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Subaxial Cervical Spine Injury or Injury to C3-C7 vertebrae

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The term lower cervical spine injury refers to the Injury of the subaxial cervical spine or that is below axis. It includes injuries to C3-C7 vertebra and adjoining structures.

Lower cervical spine injuries are very common and are associated with substantial mortality and morbidity.

The cervical spine can get injured during motor vehicle accidents or falls.

In trauma patients, it should be assumed that there is an injury to the cervical spine unless ruled out. Therefore, the cervical spine is protected in a patient of trauma, beginning at the accident site, during extrication, examination and shifting the patient.

Cervical spine injury has been known to occur in as many as 4.5% cases of blunt trauma.

The cervical spine is a mobile region enabling mobility in various planes and during any trauma, the head can act as a significant lever arm on the cervical spine and creating a wide range of injury patterns.

These injuries, minor or major, can affect the spinal cord and nerve roots, and depending on the level of the spinal injury cause various motor and sensory dysfunctions.

The injuries to the subaxial spine have a bimodal age distribution.

High energy trauma such as motor vehicle accidents is responsible for injuries in age 15-25 years whereas falls are the most common cause for persons older than 65 years.

The relatively minor trauma is able to cause injury in the second group because the cervical spondylosis predisposes the cervical cord to injury by diminishing the space.

Anatomy, Biomechanics, and Pathophysiology

The cervical spine consists of seven vertebrae numbered C1-C7. C1 and C2 along with C2-C3 joint are considered upper cervical spine whereas below that is lower cervical spine.

[Read anatomy of the cervical spine in detail]

The subaxial cervical spine is seen as formed by two columns.

The anterior column consists of posterior longitudinal ligament and structures anterior to it [vertebral body and disc, anterior longitudinal ligament].

The posterior column includes

  • Pedicles
  • Laminae
  • Facet joints
  • Spinous processes
  • Posterior ligament complexes
    • Ligamentum flavum
    • Interspinous ligaments
    • Supraspinous ligaments

Posterior column often fails in extreme flexion or distraction and is able to resist tension. Posterior column failure may be associated with concomitant injury to the anterior column.

The zygapophyseal or facet joints are oriented at 45º to the axial plane, allowing a sliding motion. The joint capsule is weakest posteriorly.

Spinal nerves exit at the vertebral level. There are a total of eight cervical nerve roots.

The first root leaves above the atlas and last [C8] exits between the seventh cervical vertebra and the first thoracic level.

The cervical spine can get injured by various mechanisms that lead to bony or ligamentous failure.

The position of the head and neck at the time of impact and the direction of force causing injury results in the different pattern of injury seen.

Key components in cervical spine injury are force/load transmission and kinematics (motion). Mostly, cervical spine injury occurs due to both components being present in different proportions.

One can consider an axial compressive load applied to a single cervical vertebra as a fundamentally pure example of load transmission. Force can be applied in different directions like shear, torsion, tension.

Kinematics refers to cervical vertebral motion. The lower cervical spine that permits motion through intervertebral discs and facet joints and is limited by the anterior longitudinal ligament and posterior ligamentous complex. It can be in a flexion-extension plane, axial rotation and lateral flexion.

Flexion-extension motion is greatest at the C4-C5 and C5-6 segments, averaging about 20 degrees. Axial rotation ranges from 2 to 7 degrees at each of the subaxial motion segments. Lateral flexion is 10 to 11 degrees per level in C2-5 and decreases caudally.

Cervical spine injury alters both load transmission and the kinematics of the cervical spine. The cervical spinal column is extremely vulnerable to injury.

Allen described the following three common mechanisms for spinal injury in a descriptive classification. The various mechanisms described are

  •  Compression-flexion
  • Distraction-flexion
  • Compression-extension

 Motor-vehicle accidents, falls, and accidents resulting from recreational activities or sports are the leading causes of injuries to the lower cervical spine.  

Classification of Lower Cervical Spine Injury

In the past, Holdsworth, Allen, and Harris systems of classifications have been used but these had following drawbacks

  • Based on the mechanism of injury only
  • Neurological status not taken into consideration
  • Could not guide the treatment

American Association of Neurological Surgeons now recommends the use of Subaxial Injury Classification (SLIC ) and the Cervical Spine Injury Severity Score (CSISS).

[Read more about Allen Classification of Cervical Injury]

SLIC is based on three categories—morphology, discoligamentous complex (DLC), and neurologic status> Each category has subpoints which are given a score. The final score is calculated by adding all the scores.

  • No abnormality – 0
  • Compression – 1
    • Burst  +1 = 2
  • Distraction – 3
  • Rotation/translation – 4

With respect to the DLC, points are assigned as follows:

  • Intact – 0
  • Indeterminate – 1
  • Disrupted – 2

With respect to neurologic status, points are assigned as follows:

  • Intact – 0
  • Root injury – 1
  • Complete cord injury – 2
  • Incomplete cord injury – 3
  • Continuous cord compression in setting of neurologic deficit – +1

The score is used in decision making for treatment

  • < 4 Nonoperative treatment
  • 4 Operative versus nonoperative
  • 5or more –  Operative treatment

Clinical Presentation

The cervical spine injury should be suspected in every major trauma.

For best possible in any given injury, the precautions of cervical spine begin at the field or first contact and continue till the spine is managed definitely.

The neck needs to be immobilized manually, with sandbags or cervical collar. These methods and use of spine board help to prevent secondary injury. Transfers and intubation should be accomplished under strict spine precautions. Log-roll technique and spinal precautions should be observed at all times.

Airway, breathing, and circulation should always be the highest priority.

Airway security and hemodynamic resuscitation are crucial and should take precedence. Tracheal intubation and central line placement are often performed in the emergency and due to a danger of worsening of injury by manipulation, manual cervical stabilization should be maintained throughout the intubation process.

If intubation is not possible, mask ventilation can be continued until fiberoptic or nasotracheal intubation can be safely performed in a hospital.

Cricothyroidotomy might be the safest alternative for airway control when the spine is highly unstable.

History should be taken to note the circumstances of accident and forces working. Mental status and consciousness level should be assessed.

Neurological functions, regions of pain and other injuries should be noted especially abrasions and/or laceration on the scalp, face, neck, or shoulders as clues to the mechanism of injury.

The back of the neck should be palpated for any tenderness, step-off, or hematoma.

Performa neurologic examination as soon as feasible as per ASIA.

The presence of pathologic reflexes like clonus Hoffman sign, and Babinski sign.

Often, in cases of acute cord injury, there is a spinal shock present and detailed assessment could only be done at a later date when spinal shock goes. The return of the spinal function is indicated by bulbocavernous reflex. Therefore serial examination needs to be done to see if spinal shock has gone or not. It usually takes about 24 hours.

[Read more about spinal shock]

[Read more about spinal cord injury]

Depending on the spinal cord injury, different incomplete patterns of spinal injury may be seen.

[Bilateral facet dislocations have the highest incidence of spinal cord injury often resulting in incomplete/complete injury paterns]

Special attention should be paid to examine sacral roots and reflexes. Return of sacral reflexes indicates the end of the spinal shock.

Secondly, the return of the sacral reflexes indicates the passing of spinal shock. The bulbocavernosus reflex and anal wink are good tests of the sacral reflex arc.

The neurological examination should be regularly done to find if the lesion is improving or worsening. This helps in the guidance of the treatment.

The neurogenic shock when present should be recognized and managed.

Lab Studies

In the initial acute stage hemoglobin level and typing/cross matching are required in case the patient requires a blood transfusion.

During acute management, the lab tests are done as the need arises during management.

After the patient is stabilized, routine lab studies are indicated which include

  • Complete blood count
  • Urine analysis,
  • Biochemistry tests of blood
  • Serum electrolyte levels
  • Liver and renal function testing

Imaging

X-rays and CT

The standard x-ray imaging is a cross-table lateral view of the cervical spine that helps to gauge the cervical alignment. Other x-rays that could be included are odontoid view, and AP view.

A swimmer’s view may be needed to complete the evaluation.

In case, the x-rays are not able to visualize the spine properly, CT must be done to exclude the neck injury.

CT scan is helpful in imaging of the cervicothoracic junction and identification of posterior-column injuries such as lamina or facet fractures.

American Association of Neurological Surgeons (AANS) recommendations

Awake, Asymptomatic Patient

No radiographic evaluation not required if the patient has no neck pain or tenderness, has no neural deficit and is able to complete a functional range of motion.

However, the patient should not have an injury that detracts from accurate evaluation.

Awake, Symptomatic Patient

High-quality computed tomography (CT) imaging of the cervical spine is recommended.

If high-quality CT imaging is not available, a 3-view cervical spine series (anteroposterior, lateral, and odontoid views) is recommended. This should be supplemented with CT =when it becomes available.

Obtunded or unevaluable Patient  

High-quality CT is indicated and if not available, 3 view cervical series is recommended and supplemented as CT becomes available.

MRI

MRI is able to visualize neural elements – cord and roots. Disc herniations can easily be seen on MRI.

A mismatch of injury levels on X-rays is another indication of MRI.

MRI should be performed in neurally intact patients of facet dislocations before closed reduction is done. The MRI is able to tell if there is any large disc herniation associated which could increase the risk of neural injury.

However, in a patient with injuries that require early surgical stabilization in the operating room, the reduction could be performed without the delay and therefore, MRI is avoided.

In the case of suspected vertebral artery injury, magnetic resonance angiography may be indicated. The artery is known to get injured in the severely degenerative cervical spine or fractures through the foramina transversarium.

Management of Cervical Injuries

Acute Management

Management of cervical injury in the emergency requires treating the multiple injuries [often associated] and treating the concomitant neurologic injury.

Though the risk-benefit ratio has been questioned, steroids are given to prevent secondary cord damage and to minimize local edema.

For a patient presenting within 3 hours of injury, the dosage is

  • 30 mg/kg loading dose of methylprednisolone given intravenously (IV) over 1 hour, followed by 5.4 mg/kg/hr for the next 23 hours.

If the patient presents after 3 hours but less than 8 hours

  • the 5.4 mg/kg/hr dosage is extended for 48 hours following the same loading dose.

After 8 hours of injury starting patient on steroid does not appear to be beneficial.

Steroids are associated with poor wound healing, the risk of infection, stress ulcers and increased sugar levels. Therefore some clinicians avoid the use of steroids. Moreover, there appears insufficient to weak evidence for their effectivity.

Histamine 2 (H2) blockers such as famotidine and ranitidine) are given to prevent stress ulcers from spinal cord injury.

Prophylaxis for deep vein thrombosis is carried using low-molecular-weight heparin (LMWH), oral warfarin.

Intermittent compression devices for the lower extremities or vena cava filters may be used when required in high-risk cases

Approach to Definitive Treatment

After the patient is stabilized, the decision for the definitive treatment is based on

  • Malalignment of the spine, with or without neural deficits
  • Progressive neurologic deterioration associated with persistent compression.

Patients without malignment or without neural deficits [minimally displaced injuries] can be managed with nonoperative treatment.

Malalignment can be managed initially with cervical tong traction. Surgery is then done as definitive treatment. Decompression, when required, may be done.

In cases where the closed reduction is contemplated before the definitive treatment, the presence of concomitant disc herniations must be considered and if feasible confirmed with MRI. The discs with postero-inferior herniations are known to pose worsening of the neural deficit. [This is also important if the open reduction is planned.]

If MRI is not feasible, a cautious reduction while performing serial neurologic examination should be done in the awake patient.

But if the patient is intoxicated or has a head injury, MRI should be sought if patient condition allows.

A disc herniation if present should be removed anteriorly before performing the reduction.

The decision for surgery depends on the type of injury.

  • For anterior column injuries
    • Anterior approach
    • Anterior decompression and reconstruction+grafting+ stabilization
  • Posterior column injuries
    • Posterior approach
    • Posterior decompression/fixation/grafting
  • Global injuries
    • Anterior and posterior fixation approaches

Early intervention [within 24-72 hours] is recommended to facilitate early decompression and rapid return of the mobilization.

Nonoperative Treatment Options

A number of lower cervical spine fractures can be managed with nonoperative means. Nonoperative means of treatment include orthoses, skull traction, and halo vest immobilization.

The basic aim of nonoperative means is to align and immobilize the cervical spine and prevent it from further stress till the fracture union occurs.

Orthoses

Orthoses can be cervical or cervicothoracic.

Orthoses decrease motion rather than effect true immobilization.

Cervical Orthoses work through padded contact areas strategically located over subcutaneous bony prominences like occiput, spinous processes, scapular spines, acromion processes, clavicles, sternum, and mandible.

Soft cervical orthoses cause little decrease in spinal motion and are most commonly used after cervical strains or sprains.

Rigid cervical orthoses can provide varying degrees of immobilization depending on the construction material and the overall design. They are commonly used for emergent in-field cervical spine immobilization.

Skin breakdown at bony prominences can occur as a complication of cervical collars.

Cervicothoracic Orthoses devices extend to the upper thorax. These provide more effective immobilization than simple cervical collars in all planes. Sternooccipito-mandibular immobilizer –(SOMI) and Minerva brace are examples of cervicothoracic orthoses.

However, they are more difficult to apply and remove and produce high resting pressures on the chin and occiput.

Both cervical and cervicothoracic devices cause increased motion at the cervicothoracic junction.

[Read more about cervical orthoses]

Cervical Traction

Traction can be used for temporary immobilization of unstable cervical spine injuries, or to realign or reduce and maintain cervical spine fractures or dislocations.  The devices used are Crutchfield’s tongs, Gardner-Wells tongs, and the halo-ring.

Halo Vest

Halo immobilization has become a less popular form of treatment for lower cervical spine injuries as the better internal fixation techniques have been developed. Despite this, halo vest immobilization remains a viable, minimally invasive method of stabilization of unstable cervical spine injuries for patients who might otherwise have contraindications to open surgical methods.

Surgical Treatment Options

With the increased choice of implants and gadgets and development of better surgical approaches & techniques, surgery is playing a greater role in the management of cervical injuries as compared to earlier times.

Anterior Surgery

The subaxial spine is reached by the interval plane between the sternocleidomastoid (lateral) and medial muscles. Following options are available with the anterior approach

  • Decompression by removing offending structure
    • Removal of the disc [discectomy]
    • Removal of vertebra[corpectomy or vertebrectomy]
  • Anterior Reduction of Dislocated Facets
    • Reduction confirmed under C-arm
    • Additional posterior surgery if reduction fails
  • Reconstruction
    • Replacement of the removed vertebra or disc.
    • Autograft/ allograft/ titanium mesh cage.
  • Stabilization
    • Anterior locking plate

Posterior Surgery

  • Midline extensile posterior approach
  • Decompression
    • Posterior decompression often not necessary
    • Laminectomy needed to remove the offending compressive elements.
  • Open reduction of dislocated facet joints can be performed using a posterior approach.
  • Posterior Instrumentation
    • Wire-based constructs
    • Variable-angle screw-rod constructs.
  • Posterior Fusion
  • Cancellous bone harvested from the posterior iliac crest

Follow-up after Surgical Treatment

Rigid postoperative external immobilization is often not required after surgery. A cervical collar is generally enough.

Postoperatively, patients usually are maintained in a rigid or soft collar for comfort.

The patient should be mobilized out of bed as soon as possible to prevent pulmonary and thromboembolic complications.

Further management of the injury is

  • Wound care in early postoperative period
  • Early mobilization
  • Physical, emotional and functional rehabilitation
  • Management of bowel and bladder dysfunction
    • Intermittent catheterizations
    • Alternate-day suppositories
    • High-fiber diet to avoid impaction.

Radiological sign of union is expected in about 2-3 months. Any deterioration in neurologic function should prompt further investigation.

Complications o Cervical Injury

  • Spinal cord or root injury
  • Pulmonary problems
    • Pneumonia
    • Atelectasis
    • Pulmonary embolus
  • Stress ulcers
  • Pressure ulcers
  • DVT
  • Depression
  • Autonomic dysreflexia

Cervical Injuries in Special Cases

Patients with the ankylosed and spondylotic spine can suffer cervical injury even after minor trauma. Therefore, the patients who present with neck pain or neurologic deficit after major or minor trauma should be considered to have a cervical spine injury until proven otherwise.

Degenerative spondylotic changes, such as vertebral body osteophytes, fixed subluxations, and facet hypertrophy can make plain films difficult to interpret. Therefore unless the injury is severe, the plain x-rays may not be helpful in detecting a level of injury.

If x-rays do not reveal much information CT or MRI should be done in these patients.

Ankylosing Spondylitis and Diffuse Idiopathic Skeletal Hyperostosis

Due to ankylosis, the spine can no longer be considered as constituted of multiple motion segments. Instead, the ankylosed spine should be considered as a long bone.

Bridging osteophytes in these diseases fuse the spine into a solid, continuous piece of bone.  If there is a break in one region, it is likely to have propagated through both the anterior and posterior elements.

Therefore any fracture in the cervical spine in these patients should be considered as unstable and treated accordingly.

Patients should be immobilized as soon as the diagnosis is made, admitted, and placed on strict log-roll precautions until definitive management.

Halo fixation, anterior fixation, and posterior fixation are the treatment options in these patients through optimal treatment has not yet been formulated in the literature.

Spinal Cord Injury In  Spondylotic Spine

There is underlying cervical stenosis in these patients following the degenerative changes which increase the risk for neural injury.

Patients often present with complete or incomplete spinal cord injury without x-ray signs. CT or MRI as desired may be asked.

Again there is a shortage of data on what is optimal treatment.

Nonoperative Treatment includes rest, collar immobilization and observation in particular for patients with central cord lesions, in which a high percentage will have a nearly complete resolution of their neural deficits. The decision for long-term definitive treatment is influenced by the presence of persistent signs or symptoms or myelopathy.

Operative treatment is indicated in unstable spine or patients who do not recover with nonoperative treatment.

The treatment depends on cervical injury level and the presence or absence of myelopathy.

Prognosis

The clinical outcome after lower cervical spinal injury generally is related to the level and severity of associated spinal cord injury.

If the neural functions do not return, the patient is left with disabilities depending on the level of injury.

A rough estimate of different injury levels and functional disabilities is given below. The level given as cord levels.

[Read this article for correlation between cord levels and vertebral levels]

  •  C3-4
    • must use a sip-and-puff (mouth)
    • Chin/head control for mobilization in a wheelchair
  • C5
    • Able to assist with upper body dressing
    • Can feed themselves with assistive devices
    • Can operate a power wheelchair
  • C6
    • Assistance with bowel and bladder programs
    • Able to feed themselves with hand or tenodesis splints
    • Can transfer to and from wheelchairs or toilets with some assistance
  • C7
    • Can transfer independently to the bed, car, or toilet
    • Can use manual or power wheelchairs
    • Cand can dress independently using assistive devices
  • C8
    • Independent in all transfers
    • Able to use a manual wheelchair
    • Can assist in some homemaking activities

[Read in detail about different levels of spinal cord injury]

References

  1. Vaccaro AR, Hulbert RJ, Patel AA, Fisher C, Dvorak M, Lehman RA Jr, et al. The subaxial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. Spine (Phila Pa 1976). 2007 Oct 1. 32 (21):2365-74.
  2. Ryken TC, Hadley MN, Walters BC, Aarabi B, Dhall SS, Gelb DE, et al. Radiographic assessment. Neurosurgery. 2013 Mar. 72 Suppl 2:54-72
  3. Toh E, Nomura T, Watanabe M, Mochida J. Surgical treatment for injuries of the middle and lower cervical spine. Int Orthop. 2006 Feb. 30(1):54-8.
  4. Furlan JC, Noonan V, Cadotte DW, Fehlings MG. Timing of decompressive surgery of spinal cord after traumatic spinal cord injury: an evidence-based examination of pre-clinical and clinical studies. J Neurotrauma. 2011 Aug. 28(8):1371-99.

 

Allen Classification of Cervical Spine Injury

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Allen classification of cervical injury is also called mechanistic classification and was given by  Allen and associates in 1982.

The translation of kinetic energy into fractures and dislocations is determined by two independent variables

  • Injury vector
  • Posture of the cervical spine at the time of accident

Allen et al presumed that identical segmental failures could result from injury vectors of the same magnitude when applied to cervical spines set in similar postures.

Based on the mechanism of injury, fractures and dislocations occur in groups, with specific anatomic derangements. These families of fractures and dislocations include

  • Compressive Flexion
  • Vertical Compression
  • Distractive Flexion
  • Compressive Extension
  • Distractive Extension
  • Lateral Flexion

The terms describe the forces upon the cervical spine at the time of injury and the magnitude of the force vector. Within each category, a series of injuries were described from mild to severe stages.

Allen classification has been commonly used over the past two decades.

This classification does not allow comparison of neurological outcome between different categories of injuries as neurologic status is not included in this classification.

It also does not explain force vectors that cause rotation and their implication in spine stability.

SCIWORA are underrepresented and may lead to mistakes in terms of management and predicting clinical outcome.

Recently SLIC system has been advised and is the preferred classification. Allen classification is hardly used now.

Main groups of Allen classification of subaxal spine injuries
Main groups of Allen classification of subaxal spine injuries, Image Credit: OUP

Classification System

Six common patterns of injury have been identified and each is further classified into stages based on the degree of injury to osseous and ligamentous structures.

Compressive Flexion

Compressive Flexion Stage 1

There is blunting of the anterosuperior vertebral margin to a rounded contour, with no evidence of failure of the posterior ligamentous complex.

Compressive Flexion Stage 2

In addition to the changes seen in stage 1, obliquity of the anterior vertebral body with loss of some anterior height of the centrum [Central portion of vertebra]. The anteroinferior vertebral body has a “beak” appearance, concavity of the inferior endplate may be increased, and the vertebral body may have a vertical fracture.

Compressive Flexion Stage 3

In addition to the characteristics of a stage 2 injury, fracture line passing obliquely from the anterior surface of the vertebra through the centrum [Central portion of vertebra] and extending through the inferior subchondral plate, and a fracture of the beak.

Compressive Flexion Stage 4

Deformation of the centrum and fracture of the beak with mild (<3 mm) displacement of the inferoposterior vertebral margin into the spinal canal.

Compressive Flexion Stage 5

Bony injuries as in stage 3, but with more than 3 mm of displacement of the posterior portion of the vertebral body posteriorly into the spinal canal. The vertebral arch remains intact, the articular facets are separated, and the interspinous process space is increased at the level of injury, suggesting a posterior ligamentous disruption in a tension mode.

Vertical Compression

Vertical Compression Stage 1

Fracture of the superior or inferior endplate with a “cupping” deformity. Failure of the end plate is central rather than the anterior, and posterior ligamentous failure is not evident.

Vertical Compression Stage 2

Fracture of both vertebral endplates with cupping deformities. Fracture lines through the centrum may be present, but displacement is minimal.

Vertical Compression Stage 3

Progression of the vertebral body damage described in stage 2. The centrum is fragmented, and the displacement is peripheral in multiple directions. Most commonly, the centrum fails, with significant impaction and fragmentation.

The posterior aspect of the vertebral body is fractured and may be displaced into the spinal canal.

The vertebral arch may be intact with no evidence of ligamentous failure, or it may be comminuted with a significant failure of the posterior ligamentous complex; the ligamentous disruption is between the fractured vertebra and the one below it.

Distractive Flexion

Distractive Flexion Stage 1

Failure of the posterior ligamentous complex, as evidenced by facet subluxation in flexion, with an abnormal divergence of the spinous process.

Distractive Flexion Stage 2

Unilateral facet dislocation. Subluxation of the facet on the side opposite the dislocation suggests severe ligamentous injury.

In addition, a small fleck of bone may be displaced from the posterior surface of the articular process, which is displaced anteriorly.

Widening of the uncovertebral joint on the side of the dislocation and displacement of the tip of the spinous process toward the side of the dislocation may be seen.

Distractive Flexion Stage 3

Bilateral facet dislocations, with approximately 50% anterior subluxation of the vertebral body.

Blunting of the anterosuperior margin of the inferior vertebra to a rounded corner may or may not be present.

Distractive Flexion Stage 4

Full vertebral body width displacement anteriorly or a grossly unstable motion segment, giving the appearance of a “floating” vertebra.

Compressive Extension

Compressive Extension Stage 1

Unilateral vertebral arch fracture with or without anterior rotatory vertebral displacement. Posterior element failure may consist of a linear fracture through the articular process, impaction of the articular process, and ipsilateral pedicle and lamina fractures.

Compressive Extension Stage 2

Bilaminar fractures without evidence of other tissue failures.

Typically, the laminar fractures occur at multiple contiguous levels.

Compressive Extension Stage 3

Bilateral vertebral arch fractures with a fracture of the articular processes, pedicles, lamina, or some bilateral combination, without vertebral body displacement.

Compressive Extension Stage 4

Bilateral vertebral arch fractures with partial vertebral body width displacement anteriorly.

Compressive Extension Stage 5

Bilateral vertebral arch fracture with full vertebral body width displacement anteriorly. The posterior portion of the vertebral arch of the fractured vertebra does not displace, and the anterior portion of the arch remains with the centrum.

Ligament failure occurs at two levels: posteriorly between the fractured vertebra and the one above it and anteriorly between the fractured vertebra and the one below it.

The anterosuperior portion of the vertebra below is sheared off by the anteriorly displaced centrum.

Distractive Extension

Distractive Extension Stage 1

Either failure of the anterior ligamentous complex or a transverse fracture of the centrum. The injury usually is ligamentous, and there may be a fracture of the adjacent anterior vertebral margin.

The radiographic clue to this injury is abnormal widening of the disc space.

Distractive Extension Stage 2

Evidence of failure of the posterior ligamentous complex, with the displacement of the upper vertebral body posteriorly into the spinal canal, in addition to the changes seen in stage 1 injuries.

Because displacement of this type tends to reduce spontaneously when the head is placed in a neutral position, radiographic evidence of the displacement may be minimal, rarely greater than 3 mm on initial films with the patient supine.

Lateral Flexion

Lateral Flexion Stage 1

symmetrical compression fracture of the centrum and ipsilateral vertebral arch fracture, without displacement of the arch on the anteroposterior view. Compression of the articular process or comminution of the corner of the vertebral arch may be present.

Lateral Flexion Stage 2

lateral asymmetrical compression of the centrum and either ipsilateral displaced vertebral arch fracture or ligamentous failure on the contralateral side with separation of the articular processes.

Ipsilateral and compressive and contralateral disruptive vertebral arch injuries may be present.

Subaxial Cervical Spine Injury Classification System or SLICS

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The Subaxial Cervical Spine Injury Classification (SLIC) system is a classification system for subaxial cervical spine injury.

This is one of the recommended classification systems for lower cervical injury.

Not only it helps to determine the injury pattern and its severity but also it guides the treatment considerations and prognosis.

The classification is similar to TLICS for the thoracic and lumbar spine injuries.

The classification was given by Spine Trauma Study Group [Vaccaro et al, 2007] and is based on the following three characteristics.

  • Injury Morphology
  • Status of discoligamentous complex
  • Neurological Status

Under each characteristic, points are given in order of increasing severity as given below.

Each of the 3 main categories is identified as integrally important to injury classification was assigned a weighted score.

Categories of Injury Morphology

Morphology of sub-axial cervical spine trauma was divided into three main categories referenced to the relationship of the vertebral bodies with each other (anterior support structures):

  • Compression
  • Distraction
  • Translation/rotation.

Classification into each of the three groups can be determined through traditional radiographic imaging studies such as plain X-ray, CT scan and MR images.

Compression

Injury appearances compatible with compression were defined as a visible loss of height through part of or an entire vertebral body, or disruption through an end-plate. This morphology includes

  • Compression fractures
  • Burst fractures
  • Sagittal or coronal plane fractures of the vertebrae
  • Tear-drop or flexion compression fractures primarily involving the vertebral body.
  • Undisplaced minimally displaced lateral mass and/or facet fractures

Concomitant fractures of the posterior cervical elements may exist with axial loading is more evenly distributed between anterior and posterior support structures.

Compression injuries of cervical spine for SLICs
Compression injuries of cervical spine

Distraction

These injuries occur less commonly than compression injuries but signify degree disruption and potential instability.

The distraction injuries are primarily identified by evidence of anatomical dissociation in the vertical axis.

This injury pattern often involves ligamentous disruption propagating through the disk space or through the facet joints, such as that seen in facet subluxation or dislocation (without fracture and translation or rotation).

A hyperextension injury disrupting the anterior longitudinal ligament and widening the anterior disk space is another form of distraction injury.

An extension force may also result in concomitant compression injury to posterior elements or cord compression due to inward buckling of the ligamentum flavum.

MRI may detect subtle distraction injuries.

Distraction injuries of cervical spine for SLICs
Distraction injuries of cervical spine

Facet capsules and bony anatomy of the facet joints are likely the primary posterior determinants of stability and must be considered for distraction injury evaluation.

Translation/Rotation

These injuries are based on radiographic evidence of horizontal displacement of one part of the sub-axial cervical spine with respect to the other exceeding physiological ranges.

This may be evidenced on either static or dynamic imaging.

A suggested threshold of rotation is a relative angulation of 11 degrees or greater.

Translation injuries are

  • Facet fracture-dislocations [unilateral, bilateral]
  • Fracture separation of the lateral mass (floating lateral mass)
  • and bilateral pedicle fractures.

Translational and rotational injuries imply disruption to both anterior and posterior structures as demonstrated in several studies

Rotational-translational injuries of cervical spine for SLICs
Rotational-translational injuries of the cervical spine

Disco-ligamentous Complex

The discoligamentous complex includes the following structures

  • Intervertebral disc
  • Anterior and posterior longitudinal ligaments
  • Ligamentum flavum
  • Interspinous and supraspinous ligaments
  • Facet capsules

Facet joint capsules are the strongest component of the posterior tension band while the anterior longitudinal ligament is the strongest anterior ligamentous structure

The complex provides significant restraint for the spine against deforming forces while allowing movement under normal physiological loads.  If its integrity is broken, spinal instability occurs.

Instability and deformity can lead to long-term impairment, including paralysis.

Disruption is inferred by abnormal bony relationships on imaging and includes

  • Widened inter-space between two adjacent spinous processes
  • Malalignment or dislocation of facet joints
  • Subluxation of the vertebral bodies
  • Abnormal widening of a disc space

Distraction and translational injuries are almost always associated with some degree of discoligamentous complex compromise.

Neurological Status

Neurological injury is inherently an important indicator of the severity of spinal column injury. Significant neurologic injury infers a significant force of impact and potential instability to the cervical spine. Moreover, the neurological status may be the single most influential predictor of treatment.

Score Calculation

Morphology

The injury is scored depending on the visible morphology

  • No abnormality is given a score of Zero – 0
  • Compression – 2
  • Distraction – 3
    • Perched facet
    • Hyperextension
  • Rotation/translation – 4
    • Facet dislocation
    • Unstable teardrop fracture
    • Advanced-stage flexion compression injury

Thus, the minimum possible score is zero and the maximum 4 under these characteristics.

Discoligamentous Complex

  • Intact – 0
  • Indeterminate – 1
    • Isolated interspinous widening
    • MRI signal indicating injury
  • Disrupted – 2
    • Widening of disk space
    • Perched facet joint
    • Facet dislocation

Neurological Status

  • Intact- 0
  • Root injury – 1
  • Complete cord injury – 2
  • Incomplete cord injury – 3
  • Continuous cord compression in the setting of the neural deficit (Neuro Modifier)

In this category score of 1 is added in case there is continuous cord compression in the setting of neurological deficit. This is called neuro modifier.

Final Score

The total score is calculated by adding scores from all the categories.

Interpretation and Treatment Guidance

  • A score of less than 4 is suitable for nonoperative treatment
  • If score is 4, the patient may be treated without or with surgery and other factors might influence treatment decision
  • If score is 5 or more, operative treatment should be considered.

The system does not pay attention to the level of injury which can be important in determining prognosis or surgical approaches. This could be a drawback of the system.

References

  • Vaccaro AR, Hulbert RJ, Patel AA, Fisher C, Dvorak M, Lehman RA Jr, et al. The subaxial cervical spine injury classification system: a novel approach to recognize the importance of morphology, neurology, and integrity of the disco-ligamentous complex. Spine (Phila Pa 1976). 2007 Oct 1. 32(21):2365-74.

** All the images used have been taken from the referenced article and labeled for easier grasp.

Spinal Cord Stimulation- Concept and Use

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Spinal cord stimulation or neurostimulati is a pain-relief technique that works by masking the pain signals before they reach the brain by delivering a low-voltage electrical current, by a surgically implanted device, to the spinal cord.

The spinal cord stimulation device is the most commonly used implantable neurostimulation technology for management of chronic pain.

They can be used for many conditions but mostly used for chronic back pain or radiating pain in arm or leg.

Types of Spinal Cord Stimulators

Spinal cord stimulator device is similar to pacemaker devices and is implanted under the skin.  A small wire carries the current from a pulse generator to the nerve fibers of the spinal cord. The electrical pulses mask the perception of pain signals or are replaced by a tingling feeling.

It is noteworthy that stimulation does not eliminate the source of pain, but simply interferes with the signal to the brain.

Therefore, the pain relief received is different in different people.

A trial stimulation is performed before the device is permanently implanted.

Spinal cord stimulator consists of following parts:

  • Pulse generator with a battery
  • Lead wire with electrodes to deliver electrical pulses to the spinal cord.
  • A hand-held remote control

Two types of systems are available.

  • One type has a non-rechargeable battery and needs to be surgically replaced every 2 to 5 years.
  • Other type is with a rechargeable battery which may last 8-10 years or longer.  But this kind needs regular charging.

Some devices are able to sense a change in body position and can adapt the stimulation level to your activity.

The pulse generator has programmable settings like rate of stimulation [frequency], area that stimulation will cover [pulse width] and how strong the pulse is [amplitude [determines the threshold of pain perception].

The adjustment can be made by by handheld remote to achieve the best possible pain relief.

There could be a difference in  stimulation intensity depending on due to variations in  the spread of electricity with change in position.

A device using radiofrequency systems can  sustain therapy over long periods but the patient must wear an external power source to activate stimulation.

Patient Selection

Following patients can be considered for treatment by neurostimulation

  • Pain not associated with malignancy
  • Poor response to conservative treatment [minimum of six months]
  • No pacemaker or other medical contraindications
  • No major psychiatric disorders, depression or drug addiction
  • A successful spinal cord stimulator trial.

Indications

The conditions in which Spinal cord stimulation may be used are

    • Degenerative disease
    • Spinal stenosis
    • Nerve compression or neuropathy

Trial Procedure of Spinal Cord Stimulation Device

The trial procedure is conducted to find if the device is suitable for the patient or not.

For the trial, under local anesthesia, a hollow needle is inserted through the skin into the epidural space. The trial lead is inserted and positioned over specific nerves. The wires are attached to an exter­nal generator worn on a belt. The trial stimulator is programmed with one or more stimulation programs customized to the pain requirement of the patient.

Over the next few days, patient analyzed whether the device is effective and if he would be able to carry it permanently. It also helps the patient to the type of spinal cord stimulation technology works best.

You will be sent home with instructions on how to use the trial stimulator and care for your incision site. Keep a written log of the stimulation settings during different activities and the level of pain relief. After 4 to 7 days, you will return to the doctor’s office to discuss permanently implanting the stimulator or removing the trial leads.

Implantation of SCS device

If the trial was successful, then a permanent system may be implanted. In spite of the name permanent, it is a reversible procedure and can be discontinued by removing the implant.

With the patient under sedation or anesthesia and trial leads are removed and the new leads are inserted in the epidural space above the spinal cord using a small needle or through a small incision.

[Sometimes, the leads implanted during the trial are perfect in position and are used for a permanent system as well.]

Laminotomy may be needed to allow room to place the leads. The leads are secured with sutures in the epidural space above the spinal cord.

The actual location of the leads would depend on the pain profile of the patient.

After leads are placed, the patient is awakened to get feedback the stimulation patterns and whether the placement works for the pain region involved.

After ascertaining, the lead wire is passed under the skin from the spine to the buttock, where the generator will be implanted.

The generator can also be implanted in the abdominal region.

[Once healed, most the patients do not feel the device]

Incisions are closed and dressed. The patient can be discharged on the same day or kept overnight.

The patient is instructed not to lift, bend, stretch or twist for at least two weeks. Walking and other light exercises are prescribed for strength building.

Strenuous activity should be avoided for the next few weeks.

Follow up is done for suture removal and adjustment of the device settings if required.

Complications/Risks of SCS Implantation

General Risks

  • Allergic reaction
  • Hematoma or seroma formation
  • Spinal cord compression
  • CSF leakage
  • Wound infection
  • Paralysis or weakness
  • Spinal fluid leakage
  • Worsened pain

Specific Risks

  • Device malfunctions requiring revision surgery
  • Undesirable changes in stimulation –  stops or works intermittently, wrong location or overstimulation
    • Scar tissue around electrodes
    • Changes in electrode position
    • Loose electrical connections
    • Lead failure/migration
  • Battery failure and/or battery leakage
  • Persistent pain at the electrode or stimulator site
  • Generator migration
  • Local skin erosion

Precautions

  • Avoid using heavy equipment when the stimulator is active
  • Avoid driving when the stimulator is active
  • The device can set off metal detectors at security gates and physician provided ID should always be carried
  • Anti-theft devices may temporarily increase stimulation if the system is on
  • Magnet on the device may damage magnetic strips as in including credit cards, video or audiocassettes, and computer disks.
  • Adverse effects of MRIs, ultrasound, defibrillators, electrocautery, diathermy, and cardiac pacemakers. The use should be restricted as directed by device type

Outcome

About 60 percent of people who received spinal cord stimulator have reported pain reduction/relief.

In case of failed back surgery syndrome, early treatment has a better outcome.

References

  • Verrills P, Sinclair C, Barnard A. A review of spinal cord stimulation systems for chronic pain. J Pain Res 9:481-92, 2016
  • De la cruz P, Fama C, Roth S, et al. Predictors of Spinal Cord Stimulation Success. Neuromodulation 18(7):599-602, 2015
  • Eldabe S, Buchser E, Duarte RV. Complications of Spinal Cord Stimulation and Peripheral Nerve Stimulation Techniques: A Review of the Literature. Pain Med 17(2):325-36, 2016
  • Sundaraj SR, et al: Spinal cord stimulation: A seven-year audit. J Clin Neurosci 12:264-270, 2005

 

TLICS- Thoracolumbar Injury Classification and Severity Score

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Thoracolumbar injury classification and severity score or TLICS  is a scoring system for thoracolumbar fractures which classifies and provides guidance to the treatment as well.

TLICS is based on three major categories

  • Morphology of the injury
  • Integrity of the posterior ligamentous complex
  • Neurologic status of the patient.

Denis classification of spinal injuries which is based on the three column concept emphasized that that mechanical instability and progressive neurologic deterioration could occur separately or together. It is the most popular classification but it fails to provide useful treatment guidance.

For example, not all two column injuries would require surgery but the simplification of Denis classification has been widely accepted so. But studies have shown repeatedly that conservative treatment works well for some two column injuries.

Moreover, the Denis’ classification is not clear on how ligamentous injuries can be identified.  These, if present could lead to progressive instability. These patients require surgical intervention to prevent progressive deformity or progressive neurologic deficit. These patients may be missed.

These can be identified with MRI and TLICS incorporates its use quite well.

Thoracolumbar injury classification and severity score or TLICS

The thoracolumbar injury classification and severity score  or TCLICS)  is based on three major categories

  • Morphology of the injury
  • Integrity of the posterior ligamentous complex
  • Neurologic status of the patient.

The morphology of injury and the integrity of the posterior ligamentous complex are both defined by the appearance of the injury on imaging studies. Neurologic status is determined clinically.

Each category is given a score depending on the severity.

The total score is calculated by addition of scores from individual categories.

Based on the severity of these categories, specific points are allocated, and the sum of the points defines the possible treatment alternatives. Higher total points indicate a more severe injury, and those injuries are more likely to benefit from surgical intervention based on the opinions of the Spine Trauma Study Group.

Morphology of injury

The three major morphologic subcategories are

  • Compression injuries
  • Burst Fractures
  • Translational/rotational injuries
  •  Distraction injuries

If there are injuries at multiple levels, only the more severe morphology is counted. If multiple primary morphologies are involved at a single level, only the most severe is counted.

Compression fractures [score 1]are most common thoracolumbar injuries and result from an axial loading of the spine transferred to the anterior vertebral body. This results in wedge deformity of the vertebral body because of the collapse of the anterior vertebral body while the posterior vertebral body remains intact.

Compression fracture get a score of 1

The burst fracture [score 2]is more severe injury and in this, the axial load is transferred to both the anterior and posterior vertebral walls resulting in disruption of anterior and posterior cortex.

Score 2 is assigned to these fractures

Translational/rotational injuries [score 3] occur from violent torsional, shear forces, or both and often cause significant ligament injury. or osseous damage. These injuries are frequently unstable and a score of 3 is assigned to these injuries.

Distraction injuries [score 4] are the severest form of injury to the spine and occur due to spine failing under tensile forces.

Score assigned is 4.

For proper scoring, the injury should be well identified.

Neurologic injury

There are five categories of neurologic injury

  • Intact – score is zero
  • Nerve root injury- 1
  • Complete spinal cord injury -2
  • Incomplete spinal cord injury – 3
  • Cauda equina syndrome- 4

One of the surprising element is assigning a lesser score to complete spinal injury whereas incomplete spinal injuries like cauda equina syndrome are assigned the higher score.

This is because of the therapeautic significance of scoring. Surgery has greater relative value in incomplete injury and patients with a higher score are the candidate for surgery in this scheme of scoring.

Posterior ligamentous complex

Injury to the posterior ligamentous complex is seen in three categories.

  • Intact – Zero point
    • The absence of a palpable gap between spinous processes
    • No interspinous widening on plain x-ray or CT
    • Absence of posterior ligamentous hyperintensity on fat-suppressed MRI images [T2-weighted ]
  •  Indeterminate disruption of the posterior ligamentous complex – 2 points
  • Definite disruption – 3 points.

Total Score and Its Applicaton

The total score is calculated by adding points in all the major categories.

  • Score less than 3
    • Nonoperative
  • Score of 4
    • Indistinct category
    • Either nonoperative or operative treatment
  • 5 or more Score
    • Surgery

Use of TLICS

The TLICS can serve as a guide to help determine possible treatment options.

However other factors important for decision making, like medical co-morbidities, other injuries, skin condition of the intended incision site, the preexisting bony disorders like ankylosing spondylitis, DISH etc. may also affect treatment decisions.

References

  • Lee JY, Vaccaro AR, Lim MR, et al. Thoracolumbar injury classification and severity score: a new paradigm for the treatment of thoracolumbar spine trauma. J Orthop Sci. 2005;10(6):671-5.
  • Blauth M, Bastian L, Knop C, Lange U, Tusch G. Inter-observer reliability in the classification of thoraco-lumbar spinal injuries. Orthopade. 1999;28:662–81. doi: 10.1007/s001320050397.

Vertebra Prominens or Seventh Cervical Vertebra [C7]

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Vertebra prominens is the common name for 7th cervical vertebra or C7, the largest and most inferior vertebra of the cervical region of the spine.

It is named because it has a large spinous process that protrudes posteriorly and can be felt prominently on palpation.

Vertebra prominens is easily recognized on palpation of the back of the neck from above downwards because of its palpation.

Cervical spine is formed by seven vertebras named as C1 to C7.  First vertebra is known as atlas and second as axis. Third to sixth cervical vertebra are typical in anatomical structure. But as the cervical spine approaches its end, its last vertebra or seventh cervical vertebra, C7 changes in shape.

[read more on cervical spine anatomy]

This vertebra prominens is used as a landmark in the clinical examination for numbering the vertebra during spine examination

c7.png

Structural Features

The transverse processes are comparatively large in size, the posterior root is larger than the anterior. The anterior tubercle is absent. The foramen transversarium is relatively small, sometimes double, or may be entirely absent.

The anterior root of the transverse process may sometimes be separate and form cervical rib.

The upper surface of transverse processes usually bears a shallow sulcus for the eighth spinal nerve.

The spinous process is thick, long and nearly horizontal going straight back. Unlike other cervical vertebrae, It is not bifid but ends in a tubercle.

C7 vertebra forms joints with C6 vertebra above and T1 vertebra below.

Attachments

  •  Tip of spinous process-
    • Ligamentum nuchae
    • Trapezius
    • Rhomboideus minor
    • Serratus posterior superior
    • Splenius capitis
    • Semispinalis thoracis
    • Spinalis cervicis
    • Interspinales
    • Multifidus.
  • Transverse process
    • Transmits only an accessory vertebral vein
  • Posterior tubercle
    • Suprapleural membrane
  • Lower border
    • Levator costarum.

Clinical significance

Anatomical Landmark

In most of the people, C7 is most prominent vertebra and is considered as a landmark in clinical examination of spine. This gives a landmark to count vertebrae above and downward.

But it must be borne in the mind that only 70% of people have C7 as most prominent. In the rest, either C6 or T1 can make the most prominent vertebra. Therefore, it introduces a chance of error in such cases.

Cervical Rib

Anterior root of the C7 vertebra can form the cervical rib. It could be asymptomatic in most of the people but can give rise to Thoracic outlet syndrome.

 

Lumbosacral Plexopathy – Causes and Management

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Lumbosacral plexopathy is an injury to the nerves in the lumbar or sacral plexus.

Lumbosacral plexopathy can be caused by many disorders. The prevalence of lumbosacral plexopathies is unknown and is much less common than brachial plexopathies.

Risk factors vary based on cause.

Relevant Anatomy

Lumbar plexus details, PD wiki

The lumbar and sacral plexuses together make lumbosacral plexus which is formed from the anterior (ventral) rami of the L1 through S4 nerve roots

The lumbar plexus is derived from the anterior rami of the L1 through L4 nerve roots. These rami pass downward and laterally along the psoas major muscle where they eventually form the plexus.

While within the psoas, they divide into anterior and posterior branches.

The posterior branches of anterior rami, L2-L4, become the femoral nerve, which exits from the lateral aspect of the psoas, traveling through the iliacus and under the inguinal ligament to the anterior thigh.

The anterior branches become the obturator nerve, that exits through the obturator foramen to the medial thigh. The lumbar plexus also gives off the lateral femoral cutaneous nerve of the thigh, iliohypogastric, ilioinguinal, and genitofemoral nerves.

The lumbar plexus and sacral plexus are united via the lumbosacral trunk, which is comprised of a part of L4 nerve root anterior rami, and all L5 anterior rami. The lumbosacral trunk passes over the sacral ala and joins the anterior rami of the S1-4 nerve roots to complete the sacral plexus.

sacral plexus or lower lumbosacral plexus

The sacral plexus lies more inferiorly and posteriorly within the pelvic outlet. It is made up of ventral primary spinal nerve branches from L4 to S4, which form several branches including the following:

  • Proximal branches to the pelvic musculature and buttock region, including nerves to the quadratus femoris, Gemelli, obturator internus, piriformis, and superior and inferior gluteal nerves.
  • Posterior femoral cutaneous nerve, which has multiple sensory branches to the genitals and thigh.
  • Sciatic nerve

Read detailed anatomy of Lumbosacral Plexus

Causes of Lumbosacral Plexopathy

Structural

  • Retroperitoneal hemorrhage (anticoagulation, hemophilia)
  • Pelvic or abdominal tumor
  • Aneurysm (common or internal iliac artery)
  • Endometriosis
  • Trauma

Nonstructural

  • Inflammatory (plexitis)
  • Infarction
  • Postpartum [during childbirth]
  • Diabetes (diabetic amyotrophy – most common non-structural cause)
  • Radiation
  • Postsurgical (retractor injury)

Pattern of Injury or Plexopathy

Lumbosacral plexus lesions usually are divided clinically into

  • Upper lumbar plexus [anatomical lumbar plexus]
  • Lower lumbosacral plexus [anatomical sacral plexus]

Lumbar plexopathies

It predominantly affects the L2–L4 nerve fibers. Pain, if present, usually is located in the pelvis with radiation into the anterior thigh.  Quadriceps, iliopsoas, and hip adductor muscles ( femoral and obturator nerves) are the affected muscles.

The knee reflex is frequently depressed or absent.

Sensory loss and paresthesias occur over the lateral, anterior, and medial thigh and may extend down the medial calf

Sensory abnormalities are

  • Over the lateral thigh (lateral femoral cutaneous nerve)
  • Anterior thigh (the intermediate cutaneous nerve of the thigh from femoral nerve
  • Medial thigh (the femoral branch of the genitofemoral nerve, the medial cutaneous nerve of the thigh [femoral branch] and obturator nerve)
  • Medial calf (saphenous nerve [femoral]).

Lower Lumbosacral  Plexopathy

It predominantly affects the L4–S3 nerve fibers.

There is a complaint of a deep boring pain in the pelvis that can radiate posteriorly into the thigh with extension into the posterior and lateral calf.

The ankle reflex may be depressed or absent.

Sensory symptoms and signs may be seen over the posterior thigh and posterior-lateral calf and in the foot.

Muscles affected are

  • Hip extensors (gluteus maximus)
  • Hip abductors and internal rotators (gluteus medius and tensor fascia latae).
  • Hamstrings
  • All leg muscles supplied by the peroneal and tibial nerves.

Nerve fibers that would go to form the peroneal nerve often are preferentially affected in lumbosacral plexopathies. Therefore the patient may have foot drop and sensory disturbance over the dorsum of the foot and lateral calf. In some cases, the pattern of weakness and numbness may be difficult and electrodiagnostic studies are needed to differentiate.

Clinical Presentation

The patient typically presents with unilateral weakness, sensory loss, and pain.

The presentation may be acute or subacute depending on the cause

The Plexopathy is generally unilateral but the bilateral disease is possible (massive traumas, autoimmune diseases, or radiation-induced).

The symptoms of plexopathy would be accompanied by other symptoms of the associated conditions. For example in autoimmune disease, the skin lesions or other symptoms and signs suggestive of autoimmune disease may be present.

Systemic symptoms like weight loss, fever may be present in some conditions.

The affected limb would have signs suggestive of lower motor neuron injury.

There would be decreased muscle bulk in the distribution of the affected nerves. Muscle tone is decreased in the affected muscles, and reflexes are usually absent or greatly diminished.

[Patellar reflex is present in intact lumbar plexus whereas hamstrings reflex and Achilles reflex are affected [ supplied by the sacral plexus.]

The pattern of weakness would indicate root affected and thus guide to the part of the plexus involved.

Differential Diagnoses

Lab Studies

Lab studies would depend on the causation.

In general

  • Blood glucose and glycosylated hemoglobin  in diabetic lumbosacral plexopathy
  • Erythrocyte sedimentation rate
  • White blood count if an abscess is suspected
  • Prothrombin time and platelets to know blood disorders

Imaging

X-rays would reveal any bony trauma.

MRI/CT can identify space occupying lesions (eg, cancer, hematoma, abscess) that may be compressing the plexus. MRI neurogram can be done evaluate if nerve root avulsion has occurred.

Neural Studies

Electrodiagnostic testing is used to localize the nerve injury and characterize the process.

Nerve Conduction Studies

Fibular and tibial motor nerve conduction studies with F waves would be absent or of low amplitude in sacral plexus involvement.

Sural, saphenous, and lateral femoral cutaneous sensory nerve conduction studies would be expected to be absent or of low amplitude, with normative distal latency unless the amplitudes are very low, in which case there may be prolonged distal latencies.too.

It must be noted that sensory nerve conduction would be normal in root avulsion too because the dorsal root ganglion cell body remains intact.

Comparison with an opposite limb or upper limb may help.

Needle electromyography

Multiple muscles innervated from L2 to S1 with multiple peripheral nerves are tested. Lumbar paraspinals should also be tested to search for radiculopathy. No motor recruitment will be seen in case the plexus is severely damaged or there is root avulsion.

Management of Lumbosacral Plexopathy

The management of plexopathy would depend on the cause. Following options are available

  • Pain management
    • Drugs
    • Spinal cord stimulators
    • Intrathecal therapies.
  • Physical therapy
    • Strengthening  of  partially affected muscles
    • Correction of  address muscular imbalances
    • Maintain flexibility
    • Improve balance and gait.
  • Assistive devices and braces  like AFO to correct foot drop and weakness
  • Surgery in selected cases of severe nerve injury
    • Preferred in  root avulsions and sharp lacerations

Prognosis

The clinical course depends on the cause.

Except in root avulsion, traumatic plexopathies partial recovery normally, and many patients will have a full or nearly full recovery.

Recovery may take about 18 months after injury.

For lumbosacral plexopathy caused by compression such as (eg, retroperitoneal hematomas), outcomes can be excellent but patients may have lingering symptoms.

Similarly, for diabetic lumbosacral plexopathy, significant improvement with time occurs through some non-progressive deficits may remain.

In radiation-induced plexopathies, unfortunately, a slow but progressive loss of function is expected.

Patients of plexopathy may be left with decreased function and an abnormal gait related to muscle weakness including foot drop. There could be sensory deficits [ insensate skin].

Chronic pain may also be present.

Neoplastic plexopathy generally has a very poor prognosis when they are not resectable and resistant to radiotherapy.

Needle electromyography may be used to monitor the progress.

Common Lumbosacral Plexopathies

Retroperitoneal Hemorrhage

Retroperitoneal hemorrhage is most commonly seen in

  • Complication of anticoagulation
  • Hemophilia
  • Aortic aneurysm rupture.

Such hemorrhages usually are located within the psoas muscle itself, where they can compress the lumbar plexus.

The presentation is of acute severe pain where the hip is flexed and slightly externally rotated.

The major neurologic deficit usually is in the femoral nerve territory, with the weakness of hip flexion and knee extension and a reduced or absent knee-jerk. However, the examination would reveal some dysfunction in the obturator or lateral femoral cutaneous nerve or both.

The treatment would depend on the cause but a decompression is almost always required.

Mass Lesions

Tumors from the bladder, cervix, uterus, ovary, prostate, colon, or rectum may compress the lumbosacral plexus leading to lumbosacral plexopathy.

Lymphoma and leukemia can directly infiltrate nerves, even in the absence of a mass lesion on imaging studies.

Aneurysms or pseudoaneurysms of the internal iliac or common iliac artery have been reported to compress the lumbosacral plexus.

In women, endometriosis can cause implantation of abnormal tissue on the plexus and cause compression. These lesions more often affect the lower lumbosacral plexus.

Endometriosis may result in intermittent symptoms but other lesions are usually slowly progressive.

Idiopathic Lumbosacral Plexitis

Idiopathic plexitis pathology is not completely known. It is thought to be inflammatory, often occurring within a few weeks of a possible inciting immunologic event, such as a cold, flu, or immunization.

There is a severe deep pain in the pelvis or in the upper leg. It characteristically persists for 1 to 2 weeks but may last many months. Because both the upper and lower plexus may be involved leading to different patterns of weakness and sensory loss.

The weakness recovers over many months to years.

Postpartum Plexopathy

Other names for this compression injury to the lumbosacral plexus during labor and delivery are maternal peroneal palsy, maternal birth palsy, neuritis puerperalis, and maternal obstetric paralysis. Although most large series place the incidence of this disorder at one in 2600 births, there are likely many milder cases that never reach medical attention.

The mechanism involves compression of the fetal head against the underlying pelvis and lumbosacral plexus. The compression primarily occurs at the lumbosacral trunk which is vulnerable as it crosses the pelvic outlet and no longer protected by the psoas muscle as they rest against the sacral ala near the sacroiliac joints.

The origin of the superior gluteal nerve lies which is close can also get compressed.

As the fibers that eventually form the peroneal division of the sciatic nerve lie posteriorly, closest to the bone, and are more vulnerable. It should be kept in mind when women present with foot drop after delivery [It can be misdiagnosed as peroneal palsy at the fibular neck.]

Weakness may be noticed immediately or within the first few days after delivery.

In addition to peroneal weakness, the examination would reveal mild weakness hamstrings; hip abduction, extension, and internal rotation indicating a higher lesion than just foot drop.

A sensory deficit is marked over the dorsum of the foot and lateral calf but may be patchy.

Diabetic Lumbosacral Plexopathy

Diabetic lumbosacral plexopathy is most common non-structural lumbosacral plexopathy. Patients develop severe aching or burning and lancinating pain in the hip and thigh, followed by weakness and wasting of the thigh muscles

It occurs in type 1 and 2 diabetes mellitus. 

Often,  the root and nerve levels are also involved and the disorder is called lumbosacral radiculoplexus neuropathy.

Control of sugar by adjustment of diabetes medication is important.

The management includes neuromodulator medications like gabapentin or pregabalin for neuropathic pain and selective norepinephrine reuptake inhibitors such as duloxetine.

References

  • Jaeckle KA. Neurological manifestations of neoplastic and radiation-induced plexopathies.Semin Neurol.2004;24:385-393.
  • Laughlin RS, Dyck JB. Electrodiagnostic testing in lumbosacral plexopathies.Phys Med Rehabil Clin N Am. 2013;24:93-105.
  • Garozzo D, Zollino G, Ferraresi S. In lumbosacral plexus injuries can we identify indicators that predict spontaneous recovery or the need for surgical treatment? Results from a clinical study of 72 patients.J Brachial Plex Peripher Nerve Inj.2014;9:1.
  • Kent KC, Moscucci M, Gallagher SG, DiMattia ST, Skillman JJ. Neuropathy after cardiac catheterization: incidence, clinical patterns, and long term outcome. J Vasc Surg.1994;19:1008-1013.

Transitional Vertebra Definition and Types

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Transitional vertebra at any junction is characterized by features retained from two adjacent regions in the vertebral column. For example in the lumbosacral transitional vertebra, there is an L5 vertebra can become like S1 vertebra or S1 can leave the sacrum and become L6.

As we know from our knowledge of the anatomy of the spine, the anatomy of vertebrae varies according to the region and function.

Thus cervical vertebrae have different anatomy than thoracic and lumbar and sacral. The size shape and different features are different. Most of the typical vertebrae behave like that.

The issue of transitional vertebra arises when there is a change of region. These regions are from skull to cervical vertebrae, cervical to thoracic, thoracic to lumbar and lumbar to sacrum.

Out of these lumbosacral transitional vertebrae is most common.

Thus the transitional vertebra is found in  cervicothoracic, thoracolumbar, or lumbosacral junction.

The transitional vertebra has indeterminate characteristic and features of vertebrae from adjacent vertebral segments.

This transitional vertebra causes a change in anatomy and biomechanics. These may cause symptoms and can lead to confusion when describing findings [the difficulty in labeling the correct number of the vertebra].

Different Types of Transitional Vertebra

Following are the different transitional vertebrae

Atlanto-occipital Junction

Transitional vertebra here can present as

Atlanto-occipital assimilation

Complete or partial fusion of C1 and the occiput

Occipital vertebra

Here there is an additional bone present between C1 and the occiput

Cervicothoracic junction

Cervical rib arising from C7 is an example of transition. Normally, the ribs begin from T1 vertebra and arising from C7 indicates transition.

Thoracolumbar junction

Here, there may be a lumbar rib or 13th rib arising from T13 vertebrae or  L1 vertebra( the label varies according to the method of numbering chosen.

Other examples of transition are

  • Aplasia or hypoplasia of the transverse process
  • Irregular orientation on the superior articular process
  • Atypical mammillary bodies [Mamillary body is a  small apophysis or tubercle on the dorsal margin of the superior articular process of each of the lumbar vertebrae and often of T12 too].

Lumbosacral junction

Lumbosacral transitional vertebra

It is the most common transitional vertebra and most researched also. Its spectrum ranges from complete lumbarization to sacralization.

In lumbarization,  there are six lumbar vertebrae and four sacral because first sacral vertebrae have left the sacrum during development and became like the lumbar vertebra.

Sacralization is the opposite of the above. The last lumbar vertebra gets fused with the sacrum. Now sacrum has six vertebrae and lumbar spine has only 4.

Transitional lumbosacral is also thought to be the cause of back pain. Bertolotti syndrome is symptomatic transitional lumbosacral vertebra.

In presence of LSTV, the numbering of vertebrae has to be done carefully to ascertain correct levels and confirmed using more than one methods.

Detection

These vertebrae are best identified on MRI on sagittal T1W and T2W images. For correct identification, the entire spine is imaged.

Clinical Significance

Transitional vertebrae could be found on images incidentally or could present as a set of symptoms as defined by the area where they are present.

It is important to mention that just the presence of transitional vertebra doe does not mean that, it is the originator of the symptoms. Therefore clinical relevance and correlation of the findings are very necessary.

The presence of transitional vertebra could confuse the numbering of the vertebral levels. Therefore, it is important to ascertain the correct levels by using more than one method to count the vertebrae.

In some case, the whole spine may be needed to be imaged to ascertain the correct level.

 

Lumbosacral Transitional Vertebra or LSTV

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Lumbosacral transitional vertebra refers to a spectrum of are congenital spinal anomalies involving L5 and adjacent vertebrae and varies from complete fusion of L5 with the sacrum, called sacralization to complete separation of S1 from the sacrum and present as L6, called lumbarization.

When the L5 vertebra fuses completely to the sacrum, 4 lumbar vertebrae exist, whereas when S1 separates entirely from the sacrum, 6 lumbar vertebrae exist

Many intermediate incomplete transitions have also been recognized and classified as LSTV.

The prevalence of LSTV in the general population varies from 4.0% -35.9% with a mean of 12.3%.

In unilaterally occurring malformations, the incidence is significantly higher on the left side, a finding which remains unexplained.

The prevalence of LSTV is higher in men. Sacralization is common in males while lumbarization of S1 is more common in women.

A genetic component involving HOX10/HOX11 has been suggested.

The presence of an LSTV is associated with a higher incidence of a concomitant thoracolumbar transitional vertebra and vice versa.

Types of Lumbosacral Transitional Vertebra

Castellvi Classification

Classification of Lumbosacral transitional vertebra
Classification of Lumbosacral transitional vertebra

Type I

It includes unilateral (Ia) or bilateral (Ib) dysplastic transverse processes, measuring at least 19 mm in width in craniocaudal dimension.

 Type II

Incomplete unilateral (IIa) or bilateral (IIb) lumbarization/sacralization with an enlarged transverse process that has a diarthrodial joint between itself and the sacrum.

Type III

Unilateral (IIIa) or bilateral (IIIb) lumbarization/sacralization with a complete osseous fusion of the transverse process(es) to the sacrum.

Type IV

Unilateral type II transition with a type III on the contralateral side.

Mahato Classification

There is an association between lumbosacral transitional vertebra with morphological alterations of neural arch elements and auricular surfaces is well established.

Mahato classification takes these things into account.

Type I – Dysplastic L5 Transverse Process

Type I A

Unilateral TP  less than 19 mm in width

Type I B

Bilateral TPs more than 19 mm in width

Type I A F (i/c) or Type I B F(i/c)

With the presence of ipsilateral/contralateral rudimentary facet to the side of the L5 enlargement

Type I A F2 or Type I B F2

With the presence of bilateral rudimentary facets

Type II – Accessory articulations

Type II A

Unilateral L5-S1 accessory articulation

Type II B

Bilateral L5-S1 accessory articulations

Type II A F(i/c) or Type I B F(i/c)

With the presence of ipsilateral/contralateral rudimentary facet to the side of the diarthrosis.

Type II A 2F or Type II B 2F

With the presence of bilateral rudimentary facets

Type III – Sacralisation

Type III A

Unilateral L5-S1 sacralization

Type III B

Unilateral complete sacralization with contralateral L5-S1 pseudoarthrosis

Type III C

Bilateral complete L5-S1 sacralization

Type III A F (i/c) or Type III B F(i/c) or Type IIIC F

With the presence of ipsilateral/contralateral rudimentary facet to the side of the sacralization

Type III A 2F or Type III B 2F or Type III C 2F

With the presence of bilateral rudimentary facets

Lumbarization

Type IV A

Incomplete/partial lumbarization of S1 as an accessory S1-2 articulation

Type IV B

Unilateral complete separation of S1 from sacral mass

Type IV C

Bilateral S1-2 accessory articulation

Type IV D

Complete sacralization with residual four segment sacrum

Type IV A F(i/c) or Type IV B F(i/c) or Type IV C F or Type IV D F

With the presence of ipsilateral/contralateral rudimentary facet to the side of the diarthrosis

Type IV A 2F or Type IV B 2F or Type IV C 2F or Type IV D 2F

With the presence of bilateral rudimentary facets

Biomechanical and Structural Changes

The presence of a lumbosacral transitional vertebra alters normal spine biomechanics.

The function of the sacrum is to optimize the transfer of the weight of the upper body toward the sacroiliac joint. This function depends on the size and its surface area with the SI joint.

HOX genes regulate segmentation of the vertebral column into individual vertebral segments.

But the formation of transitional states at the lumbosacral junction is thought to be influenced by the functional requirements of load transmission at the sacroiliac junction.

It has been found that in sacrum in the sacralized specimen is smaller in height than the normal sacra if the fused L5 vertebra is excluded from the measurement.

This addition or separation of segments to or from the sacrum depends on the load-bearing capacity of the normal sacrum at a very rudimentary stage of its formation.

Small sacrum with inadequate sacroiliac joint surface area may incorporate L5 to enhance load-bearing capacity, while a sacrum with over competent load bearing capacity may release S1.

Bony abnormalities are associated with the lumbosacral transitional vertebra.

In sacralization, all dimensions, including pedicle height, sagittal and transverse dimensions, and sagittal angulation are reduced, and the downward slope is increased.

The height of the pars interarticularis and the widths of laminae are significantly smaller in the terminal lumbar segment of sacralized specimens, predispose spondylolysis and spondylolisthesis at the lumbosacral junction.

Lumbarization of S1 results in a shorter distance between the facet and sacral promontory, more obtuse pedicles in the sagittal plane and less steep in front.

The orientations and anatomy are important from the surgical viewpoint.

Facet asymmetry is seen in all subtypes.

The disc height below a lumbosacral segment is significantly decreased in types II, III, and IV and may be confused with degeneration or displacement.

The weakness of the iliolumbar ligaments has been noted at the level immediately above transitional vertebrae. It could be responsible for vertebral segment instability and could subsequently lead early disc degeneration.

It is suggested that the articulation or bony union between vertebra and sacrum through the transverse process may represent an adaptive mechanism to compensate for a weak iliolumbar ligament and to preserve stability.

Terminal level of the conus medullaris is significantly higher in the presence of a sacralized L5 and significantly lower in the presence of a lumbardized S1. This might be the reason for the neurological discrepancies observed among neurologic injuries at the thoracolumbar junction.

Due to altered vertebral, neural and possible vascular anatomy, modification of surgical approaches may be necessary.

Pain in the presence of an LSTV may arise from disc herniation or degeneration [also occurs at a younger age than people without LSTV] , facet joint arthrosis, or spinal canal or foraminal stenosis.

LSTV are more likely to be present in patients with clinically significant spinal symptoms and even more so in those operated on for disc herniation of the last mobile disc.

Hypermobility and abnormal torque moments at the level immediately above the transitional vertebra and restricted movement between the L5 and S1 vertebra result in degenerative changes at the level above the anomalous articulation.

Disc protrusion and/or extrusion occurs more often at the level which is suprajacent.

Disc bulge or herniation is exceedingly rare at the interspace below a transitional vertebra.

The incidence of spinal stenosis and spondylolysis is not significantly higher in patients with an LSTV. Though anterior slippage can be more severe when it occurs.

Unilateral LSTV result in asymmetrical biomechanical alterations. The side bearing the additional L5/S1 relationship supports a larger proportion of load, resulting in lateral tipping of the iliac crest. There is convexity of a scoliotic curve towards the side of the articulation.

Asymmetry can cause early degenerative changes and influence disc degeneration.

S1 lumbarization has been implicated in compression neuropathy of the S1 nerve root. Lumbar spinal nerve between the transverse process of the 5th lumbar vertebra and the sacral ala is called  Far-Out Syndrome. Extraforaminal entrapment of the spinal nerve leading to radiculopathy.

Neural compression by new bone formation below an LSTV may occur.

Imaging of Lumbosacral Transitional Vertebrae

X-rays

X-rays in a saggital plane[lateral projection] features suggestive are “squaring” of the transitional vertebral body and reduced height of the transitional disc.

Axial images depict pseudoarthrosis or fusion of the last lumbar vertebra with the sacrum.

The pseudoarticulation between the transverse process and the sacrum may be indicated by sclerotic changes and osteophytes near the false joint.

Standard AP radiographs demonstrate 76%-84% accuracy for lumbosacral transitional vertebra detection.

The 30° angled AP radiograph (Ferguson radiograph) serves as the reference standard method to detect LSTV.

MRI

Exaggerated lumbar lordotic curvature and a lack of sharp angulations at the lumbosacral junction on mid-sagittal MRI suggest lumbosacral transitional vertebra.

An angle formed by a line parallel to the superior surface of the sacrum and a line perpendicular to the axis of the scan table on mid-sagittal T2-weighted MRI is calculated. A value >39.8° suggests LSTV.

The angle formed by a line parallel to the superior endplate of the L3 vertebra and a line parallel to the superior surface of the sacrum, if  >35.9° suggests lumbosacral transitional vertebra.

Paraspinal structures in positions outside their frequent location may signify the presence of a transitional vertebra.

Aortic bifurcation, IVC confluence, right renal artery, celiac trunk, and superior mesenteric artery root are located 1-3 levels more caudal than normal in the case of lumbarization, and 1-3 levels more cephalic than normal in the case of sacralization.

But it must be kept in mind that nonspinal landmarks have a variable location and also changes with age.

Correct Numbering of the vertebrae

A lumbosacral transitional vertebra can make correct numbering of lumbar and sacral vertebra difficult on imaged

It is important to ensure a correct number of the vertebra to avoid intervention or surgery at the incorrect level.

On x-rays, by convention, on a sagittal radiograph, the last vertebra with a rectangular shape is generally considered to be L5, and then the vertebral bodies are numbered from the bottom to the top.

In the presence of an LSTV the rectangular shaped last vertebra can be L4 or L6.

This is confirmed by counting from above, T12 downwards. The vertebra with the last rib is deemed as T12 [ But that can be fallacious as many persons have last rib absent]

In such cases/doubt, whole spine images including cervical spine can be used for confirmation, starting from C2 downward.

On MRI, whole spine sagittal T2W images play an essential role in accurate vertebral numbering. Numbering is done caudally from C2 on whole-spine MR images.

In a child, sagittal images of the sacrum and coccygeal bone on T2 weighted can help. The counting is done up from S5 and S1 is determined correctly.

Determination of S1 enables detection of the L5 and, in turn, all other vertebrae.

Clinical Significance of LSTV

Low back pain in the presence of an LSTV was originally noted by Mario Bertolotti in 1917 and termed Bertolotti’s Syndrome.

The potential association between LSTV and low back pain has been debated.

Some authors suggest that lumbosacral transitional segments are quite common and may not be seen with higher prevalence in patients reporting low back pain.

A third opinion suggests that low back pain complaints might be worse, but not more frequent when a lumbosacral transitional vertebra is present.

A diagnosis of Bertolotti’s syndrome should be cautiously considered with appropriate patient history, imaging studies, and diagnostic injections.

References

  • Hughes RJ, Saifuddin A. Imaging of lumbosacral transitional vertebrae. Clinical radiology. 2004;59(11):984–91.
  • Mahato NK. Redefining lumbosacral transitional vertebrae (LSTV) classification: integrating the full spectrum of morphological alterations in a biomechanical continuum. Medical hypotheses. 2013;81(1):76–81.
  • Konin GP, Walz DM. Lumbosacral transitional vertebrae: classification, imaging findings, and clinical relevance. AJNR American journal of neuroradiology. 2010;31(10):1778–86.
  • Luoma K, Vehmas T, Raininko R, Luukkonen R, Riihimaki H. Lumbosacral transitional vertebra: relation to disc degeneration and low back pain. Spine. 2004;29(2):200–5
  • Kim YH, Lee PB, Lee CJ, Lee SC, Kim YC, Huh J. Dermatome variation of lumbosacral nerve roots in patients with transitional lumbosacral vertebrae. Anesthesia and analgesia. 2008;106(4):1279–83. table of contents.
  • Hughes RJ, Saifuddin A. Numbering of lumbosacral transitional vertebrae on MRI: role of the iliolumbar ligaments. AJR American journal of roentgenology. 2006;187(1): W59–65.

Adjacent Segment Disease Causes and Treatment

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Adjacent Segment Disease is defined as new degenerative changes at a spinal level adjacent to a surgically treated level or levels in the spine, leading to symptoms of radiculopathy, myelopathy, or instability. It is denoted as ASDis

This condition may or may not result in any symptoms.

The term adjacent segment degeneration (ASDeg) is used to represents the radiographic changes without the symptoms.

At present, there is no clearcut or accurate definition of an adjacent segment disease. It refers to a condition in which after a cervical or lumbar spinal fusion, the levels adjacent to the fused level show degeneration which are readily seen radiographically. Thus it is a broad term encompassing many complications of spinal fusion, listhesis, instability, herniated disc, facet hypertrophy and compression fracture of the vertebra.

Due to this complication, current studies are encouraging motion sparing spinal surgery though long-term data are required.

Cervical Spine Fusion - Adjacent segment disease is known complication
Cervical Spine Fusion, Image from Wikipedia, in public domain

In contrast to adjacent segment degeneration, which is a common radiographic finding, adjacent segment disease is less common. The incidence of ASDis in both the cervical and lumbar spine is between 2% and 4% per year, and ASD is a significant contributor to reoperation rates after spinal arthrodesis.

Why does Adjacent Segment Disease Occur?

 ASD is seen more in people who have other risk factors like arthritis or other condition that predispose them to disc degeneration or disease.

The etiology is probably multifactorial, stemming from existing spondylosis at adjacent levels, the predisposed risk to degenerative changes, and altered biomechanical forces near a previous fusion site. Numerous studies have sought to identify both patient and surgical risk factors for ASD, but a consistent, single predictor is not found yet to be found.

Some researchers have pointed out that a damage done to the structures of the spine, during the surgery may be responsible.

The unanswered question is whether the degeneration is due to degenerative changes caused by further aging or fusion of the adjacent level or levels which have put excessive stress.

The answer is not confirmed yet and research is still going on.

Studies have shown that after fusion surgery, there is an increased load on adjacent segments.

This is seen in both cervical and lumbar spine after fusion.

Although no conclusive etiology exists, natural history seems to be an important factor.

Spinal fusions are used for treatment of back pain and/or instability of the spine.

Soft tissue disruption adjacent to the surgical level is considered a potential cause.

Fusion kills the painful motion and therefore, the pain generator. But it also means loss of a motion segment.

This creates abnormal loads for the spine segments above and below the fusion leading to stress to the nearby facet joints and discs. Wear and tear also cause thickening of the spinal ligaments, which could lead to spinal stenosis.

Disc herniation may occur and spinal instability could result leading to spondylolisthesis.

The patient symptoms would be back pain, radiation of the pain and that of myelopathy.

Treatment of Adjacent Segment Disease

Treatment strategies for ASDis are initially nonoperative.

Conservative treatments can help ease the pain in the early stages.

Physical therapy exercises, injections, anti-inflammatory medications, and modification of activities will all address the symptoms.

But the disease may progress and when severity increases, another fusion surgery may become necessary.

Prevention of Adjacent Segment Disease

Spinal motion preserving surgeries are thought to help by preserving the motion of the spine which spinal fusion blocks. It should minimize the risk but long-term clinical outcome studies are needed to quantify its efficacy.

References

  • Cho SK, Riew KD. Adjacent segment disease following cervical spine surgery. J Am Acad Orthop Surg. 2013 Jan;21(1):3–11.
  • Matsumoto M, Okada E, Ichihara D, et al. Anterior cervical decompression and fusion accelerates adjacent segment degeneration: comparison with asymptomatic volunteers in a ten-year magnetic resonance imaging follow-up study. Spine (Phila Pa 1976) 2010 Jan 1;35(1):36–43.
  • Dmitriev AE, Cunningham BW, Hu N, Sell G, Vigna F, McAfee PC. Adjacent level intradiscal pressure and segmental kinematics following a cervical total disc arthroplasty: an in vitro human cadaveric model. Spine (Phila Pa 1976) 2005 May 15;30(10):1165–1172.
  • Levin DA, Hale JJ, Bendo JA. Adjacent segment degeneration following spinal fusion for degenerative disc disease. Bull NYU Hosp Jt Dis. 2007;65(1):29–36
  • Nunley PD, Jawahar A, Kerr EJ. 3rd, et al. Factors affecting the incidence of symptomatic adjacent-level disease in cervical spine after total disc arthroplasty: 2- to 4-year follow-up of 3 prospective randomized trials. Spine (Phila Pa 1976) 2012 Mar 15;37(6):445–451
  • Radcliff KE, Kepler CK, Jakoi A, et al. Adjacent segment disease in the lumbar spine following different treatment interventions. Spine J. 2013. Jun 14.

 

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