column and its associated structures in the monkey. Anat Rec. 1956;125:139-169.
58. Yoshizawa H, O’Brien JP, omas-Smith W, et al. e neuropathology of intervertebral discs removed for low back pain. J Pathol. 1980;132:95-104.
59. Kimmel DL. Innervation of the spinal dura and the dura of the posterior cranial fossa. Neurology. 1986;11:800-809.
60. Cyriax J. Dural pain. Lancet. 1978;1:919-921.
61. Groen GJ, Baljet B, Drukker J. e innervation of the spinal dura mater: anatomy and clinical implications. Acta Neurochir (Wien). 1988;92:39-46.
62. Parke WW, Watanabe R. Adhesions of the ventral lumbar dura: an adjunct source of discogenic pain? Spine. 1990;15:300-303.
63. Blikra G. Intradural herniated lumbar disc. J Neurosurg.
1969;31:676-679.
64. Junghanns H. Der Lumboscralwinkel. Dtsch Z Chit.
1929;213:332.
65. Schmorl G, Junghanns H. e Human Spine in Health and Disease. New York: Grune & Stratton; 1959.
66. DePalma AF, Rothman RH. e Intervertebral Disc. Philadelphia: WB Saunders; 1970.
67. Brown MD. e Pathophysiology of the Intervertebral Disc: Anatomical, Physiological and Biomedical Considerations. Philadelphia: Jeerson Medical College; 1969.
68. Maroudas A. Nutrition and metabolism of the intervertebral disc. In: Ghosh P, ed. e Biology of the Intervertebral Disc. Boca Raton, FL: CRC Press; 1988.
69. Grunhagen T, Shirazi-Adl A, Fairbank JC, Urban JP. Intervertebral disk nutrition: a review of factors inuencing concentrations of nutrients and metabolites. Orthop Clin North Am. 2011;42(4):465-477, vii.
70. Holm S, Maroudas A, Urban JPG, et al. Nutrition of the intervertebral disc: an in vivo study of solute transport. Clin Orthop. 1977;129:104-114.
71. Holm S, Maroudas A, Urban JPG, et al. Nutrition of the intervertebral disc: solute transport and metabolism. Connect Tissue Res. 1981;8:101-110.
72. Maroudas A, Nachemson A, Stockwell RA, et al. Factors involved in the nutrition of human lumbar intervertebral disc: cellularity and diusion of glucose in vitro. J Anat. 1975;120:113-130.
73. Ferguson WP. Some observations on the circulation in fetal and infant spines. J Bone Joint Surg. 1950;32:640-645.
74. Willis TA. Nutrient arteries of the vertebral bodies. J Bone Joint Surg. 1949;31:538-541.
75. Crock HV, Yoshizawa H. e Blood Supply of the Vertebral Column and Spinal Cord in Man. New York: Springer-Verlag;
1977.
76. Milen MT, Bloom DA, Culligan J, et al. Albert Adamkiewicz (1850-1921)—his artery and its signicance for the retroperitoneal surgeon. World J Urol. 1999;17:168-170.
77. Parke WW. e vascular relations of the upper cervical vertebrae. Orthop Clin North Am. 1978;9:879-889.
78. Schi DCM, Parke WW. e arterial supply of the odontoid process. Anat Rec. 1972;172:399-400.
79. Jasani V, Jaray D. e anatomy of the iliolumbar vein: a cadaver study. J Bone Joint Surg Br. 2002;84:1046-1049.
80. Kaisary AV, Smith P. Spinal cord ischemia aer ligation of both internal iliac arteries during radical cystoprostectomy. Urology. 1985;25:395-397.
81. Breschet G. Essai sur les Veines der Rachis. Paris: Mequigon-Morvith; 1819.
82. Batson OV. e function of the vertebral veins and their role in the spread of metastases. Am Surg. 1940;112: 138-145.
83. Clemens HJ. Die Venesysteme der Menschlichen Wirbelsaule. Berlin: Walter de Gruyter; 1961.
84. Chaynes P, Verdie JC, Moscovici J, et al. Microsurgical anatomy of the internal vertebral venous plexuses. Surg Radiol Anat. 1998;20:47-51.
85. Parke WW, Valsamis MP. e ampulloglomerular organ: an unusual neurovascular complex in the suboccipital region. Anat Rec. 1967;159:193-198.
86. Parke WW, Rizzoli HV, Brown MD. e pharyngovertebral veins: an anatomic rationale for Grisel’s syndrome. J Bone Joint Surg Am. 1984;66:568-574.
Chapter 2 Applied Anatomy of the Spine 55
87. Wetzel FT, LaRocca H. Grisel’s syndrome: a review. Clin Orthop. 1989;240:141-152.
88. Corbib JL. Anatomie et Pathologie Arterielles de la Moelle. Paris: Masson et Cie; 1961:787-796.
89. Brewer LA, Fosburg RG, Mulder GA, et al. Spinal cord complications following surgery for coarctation of the aorta. J orac Cardiovasc Surg. 1972;64:368-379.
90. Lazorthes G, Gouaze A, Zadeh JO, et al. Arterial vascularization of the spinal cord. J Neurosurg. 1971;35:253-262.
91. Marcus ML, Heistad DD, Ehrardt JC, et al. Regulation of total and regional spinal cord blood ow. Circ Res. 1977;41:128-134.
92. Parke WW, Whalen JL, Bunger PC, et al. Intimal musculature of the lower anterior spinal artery. Spine. 1995;20:2073-2079.
93. Parke WW. Correlative anatomy of cervical spondylotic myelopathy. Spine. 1988;13:831-837.
94. Dommissee GF. e Arteries and Veins of the Human Spinal Cord From Birth. Edinburgh: Churchill-Livingstone;
1975.
95. Lasjaunias P, Vallee B, Person H, et al. e lateral artery of the upper cervical spinal cord. J Neurosurg. 1985;63:235-241.
96. Gillilan LA. e arterial blood supply of the human spinal cord. J Comp Neurol. 1958;110:75-103.
97. Hassler O. Blood supply to human spinal cord. Arch Neurol. 1966;15:302-307.
98. Herren RY, Alexander L. Sulcal and intrinsic blood vessels of human spinal cord. Arch Neurol Psychiatry. 1939;41:678-683.
99. Kadyi H. Über die Blutgefasse des menschlichen Ruckenmarkes:
Nach einer im XV Bande der Denkschrien d. math-naturw. Cl. d. Akad. d. Wissensch. Krakau erschienen Morphology, aus dem Polnischen Ubersaatz vom Verfasser. Lemberg:
Grubrnowicz & Schmidt; 1889.
100. Turnbull IM, Brieg A, Hassler O. Blood supply of cervical spinal cord in man. J Neurosurg. 1966;24:951-965.
101. Ireland WP, Fletcher TF, Bingham C. Quantication of microvasculature in the canine spinal cord. Anat Rec. 1981;200:103-113.
102. Feeney JF, Watterson RL. e development of the vascular pattern within the walls of the central nervous system of the chick embryo. J Morphol. 1946;78:231-303.
103. Lobosky JM, Hitchon PW, Torner JC, et al. Spinal cord autoregulation in the sheep. Curr Surg. 1984;41:264-267.
104. Parke WW. Arteriovenous anastomoses in the spinal cord: probable role in blood ow autoregulation [abstract]. Anat Rec. 1989;223:87A.
105. Molina JE, Cogordon J, Einzig S, et al. Adequacy of ascending-descending aorta shunt during cross-clamping of the thoracic aorta for prevention of spinal cord injury. J orac Cardiovasc Surg. 1985;90:126-136.
106. Wadouh F, Arndt CF, Opperman E, et al. e mechanism
of spinal cord injury aer simple and double aortic
cross-clamping. J orac Cardiovasc Surg. 1986;92:121-127.
107. Svensson LG, Rickards E, Coull A, et al. Relationship of spinal cord blood ow to vascular anatomy during thoracic aorta cross-clamping and shunting. J orac Cardiovasc Surg. 1986;91:71-78.
108. Gillilan LA. Veins of the spinal cord. Neurology. 1970;20:860-868.
109. Parke WW, Gammel K, Rothman RH. Arterial vascularization of the cauda equina. J Bone Joint Surg Am. 1981;63:53-62.
110. Parke WW, Watanabe R. e intrinsic vasculature of the lumbosacral spinal nerve roots. Spine. 1985;10:508-515.
111. Yamamoto H. Quantitative measurements of blood ow in cauda equina in spinal cords of monkeys by using radioactive microspheres. J Jpn Coll Angiol. 1982;22:35-42.
111a. Rydevik B, Holm S, Brown MD, et al. Diusion from the
cerebrospinal uid as a nutritional pathway for spinal nerve roots. Acta Physiol Scand. 1990;138(2):247-248.
112. Watanabe R, Parke WW. e vascular and neural pathology of lumbosacral spinal stenosis. J Neurosurg. 1986;65:64-70.
113. Watanabe R, Parke WW. Structure of lumbosacral spinal nerve roots: anatomy and pathology in spinal stenosis. J Clin Orthop Surg (Jpn). 1987;22:529-539.
114. Evans JG. Neurogenic intermittent claudication. BMJ. 1964;2:985-987.
115. LaBan MM. “Vesper’s curse”: night pain, the bane of Hypnos. Arch Phys Med Rehabil. 1984;65:501-504.
116. LaBan MM, Wesolowski DP. Night pain associated with diminished cardiopulmonary compliance. Am J Phys Med Rehabil. 1988;67:155-160.
117. Madsen JR, Heros RC. Spinal arteriovenous malformations and neurogenic claudication. J Neurosurg. 1988;68:793-797.
118. Aboulker J, Bar D, Marsault C, et al. L’hypertension veineuse intra-rachidienne par anomalies multiples du système cave: une cause majeure de sourance médullaire. Clin Obstet Gynecol. 1977;103:1003-1015.
119. Takata K, Inoue S, Takashi K, et al. Swelling of the cauda equina in patients who have herniation of a lumbar disc. J Bone Joint Surg Am. 1988;70:361-368.
120. White A, Panjabi M. Clinical Biomechanics of the Spine. 2nd ed. Philadelphia: JB Lippincott; 1990.
121. Puschel J. Der Wassergehalt normaler and degenerierter Zwischenwirbelscheiben. Beitr Pathol Anat. 1930;84:123-130.
122. Galante JO. Tensile properties of the human lumbar annulus brosus. Acta Orthop Scand. 1967;100(suppl):1-91.
123. Nachemson A. e load on lumbar discs in dierent positions of the body. Clin Orthop. 1966;45:107-122.
124. Petter CK. Methods of measuring the pressure of intervertebral discs. J Bone Joint Surg. 1933;15:365.
SECTION
I
This page intentionally left blank
AMATPAMADP PForce
++ →+ +++
Skeletal Muscle: Architectural Design,
SECTION
3
CHAPTER
Spinal muscles generate movement of the spine and provide the stability needed to protect vital anatomic structures, in coordination with the rest of the neuromusculoskeletal system (vertebrae, tendons, ligaments, and the nervous system). For example, large movements of the head require appropriate muscle strength, vertebral geometry (e.g., facet joint orienta­tion), ligament compliance, and neural control. Spinal muscles have been described as one of three subsystems (along with passive spinal column and neural control) that must work together to stabilize the spine.
Spinal musculature dysfunction is hypothesized to be the cause of a variety of pathologic conditions, such as segmental instability, low back or neck pain, and degenerative disc syn­dromes. However, the mechanisms that relate muscle function (or dysfunction) to pathologic processes are unclear. Some factors that lead to pathologic processes may be elucidated by biomechanical analyses of spine kinematics along with the associated tissue strains and loads. Such analyses rely heavily on accurate knowledge of muscle forces, moment arms, and activation patterns to calculate loads and displacements, which is frequently unavailable for spinal muscles. Oen,
spinal muscles are ignored or overly simplied (e.g., modeled together as one muscle) because the anatomy of these muscles is considered too complex to represent realistically. However, the complex anatomy and architecture of spinal muscles profoundly inuence their function; thus, this information must be incorporated into analyses in order to accurately predict the role of these muscles in spinal function and dysfunction.
In this chapter, an overview of skeletal muscle contractile properties is presented rst. en, a description of the impor­tant, and oen neglected, principles of skeletal muscle archi­tecture along with the ways that architecture determines muscle function are provided. In Chapter 4, specic informa­tion about the anatomy and architecture of the spinal muscu­lature is provided, as well as information on the implications of spinal muscle anatomy and architecture for motor control, injury, and pain.
1
Physiology, and Function
Samuel R. Ward
Anita Vasavada
Scott Delp
Richard L. Lieber

Cross-Bridge Cycle

e basic force-generating event in skeletal muscle is the cyclic formation of cross-bridges between the lamentous proteins actin and myosin. Most of our understanding of the
mechanism of muscle contraction has come from excellent biochemical studies performed in the 1950s and the decades that followed. isolating specic muscle proteins were developed, together with methods for measuring their physicochemical and bio­chemical properties. In simple terms, biochemical experiments on muscle contractile proteins have shown that, during the cross-bridge cycle, actin (A) combines with myosin (M) and adenosine triphosphate (ATP) to produce force, adenosine diphosphate (ADP), and inorganic phosphate (Pi), which can be represented as a chemical reaction in this form:
It is obvious that if ATP is either not present or is rapidly depleted with the muscle cell, the number of A-M cross­bridges, and therefore force, will decrease. is is manifested in muscles as “fatigue.” Importantly, many factors can cause ATP depletion and fatigue, which may predispose muscle tissue to injury.

Muscle Fiber Types

Overwhelming evidence indicates that skeletal muscle bers are heterogeneous. In the early 1800s, it was observed that the gross appearance of dierent skeletal muscles ranged in color from pale white to deep red. In fact, one of the earliest clas­sication schemes for muscle was based on color; thus, muscles were classied as “red” or “white” (Table 3.1). However, as experimental methods became more sophisticated, it became clear that numerous other dierences existed between muscles. For example, certain muscles contract rapidly, whereas others contract more slowly; certain muscles maintain force for a
2-4
It was during this period that methods for
i
(Eq. 1)
I
57
58 BASIC SCIENCE
TABLE 3.1 Fiber Type Classication Schemes
Basis for Scheme FIBER TYPE SPECTRUM Reference
Metabolic SO FOG FG Peter et al., 1972
Morphology and physiology Slow red Fast white Fast white Ranvier, 1873
Z-line width Red Intermediate White Gauthier, 1969
Histochemistry III II I Romanul, 1964
Histochemistry Type 1 Type 2A Type 2B Brooke and Kaiser, 1972
M-band bridging pattern Five bridges Three inner, two faint outer bridges Three bridges Sjöström et al. 1982
Immunohistochemistry Type 1 Types 2A and 2X Type 2B Schiano et al., 1989
Gene sequencing Type 1 Types 2A and 2X Type 2B Schiano and Reggiani,
FG, fast glycolytic; FOG, fast oxidative glycolytic; SO, slow oxidative.
1993
46
39
40
41
42
43
44
45
long period of time, whereas others fatigue rapidly; and certain muscles generate large forces, while others generate small forces. ese functional properties led to descriptions of
muscle as “fast twitch” or “slow twitch,” and “fatigable” or “nonfatigable.” In addition, with the advent of light microscopy and histochemistry, it became possible to classify individual bers based on their appearance following a particular stain­ing protocol. Unfortunately, many of these classication schemes did not correlate simply with muscle color. In fact, many of them did not correlate at all with one another. e main problem with ber-type classication schemes is that the classied feature may correlate with one physiologic or bio­chemical property, but may have no relationship to others.
e current view of muscle ber types is that skeletal­muscle bers possess a wide spectrum of morphologic, con­tractile, and metabolic properties.5 e appropriate view of any classication scheme, therefore, is that it is an articial system superimposed on a continuum of properties for our convenience. Probably the most useful “ber-typing” scheme is one that describes contractile speed and muscle oxidative capacity. ere are a variety of ways to do this; several schemes are listed in Table 3.1. e most denitive method for typing human skeletal muscle (not necessary the most physiologic, but very consistent among labs) is to use the type of myosin heavy chain expressed in the bers. One of the most conve­nient methods to type a muscle based on myosin heavy chains is to homogenize large-muscle biopsies and separate the myosin isoforms on protein gels.6 Using this method, it is possible to identify the three ber types in human muscle: types 1, 2A, and 2X (see Table 3.1). Although there are four human myosin heavy chain gene—type 1, type 2A, type 2X, and type 2B—only the former three are expressed.7 is strange phenomenon can make it dicult to compare animal muscle studies with human muscle studies.
Fiber Type Distribution of Paraspinal Muscles
Since ber types develop in response to functional demands, the ber type of paraspinal and lumbar extensor muscles provides insight into their function and use patterns. It has been clearly shown that the paraspinal and lumbar extensor muscles are largely composed of type 1 and type 2A bers.
us, these muscles are predicted to be relatively slow con­tracting and fatigue resistant compared to most limb muscles. In fact, recent analysis of paraspinal muscles showed that multidus, longissimus, and iliocostalis muscles comprised more than 60% type 1 muscle bers8; this proportion is greater than many limb muscles, such as exor digitorum profundus (35.5 ± 4.8%), triceps (42.4 ± 3.6%), brachioradialis (45.5 ±
6.4), or vastus lateralis (48.3 ± 9.5%), but approaching the values of other tonic, postural muscles such as soleus (88%).9 Fiber-type distributions of dierent spinal muscles are described further in Chapter 4.

Muscle Injury

Injury to muscle bers can occur as a result of trauma, disease, application of myotoxic agents (e.g., local anesthetics), inam­matory processes, or intense exercise. e degree to which muscle injury relates to low back pain or neck pain is unknown. However, muscle injury, and the pain that accompanies it, have been studied extensively. Skeletal-muscle injury and soreness frequently occur when a muscle is rapidly lengthened while it is activated. Active lengthening of muscle (also called eccentric contraction) has been used to study injuries in animals and humans for more than 30 years. Muscle pain accompanying eccentric exercise peaks 24 to 48 hours aer the exercise bout. Several studies have reported that eccentric exercise results in a signicant increase in serum creatine kinase levels 24 to 48 hours aer the exercise bout persist for 3 to 6 days, depending on the precise nature of the exercise. e appearance of creatine kinase in the serum is interpreted as a result of increased permeability, or breakdown of the muscle cell membrane surrounding the muscle cell.
Eccentric training of a specic muscle group prevents, or at least attenuates, the magnitude of muscle injury that occurs aer eccentric exercise in that muscle group. However, general increased tness does not prevent or reduce eccentric contraction-induced muscle injury.
Experimental studies of skeletal muscles directly sub­jected to eccentric exercise suggest that early mechanical events result in muscle injury.
12,13
For example, during cyclic
eccentric exercise of the rabbit tibialis anterior, signicant
10,11
that may
Chapter 3 Skeletal Muscle: Architectural Design, Physiology, and Function 59
muscle
Gluteus
ABC
biomechanical changes were observed in the rst 5 to 7 minutes of exercise.14 Other studies have revealed structural disruption of the cytoskeleton within the bers during these early time periods,
15,16
which may provide further insights into
the damage mechanism.
Animal and human studies have provided evidence for
selective damage of fast-ber types aer eccentric exercise.
17-19
In human studies, this damage was generally conned to the type 2 muscle bers; but in animal studies, damage has been further localized to the fastest of the fast-ber subtypes. Because these are also the most highly fatigable muscle bers,20 it has been speculated that the high degree of fatigability of these bers may predispose them to injury. In fact, several clinical studies have proposed that the fatigability of spinal muscles may be a predisposing factor to injury. However, it is dicult to test this idea directly because of the many other dierences between these bers and other ber types. Further studies are required to elucidate the basis for ber type–specic injury to skeletal muscle and to document the relationship between spinal muscle injury and back and neck pain.

Muscle Architecture

While muscle ber types are much more widely studied and reported (probably due to the ease with which ber-type data can be obtained), muscle functional properties are much more highly determined by muscle architecture—the number and arrangement of muscle bers relative to the axis of force generation.
21–23
Whereas muscle ber size (which is directly
proportional to force generation) is relatively consistent among muscles of dierent sizes, architectural dierences
between muscles are much more variable and much more strongly aect function. us, muscle architecture is a primary determinant of muscle function, and understanding this structure–function relationship is of great practical impor­tance not only in clarifying the physiologic basis for produc­tion of force and movement but also in providing a scientic rationale for surgery or rehabilitation. Muscle architectural studies also guide electrode placement for electromyographic measures of muscle activity, explain the mechanical basis of muscle injury during movement, and aid in the interpretation of histologic specimens obtained from muscle biopsies.
Basic Architectural Denitions
e various types of architectural arrangement are as numer­ous as the muscles themselves. For discussion purposes, however, we present three general classes of muscle-ber architecture. Muscles composed of bers that extend parallel to the muscle’s force-generating axis are described as having a parallel or longitudinal architecture (Fig. 3.1A). Muscles with bers that are oriented at a single angle relative to the force-generating axis are described as having unipennate architecture (Fig. 3.1B). e angle between the ber and force­generating axis has been measured at resting length in dierent mammalian muscles and varies from about 0 to 30 degrees. It becomes obvious when performing muscle dissections that most muscles fall into the third and most general category,
SECTION
I
medius
Vastus lateralis
ML
Biceps
FL
ML
ML = FL
FIG. 3.1 Three general types of skeletal muscle architecture. (A) Longitudinal architecture in which muscle
bers run parallel to the muscle force-generating axis. A typical example is the biceps brachii. (B) Unipennate architecture in which muscle bers run at a xed angle relative to the muscle’s force-generating axis. The vastus lateralis muscle is shown. (C) Multipennate architecture in which muscle bers run at several angles relative to the muscle’s force-generating axis. The gluteus medius muscle is shown. FL, ber length; ML, muscle length.
FL
60 BASIC SCIENCE
multipennate muscles—muscles constructed of bers that are oriented at several dierent angles relative to the axis of force generation (Fig. 3.1C). Obviously, these three designations are oversimplied, but they provide a vocabulary with which to describe muscle architecture. Because bers may not be oriented along any of the classic anatomic axes, determination of muscle architecture is impossible from a single biopsy or even magnetic resonance imaging (MRI), computed tomogra­phy (CT), or ultrasonography, because these methods cannot account for the variations in ber length and orientation that occur along the muscle length. us, other methods, which are described in some detail later, have been devel­oped to characterize the architectural properties of skeletal muscle.

Experimental Determination of Skeletal Muscle Architecture

Quantitative studies of muscle architecture were pioneered by Gans and his colleagues, ology for dening muscle architecture based on microdissec­tion of whole muscles. e parameters usually included in an architectural analysis are muscle length, ber or fascicle length, pennation angle (i.e., the ber angle relative to the axis of force generation), and physiologic cross-sectional area (PCSA). Typically, muscles are chemically xed in formalin to maintain ber integrity during dissection.
Pennation angle (θ) is measured by determining the average angle of the bers relative to the axis of force generation. Usually only the pennation angle of bers on the supercial muscle surface is measured, although pennation angles may vary from supercial to deep and also from proximal to distal. In fact, variation in pennation from supercial to deep bers has been documented in several spinal muscles (see
Chapter 4). Although more sophisticated methods could be
developed for measurement of pennation angle (e.g., diusion tensor imaging), it is doubtful they would provide a great deal more insight into muscle function because variations in pennation angle do not dramatically aect function.
Muscle length is dened as “the distance from the origin of the most proximal muscle bers to the insertion of the most distal bers.”25 Fiber length represents the number of sarco­meres in series, and experimental evidence suggests that muscle ber length is proportional to ber contraction veloc-
24,26
it y.
Muscle length and ber length are not always the same because there is a variable degree of “stagger” seen in muscle bers as they arise from and insert onto tendon plates (see Fig.
3.1). Muscle ber length can only be determined by microdis-
section of individual bers from xed tissues or by laborious identication of bers by glycogen depletion followed by serial sections along the length of the muscle.27 Unless investigators are explicit when they refer to muscle ber length, they are probably referring to muscle ber bundle length (also known as fascicle length) because it is extremely dicult to isolate intact bers that run from origin to insertion, especially in mammalian tissue. muscle suggest that individual muscle bers do not extend the
23,24
who developed a precise method-
23
27,28
Experimental studies of mammalian
entire muscle length and may not even extend the entire length of a fascicle.
27,28
Detailed studies of individual muscle
ber lengths have not been conducted in human spinal muscles, but studies in feline neck muscles illustrate that muscle bers are oen arranged in series, ending in tendinous
inscriptions within the muscle or terminating intrafascicu-
29,30
larly.
Although the terms ber length and fascicle length are oen used interchangeably, technically they are identical only if muscle bers span the entire length of a fascicle. In muscle architecture studies, bundles consisting of 5 to 50 bers are typically used to estimate ber length, which may be reported as either ber length or fascicle length.
e nal and crucial experimental step required to perform architectural analysis of a whole muscle is to measure the sarcomere length within the isolated bers. is is necessary to compensate for dierences in muscle length that occur during xation. In other words, to conclude that a muscle has “long bers” one must ensure that it was not merely xed in highly stretched position corresponding to a long sarcomere length. Similarly, muscles with “short bers” must be further investigated to ensure that they were not simply xed at a short sarcomere length. To permit such conclusions, ber length measurements should be normalized to a constant sarcomere length. Fiber (or fascicle) lengths are usually normalized to the sarcomere length at which the sarcomere generates maximum force. is normalized ber length is referred to as optimal ber (or fascicle) length and provides a reference value that can be related back to the physiologic length if the relationship between muscle length and joint position is noted. en, based on measured architectural parameters and joint proper­ties, the relationship between sarcomere length and joint angle can be calculated. As an alternative to measurements in cadav­ers, sarcomere lengths can be measured in live humans using intraoperative laser diraction31 or less invasively with micro­endoscopy.
32,33
Because sarcomere length strongly inuences muscle force generation, an understanding of the relationship between sarcomere length change and movement has been used in many studies to provide added understanding of muscle design.
31,34–37
e physiologic cross-sectional area (PCSA) is the main architectural calculation. eoretically, PCSA represents the sum of the cross-sectional areas of all the muscle bers within the muscle, and thus it is the only architectural parameter that is directly proportional to the maximum tetanic tension gen­erated by the muscle. e PCSA is almost never the same as the cross-sectional area of the muscle measured in any of the traditional anatomic planes, as would be obtained using a noninvasive imaging method such as MRI, CT, or ultrasonog­raphy. It is calculated as muscle volume divided by ber length and has units of area. Because bers may be oriented at a pennation angle relative to the axis of force generation, not all of the ber tensile force is transmitted to the tendons. Speci­cally, if a muscle ber is pulling with X units of force at a pennation angle θ relative to the muscle axis of force genera-
θ) will
actually be transmitted along the muscle axis. us, the volume/length is oen multiplied by cosineθ (pennation angle) to yield PCSA.
Chapter 3 Skeletal Muscle: Architectural Design, Physiology, and Function 61
B
40
Maximum tension (N)
120
40
Maximum tension (N)
B
540
Maximum tension (N)
120
540
Maximum tension (N)
Mechanical Properties of Muscles With Dierent Architectures
As stated earlier, muscle force is proportional to PCSA and muscle velocity is proportional to ber length. By stating that velocity is proportional to ber length, it is implicit that the total excursion (active range) of a muscle is also proportional to ber length. us, it is important to understand how these two architectural parameters, PCSA and ber length, aect muscle function.
Comparison of Two Otherwise Identical Muscles With Dierent PCSAs
Suppose that two muscles have identical ber lengths and pennation angles but one muscle has twice the mass (equiva­lent to saying that one muscle has twice the number of bers, thus twice the PCSA). For the sake of simplicity, suppose that these two muscles have identical ber-type distributions and that they generate the same force per unit area. e functional dierence between these two muscles is shown in Fig. 3.2.
e muscle with twice the PCSA has an isometric length–
tension curve with the same shape, but it is amplied upward
by a factor of 2. us, the maximal tetanic tension (Po) of the larger muscle will be twice that of the smaller muscle. Simi­larly, comparison of isotonic force–velocity curves indicates that the dierences between muscles will simply be an upward shi in Po for the larger muscle.
Comparison of Two Otherwise Identical Muscles With Dierent Fiber Lengths
For two muscles with identical PCSAs and pennation angles but dierent ber lengths, the schematic in Fig. 3.3 demon­strates that the eect of increased ber length is to increase muscle excursion and velocity. Peak force of the length–tension curves is identical between muscles, but the range of lengths over which the muscle generates active force is dierent. For the same reason that increased ber length increases the active muscle range of the length–tension relationship, it also results in an increase in the muscle’s maximum velocity (V
max
).
Interplay of Muscle Architecture and Moment Arm
In addition to its architecture, the moment generated by a muscle is inuenced by its moment arm. Moment arm, the
SECTION
I
FIG. 3.2 Two muscles with dierent physiologic cross-sectional areas
(PCSAs) but identical mass. (A) Comparison of isometric length–tension properties. (B) Comparison of isotonic force–velocity properties. The eect of increased PCSA with identical ber length is to shift the absolute length–tension and force–velocity curves to higher values, but with retention of the same range and intrinsic shape.
100
80
60
40
20
0
05 10 15 20 25 30 35
A
120
100
80
60
40
20
0
05 10 15 20 25 30 35
Muscle length (mm)
Large PCSA
Small PCSA
Muscle velocity (mm/s)
Large PCSA
Small PCSA
100
80
60
40
20
0
510152025303
A
120
100
80
60
40
20
0
510152025303
FIG. 3.3 Two muscles with dierent ber lengths but identical physiologic
cross-sectional areas. (A) Comparison of isometric length–tension properties. (B) Comparison of isotonic force–velocity properties. The eect of increased ber length is to increase the absolute range of the length–tension curve and absolute velocity of the force–velocity curve, but with retention of the same peak force and intrinsic shape. The dotted vertical line in (B) demonstrates that, for an equivalent absolute velocity, the muscle with longer bers will generate a greater force.
Muscle length (mm)
Long fibers
Short fibers
Muscle velocity (mm/s)
Long fibers
Short fibers
62 BASIC SCIENCE
Full flexion
Full extension
C
“mechanical advantage” of a muscle, is the distance from a muscle’s line of action to the joint axis of rotation and is directly related to a muscle’s change in length with joint rota­tion.38 In other words, the amount of muscle ber length
change that occurs as a joint rotates—and, consequently, the range of joint angles over which the muscle develops active force—both depend on the muscle moment arm. is idea can
be explained by comparing the situation in which two muscles with identical ber lengths have dierent moment arms at a joint (Fig. 3.4). In the case in which the moment arm is greater, muscle bers will change length much more for a given change in joint angle compared with a muscle with a shorter moment arm. As a result, the range of joint motion over which the muscle develops active force will be smaller for the muscle with the larger moment arm in spite of the fact that the mus­cular properties of both muscles are identical. e architectural design of a muscle and its placement in relation to skeletal geometry are both important determinants of its function. Although it is true that muscles with longer bers can generate force over a greater range of lengths than muscles with shorter bers (e.g., Fig. 3.3A), this does not necessarily indicate that muscles with longer bers are associated with joints that have larger ranges of motion. Muscles that appear to be designed for speed based on their long bers may not actually produce large joint velocities if they are placed in the skeleton with a very large moment arm, because joint excursion and joint angular velocity are inversely related to moment arm. A large moment arm results in a large joint moment, so that the muscle would be highly suited for torque production but at low angular velocities. Similarly, a muscle that appears to be designed for force production due to a large PCSA, if placed in a position with a very small moment arm, may actually produce high joint excursions or angular velocities. Dier­ences between muscle–joint systems thus require complete analysis of both joint and muscular properties. ese inter­related concepts of architecture and moment arm (gross anatomy) must be considered when examining the design and function of spinal muscles. is concept is fairly complex and it takes practice to become facile with such functional ana­tomic descriptions.
Summary
In this chapter, the basic functional properties of muscle sar­comeres that generate force via the cross-bridge cycle were reviewed. Muscle bers are heterogeneous, and descriptors of human muscle typically refer to types 1, 2A, and 2X, relating to the type of myosin heavy chain expressed in the bers. Finally, the major anatomic property that predicts skeletal­muscle function is muscle architecture. is arrangement of muscle bers and placement of the muscle in relation to skeletal geometry determines the moments generated at all joints—whether relatively simple, such as the elbow, or complex, such as intervertebral movement. Application of these concepts to the spine and spinal muscles is presented in more detail in Chapter 4.
(θ = 40°)
(θ = 80°)
A
Full flexion
(θ = 50°)
Full extension
(θ = 75°)
B
1.0
0.5
Relative muscle force
0.0 30 40 50 60 70 80 90
Joint angle (degrees)
FIG. 3.4 Eect of changing moment arm on active range of motion (ROM).
In this example, a schematic muscle (shown as a sarcomere in series with some tendon) is attached with two dierent moment arms. (A) 40 degrees range of motion for “normal” muscle (from 40 degrees to 80 degrees). (B) Moment arm increase results in a decrease in range of motion to 25 degrees muscle (from 50 degrees to 75 degrees). In (B), the active ROM is smaller since the moment arm is greater; therefore, more sarcomere length change occurs for a given angular rotation. (C) Comparison of force versus joint angle (ROM) for muscles with short or long moment arms.
Long moment arm (B) Short moment arm (A)

KEY REFERENCES

1. Burke RE, Levine DN, Tsairis P, Zajac FE. Physiological types and histochemical proles in motor units of the cat gastrocnemius.
J Physiol. 1973;234:723-748. This publication is the classic reference that describes the relationship between the anatomic, physiologic, and biochemical properties of the mammalian motor unit. This work helps to explain the orderly recruitment of motor neurons during normal movement.
2.
Evans WJ, Meredith CN, Cannon JG, et al. Metabolic changes
following eccentric exercise in trained and untrained men. J Appl Physiol. 1986;61:1864-1868.