Spondylolisthesis: Slip, Ouch, and Wiltse

Spondylolisthesis occurs when one vertebrae "slips" forward relative to the one below it. Spondylolisthesis is most frequently used to describe this process in the lumbar spine, but it may occur in the cervical or thoracic spine as well.

Spondylolisthesis has traditionally been divided into categories based on the underlying pathology causing the slip (ie: the Wiltse classification). These categories include: congenital, isthmic, degenerative, traumatic, pathologic, and post-surgical (aka: iatrogenic).

Regardless of the category, the end result is the same: one vertebrae slips forward relative to the one below it. Let’s talk about each category in more detail…

Congenital spondylolisthesis occurs in children. It is usually caused by malformation of the superior articulating facet of the first sacral vertebrae (S1). The facet is a portion of bone that forms a joint with the vertebrae above or below it. Therefore, in congenital spondylolisthesis the malformed S1 facet joint is unable to form a stable joint with the lowest lumbar vertebrae (L5). The end result is that the L5 vertebrae is able to slip forward relative to the sacrum.

Isthmic spondylolisthesis occurs when there is a break in the bone that connects the facet of one vertebrae to the facet of the vertebrae immediately above (or below) it. This connecting bone is known as the pars interarticularis. The defect in the pars interarticularis is known formally as spondylolysis (see image below). Spondylolysis does not necessarily cause spondylolisthesis, but when it does it is classified as "isthmic". This type of spondylolisthesis is more common in those of Inuit heritage, as well as in athletes who have had repetitive hyperextension of the lumbar spine (ie: gymnastics, tennis, football, etc).

Traumatic spondylolisthesis is exactly what it sounds like. Injury to the facet joints, pars interarticularis, or ligaments of the spine can allow one vertebrae to slip forward/dislocate relative to the one above and/or below it.

CT lumbar spondy
Pathologic spondylolisthesis occurs when the slip is caused by some underlying pathology in the bone. This category is broad and may include tumors, osteoporosis, osteopetrosis, Paget’s disease, or other diseases of bone formation or metabolism.

Post surgical (also known as iatrogenic) spondylolisthesis occurs after surgery. It most frequently develops after a laminectomy is performed. If too much bone is removed during the laminectomy it may cause instability and allow a slip to occur.

The last category, degenerative spondylolisthesis, affects people over the age of forty. It is unclear exactly what causes this type of spondylolisthesis, but it is believed to be secondary to a combination of arthritic changes in the facet joints, degenerative disc disease, and bony remodeling of the pars interarticularis. Degenerative spondylolisthesis, unlike isthmic or congenital, usually results in the fourth lumbar vertebrae (L4) slipping over the fifth lumbar vertebrae (L5).

How Do Patient’s with Spondylolisthesis Present?

Spondylolisthesis typically presents with a combination of low back pain with or without radiculopathy (ie: discomfort down the legs). The radiculopathic symptoms are due to narrowing of the intervertebral foramen and pinching of the nerves as they exit the spinal column.

Neurological symptoms such as weakness, bowel or bladder problems, or sexual dysfunction are uncommon, but can also occur. These symptoms become more common as the severity of the slip increases.

Many patient’s with spondylolisthesis also have significant hamstring tightness (ie: unable to touch their toes). Additionally, many patients will walk or stand with their torso or knees in a flexed position.

Diagnosis and Severity of Slip

Diagnosis of spondylolisthesis is based on x-rays, CT scans, and MRI imaging. X-rays and CT scans are best at delineating the bony anatomy. MRIs are frequently ordered to assess the amount of nerve compression (especially in patients with signs of neurologic dysfunction).

The severity of the slip is based on the Meyerding classification system. Type one slips occur when less than 25% of the diameter of the vertebral body slips forward relative to the one below it. Type two slips are between 26% and 50%. Type three slips are between 51% and 75% and type four slips are between 76% and 100%. If a slip is more than 100% it is referred to as a grade five slip or spondyloptosis.

Grade 1 Spondylolisthesis L5-S1

Fix Me Doc!

Initial treatment for low grade slips presenting with back pain and mild radiculopathy is usually conservative. Physical therapy, joint injections, ibuprofen (or other non steroidal anti-inflammatory medications), and bracing can be used for several months. Physical therapy should focus on lumbar flexion exercises with avoidance of lumbar extension. If symptoms continue or worsen then surgery is indicated (talk to your local spine surgeon).

Patient’s who fail conservative treatment, have high grade slips (ie: greater than 50%), or have weakness, bowel/bladder issues, or sexual dysfunction should be offered surgery. The primary goal of surgery is to prevent further slippage by fusing the vertebrae together; realigning the spine is a secondary goal, but is not absolutely necessary. In fact, attempts to realign high grade slips have been shown to increase the risk of neurological injury.

The type of surgery offered to correct spondylolisthesis may be from the front (ie: anterior), from the back (ie: posterior), or a combination of both. As of now, there is no “right” surgical approach.

The Play by Play…

Spondylolisthesis is a fancy term that describes one vertebrae slipping forward relative to the one below. There are six categories based on the underlying pathology causing the slip. These categories are congenital, isthmic, degenerative, traumatic, pathologic, and post surgical/iatrogenic. Symptoms are typically low back pain with a component of radiculopathy. Weakness, bowel/bladder or sexual dysfunction is actually uncommon unless high grade slips are present. The Meyerding system is used to determine the severity of the slip. Treatment for low grade slips is usually conservative, but surgery may be necessary for high grade slips, patients that fail conservative management, or those with hard signs of neurological dysfunction.

Additional Pathology You Might Fancy…

References and Resources

Spondylolysis and the Scotty Dog

Spondylolysis is a fancy term for a defect in a portion of a vertebrae known as the pars interarticularis. The pars interarticularis is a section of bone that connects the superior articulating facet and the inferior articulating facet of a given vertebral body. The facets (which are joints) connect adjacent vertebrae together.

The CT scan below shows the relevant anatomy of a normal pars interarticularis and one that exhibits spondylolysis. Spondylolysis occurs about 85% of the time at the fifth (L5) lumbar segment, followed in frequency by the fourth lumbar vertebrae (L4), but it can occur elsewhere in the spine.

In spondylolysis there is a fracture/defect in the pars. Fractures of the pars interarticularis typically occur after repeated extension of the lower back. Repetitive extension causes significant pressure on the pars, which in susceptible individuals can lead to weakening of the bone.

Spondylolysis is actually quite common in gymnasts, football, and tennis players because of the repetitive back extension required of these athletes.

The importance of spondylolysis is not so much the pars defect itself, but the fact that these defects can cause one vertebrae to "slip" over the top of the one below it. When this occurs a new name is given to the condition – spondylolisthesis.

Signs and Symptoms

CT lumbar spondy
Xray Scotty Dog
The most common symptom of spondylolysis is low back pain. In fact, one of the most common causes of low back pain in individuals less than 25 years old is spondylolysis, especially in athletes. It is also important to note that spondylolysis is commonly asymptomatic.

Diagnosing Spondylolysis

Diagnosis is made by looking at an x-ray or CT scan of the spine. The classic description is a defect through the neck of the “Scotty dog”, which is seen best on an oblique x-ray of the lumbar spine.

What to do About It

Treatment starts with avoidance of the motions that caused the fracture. Occasionally a brace is used to prevent extension of the spine.

Anti-inflammatory medications like ibuprofen are commonly used if pain is significant. After a period of rest, physical therapy can be useful to strengthen muscles and prevent recurrence.

Less commonly surgical repair of the pars defect may be attempted. Surgical candidates are patients who continue to have back pain despite conservative treatment. If the patient receives significant pain relief from pre-operative bupivacaine injection into the defect, then they should be considered excellent surgical candidates.


Spondylolysis is a defect in the bony pars interarticularis of the vertebrae. It commonly occurs in the lumbar spine after repetitive extension motions. Low back pain is the most common symptom. In the absence of complications like spondylolisthesis treatment is typically conservative and involves bracing, physical therapy, and anti-inflammatories. Diagnosis is made by x-ray and/or CT scan.

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Atlanto-Occipital Dislocation (Internal Decapitation)

Atlanto-occipital dislocations (AODs) occur when there is severe damage to the ligaments that connect the skull to the cervical spine. The most common cause of an AOD is trauma.

There are several classifications of atlanto-occipital dislocations. In type 1 dislocations the base of the skull moves anteriorly (ie: forward) relative to the dens of the second cervical vertebrae. In type 2 dislocations the skull moves superiorly (ie: upwards) relative to the cervical spine. In type 3 dislocations the skull moves posteriorly (ie: backwards) relative to the cervical spine.

Often times more than one classification may exist in a single patient. For example, a patient may have both a type 1 and type 2 AOD if the patient’s skull has moved forward and upwards relative to the cervical spine.

Signs and Symptoms

Most cases of complete atlanto-occipital dislocation are fatal. Severe damage to the spinal cord around the cranio-cervical junction leads to respiratory paralysis and death if mechanical ventilation is not started rapidly. Patients are often quadriplegic (ie: unable to move their upper and lower extremities) because of damage to the descending motor axons of the corticospinal tract. Incomplete injuries can also occur with varying degrees of cervical spine injury.

The lower cranial nerves are sometimes involved in the injured segment. The most commonly injured cranial nerves are the abducens (VI), vagus (X), and hypoglossal (XII) nerves. Abducens nerve injury causes an inability to deviate the eye outwards. Damage to the hypoglossal nerve causes deviation of the tongue towards the side of the injured nerve (“lick your wound”).

Surprisingly, some patients with atlanto-occipital dislocation may have no neurologic symptoms! It is therefore important to rule out ligamentous injury, especially in patients who have had severe head and neck trauma.

Diagnosis and Classification

Power's Ratio
Diagnosis is made after appropriate imaging studies are obtained. Plain films and CT scans of the cervical spine are the most commonly obtained initial imaging studies.

There are several methods for determining if atlanto-occipital dislocation has occurred. The first is the “BAI-BDI method”. Two distances are measured. The BDI, or basion-dental interval, measures the distance between the most anterior and inferior portion of the skull (ie: “basion”) and the tip of the dens, which is a superior extension of the second cervical vertebrae. The BDI should normally be less than 12mm. In the image below the BDI is 14mm and is indicative of atlanto-occipital dislocation.

The second distance that is measured is the BAI, or basion-axial interval. The BAI is the distance between the basion and a line drawn straight up from the posterior (ie: back) portion of the dens. The normal interval is less than 12mm. In the image below the BAI is 14.2mm indicating likely atlanto-occipital dislocation.

A second method of assessing atlanto-occipital dislocation is known as Power’s ratio. Power’s ratio is most useful if the dislocation is anterior (ie: the head moves forward relative to the spine). Two distances are measured. The first is the distance between the opisthion and the anterior ring of C1; the second is the distance between the basion and the posterior ring of C1. The second distance is then divided by the first to obtain the ratio. A “normal” ratio is less than 1.0; if the ratio is greater than 1.0 then suspicion for dislocation should be high.

X-rays and CT show bony anatomy very well, but do not demonstrate ligamentous injury. Many patients with suspected AOD may also get an MRI to assess ligamentous damage. MRI will usually show severe injury to the ligaments that connect the first and second cervical vertebrae to the skull base.

There are two commonly used classification systems for describing atlanto-occipital dislocations. The Traynelis system is purely descriptive and is based on which way the head moves relative to the spine.

Traynelis Classification
Type 1 Head moves forward relative to the spine
Type 2 Head moves upwards relative to the spine
Type 3 Head moves backwards relative to the spine

The Bellabarba system is based on CT findings and is used to determine stability; it is also useful because it helps guide treatment decisions. A stable injury is one in which the dislocation is within 2mm of a normal BDI/BAI value and does not get worse with a traction test. Unstable injuries are present when the dislocation gets worse with a traction test; these injuries may be reduced at baseline (ie: within 2mm of a normal BDI/BAI) or grossly abnormal. That being said, it is important to note that very few doctors perform traction tests in patients with suspected AOD as this can worsen the condition!

Bellabarba Classification
Type Description Stability
Type 1 Alignment within 2mm of normal BAI/BDI interval; distracts less than 2mm with traction Stable
Type 2 Reduced at baseline (ie: within 2mm of normal BDI/BAI), but significant distraction with traction test Unstable
Type 3 Severely misaligned relative to normal BDI/BAI values Unstable


Treatment of atlanto-occipital dislocations involves spinal immobilization. This is usually done via a surgical procedure known as an occipital-cervical fusion in which the back of the skull is fused to the cervical spine. Some patients are also put in a halo immobilization device.


Atlanto-occipital dislocation occurs after severe injury to the ligaments that connect the skull to the cervical spine. It most commonly occurs after severe head or neck trauma. Death secondary to ventilatory failure, quadriplegia, and cranial nerve deficits are common symptoms. Diagnosis is based on characteristic findings found on CT, x-rays, and MRI scans. Treatment is with spinal immobilization, either with a halo apparatus, or a surgical procedure known as occipital-cervical fusion.

Some More Useful Learning Material…

References and Resources

  • Garrett M, Consiglieri G, Kakarla UK, et al. Occipitoatlantal dislocation. Neurosurgery. 2010 Mar;66(3 Suppl):48-55.
  • Greenberg MS. Handbook of Neurosurgery. Sixth Edition. New York: Thieme, 2006. Chapter 25.
  • Deliganis AV, Mann FA, Grady MS. Rapid diagnosis and treatment of a traumatic atlantooccipital dissociation. AJR Am J Roentgenol. 1998 Oct;171(4):986.
  • Traynelis VC, Marano GD, Dunker RO, et al. Traumatic atlanto-occipital dislocation. Case report. J Neurosurg. 1986 Dec;65(6):863-70.
  • Bellabarba C, Mirza SK, West GA, et al. Diagnosis and treatment of craniocervical dislocation in a series of 17 consecutive survivors during an 8-year period. J Neurosurg Spine. 2006 Jun;4(6):429-40.
  • Horn EM, Feiz-Erfan I, Lekovic GP, et al. Survivors of occipitoatlantal dislocation injuries: imaging and clinical correlates. J Neurosurg Spine. 2007 Feb;6(2):113-20.

Denis’ Three Column Spine: A Simple Way to Think About Spinal Stability

The three column model of the spine was first introduced by Dr. Francis Denis in his aptly named paper, "The Three Column Spine and its Significance in the Classification of Acute Thoracolumbar Spinal Injuries". This paper, published in 1983, proposed a new biomechanical model for spinal stability that challenged Dr. Frank Holdsworth’s two column model from the 1960s. Although replaced by more modern grading scales (ie: the TLICS model) the three column spine is a simple way to think about spinal biomechanics.

Denis’ three column model proposes that the thoracolumbar spine can be divided into three columns. The first column includes the anterior longitudinal ligament (ALL) up to the first half of the bony vertebral body. The second column includes the second half (ie: more posterior half) of the vertebral body, up to, and including the posterior longitudinal ligament (PLL). The third column includes the pedicles, spinal cord/thecal sac, lamina, transverse processes, facet joints, spinous process, and the posterior ligaments (ie: supraspinous, interspinous, and ligamentum flavum).

The purpose of Denis’ model was to delineate which injuries to the thoracolumbar spine were considered "unstable". This delineation was important because it determined which patient’s required operative treatment of their spine.

Simply stated, an unstable spine was present if two or more of the columns were involved in the injury. However, it is important to note that every rule can be broken, so not all injuries follow this rule. Part of the "art" of practicing spine surgery is determining which two-column injuries can be left alone and managed non-operatively, and which truly require operative intervention.

Types of Injuries

Based on Denis’ model he classified specific types of injuries. Injuries to the anterior column only were called "compression fractures". Damage to the anterior and middle columns were known as "burst fractures". Injury to the middle and posterior column were known as "flexion-distraction" injuries, or more colloquially as "seat-belt type" injuries. Finally, damage to all three columns were classified as "fracture-dislocation" injuries.

Classification of Thoracolumbar Injuries Using the Three Column Model

Columns Name Stability
Anterior Compression fracture Stable
Anterior and Middle Burst fracture Unstable
Middle and Posterior Flexion-distraction injury (aka: seat-belt type) Unstable
Anterior, middle, and posterior Fracture-dislocation Unstable

Examples of Thoracolumbar Spine Fractures

Clinical Significance

In very simple terms, unstable fractures require definitive treatment. Treatment for unstable spine injuries is usually operative, although rigid immobilization with bracing is sometimes used in certain circumstances.

The treatment of each fracture type is beyond the scope of this article (and discussed in more detail elsewhere on this site), but suffice it to stay that for the most part (and again, every rule was made to be broken) two or three column injures = unstable = surgery.


Denis’ three column model of the spine revolutionized the way we think about spinal biomechanics and stability. He divided the spine into three columns. Although it has been largely replaced by more modern grading scales such as the thoracolumbar injury classification and severity score (TLICS) it is still a nice way to “think” about spinal integrity.

Other Common Spine Injuries…

References and Resources

Radial Nerve and the Saturday Night Palsy

Radial Nerve Course
In order to appreciate the radial nerve, we have to first understand the brachial plexus. The brachial plexus can be thought of as a massive highway intersection, in which numerous highways come together and then split apart again.

The "highways" merging into the brachial plexus are the 5th, 6th, 7th, and 8th cervical nerve roots, as well as the 1st thoracic nerve root. These nerve "highways" tangle together to form trunks, divisions, cords, and then branches. The radial nerve is one of the branches of the brachial plexus; it gets its input from the 5th, 6th, 7th and 8th cervical nerve roots.

The radial nerve courses along the humerus in the upper arm. It wraps around the humerus in a spot called the spiral groove. Just before wrapping around the humerus, it sends a branch that innervates the triceps muscle (long, medial, and lateral heads) in the upper arm.

After wrapping around the spiral groove, it sends additional branches to the brachioradialis, extensor carpi radialis longus, and extensor carpi radialis brevis muscles.

The first major branch in the forearm is known as the superficial radial nerve. This nerve courses along the medial/ulnar aspect of the forearm (ie: the ulnar or medial side of the forearm is closest to your body when your palms are facing forward) and heads straight for the hand. It relays sensory information from the lateral portion of the back of the hand.

The second major branch at the elbow can be thought of as the deep radial nerve, but it is formally known as the posterior interosseous nerve.

The posterior interosseus nerve sends branches to eight muscles in the forearm. They include the supinator (through which the nerve travels via a fibrous tunnel known as the arcade of Frohse), extensor digiti minimi, extensor carpi ulnaris, extensor digitorum, abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis, and extensor indicis.

Muscles Innervated by the Radial Nerve and Its Branches
Muscle Action of Muscle
Triceps brachii – Extension of the forearm away from upper arm
Brachioradialis – Helps flex the forearm closer to the upper arm
– Helps supinate (ie: palm towards the sky)
– Helps pronate (ie: palm towards the floor)
Extensor carpi radialis
(longus and brevis)
– Helps extend the wrist
– Abducts the hand (ie: hand moves away from
the body when the palms are facing forward)
Extensor digiti minimi – Helps extend the little finger (5th digit)
Extensor carpi ulnaris – Helps extend the wrist
– Adducts the hand (ie: hand moves towards
the body when the palms are facing forward)
Supinator – Allows palms to face up towards the sky
Extensor digitorum – Helps with extension of the fingers
(specifically at the metacarpophalngeal joint)
Abductor pollicis longus – Helps abduct the thumb
Extensor pollicis
(longus and brevis)
– Help extend the thumb
Extensor indicis – Helps extend the index finger

Generally speaking, the radial nerve and its branches are involved in muscles that allow joints to extend (ie: widen or separate away from one another).

Importance in Disease

Damage to the radial nerve may take the form of compression or sheering injuries, typically after traumatic events.

The most common site of injury is at the spiral groove of the humerus. The nerve may be damaged if someone breaks their humerus, or if someone leans the back of their arm on something for an extended period of time (ie: a "Saturday night palsy" is the informal term given to a drunk who falls asleep with their arms draped over a chair… they end up waking up with a radial nerve palsy!).

Injury to the nerve at the spiral groove causes a wrist drop, in which the affected person cannot extend their wrist. The triceps are not affected because nerve branches to this muscle are proximal to the spiral groove. In addition, patients also complain of decreased sensation on the back of the hand (see image to right).

Radial Nerve Sensory Distribution in Hand
Additionally, the posterior interosseous branch of the radial nerve may get compressed as it passes through the supinator muscle in the forearm. This is referred to as posterior interosseous nerve syndrome.

The compression occurs at a fibrous portion of the supinator muscle known as the "arcade of Frohse", which causes an inability to extend the fingers at the metacarpophalangeal joints; this is due to dysfunction of the extensor digitorum muscle (extension at the interphalangeal – both distal and proximal – joints is controlled by the lumbricals and interossei muscles which are innervated by the median and ulnar nerves).

In posterior interosseous nerve syndrome it is still possible to extend the wrist because the branches of the nerve to the extensor carpi radialis muscle are unaffected (ie: they branch before the arcade). However, when the wrist is extended it deviates towards the radial side of the forearm because of the unopposed action of the extensor carpi radialis muscles (in other words, the extensor carpi ulnaris is affected and cannot keep the wrist extension neutral).

Sensation is entirely normal when the posterior interosseous nerve gets compressed because it contains no sensory fibers.


The radial nerve is a terminal branch of the brachial plexus. It sends branches to most of the extensor muscles of the arm and forearm. It also provides sensation to the back side of the hand. If injured it causes either a radial nerve palsy, or posterior interosseous syndrome, in which the affected patient has an inability to extend various joints at the wrist and/or fingers.

Related Anatomy You Should Know About…

References and Resources

  • Ducic I, Felder JM 3rd, Quadri HS. Common nerve decompressions of the upper extremity: reliable exposure using shorter incisions. Ann Plast Surg. 2012 Jun;68(6):606-9
  • Colbert SH, Mackinnon SE. Nerve compressions in the upper extremity. Mo Med. 2008 Nov-Dec;105(6):527-35.
  • Reddy MP. Peripheral nerve entrapment syndromes. Am Fam Physician. 1983 Nov;28(5):133-43.
  • Calfee RP, Wilson JM, Wong AH. Variations in the anatomic relations of the posterior interosseous nerve associated with proximal forearm trauma. J Bone Joint Surg Am. 2011 Jan 5;93(1):81-90.
  • Arle JE, Zager EL. Surgical treatment of common entrapment neuropathies in the upper limbs. Muscle Nerve. 2000 Aug;23(8):1160-74.

Cervical Facet Dislocation: Houston We Have a Problem…

The spine is composed of thirty-three bony elements referred to as vertebrae. Each vertebrae connects with the vertebrae above and below it. These connection points are referred to as “facet” joints.

Each vertebrae has two bony sections known as superior articulating processes, as well as two bony sections known as inferior articulating processes. The inferior articulating processes of one vertebrae connect with the superior articulating processes of the vertebrae directly below it; the connections are held in place by ligaments.

The combination of the superior articulating process, inferior articulating process, and ligaments that connect them together form the facet joint. This arrangement makes the joints look like shingles on the roof of a house (see image below).

Normal Facet Anatomy

Like any other joint in the body, facet joints can dislocate. This is most likely to occur in the cervical spine where the facet joints are more horizontal in orientation.

Facet joint dislocations occur under conditions of severe flexion and/or rotation. The flexion injury causes disruption of the ligaments that stabilize the joint; this allows the inferior articulating process of the top vertebrae to "jump" over the superior articulating process of the bottom vertebrae. The end result is a dislocated (aka: "jumped" or "locked") facet.

Signs and Symptoms

Roughly a quarter of patients will have no signs or symptoms if one facet joint is dislocated between two vertebrae; another quarter will have incomplete spinal cord injuries. Ten percent will be paralyzed or paretic (ie: unable to move their arms or legs) and the remaining forty percent will have injury to the nerve roots exiting the spinal column. Nerve root injuries can cause paresthesias (ie: abnormal sensations) in a dermatomal pattern, as well as decreased reflexes and muscle weakness in the muscle group that the nerve serves.

The stakes for spinal cord injury increase dramatically if both facet joints are dislocated between two vertebrae. Roughly three quarters of these patients will be paralyzed! Very few people escape bilateral jumped facets without neurological injury.


X-ray jumped facet
Dislocated Facet

Diagnosis can be made with x-ray and CT imaging of the spine. The image will show the inferior articulating surface of the top vertebrae displaced anterior (ie: towards the chest) and inferior (ie: towards the feet) relative to the superior articulating surface of the bottom vertebrae.

The x-ray and CT scan to the right show a jumped facet between the fourth and fifth cervical vertebrae.


Treatment of most facet dislocations begins with external traction. This involves placing tongs on the patient’s head and applying weight to gently distract (ie: pull apart) the spine.

Continuous x-rays are taken until the inferior articulating process of the dislocated joint is perched on top of the superior articulating process of the vertebrae below. At this point the weight is gradually reduced until the joint "pops" back into the proper anatomical position.

Since facet joint dislocations involve severe ligamentous injury, patients often require surgical intervention to stabilize the neck, even after reduction with external traction.


A dislocated facet joint occurs when the inferior articulating process of one vertebrae jumps over the superior articulating process of the vertebrae below it. This usually occurs after severe flexion and rotational injuries. Diagnosis is made on x-ray or CT of the spine. Treatment is usually with a combination of external traction and surgical fusion.

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References and Resources

  • Dvorak MF, Fisher CG, Fehlings MG, et al. The surgical approach to subaxial cervical spine injuries: an evidence-based algorithm based on the SLIC classification system. Spine (Phila Pa 1976). 2007 Nov 1;32(23):2620-9.
  • Patel AA, Dailey A, Brodke DS, et al. Subaxial cervical spine trauma classification: the Subaxial Injury Classification system and case examples. Neurosurg Focus. 2008;25(5):E8.
  • Rabb CH, Lopez J, Beauchamp K, et al. Unilateral cervical facet fractures with subluxation: injury patterns and treatment. J Spinal Disord Tech. 2007 Aug;20(6):416-22.
  • Andreshak JL, Dekutoski MB. Management of unilateral facet dislocations: a review of the literature. Orthopedics. 1997 Oct;20(10):917-26.
  • [No authors listed]. Treatment of subaxial cervical spinal injuries. Neurosurgery. 2002 Mar;50(3 Suppl):S156-65.
  • Handbook of Neurosurgery. Sixth Edition. New York: Thieme, 2006. Chapter 25.
  • Baehr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Anatomy, Physiology, Signs, Symptoms. Fourth Edition. Stuttgart: Thieme, 2005.

Os Odontoideum: Floating Bone of the Axis

In order to understand what an os odontoideum is, we have to first appreciate the anatomy of the first two cervical vertebrae.

The first cervical vertebrae is known as the "atlas". It forms joints with the base of the skull and the second cervical vertebrae, which is also known as the axis. It has a an elongated structure on its ventral aspect called the “odontoid”. The odontoid of the axis connects to the atlas via numerous ligaments. This joint provides most of the flexibility that allows you to move your head in various directions.

An os odontoideum is a failure of the tip of the odontoid (ie: the part closest to the atlas) to fuse with its base on the axis.

Exactly why this occurs is still debated. The first theory is that it represents a congenital failure of the odontoid to fuse properly with the axis. The second, and more supported theory is that it may be caused by a previous fracture in early childhood that failed to heal properly. Regardless of the cause, the end result is a floating mass of bone that represents the superior (ie: top) most portion of the odontoid process.

This mass of bone may be fused to the base of the skull. If this is the case, the term "dystopic" os odontoideum is used. Or it may articulate and move with the atlas; if this is the case, the term "orthotopic" os odontoideum is used.

Signs and Symptoms

Many patients with os odontoideum are asymptomatic. However, because the tip of the odontoid is not technically connected to the base of the axis the patient may have an unstable neck. If the instability is severe, damage to the spinal cord can result causing myelopathy.

Myelopathy can manifest with several symptoms. Patients may have numbness and tingling in the upper and lower extremities. If damage to the nervous tissue responsible for motor movements occurs, patients may complain of weakness (and possibly even paralysis in extreme cases!).

On examination, patients may have both upper and lower motor neuron signs. Upper motor neuron signs refer to exaggerated reflexes – Babinski and Hoffmann signs, and clonus are all examples of this. These findings tend to be seen below the level of the actual spinal cord injury. Lower motor neuron findings typically occur at the level of the spinal cord damage, and consist of flaccid weakness with decreased reflexes.


Diagnosis of os odontoideum is made by x-rays or CT of the cervical spine. To assess the degree of instability in the joint, some doctors will get flexion and extension x-rays as well.

The image to the right is a CT of the cervical spine that illustrates the missing portion of the odontoid process (marked by arrows in the image). A normal CT of the cervical spine is shown to the left for comparison.

Os Ondontoideum

Some patients may also get an MRI to assess for spinal cord and ligamentous injury, especially when symptoms or physical examination findings are present.


Treatment depends on whether or not symptoms are present, and whether or not the cervical spine is unstable. Many patients without symptoms may be followed with serial X-rays or CT scans to assess for progression of instability.

If significant instability exists, or the patient has signs and symptoms consistent with spinal cord injury, then surgical stabilization is performed. There are numerous ways to achieve stabilization in this region surgically, which are outside the scope of this article. Regardless of which method is used, the end result is stabilization of the joint between the first and second cervical vertebrae.


Os odontoideum is an absence of part of the odontoid process. It may be due to a congenital malformation, or an early childhood fracture that fails to heal properly. Symptoms, when present, are due to spinal cord injury (ie: myelopathy) and consist of weakness, numbness, tingling, and other signs of spinal cord dysfunction. Imaging with x-rays or CT scan can show the bony defect. MRI is occasionally used to assess the spinal cord itself. Treatment depends on whether or not symptoms or significant instability is present. The best treatment options are surgical stabilization of the joint between C1 and C2 using one of several potential methods.

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Ossified Posterior Longitudinal Ligament: Its Clinical Significance

The posterior longitudinal ligament is a long ligament that runs from the base of the skull to the sacrum. It provides a significant amount of mechanical integrity to the spinal column. The ligament runs down the back of the vertebral bodies just in front of the spinal cord itself.

In some individuals this ligament becomes ossified, which means that it takes on a bone like quality. As a result, its overall size and hardness increase. Given the ligament’s location adjacent to the spinal cord, any increase in the girth or flexibility of the ligament can cause injury to the cord.

Ossification of the posterior longitudinal ligament can occur at multiple spots along the spinal column. The most common spot is in the cervical spine (usually C2 to C6), but ossification can also occur in the thoracic (usually T4 to T7) and lumbar spine as well.

Exactly why the longitudinal ligament ossifies in some people is unknown. Current thinking is that a combination of genetic and lifestyle factors play a role in its pathology. For example, family studies have shown increased rates of OPLL in first degree relatives of people known to have the disorder. OPLL is also more common in people of Japanese and Korean descent.

Both familial and racial linkage usually indicate a genetic component to the disease. In fact, patients with OPLL have higher rates of dysfunctional collagen gene regulation (specifically, type XI and VI collagens). Linkage to specific human leukocyte antigen haplotypes on chromosome 6 have also been implemented.

Lifestyle factors such as diet have also been shown to increase risk. Patient’s who are diabetic or pre-diabetic have higher rates of OPLL compared to the rest of the population. High protein diets seems to decrease the risk, whereas high salt diets seem to increase risk.

Overall, the reasons why the posterior longitudinal ligament ossifies in some people, but not others remains an area of ongoing debate and research.

Signs and Symptoms

When an ossified posterior longitudinal ligament pushes on the spinal cord it causes numerous signs and symptoms. The constellation of clinical findings seen in patient’s with symptomatic ossified posterior longitudinal ligaments is known as myelopathy.

Myelopathic patients present with a combination of weakness, clumsiness (ie: decreased ability to hold objects), bowel or bladder dysfunction, spasticity – which is manifested as increased reflexes, as well as changes in sensation (ie: numbness, tingling, etc.).

Ossified Posterior Longitudinal Ligament
Myelopathy can be subtle at first, but can become debilitating depending on how much compression of the cord is present.

Diagnosis and Classification

Diagnosis of an ossified posterior longitudinal ligament is usually made when a patient presents with myelopathic features, or after neurological injury from a traumatic event.

Imaging studies such as xrays and CT scans illustrate the bony quality of the ligament. MRIs are frequently ordered to assess how "squashed" the spinal cord is. CT myelograms also provide excellent detail of cord compression when MRI is not feasible.

The ossification is classified according to its anatomic location and continuity. There are four distinct patterns. They include a continuous pattern, in which there is ossification behind both the vertebral bodies and the disc spaces. The second pattern is known as segmental; in this type the ossification is only present behind the vertebral bodies and does not span the disc spaces. The third pattern is localized, which means that the ossified ligament is present and localized behind only one vertebral body. Finally, there is a mixed type, which is a combination of continuous and segmental.


The problem with ossification of the posterior longitudinal ligament is that it progresses over time. Slowly, the ligament will compress the spinal cord. Therefore, surgical treatment is typically offered at the first sign of spinal cord compression (ie: myelopathy).

The best surgical treatment is controversial. Approaching the spine from the front (ie: anterior approach) allows direct removal of the ossified ligament. However, it is important to note that the ligament is often stuck to the dura mater overlying the spinal cord which can make dissection extremely difficult. A cerebrospinal fluid leak is not uncommon when an anterior approach is taken, and there is an increased risk of inadvertent injury to the spinal cord. That being said, when successful, surgery from the front offers several distinct advantages. The first is that myelopathic symptoms seem to respond better to this type of approach; in addition, removal of the ossified ligament can retard further progression of the disease.

The second surgical option is to approach the spine from the back (ie: posterior approach). Removing the bone behind the spinal cord allows the cord to "drift" backwards away from the ossified ligament. This approach is considered more safe because there is no direct removal of the ossified ligament, and therefore there is a decreased risk of inadvertent cord injury. That being said, progression of the ossification can still occur and myelopathic symptoms do not respond as well to this type of surgery.

Ultimately, the type of surgery offered – anterior versus posterior – is dictated by the severity of the ossification and symptoms present, as well as the preferred approach of the surgeon.


Ossification of the posterior longitudinal ligament is seen more commonly in patients of Japanese descent. There are genetic factors that appear to increase risk. Symptoms are related to compression of the spinal cord by the ossified ligament. Ossification is progressive in nature. Treatment consists of surgery from either an anterior, posterior, or combined approach.

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Gout: Uric Acid, Negatively Birefringent, and My Big Toe

Gout occurs when uric acid crystals form in joint spaces. Everyone has some level of uric acid in their blood stream. However, it is only when the level becomes high enough that uric acid leeches into the joint spaces and crystallizes. Once there, the crystals cause signifcant inflammationand the affected joint becomes painful, red, and swollen.

The causitive agent, uric acid, is a by product of purine catabolism. Purines are an important component of nucleotides, which are the building blocks of DNA and RNA. Purines are also seen in molecules like adenosine triphosphate, which serves as a source of cellular energy. The final product of the degradation of these molecules is, you guessed it, uric acid!

The degradation pathway for both adenine and guanine (and their constituent molecules) are shown below. The key enzymes involved in this degradation are shown in red.

Purine Catabolism

When uric acid is formed, the kidneys filter it, and then excrete it into the urine. Some people are predisposed to either under-secrete or over-produce uric acid. In either case it builds up in the blood stream. This is known as "hyperuricemia". In some people hyperuricemia can cause gout. However, it is important to note that not everyone with hyperuricemia develops gout.


Gout Crystals

An official diagnosis of gout can only be made by tapping the joint (ie: sticking a needle into the joint and aspirating the contents) and looking at the fluid under a microscope.

If uric acid crystals are present, they will be "negatively birefringent", which means that they appear yellow under a parallel light source. Interestingly, if the light source is turned perpendicular the crystals turn blue (this is the exact opposite of pseudogout, which is discussed in another article).

Often times clinicians will order a blood uric acid test. In an acute attack, uric acid levels are meaningless because patients suffering from a gout flair may suprisingly have normal blood levels. However, in patients who are on medications to prevent gout, monitoring the blood uric acid levels can help guide treatment. In addition, hyperuricemia almost always precedes a gout attack.

Signs and Symptoms

As discussed above, the uric acid crystals cause inflammation in the joint space. This leads to a painful, swollen, and red joint. Gout attacks joints asymmetrically, meaning that it rarely affects the same joint on both sides of the body at that same time. Symmetric joint pain is more consistent with other rheumatological diseases.

Many joints can be affected by gout. The most common joint is the metatarsal phalangeal joint (MTP), which is a joint in the big toe. When this joint is involved the disease is referred to as "podagra".

Gout attacks usually occur quickly and unexpectedly with peaking of symptoms within 12 to 24 hours. Multiple repeated attacks of gout can lead to a chronic form of the disease known as "tophaceous gout". In chronic gout, not only are joints affected, but crystal formation can also occur in other areas of the body. For example, the achilles tendon and earlobes can be affected.

Tophaceous Gout

Patients with gout may also be at increased risk of developing uric acid kidney stones due to elevated uric acid in the urine.


Acute treatment is aimed at controlling the inflammatory process within the joint. The most common drugs used to treat acute gout flairs are non-steroidal anti-inflammatory medications (NSAIDSs). Ibuprofen, naproxen, and indomethacin are the most common NSAIDs used to treat gout flairs. Steroids are also sometimes used, especially in people with contraindications to NSAIDs such as kidney failure.

An additional second line medication used to treat acute gout flairs is colchicine. It is typically used in people who cannot tolerate NSAIDs.

To prevent gout attacks from reoccurring, or to prevent tophaceous gout, there are several medicines that are used. The first medication is known as probenecid. It is most effective in people who "under-excrete" uric acid because it inhibits the re-absorption of uric acid in the kidney.

The second medication is known as allopurinol. It is most useful in people who "over-produce" uric acid because it inhibits the enzyme xanthine oxidase (see degradation pathway above) and reduces the amount of uric acid formed from the breakdown of purines.

Allopurinol and probenecid should not be used to treat acute gout flairs. Paradoxically, they can actually worsen an acute flair and should only be used to prevent recurrent attacks.


Gout is a disease of the joints caused by deposition of uric acid crystals. The joint becomes hot, swollen, red, and extremely painful. Diagnosis is made by aspiration of the crystals from the joint space. Treatment for acute flairs is usually with non-steroidal anti-inflammatories. Colchicine is occasionally used as well. Allopurinol and probenecid are used to prevent recurrent attacks.

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Burst Fractures: Axial Loading Leading to Ouch!

Burst fractures are a specific type of spine fracture in which the body of a given vertebrae “bursts” into pieces. By definition a burst fracture involves the entire vertebral body. The image below is an example of a normal lumbar spine with the vertebral bodies outlined.

Burst fractures most commonly occur at the junction between the thoracic and lumbar spine. This junction is an area where the rigid thoracic spine transitions to the more mobile lumbar spine, and hence is an intrinsic point of weakness. This is why most burst fractures occur between the T10 through L2 vertebrae.

CT vertebral body

Axial loading of the spine is what causes burst fractures. They typically occur after a traumatic events like car accidents or falls from significant heights. Elderly individuals, and those with poor bone quality, may suffer burst fractures after minor trauma such as falling from a chair.

Signs and Symptoms

Burst fractures invariably present with back pain at the site of the fracture. Depending on the exact location signs and symptoms of nerve root compression or lower spinal cord injury may occur.

If the nerves that dangle in the lumbar spine (aka: the cauda equina) get compressed by the fragments of bone then weakness, numbness, tingling, and even bowel and bladder problems may occur.

Burst fractures between T10 and L1 can cause damage to the end of the spinal cord (the spinal cord ends at L1 or L2 in most individuals), which can lead to lower extremity weakness, or even paralysis, as well as bowel and bladder dysfunction.


Diagnosis of a burst fracture is made using a combination of x-rays, CT scans, and MRIs. These three imaging modalities serve different functions when evaluating the severity of a burst fracture.

X-rays are usually the first imaging ordered in patients with suspected spine fractures. If the plain x-rays show a burst fracture then CT scanning is usually done to further assess the degree of bony injury (see image below for an example of an L2 burst fracture).

MRI is used to detect ligamentous injury. The degree of ligamentous injury indicates a higher degree of instability; information about ligament integrity helps determine treatment options.

Burst Fracture Lumbar Spine


Treatment of burst fractures is highly dependent on the severity of the burst fracture. Treatment is either conservative with immobilization in a brace (ie: a "TLSO" or thoracolumbar sacral orthotic brace) or surgical fixation.

Burst fracture after instrumentation
As a rough rule of thumb patients with any of the following criteria should be strongly considered for surgical correction:

  • Greater than 50% vertebral body height loss.
  • Greater than 25 to 40 degrees of kyphosis.
  • Greater than 50% spinal canal compromise.
  • Significant posterior ligamentous injury.
  • Any neurological signs or symptoms referable to the injury.
  • If the patient fails conservative therapy with a brace.

Surgical correction can be achieved in a variety of ways and is often related to surgeon preference. Some surgeons will remove a significant portion of the fractured vertebral body and place a “cage” in the area, a procedure known as a “corpectomy”. This, combined with rods and screws from posteriorly provides the greatest stability, but has a higher risk of nerve injury. Not uncommonly, the fractured vertebral body is left alone and rods and screws are placed from behind only. This is especially true if the fractured level shows minimal spinal canal compromise.


Burst fractures of the thoracolumbar spine typically occur after high impact axial loading. They usually occur between T10 and L2, but can be seen anywhere in the spine. Patients will almost invariably have pain at the fracture site and may or may not have neurological signs and symptoms depending on the severity of the fracture. Diagnosis is made with CT, plain x-rays, and MRI. Treatment is highly dependent on the individual fracture and ranges from bracing to surgical fixation.

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