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C H A P T E R 1 Embryology of the Spine
5
of intersegmental mesenchyme. In addition, a pair of myotomes and accompanying segmental nerves will be associated with each sclerotome.
As the process of differentiation continues, each sclerotome will divide
into a cranial region of relatively loosely packed cells and a caudal portion of
rapidly proliferating and densely packed cells. At this point in spinal d evelopment, classic embryology texts describe a phenomenon by which the pace
of proliferation is so great that the caudal part of the one sclerotome begins
to overgrow into the cranial portion of the adjacent sclerotome and thereby
fusing to create a single mass of tissue destined to become the precartilaginous vertebral body. Parke (The Spine, 1999) suggests that this theory of
“resegmentation” may not be accurate, and provides compelling evidence
toward an alternate route of vertebral body formation. In his sum mary of
the recent evidence, Parke outlines a pathway of spinal development which
begins with a uniform layer of axial mesenchyme surrounding the notochord. The sclerotomal organization is still maintained with an intersegmental vessel, a nerve, and a peripheral layer of dermatomyotome associated
with each segment. However, the uniform mesenchyme undergoes a period
of differentiation by which densities develop within the loose tissues. These
dense regions will develop into the intervertebral discs and eventually pinch
off the notochord which will be trapped within the dense tissue to become
the nucleus pulposus.2 The loose tissues between the discs form the cartilaginous centrum, which is the precursor of the vertebral bodies. The caudal portion of the centrum undergoes rapid proliferation, and cells migrate
peripherally to surround the neural tube, forming the membranous neural
arches which will serve to protect the neural elements. In total, each bony
vertebral segment will consist of five ossification centers, one centrum, two
neural arches, and two costal elements.
Ossification of the vertebral bodies occurs around the ninth week of gestation and begins at the thoracolumbar junction. Ossification then proceeds
in both cranial and caudal directions, with the caudal segments demonstrating a quicker rate of ossification compared with the cranial segments. Ossification of the posterior arches begins at approximately the same time but
begins in the cervical vertebrae and proceeds in a caudal direction. As the
two neural arch centers approach midline, they begin to fuse, forming the
lamina and spinous process. Fusion of the neural arches first occurs in the
lumbar segments during the first year of life and proceeds cranially. Fusion
is not completed until ages of 5 to 8 years. The costal ossification centers
have a variable role in vertebral body formation. In the cervical spine, these
centers have a minimal contribution and may contribute to part of the foramen transversarium. In the thoracic spine, these ossification centers are the
precursors of the ribs. In the lumbosacral spine, the costal ossification centers are responsible for formation of the transverse processes and the anterolateral portion of the sacrum.
2
UPPER CERVICAL SPINE
The upper cervical spine must provide stable support for the cranial vault,
and must also position the head and its sensory organs in space. This region
has uniquely adapted to the evolutionary requirement of each species. In
humans, this area is well suited to support a large cranium while providing
approximately ± 80 degrees of lateral rotation and ± 45 degrees of flexion/
extension.
A detailed anatomic study of cervical spine anatomy was presented by
O’Rahilly and Meyer in a serial time reconstruction of human embryos
ranging from 8 to approximately 16 weeks of gestation.3 It is generally
believed that the most cranial 4 or 5 pairs of s omites are responsible for
the occipital-atlas complex. Development of this junction is regulated by
growth factors derived from the notochord as it crosses into the cranium.
The notochord travels through the middle or slightly anterior portion of
each centrum, and up through the future dens at the level of the axis. It then
makes an anterior directed turn to enter the skull just above the level of the
dens. At this time, each centrum is divided by a thickening of the notochord
that will develop into the nucleus pulposus. The true boundary between the
spine and cranium is not fully understood, with some authors suggesting
that the atlas is a standalone accessory cranial bone with the true head-neck
boundary being between the C1 and C2 articulation.
O’Rahilly and Meyer describe the centrum of the axis as being composed
of three axial columns which they termed X, Y, and Z. The first and most
cranial column, X, will develop an articulation with the anterior tubercle
of C1, forming the atlanto-dens joint space.4 By approximately 9 weeks of
gestation, the X column, or future dens, is already bounded posteriorly by
the transverse ligament and anchored into the occipital condyles by the alar
ligamentous complex. Columns Y and Z are separated by the remnants of
an intervertebral disc that may persist well into birth. Although it is generally accepted that column Z will form the centrum of the axis, the fate of
column Y remains uncertain. Some believe that it is incorporated into the
axis centrum, while other embryologists believe, based on reptilian studies,
that it is incorporated into the centrum of the atlas. Calcifications in the
three columns are readily visible by the time the embryo reached a length of
120 mm; however, fusion will not take place until 6 to 8 years of age. In some
instances, the tip of the dens may calcify independently without fusion to
the remaining axis; this is termed os odontoideum.
NEURAL DEVELOPMENT
The neural elements likewise form during gastrulation. Under control of
growth factors secreted by the prechordal plate, the ectoderm begins to
thicken at the cranial end to form the neural plate and the lateral edges of the
germinal disc fold to form the neural crests. This process is primary neurulation. As previously discussed, the neural crests meet in the midline to form
the neural tube. The tube has two open ends, the cranial and caudal neuropores, both of which communicate with the amniotic cavity. This communication allows for prenatal detection of central nervous system markers in
amniotic fluid if neural tube closure has failed to complete. There are likely
multiple foci at which neural tube closure initiates and progresses both cranially and caudally in a zipperlike fashion. The cranial neuropore is generally first to close, and final closure is not complete until about 25 days post
gestation.1 The caudal neuropore closes approximately 2 days later. Failure
of neuropore closure at the cranial end results in anencephaly, a deficiency
of skull, scalp, and forebrain. Failure of caudal neuropore closure results
in spina bifida. Once closure is completed, the neural tube must separate
from the ectoderm. This process is termed dysjunction; premature separation during this step of neurulation may pull primitive mesenchyme tissues
inside the developing neural tube, resulting in a lipomeningocele or lipomyelomeningocele.
communicate with the spinal canal.
Thickenings in the neural tube give rise to the proencephalon (forebrain), mesencephalon (midbrain), and rhombencephalon (hindbrain). A
cervical flexure will form connecting the rhombencephalon to the developing spine. The neural tube contains a lumen, the central canal of the spinal
cord, which is in continuity with the cerebral ventricles. The neural tube wall
consists of rapidly dividing neuroepithelial cells. These cells develop into
neuroblasts and form a thick layer called the mantle. While in the mantle
layer, the primitive neuroblast cells remain relatively apolar. Neuroblastic
differentiation involves transformation of the apolar cells into a bipolar
form, with elongation of one end to form the primitive axon and complex
specialization of the other end to form the dendrites. At the completion of
maturation, this cell will be the neuron. Axons of the neuron wil l protrude
peripherally through the mantle layer and form the marginal layer of the spinal cord. The mantle layer, which contains the cell nuclei, does not undergo
myelination and becomes the gray matter of the spinal cord. The axons in
the marginal layer will get myelinated and become the white matter.
As the neuroblast proliferates, the spherical neural tube begins to thicken
both ventrally and dorsally. The two areas of neuroblast are separated by
the sulcus limitans, which prevents cell migration between the two layers.
The ventral thickenings will form the basal plate which houses the motor
horn cells. The dorsal thickenings will form the alar plate which contains
the dorsal sensory neurons. The sympathetic chain is made up of neurons
that accumulate i n the “intermediate horn,” a small thickening of cells that
is found between the alar and basal plates at the level of the thoracic and
upper lumbar spine. Neurons of the dorsal sensory horn become known as
interneurons or associated neurons. These cells project axons that enter the
marginal zone and extend proximally or distally to form communications
between afferent and efferent neurons.
The spinal nerves begin to form in the fourth week after gestation.
Each nerve is composed of a ventral motor root and a dorsal sensory root.
Axons of the ventral motor horn cells project through the marginal zone
and coalesce outside of the neural tube into the ventral motor root. These
5
Incomplete separation may lead to cutaneous sinuses that
6
P A R T I Introduction to the Aging Spine
axons will continue to the motor endplates of the muscles formed from its
respective sclerotome.
The dorsal sensory root begins its development from neural crest cells,
which are of ectodermal origin. These cells migrate laterally during formation of the neural tube, forming the dorsal root ganglia, which contain the
cell bodies. Axons project proximally and distally from the ganglia. The
proximal axons make up the dorsal sensory roots and enter the neural tube
on its dorsal surface into the dorsal horn to communicate with the sensory
neurons. The distal axons join with the ventral motor fibers to compose the
spinal nerve. They will terminate in the end organs to bring afferent feedback to the central nervous system.
SACRUM AND CONUS MEDULLARIS DEVELOPMENT
Development of the neural structures in the caudal terminus of the spine
deserves some special attention. At their respective most distal points, the
neural tube and notochord coalesce into an undifferentiated cellular mass
that will develop into the coccyx, sacrum, and fifth lumbar vertebrae. This
process is the beginning of secondary neurulation. A single canal will form
within this mass through a process called canalization. Debate exists in the
literature as to whether this newly formed neural tube is initially continuous
with the primary neural tube or whether the two coalesce at a later point in
development. It is known that the chick embryo develops two distinct neural tubes that anastomose in the sacral region, while in a mouse embryo, the
secondary neural tube forms as an extension of the primary neural tube. The
pathway of secondary neurulation in humans is not yet elucidated; however,
it is known that the distal portion of the tube and central canal will regress
in a cephalic direction via a process called retrogressive differentiation. This
will give rise to the conus medullaris and will leave behind a thin film of pia
mater tissue called the filum terminale.5 Nerve root compression may result
when an abnormally thick filum terminale is present (usually greater than
2 mm in diameter).
As retrogressive differentiation continues, the position of the conus
medullaris relative to the bony spine continues to change. The conus ascends
from the level of the coccyx early in embryogenesis to rest at approximately
the L2-3 disc space by the time of birth. Asymmetric rates of growth
between the bony spine and the cord result in further caudal migration of
the conus during the fetal period so that it comes to its final resting place at
L1-2 by a few months after birth. Any final resting position of the cord at or
below the L2-3 disc space would imply a tethered cord.
ASSOCIATED ANOMALIES
While discussing spinal embryology, it is important to remember that spinal
development is not an isolated event. Multiple organ systems are developing
in parallel with the spine and often share the same germinal tissue source.
Any internal or external insult to the developing e mbryo may affect other
organ systems. The mesoderm is particularly involved in the genesis of several organs. Paraxial mesoderm, the precursor of the centrum and vertebral
column, is also responsible for formation of the dermis, skeletal muscle, and
the connective tissue of the head.6 The intermediate and lateral mesoderm
is responsible for formation of the urogenital, cardiac, and renal systems.
In children with known congenital spinal defects, the incidence of associated anomalies has been reported as high as 30% to 60%.7 The most common organ system to be affected is the genitourinary system. Mesoderm
tissues that make up the spinal column also contribute to formation of the
mesonephros. While it is the medial region of the mesoderm that forms
the vertebrae, the ventrolateral region forms the genitourinary organs.8 The
cardiopulmonary system is also commonly involved in conjunction with a
congenital spinal abnormality. These anomalies may be fatal and should be
diagnosed and treated before their associated problems progress. Diagnosis
of both congenital spinal defects and associated anomalies may be made on
prenatal ultrasound examination.
The timing of insult during fetal development also affects the rate of
associated anomalies. Tsou (1980) divided a group of 144 patients with congenital spinal anomalies into two groups: embryonic anomalies, defined as
those that occurred in the first 56 days post fertilization, and fetal anomalies, defined as those that occurred from day 57 of gestation to birth.9
They found that the rate of a ssociated defects was 7% in the fetal group
as compared with 35% in the embryonic group. Associated orthopedic
anomalies included Klippel-Feil syndrome, acetabular dysplasia, clubfoot,
congenital short leg, Sprengel deformity, coxa vara, radial clubhand, and
thumb aplasia. Nonorthopedic associated anomalies included dextrocardia,
hypospadia, microtia, lung aplasia, pulmonary arterial stenosis, imperforate
anus, mandibular anomalies, cleft palate, and hemidiaphragm.
9
CONGENITAL SPINAL ANOMALIES
Normal spinal development involves coordination between cellular tissues
and signaling pathways. Mesenchyme provides the cellular building blocks
for the structural tissues of the spine while the notochord provides signaling
molecules to organize normal development. Congenital spinal defects may
be the result of defects in mesenchymal building blocks, genetic defects in
the signaling pathways, or a combination of both. The most commonly used
classification system for congenital spinal defects, however, is not based on
the etiology of disease but rather on the radiographic morphology. Moe et
al. proposed a classification system that breaks congenital spinal defects into
three main groups: defects of formation, defects of segmentation, and complex defects of the neural tube.
Defects of Formation
Defects of formation are defined as absence of any structural portion of the
vertebral ring. The resultant deformity is a result of the anatomic structure
that failed to form properly. The most common morphological result of a
failure of formation is a hemivertebra or wedge vertebra. Classification of
hemivertebra depends on the presence of growth plates on either side of the
body. A fully segmented hemivertebra has growth plates on both sides and
is separated by a disc from both the cranial and caudal adjacent vertebral
body. A semisegmented hemivertebra only has one growth plate, and thus an
intervertebral disc is only found adjacent to either the cranial or caudal segment. A nonsegmented hemivertebra has no active growth plates or discs to
separate it from the body above or below. This is a stable situation with minimal potential for increasing deformity with growth. Another stable situation
may occur when plasticity of both the cranial and caudal adjacent vertebral
bodies allow the adjacent bodies to conform to the shape of a hemivertebra,
thus keeping the pedicles in line with the rest of the spine. This stable situation, in which the hemivertebra is referred to as being incarcerated, does not
result in a deformity and usually does not require treatment.
Although it is generally agreed that hemivertebrae are the result of the
failure of formation, the exact pathophysiology has not yet been elucidated.
It is helpful to separate failures of formation as those occurring during
the embryonic period and those that occur in the fetal period. During the
embryonic stage, most authors propose a theory of “segmental shift,” which
occurs during the sclerotomic pairing phase of embryogenesis.9 As the
somites join in the midline, it is assumed that each somite is in the same
developmental phase as its counterpart across the midline. This development usually proceeds in a predictable pattern from a cranial to caudal
direction. Asynchronous development of one somite in a hemimetameric
pair may prevent normal midline fusion and result in a caudal shift of the
column such that the two contralateral pairs are in a synchronous phase of
development. This would leave an isolated out-of-phase hemivertebra without a cross-midline counterpart (Figure 1-4). This segmental shift theory is
further supported by the presence of double-balanced hemivertebra where
each of the asynchronous hemi-vertebra is found on one side of the midline. The most caudal hemivertebra is commonly found at the lumbosacral
junction where there is no further room for compensation from the somite
below. Another mechanism for hemivertebra formation may result from
a physiologic insult to the somite precursor during the embryonic period.
Although midline fusion occurs between corresponding somites, the injured
hemimetameric pair may undergo growth retardation of variable severity.
Mild growth retardation may result in a hypoplastic hemivertebra in which
the growth plates are formed, but the rate of growth is not equal to the
opposite side. More severe forms of sclerotome growth retardation may
result in a failure of segmentation and will be discussed later.
Insults to the growing spine during the embryonic stage tend to globally
affect the vertebral segment, including both posterior and anterior elements.
Insults occurring during the fetal period tend to be more specific and only
FI G UR E 1 - 4 Hemimetameric pairing: a defect of formation may occur
when adjacent pairs of somites are out of developmental phase with their crossmidline counterpart. This results in a caudal shift of hemimetameric pairing. An
isolated hemivertebra is left without a cross-midline counterpart. This hemivertebra may be balanced by another hemivertebra at the sacral end of the
contralateral side, resulting in minimal overall deformity. (Reprinted from Tsou
PM et al: Clin Orthop Relat Res 152: 218, 1980.)
affect a portion of the vertebra, the centrum being the area most commonly
afflicted. Centrum hypoplasia and aplasia is described by Tsou as a spectrum of growth retardation that occurs from 2 to 7 months post fertilization during a period of normally rapid vertebral growth.9 A vascular etiology
for centrum aplasia and hypoplasia was proposed by S chmorl and Junghanns; however, this has not yet been proven. Identification of these failures
of formation is clinically important as they may often result in structural
deformity of the spine. Centrum aplasia and posterior hemicentrum have
been shown to cause an isolated kyphotic d eformity, while wedge vertebra,
posterior corner hemivertebra, and a lateral hemicentrum more commonly
cause a mixed kyphoscoliotic deformity.
6
Defects of Segmentation
Defects in segmentation occur when two or more adjacent vertebrae fail to
fully separate resulting in a complete or partial loss of the growth plate. The
extent and location of the defect largely determines the resultant deformity.
One mechanism of segmentation failure involves a more advanced form of
hemimetamer hypoplasia. As cells of the sclerotome undergo their migration, they first feed formation of the centrum, followed by the neural arches.
A deficiency in the quantity of sclerotome would f irst manifest itself as a
deficit in the neural arch formation, as they are last to receive the migrating
cells. The resultant hypoplasia ha s a variable amount of penetrance. In the
mildest form, only the lamina may be fused, followed by fusion of the facet
joints. More severe forms involve fusion of the entire hemivertebra in which
the adjacent level lamina, facet joints, and pedicles are fused into a single
posterolateral bar.
Segmentation defects may also occur during formation of the intervertebral disc or the adjacent articulations. By the late embryonic period, mesodermal cells have migrated around the notochord and formed dense collections
of tissues which will form the annulus fibrosus. In a more common form
of seg mentation defect, the anterior portion of the annulus u ndergoes first
what Tsou describes as a cartilaginous transformation, followed by osseous
metaplasia.9 A bony bar forms between two or more adjacent vertebral bodies as ossification continues into childhood. This anterior tether may result
in a severe kyphotic deformity that worsens with continued growth.
Posterior elements are also prone to failures of segmentation. The
articulating facet joints form via condensation of mesenchymal tissues that
extend in a superior and inferior direction away from the pedicle. Injury to
the developing mesenchyme in the neural arches during the later portion of
C H A P T E R 1 Embryology of the Spine
the embryonic period may interrupt normal development of the apophyseal
joints. A cartilaginous bridge forms between the superior and inferior articulating processes of two adjacent vertebral segments. This bridge undergoes
ossification during early childhood and provides a posterior growth tether.
Unilateral involvement would lead to a lordoscoliotic deformity and bilateral
bars would lead to a pure lordotic deformity.
Spina Bifida
Derived from the Latin term bifidus, spina bifida literally means a spine split
in two. Although the severity of the disease may range from a benign incidental finding on x-ray to s evere neurologic damage, the etiology remains
the same, a failure of the embryonic vertebral arches to fuse. Causes for this
lack of fusion are multifactorial. Mitchell (1997) suggested a weak genetic
component by demonstrating an increased risk in siblings of affected children and even further increased risk with multiple affected siblings.10 Environmental factors also play a role in the etiology of spina bifida. Mitchell
correlated incidence with time of season, geographic location, ethnicity, race,
socioeconomic status, maternal age and parity, and maternal nutritional status, specifically the dietary intake of folic acid and alcohol. Although the
mechanism by which folic acid aids in neural tube closure is unknown, the
role of folic acid as a substrate in DNA synthesis has been well described.
An enzyme called methyl tetra hydroxy folate reductase (MTHFR) is
involved in folate metabolism during DNA synthesis. Genetic alterations
in this enzyme may lead to decreased enzymatic activity and increase the
dietary folate requirements for proper DNA synthesis. As neural tube closure has been shown to begin early in the embryonic period, it is vital to
begin folate supplementation as early as possible in the prenatal period and
encourage dietary supplementation during family planning.
Spinal bifida occulta, one of the more benign forms of spinal bifida,
results from a failure of fusion of the lamina. This relatively common finding has a reported incidence of 10% to 24% in the general population. The
disease implies involvement of the posterior arches only and sparing of the
cord and meninges from the pathology. Patients typically do not present
with any neurological symptoms. Physical exam signs may include skin
indentation and/or patches of irregular hair growth in the region of the
lower lumbar spine. The most typical diagnosis is made an incidental finding on an x-ray of the lumbar spine. Rarely, associated defects may exist in
conjunction with spina bidifa occulta. These may include a tethered cord,
distortion of the cord by fibrous bands, syrinx, lipomyelomeningocele, a
fatty filum terminale, or diastematomyelia. Collectively, these associated disorders are grouped into a term called occult spinal dystrophism.
Spina bifida cystica refers to a more severe form of spina bifida; it can
be broken down into several subgroups based on the degree of the involved
tissue layers.6 The first group, spina bifida with meningocele, involves the
meninges as well as the posterior arches. A cystic pouch is present within
the meninges without involvement of the spinal cord or nerve roots. Patients
are typically spared neurologically. Physical exam findings may be similar to
those of spina bifida occulta, but also include subcutaneous lipomas and
hemangiomas adjacent to the lesion. Spina bifida with myelomeningocele is
the next most severe form of spina bifida. This disease results from failure
of fusion in the p osterior arches with involvement of the spinal cord and
meninges. By definition, in spina bifida with myelomeningocele, the neural
elements are not exposed to the external environment and are covered by a
membranous cerebrospinal fluid–fi lled sac. This disease typically pre sents
with neurological disorder based on the neurological level of the lesion.
Associated anomalies include Arnold-Chiari malformation, hydrocephalus,
scoliosis, and kyphosis. The most severe manifestation of spina bifida cystica is myeloschisis. In this severe presentation the neural elements are completely exposed. Neurologic injury is certain and infections are common.
CONCLUSION
Clinicians treating spinal disorders may be nefit from an understanding of
the processes that drive spinal embryogenesis and the origin of common disorders affecting the spine. The process of embryogenesis is extremely complicated, but incredibly well synchronized. Multiple events happen in series
and in parallel, all under the control of signaling pathways that are just now
becoming understood. Spine development has been widely elucidated using
7
8
P A R T I Introduction to the Aging Spine
human and animal data; however there remain many unknowns, especially
on a molecular level. It is vital to remember that disorders of spinal development may not be isolated events; other organ systems are often affected.
Awareness and early intervention may be required for optimal patient care.
References
1. T.W. Sadler, Medical embryology, ninth ed., Lippincott Williams & Wilkins, Baltimore,
2004.
2. H.N. Herkowitz, S.R. Garfin, F.J. Eismont, G.R. Bell, Rothman-Simeone the spine,
WB Saunders, Philadelphia, 1999.
3. R. O’Rahilly, D.B. Meyer, The timing and sequence of events in the development of the
human vertebral column during the embryonic period proper, Anat. Embryol. (Berl) 157 (2)
(1979) 167–176.
4. R. O’Rahilly, F. Muller, D.B. Meyer, The human vertebral column at the end of the embryonic
period proper. 2. The occipitocervical region, J. Anat. 136 (1) (1983) 181–195.
5. J.D. Grimme, M. Castillo, Congenital anomalies of the spine, Neuroimaging Clin. N. Am. 17
(1) (2007) 1–16.
6. K.M. Kaplan, J.M. Spivak, J.A. Bendo, Embryology of the spine and associated congenital
abnormalities, Spine J. 5 (5) (2005) 564–576.
7. D. Jaskwhich, et al., Congenital scoliosis, Curr. Opin. Pediatr. 12 (1) (2000) 61–66.
8. G.D. MacEwen, R.B. Winter, J.H. Hardy, Evaluation of kidney anomalies in congenital
scoliosis, J. Bone Joint Surg. Am. 54 (7) (1972) 1451–1454.
9. P.M. Tsou, Embryology of congenital kyphosis, Clin. Orthop. Relat. Res. (128) (1977) 18–25.
10. L.E. Mitchell, Genetic epidemiology of birth defects: nonsyndromic cleft lip and neural tube
defects, Epidemiol. Rev. 19 (1) (1997) 61–68.
Applied Anatomy of the Normal
and Aging Spine
Rajesh G. Arakal, Malary Mani and Ravi Ramachandran
k e y p o i n t s
Cervical disc herniations most often affect the exiting root.
Lumbar posterolateral herniations most often affect the root of the respective
lower foramen.
Acquired lateral recess stenosis is most often a result of hypertrophy of the
superior articulating facet.
Degenerative spondylolisthesis is most common at L4-5 and can entrap the
L4 nerve root.
Aging affects every aspect of the spine, from mineral density of the bones, to
the physiology of the intervertebral discs, to the muscular scaffold around the
spine.
“Chance favors the prepared mind.” The spinal column consists of 33 vertebrae and is divided into seven cervical, twelve thoracic, and five lumbar
vertebrae. The lumbar vertebrae articulate with the sacrum, which in turn
articulates with the pelvis. Below the sacrum are the four or five irregular
ossicles of the coccyx.
THE VERTEBRAE
The articulations of the spine are based on synovial and fibrocartilaginous
joints. The overall morphology of the vertebral column has a basic similarity,
with the exception of the first two cervical vertebrae and the sacrum. A vertebra consists of a cylindrical ventral body of trabecularized cancellous bone
and a dorsal vertebral arch that is much more cortical. From the cervical to
the lumbar spine, there is a significant increase in the size of the vertebral
bodies. An exception is the sixth cervical vertebra, which is usually shorter
in height than the fifth and seventh vertebrae. In the thoracic spine, the vertebral body has facets for rib articulations. The posterior aspect ofthe vertebra starts with a posterior apex or spinous process. This process then flows
into flat lamina that arch over the spinal canal and attach to the main body
through a cylindrical pillar or pedicle. The transverse processes are found at
the junction of the confluence of the laminae and pedicles and extend laterally. In the upper six cervical vertebrae, this component is part of the bony
covering of the vertebral arteries. In the thoracic spine, the transverse process
articulates with ribs. A mature and robust transverse process is found in the
lumbar spine, with the remnant neural arch structure forming a mammillary
process (Figure 2-1).
There are points of articulation between the individual vertebral
segments between an inferior and ventral facing facet and a superior
and dorsal facing facet. It is a diarthrodial, synovial joint. The shape of
the facets is coronally oriented in the cervical spine, thus allowing for
flexion-extension, lateral bending, and rotation. The facets are sagitally
oriented in the lumbar spine and thus resist rotation, while allowing for
FI G UR E 2 -1 The Vertebrae
some flexion and some translational motion.
mamillary bony prominences upon which muscles can originate and
insert.
The pedicles are the columns that connect the posterior elements to the
anterior vertebral body. The transverse pedicle widths vary in size, but generally tend to larger dimension from the midthoracic to the lumbar spine, with
a decrease of pedicle width from the lower cervical to the upper thoracic
spine. Sagittal pedicle height increases from C3 to the thoracolumbar junction and then decreases from the upper lumbar region to the sacrum. The
angles at which the pedicles articulate to the body also vary depending on
the level. The windows formed between the pedicles transmit the nerves and
vessels that correspond to that body segment.
The portion of the posterior arch most subject to stress by translational
motion is the pars interarticularis, which lies between the superior and inferior articular facets of each mobile vertebra. Clinically, fracture of this elongated bony segment in the C2 vertebra results in the hangman’s fracture; in
7 Cervical vertebrae
12 Thoracic vertebrae
5 Lumbar vertebrae
Sacrum
Coccyx
2
1
Lateral to these joints are
9
10
Spinous
P A R T I Introduction to the Aging Spine
the lower lumbar spine, it results in isthmic spondylolisthesis. The shear
forces often result in ventral displacement of the superior articular facet,
pedicle, and vertebral body and in maintenance of the attachments of the
inferior articular facets and relationships to the lower vertebrae.
eric studies, the L5 pars region was particularly susceptible to fracture, given
its smaller cross-sectional area of 15 mm
brae, which had over a fourfold increase.
2
compared to the L1 and L3 verte-
3
2
In cadav-
Cervical Vertebrae
Forward flexion and rotation are largely attributed to the first two cervical
vertebrae. The atlas is the first cervical vertebra. It is a bony ring with an
anterior and posterior arch connected with relatively two large lateral masses.
The superior articular facet of the lateral mass is sloped internally to accommodate the occipital condyles. The inferior portion is sloped externally to
articulate with the axis. This inferior articulation allows for rotational freedom while limiting lateral shifts. The posterior arch of C1 is grooved laterally
to fit the vertebral arteries as they ascend from the foramen transversarium
of C1 to penetrate the posterior atlanto-occipital membrane within 20 to
15 mm lateral to the midline. It is recommended that one remain within
12 mm lateral to midline during dissection of the posterior aspect of the
4
ring.
The anterior arch connects the two lateral masses, and the anterior
tubercle in the most ventral portion is the site of attachment for the longus
colli. The ventral side of the anterior arch has a synovial articulation with the
odontoid process. The odontoid is restrained at this site with thick transverse atlantal ligaments that attach to the lateral masses (Figure 2-2).
The axis is the second cervical vertebra. The odontoid process, a rem-
nant of the centrum of C1, projects from the body of C2 superiorly. This
anatomy, unique to the cervical spine, allows for a strong rotational pivot
with limitations on horizontal shear. Apical ligaments attach superiorly and
alar ligaments attach laterally on the odontoid to the base of the skull at
the basion. The basion is the anterior aspect of the foramen magnum. The
superior aspects of the lateral masses are directed laterally and are convex to
accommodate the atlas. The inferior articulations of the axis are similar to
the remainder of the subaxial spine with a 45 degree sagittal orientation of
the facets.
The cervical vertebrae are smaller in dimension than the lumbar vertebrae because they bear less weight than their lumbar counterparts. They
are wider in the coronal plane in relation to the sagittal plane. The superior
lateral edges of the vertebrae form the uncinate processes. The lateral processes have openings for the superior transit of the vertebral artery; these
are called the foramen transversarium. During instrumentation of the lateral masses, it should be noted that as one descends from the upper cervical levels to C6, the foramen is more laterally positioned respective to the
midpoint of the lateral mass. Anterior and posterior cervical musculature
attach to their respective tubercles in the lateral portions of the transverse
process. The seventh cervical vertebra is a transitional segment and has a
long spinous process or vertebra prominens. The vertebral arteries usually
enter the transverse foramen at C6 and omit the passage through the C7
foramen.
Thoracic Vertebrae
The thoracic vertebrae are heart-shaped and have dual articulations for both
ribs as well as for the superior and inferior vertebrae. The transverse diameter of the pedicles is smallest from T3 to T6. At T1, the transverse diameter
Vertebral
foramen
Lamina
transverse process
FI G UR E 2 -2 Cervical Vertebrae
Superior articular
process
Foramen of the
Spinous
process
process
Pedicle
Vertebral
foramen
Superior articular
process
Transverse
process
Pedicle
Lamina
Transverse
process
Facets for articulation
Vertebral body
Facet on transverse
process for articulation
with tubercle of rib
Superior vertebral
Body
with head of rib
Inferior vertebral
Superior vertebral
notch
Transverse process
Spinous
process
Inferior vertebral
notch
notch
notch
FI G UR E 2 -3 Thoracic Vertebrae
Vertebral body
Superior and
inferior articular
processes
C H A P T E R 2 Applied Anatomy of the Normal and Aging Spine
Lamina
11
Spine
Superior
articular
process
Body
FI G UR E 2 -4 Lumbar Vertebrae
Vertebral foramen
Pedicle
is larger, with an average of 7.3 mm in men and 6.4 mm in women.5 The
first thoracic vertebra has a complete facet on the side of the body for the
first rib head and an inferior demifacet for the second rib head. The ninth to
twelfth vertebrae have costal articulations with their respective ribs. The last
two ribs are smaller and do not attach to the sternum. The thoracic facets are
rotated 20 degrees forward on the coronal plane and 60 degrees superiorly
on the sagittal plane (Figure 2-3).
Lumbosacral Spine
The lumbar vertebrae are much larger in overall relative proportion. The
articular facets are concave and directed approximately 45 degrees medially
on the coronal plane. The fourth transverse process tends to be smallest in
comparison to the proximal lumbar segments. The fifth transverse process
is the most robust (Figure 2-4).
The sacrum is the complex of five fused vertebra that articulates with
the fifth lumbar vertebrae. There are both dorsal and ventral foramina. The
ventral portion is relatively larger. The dorsal aspect of the sacrum is composed of ridges that are formed from the fusion of the spinous processes of
the respective sacral vertebrae. At the superior margin, the articulation with
the fifth lumbar vertebra is almost purely dorsal. This provides necessary
restraint from a ventral translation at the lumbosacral junction.
The coccyx is the rudimentary remnant of the tail. It acts to provide
attachment for the gluteus maximus and the pelvic diaphragm.
Loss of normal bone within the vertebrae is characteristic of osteoporosis.
Primary osteoporosis affects the trabecular bone and is associated with
vertebral compression fractures. This is most commonly seen in postmenopausal women, secondary to the sensitivity of the skeleton to estrogen loss.
Secondary osteoporosis affects the trabecular and cortical bone and is a
result of aging and prolonged calcium deficiency.
INTERVERTEBRAL DISC
The fibrocartilaginous nature of the disc provides mobility while maintaining relative structural orientation in the spine. The disc is most commonly
divided into the outer annulus fibrosus and the inner nucleus pulposus.
The annulus is a concentric mesh that surrounds the nucleus and resists
tensile forces. The individual lamella can run obliquely or in a spiral manner
in relation to the spinal column. Furthermore, there can be alterations in the
direction of the fibers. On a sagittal section, the fibers are pointed slightly
to the nucleus pulposus in its proximity, find a vertical orientation moving
outward, and then finally bow out at its periphery. The fibers of the nucleus
and inner lamellae are interposed into the cancellous bone of the vertebrae.
The outer rings penetrate as Sharpey fibers with dense attachments into
the verterbral periosteum and the anterior and posterior longitudinal ligaments (Figure 2-5).
The nucleus pulposus is usually confined within the annulus. It has a
large number of fusiform cells in a heterogenous matrix. This allows for the
ability of the disc material to bulge and recoil back with pressure. The fibers
are not in any one orientation in histologic section and are the embryological
remnant of the notochord.
Superior articular
Transverse process
Transverse
process
Annulus fibrosus
FI G UR E 2 -5 Anatomy of the intervertebral disc
process
Body
Inferior articular
process
Lamellae
Spine
Nucleus pulposus
From the cervical to the lumbar spine, there are further variations at
the disc level. There are uncovertebral “joints” that develop during the first
decade; these are superior extensions of the uncinate processes with a corresponding slope from the superior vertebra. Anteriorly, the discs are wider
in the cervical and lumbar spine, which results in cervical lordosis and a
lumbar lordosis of 40 to 80 degrees. The thoracic kyphosis from 20 degrees
to 50 degrees is mostly attributed to a disproportionately larger posterior
vertebral body and smaller anterior height to contrast with a uniform disc
height.
Disc degeneration with aging may be a component of the enzymatic
activity resulting in an active breakdown of collagen, proteoglycans, and
fibronectin. Proteoglycans are diminished with aging.
6
ated by various enzymes including cathepsins, matrix metalloproteinases,
7
Aggrecan is degener-
and aggrecanases. Various mutations in genes can result in a genetic predisposition to disc degeneration, including defects of genes involving vitamin D
8
receptor,
collagen IX,9 collagen II, and aggrecan.
LIGAMENTS
The dorsal lamina articulate with the adjacent segments through the ligamentum flavum, interspinous ligaments, supraspinous ligaments, and intertransverse ligaments. The ligamentum flavum attaches superiorly on the
ventral side of the lamina, laterally on the base of the articulating facets, and
inferiorly on the superior aspect of the lamina. With aging, the fibers may
lose some of the material properties allowing for redundancy and laxity with
extension. The ligamentum is a dual-layered structure that flows along both
sides of the spine, with a central deficiency. The spinous processes are connected by the oblique interspinous ligaments. The supraspinous ligament
connects the apices of the spinous processes. In the cervical spine, this
structure is known as the ligamentum nuchae (Figure 2-6).
Intraspinal Ligaments
The anterior longitudinal ligament drapes ventrally from the axis to the
sacrum. Superficial layers span multiple segments with the deep layer spanning one spinal segment. In a similar fashion, the posterior longitudinal
12
Posterior
P A R T I Introduction to the Aging Spine
longitudinal
ligament
Ligamentum
flavum
Interspinous
ligament
Supraspinous
ligament
Facet capsulary
ligament
Intertransversus
ligament
FI G UR E 2 -6 Ligaments of the spine
Anterior
longitudinal
ligament
ligament (PLL) has superficial and deep layers. The deep layer forms a
dense central vertical strap with lateral attachments to the disc. Disc protrusions are likely more frequent posterolaterally, secondary to the stronger
tether centrally. The peridural membrane is an additional layer between the
PLL and the dura.
10
THE NERVE ROOTS
Due to the differential growth of the lower segments of the spine in relation
to the more cranial segments, the dorsal and ventral roots converge to form
the spinal nerve at a more oblique angle toward the intervertebral foramen
more distally. In the cervical region, the root and the spinal nerve are at the
same level as the disc and the intervertebral foramen. In the lumbar spine, the
contributing roots for the nerve are descending to the next lower foramen.
A posterolateral disc herniation will affect the nerve root of the respective
lower foramen. The spinal nerves typically are in close proximity to the
underside of the respective pedicle with narrower margins in the cervical
and thoracic spine, and approximately 0.8 to 6.0 mm in the lumbar spine.
11
The lumbosacral root ganglia are usually in the intraforaminal region with
variations medial and lateral to the foramina.
Anatomic variations can exist, with prevalence from 4% to 14% in various reports. Apart from anomalous levels of origin, there can be interconnections and divisions between nerves both intradural and extradural.
Furthermore, the origins of the motor segments from within the ventral
horn may allow for contributions to more than one nerve root. The description of the furcal nerve is most commonly applied to the cross-connection
between the fourth and fifth lumbar nerve roots.
12
This is relevant because
of the interconnections of the femoral and obturator nerves of the lumbar
plexus to the lumbosacral trunk of the sacral plexus. Compression can
result in mixed neurologic findings warranting careful investigation into the
underlying pathology.
THE INTERVERTEBRAL FORAMEN
The nerves traverse through the vertically elliptical window of the foramen. The borders of the foramen are defined anteriorly by the dorsal intervertebral disc and posterior longitudinal ligament. The posterior border
is bounded by the ligamentum flavum and the facet capsule. Frequently,
it is a sagittal narrowing that results in pathologic nerve compression.
Furthermore, thenerves can be tethered by transforaminal ligaments with
attachments to the capsule, pedicle, and disc.
INNERVATION OF THE SPINE
Emanating from the dorsal root ganglion are rami communicantes that connect to the autonomic ganglion. Sinuvertebral nerves emanate from the rami
communicantes close to the spinal nerve and enter back into the spinal canal
to divide into branches than may innervate the posterior longitudinal ligament,
and possibly, the dorsolateral aspects of the disc.
13
Branches may innervate more
than one disc level, leading to the nonspecific locations of back pain. Afferent
pain fibers are well documented within the histologic analysis of the sinuvertebral nerve. Meningeal fibers of these pain afferents to the ventral aspect of
the dura may allow for explanations of back pain with dural distortion. There
are intraspinal ligaments of Hoffman which normally tether the dura ventrally.
Adhesions in the ventral aspect of the dura can also be acquired, resulting in
a more anchored structure susceptible to external compression (Figure 2-7).
NUTRITIONAL SUPPORT FOR THE VERTEBRA AND DISC
Paired segmental arteries branch posteriorly from the aorta to supply the
second thoracic to the fifth lumbar vertebrae. These segmentals approach
the middle of the vertebral artery and divide into dorsal and lateral branches.
The dorsal branch courses lateral to the foramen, gives off the dominant spinal branch artery, and then supplies the posterior musculature. The spinal
branch arteries off the dorsal artery are the major arterial supply to the
vertebrae and the spinal canal. Segmentation off the dorsal branch vascularizes the posterior longitudinal ligament and dura, and enters in the center of
the concavity of the dorsal vertebra. Anastomoses are common between fine
branches from the left and right of each segment as well as from cranially
and caudally. The lateral segmental branch has offshoots that penetrate the
cortical body and the anterior longitudinal ligament.
An important variation is the contribution of segmental arteries in the
lower thoracic or upper lumbar region to form a large radicular artery of
Adamkiewicz, which joins the anterior spinal artery at the level of the conus
medullaris.
14
Although the disc has no direct arterial supply, disc nutrition
is dependent on the diffusion principles, size, and charge of particles. Specifically, the central aspect of the disc has a collective negative charge and is
reliant on effective glucose transport from the vasculature of the endplates.
Alterations of the precarious nutritional diffusion with age and pathologic
processes can initiate a degenerative cascade.
MUSCULAR ANATOMY
The muscles that are involved in spinal motion are the largest in the body.
The strength of contraction is related to size, fiber type, and number but not
limited to these factors. Other factors that may be pertinent to the competence of the muscular system with aging include the effect of neural stimulation, hormones, and conditioning. In the lumbar spine, the spinalis muscle
goes between the spinous processes. The multifidi go upward and span two
to four segments. The longissimus inserts into the tips of the spinous processes. The iliocostalis inserts into the ribs, and is the most lateral of the posterior lumbar spine intrinsic musculature. The psoas major acts anteriorly
and is an important stabilizer in standing and sitting postures. As there are
altered use patterns and conditioning with age, important stabilizers are
affected, contributing to spinal deformity and altered motion (Figure 2-8).
PATHOLOGIC CHANGES IN AGING
With aging, degenerative processes can result in the common pathologies
of spinal stenosis, spondylolisthesis, spondylosis, diffuse idiopathic skeletal
hyperostosis, and degenerative scoliosis. These changes will be discussed
in greater detail in the following chapters. Anatomic changes in the normal joints and perineural structures result in slowly progressive narrowing
and compression of the nerves. In the cervical spine, spinal stenosis can be
both central and foraminal. Central compression can result in spondylotic
myelopathy. Degenerative changes of the facet joints can result in joint laxity and instability. Such pathologic subluxation can give rise to degenerative
spondylolisthesis. Arthritic changes can result in mechanical irritation and
pain. The cluster of changes in the spinal complex can also result in a scoliotic collapse or adult degenerative scoliosis.
C H A P T E R 2 Applied Anatomy of the Normal and Aging Spine
Dorsal ramus branches
13
Dural sac
Nerve
root
Sinu-vertebral
nerve
FI G UR E 2 -7 Innervation of the spine
Transversospinalis
(semispinalis)
Posterior
longitudinal
ligament
Suboccipital
muscles
Transversospinalis
(semispinalis capitis)
(Semispinalis
cervicis)
Sinu-vertebral
nerve
Intermediate
Lateral
Dorsal
ramus
Splenius
Medial
Nerve
root
Nerve branches
C7
Sinu-vertebral
nerve
Transversospinalis
(multifidus)
FI G UR E 2 -8 Posterior musculature of the spine
Spinal Stenosis
Local pain and discomfort can result from pathologic changes in the caliber
of the spinal canal both centrally and at the foraminal level. Direct mechanical compression of the dural sac and the nerve roots can result in pain and
extremity weakness. Pain in the axial region can arise from pathologic
changes to the sinuvertebral nerve and posterior primary ramus. Cervical
stenosis is most commonly acquired or a result of degenerative spondylotic
changes. As the intervertebral discs collapse, the annular bulge can narrow
T6
Iliocostalis
Longissimus Erector
Spinalis
L1
spinae
the canal. Furthermore, posterior buckling of the ligamentum flavum can
contribute to cord compression. Osteophytes may form both centrally and
foraminally, exacerbating the compression. In the lumbar spine, similarly, the
stenosis may be both central and/or lateral. Lateral recess stenosis is usually
the result of hypertrophy of the superior articulating facet. Foraminal stenosis can result from direct osteophytic growth, facet subluxation, or a vertical
disc collapse. Degenerative synovial cysts can often result in compression
and can mimic symptoms of spinal stenosis (Figure 2-9).
14
FI G UR E 2 -9 T2 MRI saggital and axial image of spinal stenosis
P A R T I Introduction to the Aging Spine
Standing
FI G UR E 2 -1 0 Lateral radiograph demonstrating anterolisthesis
Spondylolisthesis
Degenerative spondylolisthesis is most commonly a result of the pathologic
degeneration of the facet joints. Asymmetry of this degeneration can result in
a rotational deformity, along with translation. The L4-5 level is the most common level and can result in entrapment of the L4 root. The root can be caught
between the inferior articulating facet of L4 and the body of L5 (Figure 2-10).
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
DISH predominantly affects middle-aged men and is characterized by prolific bone formation around the spine and in the extremities. Associated diseases are diabetes mellitus and gout. The most commonly affected area is the
F IG UR E 2 -1 1 Scoliosis view of adult degenerative scoliosis
thoracolumbar spine. Often large spurs form on the anterolateral aspect of
the vertebral body and flow into a contiguous bar. This is more common on
the right side. The most common complaint is stiffness. The facet joints and
sacroiliac joints are largely spared in this entity (Figure 2-12).
Degenerative Scoliosis and Kyphosis
Scoliosis, as a subset in patients with no preexisting scoliosis at the time of
skeletal maturity, can be a disease of the degenerative cascade, osteoporosis,
trauma, and/or iatrogenic from prior surgical intervention. Although any
curve has the potential for progression, large curves greater than 60 degrees
tend to progress with greater probability. One of the greatest risk factors for
kyphosis is osteoporosis and the ensuing compression fracture (Figure 2-11).