Anatomy clinical correlates: Vertebral canal

Last updated: November 30, 2025

Anatomy clinical correlates: Vertebral canal

Emergency & Trauma

Emergency & Trauma

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Anatomy clinical correlates: Heart
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Transcript

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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)