T2 weighted MRI images of patient with dislocation of C6 over C7 vertebra.

MRI Dislocation of Cevical Spine C6 Over C7 Showing Compression Of The Cord

Associated cord injury and compression is visible.

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Xray showing Cervical Diislocation C4 Over C5 Vertebra

MRI shows the dislocation and a disc compressing on the cord as well.

MRI Showing Dislocation C4-C5 and intervertebral Disc Compressing The Cord

Such patients often present with weakness of all the four limba following the injury.

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Minimum and maximum distances are measured from the posterior border of the C2 body to the posterior arc of the atlas.

The instability index is calculated by the following equation:

Instability index = maximum distance ? minimum distance + maximum distance × 100(%)

If the instability index is more than 40% the patient is very likely to have neurological symptom

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The apex, or tip, of the odontoid is derived from the most caudal occipital sclerotome, or proatlas.

This separate ossification center is  called ossiculum terminale, appears at age 3 years and fuses by age 12 years.

Blood Supply Of Odontoid

Vertebral and carotid arteries form the main source of blood supply to odontoid. Anterior ascending artery and  posterior ascending artery  are branches of vertebral artery beginning at the level of C3. They ascend anterior and posterior to the odontoid and meet  superiorly to form an apical arcade.

Cleft perforators come fron of the extracranial internal carotid artery and supply the superior portion of the odontoid.

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Intervertebral disc calcification is more common in boys than girls and usual age of presentation is 8-13 years.

It is most common in the cervical spine. When it occurs in cervical spine, it causes symptoms. Otherwise lesions have been detected in the thoracic spine in patients without any symptom.

Etiology

Not known

Pathophysiology

Calcification of the nucleus pulposus occurs and  the annular ligament is spared. The calcified nucleus pulposus may herniate anteriorly into the prevertebral soft tissues or posteriorly into the spinal canal.

Presentation

It is an acute condition and presents with complaint of

• Neck pain
• Torticollis
• Reduced range of motion.
• Approximately 25% of patients have fever

30% of patients have a history of trauma, and 15% have a history of upper respiratory tract infection.

Pain usually begins suddenly and persists for 2 to 3 weeks. 75% of children are asymptomatic by 3 weeks, and 95% are asymptomatic within 6 months. Disc herniation is rare, but posterior herniations can cause spinal cord compression, and anterior herniations may result in dysphagia.

Radicular pain or signs of nerve root compression are rare.

Imaging

Radiographs show images of calcium density in the normally radiolucent intervertebral discs. Anterior or posterior protrusion can be observed.

CT and MRI are generally not required but may be able to differentiate the lesion better.

Treatment

Appropriate treatment consists of rest, cervical immobilization, and analgesics.

Very rarely, symptomatic nerve root or spinal cord impingement requires anterior discectomy and fusion.

In its natural course the condition usually undergoes complete clinical and radiological resolution.

The radiographs show regression or disappearance of the calcified deposits in 90%.

The most common symptoms of intervertebral disc calcification are neck pain, limitation of motion, and torticollis.

The long-term effects of intervertebral disc calcification are not known.

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In these patients hypermobility of the spine is a feature but instability is that hypermobilty which jeopardizes neurological integrity.

Atlantoaxial instability occurs in approximately 10% to 20% of children with Down syndrome. Atlantooccipital instability incidence has been reported to be 60%.

Neurological symptoms are present in only 1% to 2.6% of patients with cervical instability, and the instability usually is discovered on routine screening examinations or on cervical radiographs obtained for other reasons.

Progressive instability leading to neurological symptoms is most common in boys older than 10.5 years of age.

Involvement of the pyramidal tract usually results in gait abnormalities, hyperreflexia, and motor weakness.

Neck pain, occipital headaches, and torticollis are other features.

Radiographic Findings

Basic imaging includes anteroposterior, flexion and extension lateral, and odontoid views.

An atlantodens interval  of more than 4 to 5 mm indicates instability. If the ADI is more than 6 to 7 mm, MRI or CT in flexion and extension is necessary to evaluate the space available for the spinal cord.

Treatment

Restriction of high-risk activities usually is sufficient in children with Down syndrome and ADIs of 4 to 5 mm.

If the ADI is 6 to 7 mm, however, MRI or CT should be used to evaluate the risk of neurological compromise.

If the ADI is 10 mm or more, posterior fusion and wiring are recommended after reduction of te unstable C1-2 joint . If the reduction is not achievable, an in situ fusion should be done.

Postoperative immobilization in a halo-cast or -vest should be continued for 6 months.

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An atlantodens interval that exceeds 5 mm in lateral flexion and 4 mm in lateral extension indicates instability and is suspicious for ligamentous disruption.

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The cause of this subluxation is not completely understood. It is related to increased laxity of ligaments and capsular structures caused by inflammation or trauma.

Atlantoaxial rotatory subluxation is a common cause of childhood torticollis. Both the subluxation and torticollis usually are temporary. but rarely they persist and become  atlantoaxial rotatory fixation.

Classification [Fielding and Hawkins]

Type I

simple rotatory displacement without anterior shift of C1

Type II

rotatory displacement with an anterior shift of C1 on C2 of 5 mm or less

Type III

rotatory displacement with an anterior shift of C1 on C2 greater than 5 mm

Type IV

Rotatory displacement with a posterior shift.

Classification of Atlantoaxial Rotatory Subluxation

Type I displacement is the most common and occurs primarily in children. Type II is less common, but carries higher risk for neurological damage.

Presentation

The child usually presents with torticollis following trauma or  upper respiratory tract infection. The sternocleidomastoid muscle on the side opposite to tilt is in  spasm as there is  an attempt to correct this deformity.  Head movements may cause pain in acute situations.

When the subluxation is acute, attempts to move the head cause pain.

With time, as the  muscle spasms subsides, and the torticollis becomes less painful, but the deformity persists.  Neurological examination should be carried to find compression.

Radiographic Findings

Anteroposterior and odontoid views of the cervical spine should be done.

In  open-mouth odontoid view, the lateral mass that is rotated forward appears wider and closer to the midline, and the opposite lateral mass appears narrower and further away from the midline. Apparent overlapping may obscure one of the facet joints of the atlas and axis.

On the lateral view, the anteriorly rotated lateral mass appears wedge-shaped in front of the odontoid. The posterior arch of the atlas may appear to be assimilated into the occiput because of the head tilt.

Flexion and extension views in lateral position are done to find atlantoaxial instability.

CT reveals the deformity better and CT  with the head rotated as far to the left and right as possible can  confirm the loss of normal rotation at the atlantoaxial joint.

This loss of normal rotation at atlanto axial joint confirms the diagnosis of rotatory subluxation.

Treatment

Non Operative Treatment

Nonoperative treatment should be used only if no significant anterior displacement or instability is seen on radiographic evaluation.

•  If rotatory subluxation has existed less than 1 week, immobilization in a soft collar, analgesics, and bed rest for 1 week. If reduction does not occur spontaneously, hospitalization and traction are indicated.
• If rotatory subluxation is present for longer than 1 week, hospitalization and cervical traction [Head-halter traction but if duration > 1 month, skeletal traction] may be required. Traction is maintained until the deformity corrects, then a cervical collar is worn for 4 to 6 weeks.

Operative Treatment

Operative treatment is indicated in following situations

• Neurological involvement
• Anterior displacement
• Failure to achieve and maintain correction and  deformity > 3 months
• Recurrence of the deformity after an adequate trial of conservative management

A preoperative traction for 2 to 3 weeks to correct the deformity is recommended as much as possible.

Fusion is carried out with the head in a neutral position. Six weeks of traction/immobilisation after surgery is recommended  to maintain correction while the fusion becomes solid. Immobilization is continued until there is radiographic evidence of fusion.

Image Credit : Behrang Amini

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Presentation

Most of the patients with this condition are aymptomatic. The symptoms may vary from  an incidental finding on radiographic examination to a passively correctable head tilt.

There may be suboccipital headaches or limitation of cervical motion may occur.

Imaging

On xrays abnormalities of atlas are noted. These are

• Hypertrophy of anterior arch
• Bilateral enlargement of lateral masses
• Ossification of posterior tubercle
• Total absence of posterior arch

Abnormalities of axis and other cervicle vertebrae can also b present

CT scan and three-dimensional reconstructions help to undrestand the anatomy better.

MRI is useful in identifying the potential for neurological compromise and the need for surgical stabilization.

Treatment

Most of the asymptomatic patients do not require any treatment or can be treated with conservative means.

If surgery is required for stabilization, an occiput-to-C2 fusion usually is needed.

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The severity ranges from a complete bony fusion to a bony bridge or even a fibrous band. Occipitalization occurs because of failure of segmentation between the fourth occipital sclerotome and the first spinal sclerotome.

The incidence has been reported to be 1.4 to 2.5 per 1000 children. It affects both sexes equally. and affects males and females equally.

In 70% of the cases atlantooccipital fusion is associated with congenital fusion between C2 and C3. Other associated congenital anomalies are

• Kyphosis and scoliosis
• Anomalies of the jaw
• Incomplete cleft of the nasal cartilage
• Cleft palate
• External ear deformities
• Cervical ribs
• Urinary tract anomalies

Clinical Findings

These patients have

• Low hairlines
• Torticollis
• Short necks
• Restricted neck movement.
• Dull, aching pain in the posterior occiput and the neck
• Episodic neck stiffness

Neurological symptoms usually occur in third and fourth decades and vary depending on the area of spinal cord impingement. If it is anterior, pyramidal tract signs and symptoms predominate, if the impingement is posterior, posterior column signs and symptoms  [Paresthesiae, numbness, impairment of 2 point discrimination and vibration and conscious proprioception impairment} predominate.

Nystagmus is a common finding.

Cranial nerve involvement can cause diplopia, dysphagia, and auditory disturbances.

Vertebral artery involvement may result in syncope, seizures, vertigo, and an unsteady gait.

Radiographic Findings

Routine radiographs usually are difficult to interpret, and  CT scans, or MRI may be needed to show the occipitocervical fusion.

Most commonly, the anterior arch of the atlas is assimilated into the occiput and displaced posteriorly relative to the occiput.

About half of patients have a relative basilar impression dueb to y loss of height of the atlas.

Posterior fusion usually is a small bony fringe or a fibrous band that frequently is not evident on a radiograph.

Atlantoaxial instability should be looked for by flexion and extension views of neck.

Myelography or MRI can detect areas of encroachment on the spinal cord or medulla

Treatment

Patients who have minor symptoms or become symptomatic after minor trauma or infection can be treated conservatively with immobilization in plaster, traction, or a cervical orthosis.

When neurological symptoms occur, cervical spine fusion or decompression is indicated.

Anterior symptoms usually are caused by a hypermobile odontoid, therefore preliminary reduction of the odontoid with traction, followed by fusion from the occiput to C2, relieves the symptoms.

If the odontoid is irreducible, excision of the odontoid may be taken.

Posterior signs and symptoms usually are caused by bony compression or compression from a dural band. Removal of the dural band are indicated when a band is documented by CT or MRI. Posterior fusion may be added to prevent instability.

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