Anatomy clinical correlates: Vertebral canal

Last updated: November 30, 2025

Anatomy clinical correlates: Vertebral canal

year 1

year 1

Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Sepsis
Neonatal sepsis
Abscesses
Food allergy
Anaphylaxis
Asthma
Immune thrombocytopenia
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Myasthenia gravis
Graves disease
Pemphigus vulgaris
Serum sickness
Systemic lupus erythematosus
Poststreptococcal glomerulonephritis
Graft-versus-host disease
Contact dermatitis
X-linked agammaglobulinemia
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Thymic aplasia
DiGeorge syndrome
Severe combined immunodeficiency
Adenosine deaminase deficiency
Ataxia-telangiectasia
Hyper IgM syndrome
Wiskott-Aldrich syndrome
Leukocyte adhesion deficiency
Chediak-Higashi syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Thymoma
Ruptured spleen
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Glucocorticoids
Non-corticosteroid immunosuppressants and immunotherapies
Skin histology
Skin anatomy and physiology
Hair, skin and nails
Wound healing
Introduction to the skeletal system
Introduction to the muscular system
Bones of the neck
Anatomy clinical correlates: Bones, fascia and muscles of the neck
Bones of the vertebral column
Joints of the vertebral column
Vessels and nerves of the vertebral column
Muscles of the back
Anatomy of the suboccipital region
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy of the muscles and nerves of the posterior abdominal wall
Bones of the upper limb
Fascia, vessels and nerves of the upper limb
Anatomy of the brachial plexus
Anatomy of the pectoral and scapular regions
Anatomy of the arm
Muscles of the forearm
Vessels and nerves of the forearm
Muscles of the hand
Anatomy of the sternoclavicular and acromioclavicular joints
Anatomy of the glenohumeral joint
Anatomy of the elbow joint
Anatomy of the radioulnar joints
Joints of the wrist and hand
Anatomy of the axilla
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Bones of the lower limb
Fascia, vessels and nerves of the lower limb
Anatomy of the anterior and medial thigh
Muscles of the gluteal region and posterior thigh
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Anatomy of the leg
Anatomy of the foot
Anatomy of the hip joint
Anatomy of the knee joint
Anatomy of the tibiofibular joints
Joints of the ankle and foot
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Development of the axial skeleton
Development of the limbs
Development of the muscular system
Bone histology
Cartilage histology
Skeletal muscle histology
Skeletal system anatomy and physiology
Bone remodeling and repair
Cartilage structure and growth
Fibrous, cartilage, and synovial joints
Muscular system anatomy and physiology
Brachial plexus
Neuromuscular junction and motor unit
Sliding filament model of muscle contraction
Slow twitch and fast twitch muscle fibers
Muscle contraction
Muscle spindles and golgi tendon organs
Radial head subluxation (Nursemaid elbow)
Developmental dysplasia of the hip
Legg-Calve-Perthes disease
Slipped capital femoral epiphysis
Transient synovitis
Osgood-Schlatter disease (traction apophysitis)
Rotator cuff tear
Dislocated shoulder
Winged scapula
Thoracic outlet syndrome
Carpal tunnel syndrome
Ulnar claw
Erb-Duchenne palsy
Klumpke paralysis
Iliotibial band syndrome
Unhappy triad
Anterior cruciate ligament injury
Patellar tendon rupture
Meniscus tear
Patellofemoral pain syndrome
Sprained ankle
Achilles tendon rupture
Spondylolysis
Spondylolisthesis
Degenerative disc disease
Spinal disc herniation
Sciatica
Compartment syndrome
Rhabdomyolysis
Osteogenesis imperfecta
Craniosynostosis
Pectus excavatum
Arthrogryposis
Genu valgum
Genu varum
Pigeon toe
Flat feet
Club foot
Cleidocranial dysplasia
Achondroplasia
Osteomyelitis
Bone tumors
Osteochondroma
Chondrosarcoma
Osteoporosis
Osteomalacia and rickets
Osteopetrosis
Paget disease of bone
Osteosclerosis
Lordosis, kyphosis, and scoliosis
Osteoarthritis
Spondylosis
Spinal stenosis
Rheumatoid arthritis
Juvenile idiopathic arthritis
Gout
Calcium pyrophosphate deposition disease (pseudogout)
Psoriatic arthritis
Ankylosing spondylitis
Reactive arthritis
Spondylitis
Septic arthritis
Bursitis
Baker cyst
Muscular dystrophy
Polymyositis
Dermatomyositis
Inclusion body myopathy
Polymyalgia rheumatica
Fibromyalgia
Rhabdomyosarcoma
Lambert-Eaton myasthenic syndrome
Sjogren syndrome
Mixed connective tissue disease
Antiphospholipid syndrome
Raynaud phenomenon
Scleroderma
Back pain: Pathology review
Rheumatoid arthritis and osteoarthritis: Pathology review
Seronegative and septic arthritis: Pathology review
Gout and pseudogout: Pathology review
Systemic lupus erythematosus (SLE): Pathology review
Scleroderma: Pathology review
Sjogren syndrome: Pathology review
Bone disorders: Pathology review
Bone tumors: Pathology review
Myalgias and myositis: Pathology review
Neuromuscular junction disorders: Pathology review
Muscular dystrophies and mitochondrial myopathies: Pathology review
Pediatric musculoskeletal disorders: Pathology review
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Osteoporosis medications
Fever of unknown origin: Clinical
Infective endocarditis: Clinical
Pneumonia: Clinical
Tuberculosis: Pathology review
Diarrhea: Clinical
Urinary tract infections: Clinical
Meningitis, encephalitis and brain abscesses: Clinical
Bites and stings: Clinical
Skin and soft tissue infections: Clinical
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Joint pain: Clinical
Pediatric orthopedic conditions: Clinical
Rheumatoid arthritis: Clinical
Lower back pain: Clinical
Immunodeficiencies: Clinical
Fat-soluble vitamin deficiency and toxicity: Pathology review
Water-soluble vitamin deficiency and toxicity: B1-B7: Pathology review
Zinc deficiency and protein-energy malnutrition: Pathology review
Viral hepatitis: Clinical
HIV and AIDS: Pathology review
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Seronegative arthritis: Clinical
Systemic lupus erythematosus (SLE): Clinical
Sjogren syndrome: Clinical
Inflammatory myopathies: Clinical
Vasculitis: Clinical
Preoperative evaluation: Clinical
Postoperative evaluation: Clinical
General anesthetics
Local anesthetics
Neuromuscular blockers
Laxatives and cathartics
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Insulins
Traumatic brain injury: Clinical
Neck trauma: Clinical
Chest trauma: Clinical
Abdominal trauma: Clinical
Anatomy of the vertebral canal
Anatomy of the descending spinal cord pathways
Anatomy of the ascending spinal cord pathways
Anatomy clinical correlates: Vertebral canal
Anatomy clinical correlates: Spinal cord pathways
Superficial structures of the neck: Posterior triangle
Superficial structures of the neck: Cervical plexus
Superficial structures of the neck: Anterior triangle
Deep structures of the neck: Prevertebral muscles
Anatomy of the thyroid and parathyroid glands
Anatomy of the larynx and trachea
Anatomy of the pharynx and esophagus
Anatomy of the lymphatics of the neck
Deep structures of the neck: Root of the neck
Fascia and spaces of the neck
Anatomy clinical correlates: Vessels, nerves and lymphatics of the neck
Anatomy clinical correlates: Viscera of the neck
Introduction to pharmacology
Enzyme function
Pharmacodynamics: Drug-receptor interactions
Pharmacodynamics: Agonist, partial agonist and antagonist
Pharmacodynamics: Desensitization and tolerance
Pharmacokinetics: Drug absorption and distribution
Pharmacokinetics: Drug metabolism
Pharmacokinetics: Drug elimination and clearance
Drug administration and dosing regimens
Mechanisms of antibiotic resistance

Transcript

Watch video only

Our spinal cord is protected by a strong vertebral canal; however, it’s still vulnerable to a variety of clinical conditions. Being able to recognize and identify these clinical conditions can help us understand the functional deficits that coincide with those conditions, and ultimately allow us to treat them.

The spinal cord transmits information from both motor neuron branches and sensory neuron branches between the brain and the rest of the body.

One way we can test whether there is injury to the spinal cord and disruption of these neuronal pathways is eliciting the autonomic tendon reflexes, you know, when the doctor hits your knee with a tendon hammer you automatically kick him?

This occurs because when you hit the tendon with a tendon hammer, stretch receptors in the muscle tendon send afferent impulses to the spinal cord, through their cell bodies in the dorsal root ganglion, which synapse with alpha motor neurons in the anterior horn.

These alpha motor neurons then transmit an automatic efferent signal back to the muscle leading to a contraction in the muscle.

All you have to do is locate the muscle tendon, get the individual to fully relax the muscle, and strike the tendon with a tendon hammer. Testing tendon reflexes can give important information about a patient’s condition.

Eliciting testing tendon reflexes can tell us if there is damage to a particular nerve route, to an area of the spinal cord or brain, or the general state of a patient’s entire peripheral nervous system which can be affected in things such as diabetes and motor neuron disease.

Testing tendon reflexes can also help us to determine different myotome levels that may be affected during nerve dysfunction.

Now remember, a myotome is a group of muscles innervated by a single spinal level, however it is difficult to test a single myotome as each muscle is innervated by multiple spinal levels.

Therefore, clinically when we test tendon reflexes we are gaining information on multiple myotomes.

The commonly affected tendon reflexes and their associated myotomes tested in clinical practice, as well as a little memory trick, are: The brachioradialis and biceps tendon which test myotome C5 and C6 to ‘pick up sticks’, the triceps tendon which tests C6, C7 and C8 to ‘make your arm straight’, the patellar tendon which tests L2, L3 and L4 to ‘kick the door’, and the achilles tendon which tests S1,S2 to ‘buckle your shoe’.

One of the most commonly talked about injuries to the spinal cord is disc herniation, which often results in nerve compression and spinal cord radiculopathy which affects the motor and sensory function of that nerve.

Before we get into this, let's start with some basic anatomy. The intervertebral disc has a rounded region in its center called the nucleus pulposus, and the nucleus pulposus is surrounded by a fibrous ring called the annulus fibrosus.

Disc herniation typically occurs during forward flexion of the vertebral column. This compresses the disc anteriorly and stretches it posteriorly pushing the nucleus pulposus posteriorly, and it is more likely if there is violent hyperflexion of the vertebral column.

Herniation of the nucleus pulposus usually extends posterolaterally. This is because posteriorly the annulus fibrosus is thinner and doesn’t receive support from either the posterior longitudinal ligament or anterior longitudinal ligament.

This type of herniation is more likely to cause symptoms because it’s close to the spinal nerve roots. If there is degeneration of the annulus fibrosus, then the nucleus pulposus can actually herniate into the vertebral canal itself, causing impingement of the spinal cord or cauda equina.

Posterolateral herniations of the nucleus pulposus are most common in the lumbar and lumbosacral region. More specifically they usually occur at the L4-L5 or L5-S1 levels.

When intervertebral discs herniate, that affects the nerve root corresponding to the inferior level of the herniated disc.

This is because spinal nerves in the lumbar region exit the intervertebral foramen superior to the level of the herniated disc.

So for example, a herniated disk at the L4-L5 level will not impinge spinal nerve L4 because it exits the intervertebral foramen above the intervertebral disc located between L4 and L5, however it will impinge on the L5 nerve root because it will cross this disc on its way to exiting the intervertebral foramen between L5 and S1.

Nerve impingement causes clinical symptoms such as lower back pain, paresthesia and weakness in the territory innervated by that nerve. Pain can also be referred down the back of the legs due to this nerve impingement.

Now a particular type of pain often caused by a herniated lumbar intervertebral disc is sciatica, and this results in lower back pain, as well as radiating pain to the hips, the back of the thigh and lower legs.

Individuals may also have weakness in hip extension, knee flexion, and ankle plantarflexion, as well as an absent ankle tendon reflex.

It occurs when a herniated lumbar intervertebral disc compresses any portion of the sciatic nerve from L4-S3, however it most commonly occurs at the level of L5 or S1.

Now, any maneuver that stretches the sciatic nerve can elicit symptoms clinically. Classically, the straight leg test is used to elicit symptoms.

During this test, an individual lies on their back, and their leg is lifted while straight to flex the thigh and stretch the sciatic nerve.

Normally, no pain is present until about 80-90 degrees, where if sciatica is present pain occurs at less than 60 degrees, however this test may be variable.

Now, intervertebral disc herniation can also occur in the cervical region, almost as often as in the lumbar region.

This can be caused by chronic or sudden forced hyperflexion of the cervical region, like with a head-on collision or during sports such as football if someone makes a hit with the top of their head.

In the cervical region, when the spinal nerves exit the intervertebral foramen they cross the intervertebral disc of the same level and exit inferior to it unlike the lumbar region.

Therefore, a herniated disc in the cervical region compresses the nerve that exits at that level and not the inferior level as it would in the case of the lumbar region.

With this in mind, you might expect a cervical disc herniation to therefore affect the spinal nerve above, however we must remember that there are 8 cervical spinal nerves and only 7 cervical vertebrae so each cervical spinal nerve will exit superior to the vertebrae of the same number.

For example nerve root C6 exits the intervertebral foramen above the C6 vertebrae. And because the cervical spinal nerves cross the intervertebral disc at the same level it exits, intervertebral disc herniation in the cervical area will affect the nerve root corresponding to the inferior level of the herniated disk just like in the lumbar region.

Using the two most frequent areas of cervical disc herniation as an example, herniations that occur at the C5-C6 level would impinge the C6 nerve root, and herniation of the C6-C7 level would affect the nerve root of C7.

To make things easy, just remember no matter where you have a disc herniation, the nerve root affected typically corresponds with the same vertebral level as the vertebral body below, so like we said an L4-L5 herniation will impinge on the L5 nerve root, and a C6-C7 herniation will impinge on the C7 nerve root.

Disc protrusions resulting in cervical radiculopathy can cause pain in the neck, shoulder, arm and hand, as well as cutaneous deficits of the nerve roots affected.

Alright, lets review! Where do lumbar disc protrusions mostly occur & where do cervical disc protrusions mostly occur?

We also have two more syndromes that can affect the spinal cord, either of which can be the result of intervertebral disc herniation, fractures or other trauma, and tumor invasion.

The first involves the conus medullaris, which is the point where the spinal cord tapers and terminates in adults at the L1-L2 vertebrae, 1:50 and the branching nerves of L3 to S4 below this point which are collectively known as the cauda equina.

A lesion at the level of L1/L2 can result in conus medullaris syndrome, where a lesion below this can result in cauda equina syndrome.

Any lesion from T12 to S4 can cause damage to both the conus medullaris or cauda equina, and can result in numerous symptoms such as radicular low back pain radiating down the legs, and lower extremity .

Conus medullaris syndrome, however, typically causes symmetric bilateral lower extremity weakness in addition to a potential mixed picture of both upper and lower motor neuron signs, with a preference for upper motor neuron signs, including things such as spasticity and hyperreflexia.

This is in contrast to cauda equina syndrome which typically affects both legs but is more likely to present with asymmetric lower extremity weakness, as well as the potential for loss of the knee and ankle reflex indicative of a lower motor neuron deficit.

Furthermore, lesions in the T12 to S4 region resulting in either conus medullaris and cauda equina syndrome can cause more severe symptoms such as loss of bladder and anal sphincter control due to compression of parasympathetic innervation traveling through the pelvic splanchnic nerves in S2 to S4, as well as the classic finding of saddle anesthesia, meaning that there’s a lo

As these syndromes have the potential for severe neurological dysfunction, they require urgent evaluation, and may ultimately need surgical decompression.

Typically, when we think of damage to the nerves of the spinal cord we think of some sort of trauma or compression.

Sources

  1. "Radiologic Anatomy of the Spine" Minimally Invasive Percutaneous Spinal Techniques (2010)
  2. "EPIDURAL ADHESIOLYSIS" Current Therapy in Pain (2009)
  3. "Prevalence of annular tears and disc herniations on MR images of the cervical spine in symptom free volunteers" European Journal of Radiology (2005)
  4. "Imaging the Intervertebral Disk" Radiologic Clinics of North America (2012)
  5. "Manipulative Therapy" Churchill Livingstone (2008)
  6. "Pain Management" Elsevier Inc. (2006)
  7. "Human Embryology" Elsevier España (2000)
  8. "Orthopedic Physical Assessment" Saunders (2005)
  9. "Deep tendon reflexes" Butterworths (1990)
  10. "The association between post-dural puncture headache and needle type during spinal anaesthesia: a systematic review and network meta-analysis" Anaesthesi (2021)