Vertebral Column and Back

Part 4 · The trunk

The curves, the disc, the facet joints and the back muscles

The central problem

The vertebral column has to be a rigid mast that supports the head and transmits load to the pelvis, a flexible rod that permits movement in three planes, and an armoured tube that protects the spinal cord — all at once, in a structure that is loaded every waking hour.

It solves the problem by segmentation: 33 vertebrae, each moving only a few degrees, summing to a large total range. Segmentation also creates the vulnerability: 23 intervertebral discs, 46 facet joints, and dozens of ligaments and nerve roots, any one of which can become a symptom generator.

Low back pain is the leading cause of years lived with disability worldwide. Neck pain is not far behind. No other region in this book has a comparable clinical footprint, and none is more surrounded by outdated teaching. This chapter covers both the anatomy and the corrections.

Learning outcomes

• Describe the regional and functional organisation of the vertebral column and the curvatures.
• Describe a typical vertebra and the distinguishing features of cervical, thoracic and lumbar vertebrae.
• Describe the atypical vertebrae, the atlanto-occipital and atlanto-axial joints, and the sacrum and coccyx.
• Describe the intervertebral disc in structural, biochemical and mechanical detail, including its nutrition.
• Describe the zygapophysial (facet) joints, their orientation by region, and the consequences for movement.
• Describe the ligaments of the column and their functions.
• Describe the back muscles in three layers and explain the thoracolumbar fascia.
• Describe the vertebral canal, its contents, the spinal nerve and its rami, and the blood supply of the cord.
• Explain coupled motion, the lumbopelvic rhythm and segmental instability.
• Explain disc herniation, spondylolysis and spondylolisthesis, stenosis, scoliosis, whiplash and cauda equina syndrome — and apply current evidence to low back pain management.

Organisation and curvatures

Figure 1 · The five regions

Curvatures

Primary curves follow the shape of the fetal C-curve and are due to vertebral body shape; secondary curves develop with postural milestones and are maintained largely by disc wedging.

Functional value of the curves: a curved column resists axial compression far better than a straight one. The classic engineering approximation is resistance ∝ (number of curves)² + 1 — giving a curved column roughly ten times the resistance of a straight rod. Whether or not the formula is exact, the principle is sound and it explains why the loss of lordosis under sustained flexion is mechanically costly.

Abnormal curvatures: excessive kyphosis (Scheuermann’s disease in adolescents, osteoporotic vertebral wedging in the elderly), excessive lordosis (hyperlordosis), scoliosis (§17.11) and gibbus (an angular kyphosis, classically from spinal tuberculosis — Pott’s disease — still relevant in India).

The typical vertebra and regional variation

Figure 2 · A typical vertebra, and the ones that break the plan

Typical vertebra

Regional distinguishing features

Facet orientation is the whole story of regional movement

The facets act as bony guides. In the cervical spine their oblique frontal orientation permits flexion, extension, lateral flexion and free rotation. In the thoracic spine their frontal orientation permits rotation but the ribs restrict everything else. In the lumbar spine their sagittal orientation permits substantial flexion and extension but blocks rotation — total lumbar axial rotation is only about 10–13° across all five segments, and forcing rotation there loads the facets and the anulus in a way they are not designed for.

This single fact explains why lumbar rotation manipulations must be applied with care, why “rotate from the hips and thoracic spine” is sound advice for golfers and throwers, and why thoracic mobility deficits so often present as lumbar or cervical symptoms.

Atypical vertebrae

Transitional anomalies are common and clinically relevant: sacralisation of L5 (fused to the sacrum) and lumbarisation of S1 (a free S1) occur in around 4–8% of people, and mis-numbering the segments is a well-documented source of wrong-level surgery.

The craniovertebral joints

The alar ligaments (dens to the occipital condyles) limit rotation and are tested by the alar ligament stress test. Upper cervical instability — from rheumatoid arthritis, Down syndrome, Marfan syndrome, os odontoideum, or trauma — is an absolute contraindication to cervical manipulation and must be screened for.

The intervertebral disc

Figure 3 · The intervertebral disc

23 discs, from C2–C3 to L5–S1 (none between C1–C2 or within the sacrum). The largest avascular structure in the body.

Structure

The alternating fibre orientation matters: in any given rotation, only about half the lamellae are engaged — those oriented with the direction of twist. This halves the anulus’s torsional strength compared to its tensile strength, and is why rotation combined with flexion and compression is the most damaging loading pattern for the disc, and why lumbar segments (which cannot rotate much anyway) are damaged by it.

Nutrition

The adult disc has no blood supply of its own beyond the outer few millimetres of anulus. Nutrition reaches the nucleus by diffusion through the vertebral endplates (the dominant route) and through the outer anulus, driven by convection from cyclical loading exactly as in articular cartilage (Chapter 3).

Consequences:

• Movement is nutrition. Sustained static loading — prolonged sitting, prolonged standing, prolonged bed rest — impairs disc nutrition. This is one of the strongest anatomical arguments for movement variety rather than “correct posture”
• Endplate calcification with age progressively blocks the diffusion route, which is the principal driver of age-related disc degeneration
• Smoking reduces endplate perfusion and is an independent risk factor for disc degeneration

Diurnal variation and creep

Disc height falls through the day as fluid is expressed under load and recovers overnight. Adults lose 1–2 cm of stature over a day, most of it in the first few hours of being upright.

Clinically: disc pressure, bending stresses and the risk of anular strain are highest in the first hour or two after rising. Advising a patient with disc-related pain to avoid heavy lifting and end-range lumbar flexion first thing in the morning is anatomically sound advice, and it is one of the few genuinely mechanical pieces of advice worth giving.

Disc pressures (Nachemson, and later in-vivo work)

Approximate intradiscal pressure relative to standing (=100%):

The classical teaching that “sitting is worse than standing” is broadly supported, though later in-vivo measurements (Wilke et al.) found smaller differences than Nachemson’s original figures. The clinically defensible message is not “sit correctly” but “change position regularly” — sustained loading in any posture is the problem.

The zygapophysial (facet) joints

Figure 4 · Why each region moves the way it does

Paired plane synovial joints between the superior articular process of one vertebra and the inferior articular process of the one above, with a capsule, synovium, and small intra-articular meniscoids (fibro-adipose folds implicated in acute locking).

Functions: 1. Guide and limit movement by their orientation (§17.3). 2. Share load: normally carrying ~16–20% of compressive load, but rising to ~40–70% in extension and in disc-degenerated segments — which is why extension-based pain suggests facet involvement. 3. Resist shear, particularly the anterior shear at L5–S1 imposed by the lumbosacral angle. 4. Proprioception — they are richly innervated.

Innervation: by the medial branch of the posterior (dorsal) ramus, with each joint supplied by the medial branches of two adjacent levels — the reason medial branch blocks and radiofrequency denervation must target two levels per joint.

The three-joint complex (Kirkaldy-Willis): each motion segment is a functional triad — one disc and two facet joints. Degeneration in any one loads the others. The degenerative cascade proceeds through dysfunction → instability → stabilisation (restabilisation by osteophytes and stiffening), which is why an elderly degenerate spine is often stiff but less painful than a middle-aged one in the instability phase.

Note: the uncovertebral joints (of Luschka) in the cervical spine (C3–C7) form between the uncinate processes and the vertebra above. They guide cervical motion, limit lateral translation, and — importantly — osteophytes here narrow the intervertebral foramen and are a common cause of cervical radiculopathy.

Ligaments

Craniovertebral ligaments: the transverse ligament of the atlas (the crucial one), the alar ligaments, the apical ligament, the tectorial membrane (the upward continuation of the PLL), and the atlanto-occipital membranes.

The back muscles

Figure 5 · The muscles of the back, layer by layer

Organised in three groups. The key discriminator is nerve supply: the true (intrinsic, deep) back muscles are supplied by posterior (dorsal) rami; every other muscle in the back is an immigrant, supplied by anterior (ventral) rami.

Superficial (extrinsic) — appendicular, all ventral rami

Intermediate — respiratory, ventral rami

Serratus posterior superior (elevates ribs) and serratus posterior inferior (depresses ribs) — of doubtful respiratory significance, but they define the layer.

Deep (intrinsic, true back muscles) — all posterior rami

Multifidus deserves separate mention. It is the largest and most medial of the lumbar transversospinalis group, contributing substantially to segmental stiffness. It shows rapid, segmental, side-specific atrophy after low back injury, with fatty infiltration that does not recover spontaneously with resolution of pain. This is a real and replicated finding. What the evidence does not support is the inference once drawn from it — that targeted multifidus/transversus retraining is superior to general exercise for chronic low back pain (Chapter 6).

The thoracolumbar fascia

Three layers enclosing erector spinae and quadratus lumborum. The posterior layer receives latissimus dorsi, the contralateral gluteus maximus, and the aponeuroses of transversus abdominis and internal oblique — forming the posterior oblique sling that transmits force diagonally across the body during gait and rotation. It is also densely innervated and is a plausible primary source of low back pain in its own right.

The vertebral canal, cord and nerves

Contents

From outside in: epidural (extradural) space (fat, the internal vertebral venous plexus of Batson, and the target of epidural injection), dura mater, arachnoid, subarachnoid space with CSF, pia mater, and the spinal cord.

Key levels:

The spinal nerve

Formed in the intervertebral foramen by the union of the dorsal (sensory) root, bearing the dorsal root ganglion, and the ventral (motor) root. It divides almost immediately into:

• Posterior (dorsal) ramus — the true back muscles and the skin of the back
• Anterior (ventral) ramus — everything else: limbs, and the anterolateral trunk; forms the plexuses
• Meningeal (recurrent, sinuvertebral) branch — re-enters the canal to supply the PLL, outer anulus, dura and periosteum; the anatomical route for discogenic pain
• Rami communicantes — to the sympathetic chain

Nerve root numbering — a perennial confusion, and worth stating precisely:

• There are 8 cervical nerves but 7 cervical vertebrae. C1–C7 exit ABOVE their corresponding vertebra; C8 exits between C7 and T1; and from T1 downwards, nerves exit BELOW their corresponding vertebra.
• In the lumbar spine, because roots descend obliquely, a posterolateral disc herniation compresses the TRAVERSING root, not the exiting one. So an L4–L5 posterolateral herniation compresses the L5 root (which exits below L5), while a far-lateral herniation at the same level compresses the exiting L4 root. This distinction accounts for most of the confusion in clinical reasoning about radiculopathy and is worth committing to memory.

Blood supply of the cord

• One anterior spinal artery (from the vertebral arteries) supplying the anterior two-thirds — motor tracts and spinothalamic tracts.
• Two posterior spinal arteries supplying the posterior third — dorsal columns.
• Segmental radicular arteries, of which the largest is the artery of Adamkiewicz (usually T9–T12, usually left), the principal supply to the lower thoracic and lumbar cord.

Anterior spinal artery syndrome therefore produces bilateral motor loss and loss of pain and temperature with preserved proprioception and vibration — a pattern that makes sense only if you know the vascular territories.

Movement of the column

Figure 6 · What keeps a spine stable

Ranges (approximate, whole region)

Coupled motion

Lateral flexion and axial rotation are mechanically linked, and the direction of coupling differs by region:

• Cervical (below C2): lateral flexion and rotation couple to the same side — consistent and predictable, because of the uncovertebral joints and facet orientation.
• Lumbar: coupling is variable and posture-dependent; the older teaching of fixed Fryette laws is not supported by contemporary in-vivo studies. Treat lumbar coupling as a tendency, not a rule.
• Upper cervical (C1–C2): rotation to one side is accompanied by lateral flexion to the opposite side.

Lumbopelvic rhythm

Forward bending is a coordinated sequence: the first ~40–60° comes from lumbar flexion, followed by progressive anterior pelvic rotation on the femoral heads, in a roughly 1:1 to 2:1 lumbar-to-hip ratio depending on the phase. Returning to upright reverses it, hips first.

The flexion–relaxation phenomenon: at full trunk flexion, the erector spinae become electrically silent, and load is borne passively by the posterior ligaments and the thoracolumbar fascia. This phenomenon is absent in most people with chronic low back pain, who maintain erector spinae activity throughout — a robust and reproducible finding, and a useful marker of guarding.

Low back pain: what the evidence actually says

This section exists because the anatomy in this chapter is routinely used to justify practices the evidence does not support.

What is well established:

• Around 85–90% of low back pain is “non-specific” — no single patho-anatomical source can be identified with confidence. This is not a failure of examination; it reflects the fact that multiple structures share innervation and produce indistinguishable pain patterns.
• Imaging findings are extremely common in asymptomatic people. Disc degeneration is present in ~37% of asymptomatic 20-year-olds and ~96% of 80-year-olds; disc bulges in ~30% at 20 and ~84% at 80 (Brinjikji et al., 2015). Routine imaging for non-specific low back pain is not recommended and is associated with worse outcomes, more surgery and greater disability, probably through the effect of the report on the patient’s beliefs.
• Red flags must still be screened: cauda equina syndrome, fracture, malignancy, infection, and inflammatory spondyloarthropathy.
• First-line management is education, reassurance, staying active, and exercise — with the type of exercise mattering less than the fact of it and the patient’s adherence. Manual therapy, if used, is an adjunct within a broader active plan.
• Posture and “core weakness” are far weaker predictors than once believed. Sitting posture, standing posture, lumbar lordosis magnitude and leg-length discrepancies show weak or absent associations with back pain. Sleep, stress, physical activity, psychological factors and previous episodes are stronger predictors.
• Language matters. Telling a patient their spine is “degenerated”, “crumbling”, “out of alignment” or that they have “the back of a 70-year-old” has measurable adverse effects on outcome.

What this does not mean: anatomy is not irrelevant. It is what allows you to recognise the 10–15% who do have a specific, identifiable and sometimes serious cause, and it is what allows you to explain to a patient, accurately and reassuringly, what their structures actually are and are not doing.

Cauda equina syndrome — the emergency you must never miss

Compression of the lumbosacral roots below the conus, most often by a large central disc herniation.

Features: bilateral (or alternating) leg pain, weakness or numbness; saddle (perineal) anaesthesia; bladder dysfunction — beginning as difficulty initiating or reduced sensation of flow, progressing to painless retention with overflow incontinence; bowel incontinence; and loss of anal tone and sexual dysfunction.

Ask about these directly in every acute low back presentation — patients do not volunteer them. Bladder symptoms are the ones that matter most, and reduced urinary sensation is an earlier and more useful question than frank incontinence.

This is a surgical emergency. Decompression within 24–48 hours substantially improves outcome. Do not arrange a follow-up appointment; arrange immediate hospital assessment.

Other clinical conditions

Disc herniation

Grading: bulge (circumferential, ≤25% of circumference) → protrusion (base wider than the dome) → extrusion (dome wider than the base) → sequestration (a free fragment).

• Location: most commonly posterolateral, because the PLL is narrow there and the anulus is thinnest posterolaterally. Central herniations threaten the cauda equina; far-lateral (foraminal) herniations compress the exiting root.
• Level: L4–L5 and L5–S1 account for ~90–95% of lumbar herniations; C5–C6 and C6–C7 dominate in the neck.
• Natural history is favourable: the majority of herniations resorb spontaneously, and larger extrusions and sequestrations resorb more readily than small bulges (because they provoke a greater inflammatory and vascular response). This is a genuinely reassuring fact to give patients.
• Radicular pain arises from a combination of mechanical compression and chemical irritation by nuclear material — which is why pain can be severe with minimal compression and why anti-inflammatory strategies help.

Nerve root levels worth having automatic:

Spondylolysis and spondylolisthesis

• Spondylolysis — a defect (usually a stress fracture) of the pars interarticularis, most often at L5, and the commonest identifiable cause of low back pain in the adolescent athlete. Caused by repetitive extension and rotation — gymnastics, fast bowling, tennis serving, diving. Presents as unilateral extension-related pain; the single-leg hyperextension (stork) test is suggestive but not diagnostic; MRI is the imaging of choice (it detects the stress reaction before the fracture).
• Spondylolisthesis — forward slip of one vertebra on another. Wiltse types: I dysplastic, II isthmic (from spondylolysis), III degenerative (typically L4–L5, in older women, from facet degeneration), IV traumatic, V pathological. Meyerding grades I–IV by quartile of slip. Managed with activity modification, extension avoidance in the acute phase, and progressive trunk and hip strengthening.

Spinal stenosis

Narrowing of the central canal, lateral recess or foramen, usually degenerative — from disc bulging, facet hypertrophy and ligamentum flavum buckling acting together.

Neurogenic claudication is the characteristic syndrome, and distinguishing it from vascular claudication is a core clinical skill:

The “shopping trolley sign” — relief when leaning on a trolley — is a classic and useful observation.

Scoliosis

A three-dimensional deformity: lateral curvature with vertebral rotation, producing the rib hump seen on Adam’s forward bend test and quantified with a scoliometer.

• Types: idiopathic (~80%: infantile, juvenile, adolescent — the commonest, predominantly girls), congenital, neuromuscular (cerebral palsy, muscular dystrophy, spina bifida), and degenerative (adult de novo).
• Cobb angle defines severity: <10° is not scoliosis; 10–25° observe; 25–40° with remaining growth → bracing (the BrAIST trial showed bracing significantly reduces progression to surgery, with a clear dose–response by hours worn); >45–50° → surgical consideration.
• Risser sign (iliac apophyseal ossification, 0–5) estimates remaining growth and hence progression risk.
• Physiotherapy scoliosis-specific exercises (PSSE — Schroth, SEAS and others) now have supportive evidence for reducing curve progression as an adjunct, reversing decades of therapeutic nihilism.

Whiplash-associated disorder

An acceleration–deceleration injury of the neck. Quebec Task Force grades 0–IV. Structures implicated include the facet joints (the best-supported single source, on medial branch block studies), capsules, discs, muscles and ligaments.

The predictors of poor outcome are largely non-anatomical: high initial pain intensity, high initial disability, cold hyperalgesia, and post-traumatic stress symptoms. Early return to normal activity with advice and exercise outperforms immobilisation — soft collars are not recommended, and prolonged rest worsens outcomes.

Where students consistently go wrong

• Forgetting that C1–C7 exit above their vertebra and T1 downwards exit below.
• Confusing traversing and exiting roots. A posterolateral L4–L5 herniation hits L5.
• Saying the cord ends at S2. The cord ends at L1–L2; the dural sac ends at S2.
• Attributing lumbar rotation to the lumbar spine. It is only ~10–13° in total; rotation is thoracic and hip.
• Forgetting the disc has no blood supply. Nutrition is by diffusion through the endplates, driven by movement.
• Assuming large herniations do worse. Extrusions and sequestrations resorb more readily.
• Ordering or over-interpreting imaging for non-specific low back pain.
• Missing cauda equina syndrome by not asking about bladder sensation and saddle anaesthesia.
• Confusing neurogenic and vascular claudication. Flexion relief versus rest relief.
• Manipulating a cervical spine without screening for upper cervical instability in rheumatoid arthritis or Down syndrome.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 17 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 18 — Thoracic Wall and Diaphragm: the cage, the intercostals and the mechanics of breathing.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents