Spine

Spinal Cord Injury Levels

Spinal cord injury levels can be expressed in many ways and it is important to understand the correlations.

This has an important bearing in marking the level of injury and correlating with the anatomy. For example, if an injury occurs at T10-11 vertebral level, it is going to damage her lower thoracic as well as lumbar spinal segments.

Few definitions first

Spinal cord Injury Levels — Image credit

Neurologic level

The most caudal segment with normal sensory and motor function on both sides

Sensory level

The most caudal segment with a normal sensory function on both sides

Motor level

The most caudal segment with a normal motor function on both sides

Skeletal level

Radiographic level of greatest vertebral damage

Spine

The spine consists of a series of vertebral segments. The spinal cord itself has neurological segmental levels marked by the spinal roots. A spinal root is named after the vertebra it exits from. When traced back to cord spinal cord segmental levels do not necessarily correspond to the bony vertebral level.

Let us have a look at vertebrae and nerve root numbers

Cervical – 7 vertebrae and 8 cervical roots. This discrepancy is because there are total 8 nerve roots exiting from the cervical vertebrae
Thoracic 12 vertebrae and 12 roots
Lumbar – 5 vertebrae and 5 nerve roots
Sacral – 5 vertebrae and 5 nerve roots

The spinal cord segments are not necessarily situated at the same vertebral levels. This has been caused by a difference in vertebral height and height of the spinal segment. Thus while the first cervical spinal segment is within C1 vertebra, the T12 cord comes to lie at the T8 vertebra.

Similarly, the entire lumbar spinal segment lies between T9 and T11 vertebrae and the sacral cord is between the T12 to L2 vertebrae.

Course of Spinal Roots

C1 spinal root exit the spinal column at the atlanto-occiput junction. C2 root exits at the atlanto-axis. The C3 roots exit between C2 and C3. The C8 root exits between C7 and T1.

The first thoracic root or T1 exits the spinal cord between T1 and T2 vertebral bodies. The T12 root exits the spinal cord between T1 and L1. The L1 root exits the spinal cord between L1 and L2 bodies. The L5 root exits the cord between L1 and S1 bodies.

Relation of Spinal and Vertebral Segments – Spinal Level vs Vertebral Level

First two cervical cord segments roughly match the first two cervical vertebral levels.
C3 – C8 segments of the spinal cords are situated between C3 through C7 bony vertebral levels.
Likewise, in the thoracic spinal cord, the first two thoracic cord segments roughly match first two thoracic vertebral levels.
However, T3 through T12 cord segments are situated between T3 to T8. The lumbar cord segments are situated at the T9 through T11 levels while the sacral segments are situated from T12 to L1. The tip of the spinal cord or conus is situated at L2 vertebral level. Below L2, there is only spinal roots, called the cauda equina.

A rough calculation can be done as follow to obtain a relation between vertebral and segmental level.

From C2-C6 vertebra add 1 to obtain the spinal segment level
From T1-T6 vertebra add 2 to obtain the spinal segment level
From T7-T9 vertebrae add 3 to obtain the spinal segment level
T10-T12 vertebrae have the whole of lumbar segments
L1 vertebra has sacral & coccygeal segments
L2 onwards is cauda equina

Spinal Cord Injury Levels Regionwise

High-Cervical Injury (C1 – C4)

Most severe of the spinal cord injury levels
Leads to quadriplegia and trunk paralysis may affect respiration too and the patient may require a ventilator.
The patient may have speaking problems, bladder and bowel incontinence and would always require assistance if no recovery occurs.
Patients may be able to use a power wheelchair controlled with the chin or the breath.
Patients are also able to control adaptive devices for light switches, bed controls, televisions and so with the help of adaptive devices. They will require a caregiver’s assistance for most or all of their daily needs.

Low-Cervical Injury(C5 – C8)

This spinal injury level involves C5 to C8 nerve roots.
There would be no breathing or speech problems
The disability depends on the spinal injury level

C5

C5 injury has to have some or total paralysis of wrists, hands, trunk, and legs, will require assistance with most activities of daily living but can move from one place to another independently in a wheelchair.

These patients are able to flex their elbows. They can learn to feed and groom themselves with help of assistive devices.

With some supervised help, they can dress their upper body and change positions in bed. These patients are able to use a power wheelchair equipped with hand controls.

These patients require help in transfers from bed to chair and so forth, and for assistance with bladder and bowel management. Bathing and dressing, especially in the lower part also require assistance.

They are able to drive to drive a vehicle equipped with hand controls.

C6

This results in C6 injury – Paralysis in hands, trunk, and legs, should be able to bend wrists back, can move in and out of wheelchair and bed with assistance/aid, no voluntary control of bowel/bladder, but may manage on their own with special equipment.

These people can use elbows and writs and are able to grasp objects with support.

Some are able to transfer themselves without help using a slide board.

They can learn to feed, groom, and bathe themselves with the help of assistance devices, are able to operate special vehicles.

C7

Most have normal movement of their shoulders, can do most activities of daily living, but need assistance with more difficult tasks, may be able to drive an adapted vehicle, no voluntary control of bowel or bladder but, may be able to manage on their own with special equipment.

C8

C8 injury – Able to grasp and release objects, can do most activities of daily living by themselves, but may need assistance with more difficult tasks, may also be able to drive an adapted vehicle, little or no voluntary control of bowel or bladder, but may be able to manage on their own with special equipment

Upper Thoracic Injury (T1 – T5)

These spinal cord injury levels affect muscles of the upper chest, mid-back, and abdomen. Arm and hand function is usually normal, paraplegia is present. Patients are able to use a manual wheelchair. Some can stand in a standing frame, while others may walk with braces.

Lower Thoracic Injury(T6 – T12)

This spinal cord injury level affects muscles of the trunk, usually results in paraplegia and there is normal upper-body movement, there is little or no voluntary control of bowel or bladder but can manage on their own with special equipment, can use a manual wheelchair, learn to drive a modified car, stand in a standing frame, while others may walk with braces.

Lumbar Injury(L1 – L5)

These generally result in some loss of function in the hips and legs. Little or no voluntary control of bowel or bladder, but can manage on their own with special equipment. Depending on strength in the legs, may need a wheelchair and may also walk with braces

Sacral Injury(S1 – S5)

Injuries generally result in some loss of function in the hips and legs. Little or no voluntary control of bowel or bladder, but can manage on their own with special equipment. Most likely will be able to walk

Note: For all practical purposes whenever lesion in the spine is examined, it is always good to mention injured vertebral and spinal levels separately.

If they roughly match, the level has been ascertained. if they grossly mismatch something might have been missed. There might be another lesion or cord edema.

Correlation between the level of spinal cord lesion and eventual deficits has been discussed before. This article concentrates on functional abilities after spinal injuries at the different levels which means what the patient is expected to do and what she would be unable to do after the injury.

In the absence of medical complications, the most important factor in functional disability is the amount of muscle power remaining to the individual.

However, there are certain factors which can affect the functional outcome. The most important factors are the spasm, decubitus nature, insufficient motivation, deformity, urinary and fecal incontinence.

We would discuss seven critical levels of injury which are

C5
C6
C7
T1
T6
T 12
L4

We would begin with C5 and move downward.

The level mentioned denotes the spared level

Chart of Activities Possible at Different Levels

Functional Abilities After Spinal Injury Patient at Different Levels

C5 Functional Abilities

The patient below C5 [C5 is spared] has full innervations of trapezius, sternocleidomastoid and upper paraspinal muscles.

The patient can stabilize and rotate his neck.

The patient can also elevate and externally rotate the scapulae.

Rhomboids, deltoids and all of the major muscles of the rotator cuff are still functional though these are partially innervated [from C6].

These muscles can provide scapular adduction, glenohumeral joint abduction, internal and external rotation, flexion and extension of the shoulder.

However, the shoulder is not able to perform strong depression, flexion, protraction, and adduction.

But it has been seen, that in absence of prime movers of shoulders [latissimus, pectoralis and serratus muscles] and incomplete innervation of stabilizers prevent remaining from becoming functional.

Elbow flexion is present as biceps and brachioradialis remain partially innervated.

There is no muscular function in hand or wrist.

The patient is unable to roll over or come to a sitting position in the bed.

She may in certain cases eating using special hand devices.

The patient is unable to push the wheelchair.

Endurance is low due to reduced respiratory reserve.

The patient cannot ambulate and is confined to a wheelchair. She requires an attendant for life who would assist in self-care, to lift and transport to back chair.

Removable armrests, swinging removable footrests and detachable back make shifting easier.

A gatch bed for care. It is a bed with a frame in three movable sections equipped with mechanical spring parts that permit raising the head end, foot end, or middle as required.

Tilt board is used for an hour daily to maintain vascular tone and bone density for compensating inability to stand.

Patient with C% injury is not able to earn a living by use of his hands.

C6 Functional Abilities

As compared to C5, a substantial functional increase occurs at C6 level. Rotator cuff of the shoulder becomes fully innervated whereas serratus, latissimus and pectoralis major receive partial but significant innervations. Nerve supply to biceps becomes complete. Muscles appear at the wrist particularly extensor carpi radialis and sometimes flexor carpi radialis.

There is good rotation and abduction of the glenohumeral joint.

As prime movers are working, true adduction, flexion, extension and scapular protraction is possible.

However, as the nerve supply of prime movers is partial only, the strength varies.

The respiratory reserve would still be low.

Biceps and brachioradialis provide strong flexion. Extensor and flexors of the wrist work and extensors of the wrist could utilize the remaining elasticity of the flexors to provide a weak closure of the hand.

However, more elaborate hand devices are required.

Even with absent grasp, the patient may take advantage of elbow flexors to sit up independently.

Rolling over in the bed is permitted by shoulder strength.

But the patient cannot move in the bed while recumbent without help.

An attendant is essential in lifting the patient to and from the wheelchair.

The patient may be able to feed himself with help of hand devices. She can perform part of his toilet and dressing activities.

But the patient cannot be termed as independent in self-care. Use of Gatch bed and tilt board is recommended.

Ambulation is not possible and the patient is confined to the wheelchair but can propel his own wheelchair on a smooth leveled floor.

The grasp is absent but she uses elbow flexors and shoulder adductors for this.

The patient is not able to do any job with hands though some may develop sufficient skill to use specially

some may use the specially adapted machinery.

C7 Functional Abilities

The patient with spared C7 has three important additions

Triceps
Common finger extensors
Long finger flexors

Primary innervation for each of these groups varies between C7 and C8.

Triceps is especially strong as the innervations come as high as C6.

This enables the patient to stabilize the elbow in extension and can assist in lifting the body weight.

Finger extensors and flexors offer grasp and release but not powerful.

As the intrinsic muscles of the hand are not yet significantly innervated, the hand lacks the strength and dexterity.

The patient is more independent in bed and wheelchair than C6 patients.

Exceptional individuals may be able to make the transition to wheelchair independence.

These patients can roll over, sit up in the bed, and move about in sitting position.

Assistance is required to lift the pelvis while recumbent, as in putting the trousers.

Most of the patients require help in transferring to and from the wheelchair but the help is just an assistive push than real lift.

Some assistance is required for toileting and dressing activities.

Eating can be done independently.

If adequately braced, some C7 lesions are able to ambulate with crutches to some extent. The fingers permit grasping the crutches and triceps provides stability to the elbow.

To maintain the upright posture, the patient needs long leg braces with the pelvic band and a high spinal attachment.

The only independent gait possible is the “drag to” gait.

As applying braces and attaining the erect position cannot be done without a great deal of assistance, this kind of ambulation cannot be considered functional.

C7 quadriplegic is still confined to a wheelchair, needs a part-time and in many cases, full-time attendant. Endurance is affected by a low respiratory reserve.

Occupations requiring the use of hands are more feasible since finger flexors and extensors are functional.

The type of work is limited by the weakness of grasp. The activities involving tight grasp such are not recommended.

Possible vacations include bookkeeping, telephone services, and mimeographing or typing.

T1 Functional Abilities

The patient in whom T1 is spared by a complete lesion as full innervations of the upper extremity musculature, including essential intrinsic muscles of the hand.

This patient would have strength, dexterity and fully innervated proximal musculature.

As the ulnar side of the wrist has full blood supply now, crutch walking is better controlled.

The patient still lacks trunk stability, a respiratory reserve of intercoastal origin and trunk fixation [required for prime movers of upper extremity]

The patient is functional in bed activities. She is able to transfer to and from the wheelchair without aid, requiring assistance sometimes.

T1 patient is independent in all activities of self-care, excluding those of requiring lifting of the body while recumbent.

The patient is able to carry himself with help of crutches with a drag to or swing to gait.

Because of full body bracing, attaining an erect position is laborious requiring help. Ambulation, therefore, cannot be considered functional and a well-adapted wheelchair is essential. The patient is able to carry homebound jobs requiring the use of the hand. Some patients develop sufficient sitting balance to drive a hand-controlled car though in and out the transfer from the car may require assistance.

T6 Functional Abilities

T6 paraplegic has complete control of thoracic and upper extremity musculature, stabilized against a well-coordinated pectoral girdle including intercostals, long muscles of the upper back and transverses throracis.

The patient has a tight grasp, supported by proximal musculature which in turn is stabilized against thorax.

Added intercostals innervations help increment in respiratory reserve.

All these factors translate into better self-care, enough to provide independence in all phases of self-care.

Even application of full body bracing becomes possible as the patient can adequately stabilize his upper extremities to use them to lift the pelvis in applying braces.

The patient can independently transfer in and out of the wheelchair by using strong pectoral girdle and triceps.

The patient usually needs no attendant but adaptation and customization of a wheelchair may be required.

The patient is braced with low spinal attachment, pelvic band, and double long leg braces.

With these braces, the patient is able to stand erect for indefinite periods. She is also able to ambulate with a swing through the gate. Ambulation gets restricted by slow and laborious attainment of erect position.

Door –bars, parallel or stall bars are prescribed for assisting in getting to an erect position.

Even if the ambulation is not very functional the patient is encouraged to stand for at least one hour daily. The use of tilt board is not required.

For those who are comfortable while standing, special standing apparatus of work equipment may be considered.

The patient is unable to do elevation activities as hip and knee are locked and all the elevation activities must be accomplished by pure push-up in the shoulder girdle.

This push up is adequate in most of the patients only for the ascent of very low stairs with a handrail but not the standard 20 cm stairs, thus making public transportation impossible.

Work outside the home could be reached by private hand controlled or chauffeured car. Most of the T6 patients have sufficient sitting balance to drive a hand-controlled car.

The patient is able to transfer from wheelchair to car.

T12 Functional Abilities

This patient has full innervations to rectus abdominis, oblique muscles of the abdomen, the transverses abdominis and all muscles of the thorax.

As lumbar innervations are absent, lower back muscles are weak. So are primary hip lifters i.e. quadratus lumborum and lower erector spinae muscles. Hip hiking can be accomplished by secondary hip hikers namely internal and external obliques and latissimus dorsi.

For ambulation, the patient is braced with bilateral long leg braces and may or may need a pelvic band, depending on his skill. The patient may use a two-point alternate or four points or swing through gait as suits her convenience. Using these gaits, she can ambulate freely on reasonably rough surfaces, negotiate curbs as well negotiate 200 mm [achieved by pelvic tilt] stairs with handrails. This would also enable the use of public transportation.

T 12 patients have very few limitations in sedentary or semisedentary jobs away from home.

The patient ’s wheelchair should be customized as per needs.

L4 Functional Abilities

The patient with a lesion below L4 has the functional assistance of quadratus lumborum, erector spinae, quadriceps, and primary hip flexors. Ankle remains flail.

Long leg brace becomes unnecessary as quadriceps extension is present. Flail ankle can be supported by a short leg brace.

The patient’s gait is bilateral maximus-medius gait with the added disability of flail ankles. Lumbar lordosis and genu recurvatum may develop as extended pelvis and extended knee becomes necessary during ambulation.

Crutches are prescribed to prevent long-term effects though the patient may be able to walk without them.

The patient is independent in all phases of self-care and ambulation. A wheelchair may be a convenient addition at home or work.

Spine Injuries – Presentation, Imaging and Treatment

By Arun Pal Singh

Spine injuries are most commonly caused by motor vehicle injuries followed by fall and gunshot injury. Most of the spine injuries occur in cervical spine followed by thoracic and lumbar. Injuries of the cervical spine occur in more than half of all spine injuries in trauma patients.

Most isolated thoracic and lumbar spine injuries are related to osteoporosis. Thoracic and lumbar fractures account for 30% to 60% of all spine injuries.

Care of Spine Injuries

All trauma patients are at risk for spine injuries including spinal cord injury. Therefore proper extrication of the patient and immobilization of the cervical spine at the accident scene are critical to avoid further neurologic injury. The neck movements are to be avoided when taking out the person out of the car or shifting the person. For this, the head and neck need to be aligned with the long axis of the trunk and immobilized in this position.

The cervical spine needs to be immobilized to prevent further movements that can cause damage to the spinal cord. Immobilization with a cervical collar, sandbags, tape, and spine board is superior to immobilization with a collar alone. Neutral flexion-extension head and neck alignment are optimal during prehospital transport. To maintain neutral head-neck alignment. in children, the relatively larger head of should is accommodated by elevating the trunk on padding or using a special pediatric spine board. Helmet and shoulder gear should be left in position until personnel trained in safe removal techniques are available.

In either case, initial evaluation of the patient must include spinal injury evaluation which might go concurrently with resuscitative measures.

Gross neurological assessment with movement and sensation in all extremities
Assessment of gross neurological function.
Direct examination to get a clinical idea of a level of injuries
Cervical spine x-ray, anteroposterior chest x-ray, and x-ray of any other injured part
Analysis of hemodynamic parameters

Any condition which needs immediate treatment should be part of the side by side ongoing resuscitation.

Hypotension, bradycardia, warm extremities in presence of normal urine output suggests neurogenic shock and should be differentiated from hemorrhagic shock as the treatment approach differs.

After the patient has been resuscitated, a detailed examination of the patient follows.

Detailed Examination After Resuscitation of Spine Injuries

After an initial examination, complete spine examination and neurological assessment follow resuscitation.

If the patient is responsive, a detailed history is obtained regarding acute symptoms and past history.

For unresponsive patients, a past history is obtained from family members or available previous medical records.

The patient must be rolled on his or her side using a log-rolling maneuver. For this, The patient’s head and neck are supported by one person and the trunk by two to three other assistants. The head and trunk are then rolled in unison to facilitate the examination of the spine by a physician.

Following things are noted

Areas of hemorrhage
Abrasion
Laceration
Alignment of the spine
Gross deformity
A palpable gap in the spinous processes
Tenderness

Trunk and abdomen are also examined for injury.

After local examination of the spine neurological examination is performed.

The neurological examination would vary in awake-cooperative and unresponsive patients. Awake and cooperative patients require a complete neurological examination. There are many methods and gradings to assess the neurological deficit whose basic purposes are following

Presence of spinal shock
Localization of the lesion level
To determine whether the injury is complete or incomplete
To determine if the injury fits into a particular pattern

This is achieved by the detailed motor and sensory examination.

In a case of an unresponsive patient, radiographic studies are the primary modalities for identifying spine injuries. Spine injury precautions must be observed until the spine is cleared. If a spinal column injury is identified, the neurological deficit should be assessed.

Imaging in Spine Injuries

After clinical evaluation, radioimaging is a very important part of spine assessment in spine injuries. Radiographs or X-rays are the first imaging modality used however radiographs do not provide complete information due to their inherent limitations of two-dimensional views.

Radiographs

Following xrays are essential in a patient who has multiple injuries

Chest x-ray anteroposterior view
Pelvis x-ray anteroposterior view
Lateral cervical spine x-ray.

Rest of the imaging for the spine is done after the patient has been stabilized.

Cervical Spine

After the patient is stabilized, a complete imaging of cervical spine views should be obtained. Following views are generally ordered.

Open mouth
Anteroposterior
Right and left oblique.

Lateral radiograph allows visualization of the spine from the occiput to C6 vertebra and C7 if shoulders are pulled during the x-ray. A swimmer’s lateral view or a CT scan may be needed if lower cervical spine cannot be visualized.

Lateral View

Alignment of the cervical vertebrae- Assessed by examining longitudinal lines along vertebral bodies, lamina, and spinous processes.
The prevertebral soft tissues are also examined for swelling related to acute hemorrhage. If increased, it suggests acute cervical spine injury.

Anteroposterior View

Shows the C3 to T4 segments. A change in alignment of the uncovertebral joints (Small synovial joints between adjacent lateral lips of the bodies of the lower cervical vertebrae) and spinous processes can indicate an acute injury.

Open mouth view

It is essential for excluding a C1 arch or odontoid process fracture.

Oblique views

To identify injuries of the facet joints, pedicles, and lateral masses.

Thoracic, Lumbar and Sacral Spine Injuries

Anteroposterior and lateral thoracic and lumbar radiographs and a pelvis AP view are standard x-rays. Alignment, destruction of vertebrae or reduction in height of vertebra, vertebral fractures are signs of injury.

Computed Tomography in Spine Injuries

CT scans are done for

Patients with suspected spinal fracture and/or dislocation
Difficult visualization of their spinal column on radiographs.
Preoperative planning
Substitute for the open mouth view in unresponsive person
Junctional injuries – Cervicothoracic area, Thoracolumbar junction

CT is superior to MRI in demonstrating bony injury.

Magnetic Resonance Imaging

It is done in patients with cervical level spinal cord injury, incomplete spinal cord injury, and for assessment of disc or ligament injuries. The purpose of MRI is to look for the integrity of the cord and severity of injury to the cord.

Treatment of Patient With Spine Injuries

All trauma patient must be provided protection and immobilization of the spine until spinal injuries have been ruled out or treated definitively.
This general principle and implications are commonly referred to as spine precautions. These precautions include

All trauma patients should be maintained in the supine position at strict bed rest with the bed flat
Transfers should be done with a spine board
Patients with cervical injury must be stabilized with hard cervical collar
Log-rolling should be don to turn the patients

Further course of events depends upon the clinical and radiological assessment of the injury.

Patients under intoxication and normal total spine radiographs/computerized tomography shouold remain in bed until a clinical exam can be performed to reliably.

After initial care of the patient with spinel injuries, decision is made about the definitive care.

A definitive care aims at making the injured spine stable and removing any decompression on the spinal cord.

Because not all patients would have a neural injury and not all patients would have instability of the spine, the definitive treatment has a spectrum from immobilization with a collar to surgery. There are indications for each method and one treatment cannot treat all kind of injuries.

Following are the ways of treating a spinal injury

- Conservative or nonoperative treatment

Operative treatment
Closed reduction with or without surgery (in cervical spine only)

Non-operative Treatment of Spine Injuries

Non-operative treatment remains the standard of care for spine injuries. Most of the injuries can be treated with these methods.

Closed treatment options are

Traction – In case of cervical spine injuries
Bed rest with regular periodic turning to avoid bed sores.
Halo apparatus, external orthosis, or cast.

Bed rest is advised for the initial few weeks and is followed by bracing. This option can be used in unstable injuries too. The external orthosis is chosen as per level of the injury.

Bracing is continued for 8–12 weeks in cervical injuries and 12–24 weeks in thoracolumbar injuries. This is the time taken for the fracture to heal sufficiently to bear the load.

Prolonged bed rest as definitive treatment may be advised in rare cases of patients unwilling to undergo bracing or surgery or are unsuitable for that treatment because of severe preexisting deformity, morbid obesity, or medical problems etc.

In some patients, nonoperative treatment may lead to chronic pain at a later date.

Operative Treatment of Spine Injuries

Surgical stabilization of the spinal column aims at

Prevention of further mechanical injury
Decompress spinal cord by removing the structures causing compression e.g. bone fragments pressing on the spinal cord

Following patients should be considered for surgery

Skeletal instability with a neurologic deficit.
Unstable ligamentous injury in an adult patient where nonoperative treatment does not restore sufficient strength for stability
Patients with multiple injuries
Multiply injured patients

The surgery of injured spine varies as per level of the injury but the principles followed are

Decompression
Fixation of the injured segment with an implant
Fusion of the segment with bone graft

The purpose of the implant is to hold the segment in the position till the time fusion occurs. If not fused, the implant would fail someday and spine would again become unstable.

There are various gadgets available for spine surgery and each has its own advantages and disadvantages.

Closed Reduction

This method is used in cervical spine dislocations. The principle behind this is to use heavy weights to distract the injured area so that a slow maneuver can be performed to reduce the spine. It is quite a safe method. Neurologic deterioration during reduction is a risk but is quite rare if done meticulously.

This needs insertion of Crutchfield tongs or Gardner-Wells tongs.

In alert cooperative patients, imaging is not necessary prior to reduction
An unconscious patient should be undergo an MRI scan before reduction.
Injuries such as craniocervical dissociation or a cervical injury that shows distraction should not be put on traction.

Benefits of closed reduction

Decreases the need for complicated surgical procedures
Improves stability, prevent neurologic deterioration or can improve the neurologic status
Reduction within the first few hours of injury may lead to dramatic improvement in neurologic status.

There is no effective closed reduction technique for the thoracolumbar spine.

Spinal Shock Definition and Significance

By Arun Pal Singh

Spinal shock is a state of total sensory, motor power loss and loss of all reflexes for a period which is followed by the gradual recovery of reflexes. Spinal shock can occur in case of spinal cord injury.

Spinal shock begins within a few minutes of the injury, it may take several hours before the full effects occur. During spinal shock, the nervous system is unable to transmit signals from the brain to end organs as they are not routed by the spinal cord.

Usually, the spinal shock recovers within 24 hours but may last over a few weeks in less common cases. In some rare cases, spinal cord shock can last for several more months.

Pathophysiology of Spinal Shock

The exact cause of the spinal shock is not known. It is thought that acute injury causes depolarization of axons due to the transfer of kinetic energy.

There are three phases of spinal shock

Phase 1

A complete loss or weakening of all reflexes below the level of spinal cord injury. This phase lasts for a day. The neurons involved in various reflex arcs the neural input from the brain due to spinal concussion become hyperpolarized and less responsive.

Phase 2

It occurs over the next two days and is characterized by the return of some, but not all, reflexes. The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex.

Bulbocavernosus reflex can be checked by noting anal sphincter contraction in response to squeezing the glans penis or tugging on the Foley. It involves the S1, S2, S3 nerve roots and is spinal cord mediated reflex. Its presence signals the end of the spinal shock.

Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until Phase 3.

The reason reflexes return is the hypersensitivity of reflex muscles following denervation — more receptors for neurotransmitters are expressed and are therefore they are easier to stimulate.

Phases 3 and 4

These are characterized by hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation following sprouting of interneurons and lower motor neurons below the injury begin to attempt to the reestablishment of synapses.

Identification of Spinal Shock

There is total paralysis, hypotonia & areflexia, and at its conclusion, there may be hyperreflexia, hypertonicity, and clonus.

Return of reflex activity below the level of injury (such as bulbocavernosus) indicates an end of the spinal shock.

Return of the of bulbocavernosus reflex signifies the end of the spinal shock, and if the injury is complete, any further neurological improvement will be minimal. The complete absence of distal motor function or perirectal sensation, together with recovery of the bulbocavernosus reflex, indicates a complete cord injury, and in such cases, it is highly unlikely that significant neurologic damage will return.

Spinal shock does not occur in the lesions that occur below the cord, and therefore, lower lumbar injuries should not cause spinal shock. If bulbocavernosus reflex is absent in such cases may indicate a cauda equina injury

The significance of Spinal Shock

There is a loss of signal transmission and the loss of these signals will result in loss of movements, sensations other body function. Complete loss of movement and sensation below the level of the spinal cord injury makes it difficult to assess the exact quantum of injury. Thus it is not possible to find the level, extent, and severity of the injury as patients would show a complete neural loss.

The only way to find that is to wait for the spinal shock to recover. Over the first few weeks, the somebody systems adjust to the effects of the injury and their function improves. Therefore, during this time it is unlikely that an accurate prediction of any recovery or permanent paralysis can be made.

Neurogenic Shock Causes, Symptoms and Treatment

By Arun Pal Singh

Neurogenic shock is a type of shock caused by the sudden cessation of autonomic regulatory signals to the smooth muscle in vessel walls.

It is a type of distributive shock which leads to hypotension, bradycardia, and peripheral vasodilatation [decreased blood pressure, low heart rate and dilatation of peripheral blood vessels resulting in pooling of blood and deficiency of supply to vital organs, leading to shock.

It is very commonly associated with injuries causing damage to the central nervous system damage (brain injury, cervical cord injury or high thoracic cord injury] but could be due to many other reasons as well [see below].

The shock occurs because of the loss of background sympathetic stimulation, which is responsible for maintenance of the tone of blood vessels. As a result of the loss of vascular tone, the vessels suddenly relax resulting in a sudden decrease in peripheral vascular resistance and decreased blood pressure.

Neurogenic shock is also known as vasogenic shock.

It should not be confused with spinal shock [especially in cases of neurogenic chock with spinal injury].

Spinal shock is a different entity and is a reversible cessation of sensory and motor function following spinal cord injury.

[Read more about Spinal Shock]

Due to associated hemorrhagic shock and other hemodynamic effects, the exact incidence is difficult to determine.

It is still unknown how hemorrhagic shock and other injuries impact the hemodynamic effects of spinal cord injury

Definition of Neurogenic Shock

The joint committee of the American Spinal Injury Association and the International Spinal Cord Society have proposed the following definition

Neurogenic shock is a general autonomic nervous system dysfunction that also includes symptoms such as orthostatic hypotension, autonomic dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the diagnosis of neurogenic shock.

Universal hemodynamic parameters for neurogenic shock have not been defined but most of the studies consider systolic blood pressure less than 100 mmHg and heart rate less than 80 bpm for labeling the condition as the neurogenic shock.

Causes of Neurogenic Shock

Neurogenic shock occurs due to insult/injury to the spinal cord with associated autonomic disturbances. The autonomic dysregulation occurs due to a loss of sympathetic tone that cannot oppose a parasympathetic response.

Traumatic spinal cord injuries are the most common cause, with 19% of cervical spine injuries and 7% of thoracic spine injuries are associated with neurogenic shock. Traumatic brain injuries are associated to a lesser extent.

Other causes of neurogenic shock less common. These include

Spinal anesthesia
Administration of autonomic blocking agents.
Transverse myelitis
Guillain-Barre syndrome

In children, there is an association of neurogenic shock with Trisomy 21, skeletal dysplasia, and tonsillopharyngitis.

In acute trauma, the cause of shock primarily is the hemorrhagic shock is the more common cause of the decrease in blood pressure. Once that has been managed, and the patient is still not improved, the neurogenic shock should be considered.

Pathophysiology of Neurogenic Shock

The shock results when descending sympathetic tracts are disrupted in the spine both in primary and secondary spinal injury. [Primary injury is direct damage and occurs within seconds whereas secondary injury is a result of vascular insult, electrolyte imbalance, and edema, and occurs hours to days after the initial insult.]

A loss of sympathetic tone and thus unopposed parasympathetic response driven by the Vagus nerve occurs. The cardiac output decreases because the venule and small veins lose tone. There is a pooling of the blood in the periphery leading to falling of blood pressure.

In the normal situation, a reflex increase in heart rate will occur to compensate for the peripheral pooling of blood. However, in neurogenic shock, blocked sympathetic pathways fail to check bradycardia. Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation.

Presentation, Evaluation, and Diagnosis of Neurogenic Shock

The surroundings leading to shock are very important in making the diagnosis.

The neurogenic shock could be difficult to diagnose especially in acute traumatic situations. In acute injuries, identification spinal cord trauma is important to consider the diagnosis.

The condition should be considered only after a hemorrhagic shock has been ruled out in a trauma patient.

The features suggesting neurogenic shock are

Hypotension – Decrease in Blood Pressure
Bradycardia – Slow heart rate
Warm, dry extremities
Peripheral vasodilation and venous pooling
Poikilothermia (Cold Body)
Decreased cardiac output (with cervical or high thoracic injury)

The presence of spinal vertebral fracture or dislocation should raise the concern for neurogenic shock.

Treatment of Neurogenic Shock

Management of neurogenic shock includes hemodynamic stabilization and measures to protect spine further injury in case of acute trauma.

Hemodynamic Stabilization

This aims to normal blood pressure and cardiac output.

Low blood pressure or hypotension should be treated as soon as possible so that secondary injury to the cervical spine is prevented. It is done by fluid administration and drugs.

It is recommended to keep the mean arterial pressure at 85–90 mmHg for the first 7 days to improve spinal cord perfusion.

Intravenous fluid resuscitation

It is the first line of treatment. The fluid administered and works Allow appropriate compensation for the dilatation that vasogenic shock has resulted.

Vasopressors and inotropes

These drugs are second line options given if there is no response to fluid administration

Phenylephrine is the commonly given drug. It is a pure alpha agonist that leads to constriction of the vessels and increases blood pressure

Reflex bradycardia is an undesirable effect because it does not have any beta activity. It adds to the already unopposed vagal tone.

Norepinephrine has both alpha and beta agonist activity. It can control low blood pressure and does not produce reflex bradycardia as well.

In refractory cases, epinephrine is used but rarely needed. Caution should be used when using vasopressors as there may be co-existing injuries exacerbated with vasoconstriction.

Atropine and glycopyrrolate oppose vagal tone and are used for countering severe bradycardia.

Isoproterenol may also be considered for countering bradycardia.

Methylxanthines such as theophylline and aminophylline are used in refractory cases of bradycardia.

Spinal Immobilization

Initial c-spine immobilization is important to prevent further spinal cord injury especially in cervical injuries

References

Taylor MP, Wrenn P, O’Donnell AD. Presentation of neurogenic shock within the emergency department. Emerg Med J. 2017 Mar;34(3):157-162
Fox AD. Spinal shock. Assessment & treatment of spinal cord injuries & neurogenic shock. JEMS. 2014
Summers RL, Baker SD, Sterling SA, Porter JM, Jones AE. Characterization of the spectrum of hemodynamic profiles in trauma patients with acute neurogenic shock. J Crit Care. 2013 Aug;28(4):531.e1-5

Muscle Power Grading

By Arun Pal Singh

Muscle power grading is a frequent and important part of the neurological examination. The neurological examination consists of sensory and motor examination. Muscle power grading is part of motor system examination.

Before muscle power grading is done, limbs or trunk are examined for the tone of the muscles, the bulk of the muscles.

The limbs are inspected for their resting posture, deformity or clawing and whether they are symmetrical. Is there any wasting or hypertrophy. Any involuntary movements, jerks etc should be noted.

Muscle fasciculation is a sign of lower motor neuron disease process. Muscle fasciculations are subcutaneous twitches over a muscle belly at rest.

Muscle tone is checked by moving the joints passively. A loss of tone suggests lower motor neuron lesion and hypertonia suggests upper motor neuron lesions.

After this comes the turn of muscle power grading. In muscle power grading individual muscle can be tested as in hand or feet. But in large joints like hip or knee joint, group of muscles like flexors, extensors or abductors are tested.

The patient is asked to contract the muscle group being tested and then examiner resists the movement of that muscle group. Muscle power grading is done as per the following chart.

Here are the grades of muscle power as examined clinically

Grade 0– complete paralysis

Grade 1 -flicker of contraction present

Grade 2– active movement with gravity eliminated

Grade 3-Active movement against gravity

Grade 4-Active movement against gravity and some resistance described as poor, fair, moderate strength.

Grade 5– Normal power.

Muscle power grading is useful in localizing the lesion and to differentiate the groups of muscles affected so that treatment can be affected.

Muscle power grading can give false results in case of very weak muscles, joint contractures, and exhaustion from repeated testing for muscle power grading.

Muscle power grading is not entirely objective and subjective errors can creep in especially in very extreme grades. For example, it may be difficult to differentiate between grade 0 and 1 or 4 and 5.

Cast Syndrome or Superior Mesenteric Artery syndrome

By Arun Pal Singh

Cast syndrome is also known as superior mesenteric artery syndrome. It is an uncommon complication in the treatment of orthopedic conditions. It results from obstruction of the third portion of the duodenum by superior mesenteric artery leading to high intestinal obstruction.

It should be kept in mind that this obstruction can occur in absence of plaster also because there are many causes to mesenteric artery obstruction.

Cause of Cast Syndrome

Most cases involve young adults with more than half of these cases have patients with scoliosis or kyphosis or treatment of hip conditions. It has been seen after casting with body jackets, shoulder spicas, and hip spicas where the common denominator is extensive coverage of the abdomen and chest.

The problem usually is located at the junction of the third and fourth parts of the duodenum, where the duodenum is bound by the ligament of Treitz. The duodenum passes across the anterior aspect of the lumbar spine from right to left at the level of the first and second lumbar vertebrae. Just above this point, the superior mesenteric artery arises from the abdominal aorta and passes downward with its accompanying veins in the mesentery.

Cast Syndrome - Compression of Duodenum By Superior Mesenteric Artery — Compression of Duodenum By Superior Mesenteric Artery

There is the potential for compression of the third portion of the duodenum between lumbar spine and aorta posteriorly and the mesentery and vessels anteriorly.

Two contributing factors are recumbency, which causes the weight of the mesentery to lie against the duodenum, and increased lumbar lordosis, which tends to displace the duodenum anteriorly.

Gastric distention may aggravate the situation by forcing the remainder of the abdominal contents more distally and stretching the mesenteric vessels further.

Clinical Presentation

The signs and symptoms of cast syndrome are typical of upper intestinal obstruction. They may come on insidiously or after several weeks after cast application or surgery.

The initial symptom is a feeling of fullness followed by nausea and vomiting.

Abdominal distention is obscured in the presence of a body jacket. Vomiting, which may be intermittent in the early stages, becomes pernicious, with dehydration and metabolic alkalosis. Progressive metabolic derangement, oliguria, and shock may occur.

When these signs and symptoms occur in a patient who is in a body cast or who has had spinal trauma (including surgery), the diagnosis should be suspected.

Xrays of the abdomen may show early gastric dilatation. Contrast may help to reveal the distention of the stomach and the proximal portion of the duodenum. Usually, there is a sharp cutoff pattern at the region where the arteriomesenteric pedicle crosses the duodenum. Xrays help to differentiate this syndrome from cholelithiasis, pancreatitis, gastric or duodenal ulcer, and high intestinal obstruction.

Treatment of Cast Syndrome

Removal of the offending plaster if any
The absolute dietary restriction should be imposed, supplemented by nasogastric suction.
Intravenous fluids are essential to maintain hydration and to correct any electrolyte or acid-base abnormalities.
Positioning the patient on the left side or prone relieves some of the effects of gravity in pulling the mesenteric pedicle against the duodenum. With the patient prone, tipping the bed to tilt the head down further decreases pressure from the pedicle.
If these conservative measures are not sufficient to reverse the process, the treatment of choice is surgery duodenojejunostomy or gastrojejunostomy.

Prevention

Cast syndrome may be prevented by avoiding constrictive body casts that accentuate lumbar lordosis or prevent normal changes in abdominal contour. Patients at risk should be turned frequently or encouraged to move from side to side.

Coccydynia – Causes, Symptoms and Treatment

By Arun Pal Singh

Coccydynia, also called coccygodynia refers to pain in the coccyx region. The term was given by Simpson in 1859. However, the condition has been reported in the literature before that period too.

The coccyx is lowermost part of the spine and is also called tailbone. One can feel the lower end of the coccyx in the proximal part of the gluteal cleft [The groove between the buttocks]. It is right there where a tail would be in animals.

Other names for the condition are tailbone pain or coccyx pain, coccygeal pain, coccyx pain, coccyaglia or tailbone pain.

Coccydynia is much more common in women than in men.

Coccydynia is rare, accounts for less than 1% of back pain conditions.

Anatomy of Coccyx

The word coccyx is derived from the Greek word for the beak of a cuckoo bird

The coccyx is the terminal portion of the spine and consists of 3-5 fused vertebrae. The largest one that articulates with sacrum through a rudimentary articular process called the coccygeal cornua [the other part is called the sacral cornua.]. The coccyx attaches the sacrum. The attachment could be a symphysis as a true synovial joint, There is very limited movement between the coccyx and the sacrum.

The coccyx represents a vestigial tail (so the term tailbone). The ventral side of the coccyx is slightly concave whereas the dorsal aspect is slightly convex.

The coccygeal ligament is the name given to the lower part of the filum terminale and it inserts onto this first segment.

Anteriorly, the coccyx is bordered by the levator ani muscle and the sacrococcygeal ligament.

Anterior to posterior, the lateral edges serve as insertion sites for the coccygeal muscles, the sacrospinous ligament, the sacrotuberous ligament, and fibers of the gluteus maximus muscle.

The iliococcygeus muscle tendon inserts onto the tip of the coccyx.

The attached ligaments and muscles support the pelvic floor and also contribute to voluntary bowel control.

Types of Coccyx

Postacchini and Massobrio described four orientations of coccyx wherein anterior angulation of the coccyx may be a normal variant.

Type I

The coccyx is curved slightly forward, with its apex pointing caudally. It is the most common type and found in 15% of the people.

Type II

The coccyx is curved more markedly anteriorly, with its apex pointing straight forward. This type is found in approximately 15% of people.

Type III

The coccyx is sharply angulated forward between the first and second or the second and third segments. It occurs in 5% of the people.

Type IV

The coccyx is subluxed anteriorly at the level of the sacrococcygeal joint or at the level of the first or second intercoccygeal joints. This type is found in about 10%.

Patients with a type II-IV coccyx are more prone to develop idiopathic coccygodynia than those with a type I configuration.

Causes of Coccydynia

Coccydynia occurs if there is an injury or excess pressure on the area causing the bones to move beyond their normal very limited range of motion. This results in inflammation and localized pain. Ligaments, the vestigial and bones of the coccyx can source of pain. Infection of coccyx can also lead to pain.

Trauma

A fall on the coccyx causes injury to ligaments or bone. It is the most common cause of coccydynia.

Childbirth

During delivery, the baby’s head passes over the top of the coccyx, and the pressure created against the coccyx can sometimes result in injury to the coccyx structures.

Pressure

Horse riding and sitting on a hard surface for long periods of time may cause the onset of coccyx pain.

Tumor or Infection

Rarely, coccydynia is due to a tumor or infection in the coccyx area that puts pressure on the coccyx.

Idiopathic Coccydynia

It is not clearly understood which portions of the anatomy can cause coccyx pain. In many cases, the exact cause of the pain is not known (called idiopathic coccydynia), and in these cases, the symptoms are managed.

Clinical Presentation of Coccydynia

A localized pain over the coccyx which is worse with sitting is the classic presentation of coccydynia. The pain will usually worsen with prolonged sitting, leaning back in seated position, worse with prolonged sitting, leaning back while seated and moving from sitting to standing position.

The patient may complain of pain during sexual intercourse or defecation.

There could be a presence of significant recent trauma that resulted in acute pain or the pain may have begun insidiously with no clear inciting factor.

The patient should be enquired about sitting tolerance [Time of sitting can be tolerated before the pain forces to change position].

The patient should be enquired about cushions tried, medications taken or interventions done previous to the visit.

In females, any events around the childbirth become important to note.

On examination, the coccyx would be tender to touch. If the coccyx is not tender, consider the possibility of the pain referred from other sites as well.

The rectal examination would allow checking for coccyx mobility [sacrococcygeal joint, normal appx 13 degrees.]

The examination includes lumbar spine examination and other probable causes of pain like ischial bursae, sacroiliac joints, lumbosacral facet joints, and lumbosacral or gluteal muscles.

The skin over the spine should be examined for sinus [pilonidal sinus] and any other notable deformity.

Differential Diagnoses

Lumbar pain
Endometriosis
Hemorrhoids

Lab Studies

Not required for diagnosis except to rule out infection.

Imaging

Plain Radiographs

X-ray is an initial investigation especially in patients with a history of trauma. AP and lateral view are most commonly done. Coned-down view of coccyx gives better exposure.

X-rays may reveal

Fractures
Osteophytes
Abnormal sacrococcygeal curvature
Sacrococcygeal or intracoccygeal dislocation.

Dynamic stress films [sitting and standing positions] can detect the sagittal rotation of the pelvis.

CT/ MRI

CT of Coccyxis rarely indicated for objective evidence of fractures in medicolegal cases.

MRI coccyx is usually not required but can be included in the lumbosacral MRI if the pain is thought to originate from anatomic structures located more superiorly within the spine.

CT/MRI can be useful in intrapelvic pathologies.

In a typical case, all imaging studies will be negative.

Injections for Localization of Pain

The injections of local anesthetic with without steroid can be used for diagnosis of pain source whether it is coccyx or some other structure. If injection to the coccyx results in pain relief, most likely the coccyx is responsible for pain.

These injections can also help identify patients who might benefit from a coccygectomy when contemplated.

Treatment of Coccydynia

Most of the patients of coccydynia can be treated by conservative treatment.

Posture and Avoidance

The patient is educated about correct sitting posture and avoid leaning back while sitting. Activities that worsen pain such as prolonged sitting, bike riding, horse riding etc should be avoided.

Local heat/Cold Application

The patient can apply local heat or cold [both have been found to be equally effective]. The best way to do this is by Sitz bath where water is filled in the tub or Sitz kit [commercially available] and patient immerses perineum and hip.

Cushions

Cushions help to relieve the pressure of the coccyx.

Modified wedge-shaped cushions or coccygeal cushions which can relieve the pressure on the coccyx when the patient sits are recommended. These are available over the counter.

Drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to relieve pain and inflammation.

Topical analgesic creams are also used and help to avoid side-effects of oral medications.

Pelvic Floor Physical therapy

Pelvic floor rehabilitation can be helpful for coccydynia that is associated with pelvic floor muscle spasms.

Tight, painful muscular structures such as the levator ani, coccygeus, or piriformis muscles are targeted. Myofascial release techniques may be used. Local modalities also may be helpful.

Pelvic floor physical therapy has been reported to be an effective treatment for chronic pain including those who have chronic coccydynia even after coccygectomy.

Manual manipulation and massage

This refers to intrarectal manipulation under anesthesia. Many authors have claimed it to be mildly effective through the clear evidence is lacking.

Ganglion Blocks

The ganglion impar is also called ganglion of Walther and is the unpaired terminal ganglion of the paravertebral sympathetic nervous system usually located anterior to the sacrococcygeal junction or near.

Hypersensitivity of the ganglion impar is thought to be responsible for persistent chronic pain which is sympathetically maintained.

Local injection of an anesthetic can effectively block the ganglion impar and thereby relieve coccyx pain.

Repeat ganglion impar blocks may be required and have been shown to provide additional benefit.

Steroid Injections

Steroid injections mixed with local anesthetics are given around the coccyx, usually at the sacrococcygeal junction or around the sacrococcygeal ligaments.

Repeat injections may be required.

Nerve Ablation

Nerve ablation [uses heat or cold or current to destroy nerve fibers] is reserved for patients for chronic pains where none of the treatment has relieved pain [before coccygectomy].

The site of pathology would depend on the specific site of coccygeal pathology. A diagnostic injection of local anesthetic prior to ablation is performed to ascertain the site of pain.

If one sitting of ablation does not provide relief, it may be repeated.

Some patients may have a recurrence of pain after months or years due to collateral reinnervation. A repeat ablation may be performed in such cases.

Surgery

Surgical treatment for coccydynia is partial or complete coccygectomy [removal of coccyx].

Surgical procedures for the treatment of coccydynia are used only as a last resort. The procedure has been associated with a high complication rate.

It is recommended that non-surgical options must be exhausted before considering surgery.

Other Treatments

Transcutaneous electrical nerve stimulation or TENS could be of benefit in selected cases.

If a non-organic cause is suspected, psychotherapy is indicated.

References

Lirette LS, Chaiban G, Tolba R, Eissa H. Coccydynia: an overview of the anatomy, etiology, and treatment of coccyx pain. Ochsner J. 2014 Spring. 14 (1):84-7.
Kim NH, Suk KS. Clinical and radiological differences between traumatic and idiopathic coccygodynia. Yonsei Med J. 1999 Jun;40(3):215–220.
Maigne JY, Doursounian L, Chatellier G. Causes and mechanisms of common coccydynia: role of body mass index and coccygeal trauma. Spine (Phila Pa 1976)2000 Dec 1;25(23):3072–3079.
Foye PM, Buttaci CJ, Stitik TP, Yonclas PP. Successful injection for coccyx pain. Am J Phys Med Rehabil. 2006 Sep;85(9):783–784.
Wray CC, Easom S, Hoskinson J. Coccydynia. Aetiology and treatment. J Bone Joint Surg Br. 1991 Mar;73(2):335–338.
Foye PM. Finding the causes of coccydynia (coccygeal pain). J Bone Joint Surg Br. Jan 18 2007.
Buttaci CJ, Foye PM, Stitik TP, et al. Coccydynia successfully treated with ganglion impar blocks: a case series. Am J Phys Med Rehabil. Mar 2005. 84(3):218.
Gopal H, McCrory C. Coccygodynia treated by pulsed radiofrequency treatment to the Ganglion of Impar: a case series. J Back Musculoskelet Rehabil. 2014 Feb 20.

Spina Bifida Presentation and Treatment

By Arun Pal Singh

Spina bifida is a neural tube defect that leads to a congenital defect in the posterior bony wall of the spinal canal [vertebral arch] involving the laminae and spinal cord malformation that occurs in varying degrees of severity and range of presentation from an incidental finding on x-ray to stillbirth.

Spina bifida is most commonly seen in the lumbosacral region. Sometimes the contents of the canal may protrude through the defect.

The average worldwide incidence of spina bifida is 1 case per 1000 births, but marked geographic variations occur.

The term bifida is derived from the Latin bifidus which means “in 2 parts.”

Development of the spinal cord

During the 2nd week of intrauterine life, a dorsal groove appears on the surface of the embryo, which is known as the neural groove. The margins of the neural groove unite into a tube known as the neural tube and the lumen, within it, is called the neural canal.

The neural tube becomes separated from the surface by an ingrowth of the mesoderm.

In front of the neural tube, there is a solid rod of cells, known as the notochord. Around the notochord, the vertebral bodies develop.

From each of the bodies, there extend two projections which grow around the neural tube to form the vertebral arch or neural arch.

Failure of fusion of these arches gives rise to spina bifida.

Etiology

Neural tube defects result from failed closure and abnormal differentiation of the embryonic neural tube. These occur between the 17th and 30th day of gestation.

Anencephaly and myelomeningocele are the most common neural tube defects.

Myelomeningocele occurs due to a failed closure of the caudal end of the neural tube resulting in a sac which contains dysplastic spinal cord, nerve roots, meninges, vertebral bodies, and skin.

The etiology in most cases of spina bifida is multifactorial.

Most infants born with spina bifida are born to mothers with no previously affected children

Genetic

Up to 10% of fetuses with a neural tube defect detected in early gestation have an associated chromosome abnormality.

Maternal risk factors

Folic acid deficiency [about 50% of cases are attributed]
Pregestational diabetes – increases the risk of CNS malformation
Maternal obesity
Hyperthermia
Maternal diarrhea
Intrauterine exposure to antiepileptic drugs and drugs used to induce ovulation
Maternal exposures to
- Fumonisins [toxins produced by fungi]
- Electromagnetic fields
- Hazardous waste sites
- Disinfection by-products found in drinking water

Note on the tethered cord

A fibrous band, the membrana reunions connects the skin to the spinal theca.

At one stage the spinal cord reaches the distal end of the vertebral column. Gradually the cord lags behind in growth in comparison to the vertebral column in intrauterine life so that at birth the distal end of the cord lies at the third lumbar vertebra.

Later on, due to more development of the vertebral column, the distal end of the cord lies at the lower end of the first lumbar vertebra in adults. With the growth of the body, the membrana reunions pull on the theca and nerve roots. This causes some neurological deficiencies e.g. foot drop, nocturnal enuresis or a backache. Such symptoms appear late in childhood or in adult life.

Types of Spina bifida

Spina Bifida Occulta

In Spina Bifida Occulta, though there is a failure of the neural arches to unite, and a small gap exists in one of the vertebral arches, usually in the lumbar or sacral regions. There is no protrusion of the cord or membranes. Frequently only one vertebra is affected and the gap is filled with fibrous tissue.

Subtle signs of underlying abnormality in bifida occulta are dimple, skin pigmentation or hairy patch. Otherwise, spina bifida occulta is almost always without consequences.

A spinal cord lipoma or a fibrous cord may be present underneath these subtle signs.

Problems with micturition or a foot deformity may be seen in some cases of occulta.

In later ages, the patient may present with tethered cord.

Many cases of spinal bifida occulta are symptomless. Either they remain undiagnosed or diagnosed by accident when an x-ray taken for some other reasons.

Clinical Presentation

Present since birth
There is some abnormality in the local skin either a skin dimple or a local patch of hair or a naevo-lipoma or simple lipoma.
Neurological examinations must be performed, as in adolescent or in adult life manifestations of such deficiency may be revealed in the form of a backache, nocturnal enuresis, local anesthesia, local paresis or even foot drop.
X-ray is often confirmatory as it will show the bony defect.

Treatment

Presence of tuft of hair or lipoma may lead to a cosmetic complaint and this is treated by excision of these lesions.
If there are neurological symptoms due to membrana reunions, [tethered cord syndrome] the membrana reunions is excised in its whole length from the skin through the vertebral gap to the spinal meninges.
Extradural or intradural lipomas causing compression of neural tissue should be excised.

Spina bifida cystica

In this type, the spine is bifid and a cyst forms. Meningocele actually refers to a cystic swelling of the dura and arachnoid which protrudes through the spina bifida defect in the vertebral arch. A person with a meningocele may have no neurologic sequelae.

When cord tissue extends into the meningocele, it is called a myelomeningocele. Meningomyelocele is a form of spina bifida cystica is the most common type of spina bifida, accounting for 94% of cases. [Spina bifida occulta not included in this figure]

The most severe type of spina bifida cystica is the myelocele [also called myeloschisis] where the open neural plate has spread out onto the surface and is covered just by epithelium.

Meningocele

In this condition protrusion of meninges occurs through the defect in the neural arch. Such protrusion contains only cerebrospinal fluid. So it gives rise to a cystic swelling.

Usually the duramater stops at the margin of the defect and usually the pia and arachnoid protrude. The overlying skin remains intact.

It is common in the lumbosacral region. Meningocele also occurs in the skull, where it is more common in the occipital region or at the root of the nose.

Clinical Features

It is present since birth
It is a cystic swelling, highly translucent, compressible swelling
Expansile impulse is present when the child cries or coughs
The overlying skin is normal and free
On careful palpation the edge of the bony defect is palpable
Neurological manifestations are usually absent (Compare with myelomeningocele, where neurological manifestations are usually present).
This condition may be associated with hydrocephalus and this combination is known as Arnold-Chiari syndrome.
X-ray is confirmatory and will show the bony defect
Infection and rupture are possible complications

Treatment of Meningocele

An operation should be performed as early as possible, but the child’s condition and strength should be sufficient to withstand the operation. This operation is often performed within a few days of birth.

The skin and the sac are opened with incisions perpendicular to each other. This will minimize the chance of postoperative C.S.F. leakage.
The redundant part of the sac is excised
The margins of the excised sac are sutured together in the midline
To strengthen the bony gap, the adjacent erector spinae muscle and the overlying fasciae are approximated over the gap with the help of lateral release incisions (to minimize tension in the suture line).
The skin is closed.

Meningomyelocele

Clinical Features

Meningomyelocele is the commonest variety of spina bifida in the living children.
The bony defect may usually extend over 3 or more segments.
Skin may be absent or atrophic, and meninges may be exposed.
Patient can have spastic or flaccid paralysis.
Neurological manifestations are almost always present.
X-ray will show the bony defect. There may be other abnormalities of the vertebrae, like scoliosis or kyphosis or even hemivertebra.
Other symptoms in infants – lethargy, poor feeding, irritability, stridor or eye coordination problem.
Older children may present with cognitive changes, motor weakness, spasticity, problems of bladder/bowel, cranial nerve dysfunction, backache or deformities of the lower limb.
Increase in foot deformities, worsening of spinal deformity or new onset of hip dislocation, progressive neurologic defects in growing children may suggest a tethered cord [tissue attachments cause stretching of spinal cord.]

Based on the level of involvement, myelomeningocele patients frequently can be classified as belonging to one of the following groups, based on the neurosegmental level of the lesion:

Thoracic

upper limb and neck musculature well innervated
Function of trunk musculature variable
No power in lower limbs.

High lumbar

Variable hip flexor and hip adductor
Absence of hip extension, hip abduction,
Absent knee and ankle movements

Thoracic and high-lumbar groups tend to have increased prevalences of lumbar lordosis, abduction and external rotation contractures of hip, flexion contracture of knee and foot equines.

Low lumbar

Present – hip flexors and adductors, medial hamstring, and quadriceps
Variable – lateral hamstrings, hip abductors, and ankle dorsiflexors
Absent – Ankle plantar flexors

These often have hip and knee flexion contractures, increased lumbar lordosis, genu valgum, calcaneo-valgus and overpronation of foot.

Sacral

Hip, knee normal
Ankle plantar flexor strength is variable.

These patients often exhibit mild hip and knee flexion contractures and increased lumbar lordosis with variable foot and ankle deformities with various ankle and foot positions.

Associated Findings

Complications of hydrocephalus
Symptoms of Chiari II malformation- Lower brainstem and/or upper cervical spinal cord compression causing apnea, dysphagia, stridor, nystagmus or upper limb weakness.
Spinal deformities
- Congenital – vertebrae and rib anomalies
- Acquired due to muscle imbalance
Lower limb deformities
Short Stature
Cranial nerve dysfunction – Ocular muscle palsies, dysphagia and dysphonia.
Tethered spinal cord – pain, sensory changes, spasticity, and progressive scoliosis.
Syringomyelia
Renal Problems
- Neurogenic bowel and bladder
- Bladder incontinence
- Hydronephrosis due to a contracted bladder
- Infections and renal failure
- Vesicoureteral reflux
Congenital Abnormalities
- Facial clefts
- Heart malformations
- Genitourinary tract anomalies

Treatment of Myelomeningocele

The operation must be performed as early as possible. Child’s condition should also be considered, as it should withstand the operation.

Delay in operation may cause

Infection within the sac and postoperative problems.
The sac may rupture and will make operation extremely difficult with infection spreading throughout the subarachnoid space.
There will be more adhesion of nerves with the wall of the sac, which will be difficult to separate.
Gradually extensive paralysis of the legs and incontinence may occur, so that surgical intervention may become contraindicated.

Additional Management which may be needed

Bladder and bowel management
Bracing and orthotics
Physical Therapy/ occupational Therapy/ recreational Therapy
Shunting for hydrocephalus and syringomyelia
Chiari malformation repair
Hip relocation and other deformity correction procedures

Syringomyelocele

In this condition, the central canal of the spinal cord is dilated and the spinal cord lies within the sac together with the peripheral nerves arising from the cord.

This is the rarest variety of spina bifida.

Gross neurological deficits and paralytic manifestations are present.

Myelocele

This is the gravest form of spina bifida, in which besides the bony defect there is also a defect of development of the spinal cord. The development is arrested before the time of closure of the neural furrow. So that the posterior part of the spinal cord is not developed.

The elliptical raw surface of the neural furrow can be seen, deep to which lies the anterior part of the spinal cord. At the top end of the defect, the central canal of the spinal cord opens on the surface and discharges the cerebrospinal fluid constantly.

Majority of the cases are stillborn. Even if a few born alive, they die within a few days from infection of the cord and meninges.

Evaluation of Spina Bifida

As the most common type of spina bifida is myelomeningocele, the evaluation discussion is centered around that.

Screening test for neural tube defects can be performed by blood tests or amniocentesis for alpha-fetoprotein estimation combined with ultrasonography. The fetal presence of an open neural tube defect is marked by an elevated alpha-fetoprotein level.

In children with spina bifida, apart from routine laboratory screening examination, urine studies for culture, urodynamic studies for bladder evaluation and latex sensitivity tests become important.

X-rays provide information for early evaluation when an infant is born.

Most of the children on MRI would show a tethered cord but only about 20% are symptomatic.

CT is useful for tracking hydrocephalus.

Prevention of Spina Bifida

Increased use and accuracy of prenatal diagnosis and option for early pregnancy termination and the introduction of primary prevention in the form of folic acid therapy has resulted in a decline of cases of spina bifida.

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Tuberculosis of Spine Presentation and Treatment

By Arun Pal Singh

Tuberculosis of spine or TB spine or spinal TB was first described by Percivall Pott. He noted this as a painful kyphotic deformity of the spine associated with paraplegia. Since then condition is also referred to as Pott’s disease or Pott’s spine. It is also called vertebral tuberculosis. Because tuberculosis is also called Koch’s lesion, the term spinal Koch’s is also used. Another term used is caries spine or spinal caries.

Spine tuberculosis is the commonest form of skeletal tuberculosis. It constitutes about 50 percent of all cases of bone and joint TB.

Spine TB is most commonly found in the first three decades of life but can occur in any age group.

There is no gender predilection.

Tuberculosis of the spine occurs most commonly in the lower thoracic region. It is followed by lumbar, upper dorsal, cervical and sacral regions in decreasing order of frequency.

Tuberculosis of spine is also referred to as tuberculous spondylitis. Tuberculosis of the spine used to be a disease of early childhood in the past. But with improved public health measures, this age incidence has changed, and adults are more frequently affected.

Before the availability of modern antitubercular drugs, the mortality rate of the patients was about 30 percent. With the use of modern antitubercular drugs, the outcomes of the treatment have been changed.

Anatomy of Spine

Detailed anatomy of spine is discussed separately. Here A general overview with terms is presented.

Human spine or vertebral column is a structure made of multiple small units called vertebra and extends from just below the base of skull to a point just below the beginning of gluteal cleft.

A vertebra is the smallest unit of vertebral column. Plural term is vertebrae. Vertebrae have been modified according to the function they are expected to serve in different parts of the spine.

Spine appears straight in anteroposterior view (That means looking from front or back) but in lateral view or looking from a side, we can see multiple curves in the spine in different regions.

These curves are called kyphotic if they are concave in anterior(front) and convex on posterior (back) and lordotic if they are convex in anterior and concave on posterior.

Spine is divided into five regions

Cervical Spine

This part of the spine is present in the neck and consists of first seven vertebrae. Thus the first vertebra is called C1 and last vertebra is called C7. The cervical spine has a normal lordotic curve.

Thoracic Spine

Also called dorsal spine, it is below the cervical spine and spans upper trunk or thorax or area corresponding to the chest. It contains a total of 12 vertebrae which are designated as T1 to T12

Thoracic spine has a normal kyphotic curve.

Lumbar Spine

It follows thoracic spine and consists of 5 vertebrae, L1 to L5. Anatomical variations in which 4 or 6 vertebrae might be present in lumbar spine are known.

Sacral Spine

Sacral spine is composed of five sacral vertebrae S1 to S5. Vertebrae in sacral spine are fused to each other. This part of spine follows lumbar spine and is present in the pelvic area.

Coccyx or Coccygeal Spine: This is also known as tailbone. It consists of four fused vertebrae (the coccygeal vertebrae) below the sacrum.

Vertebra

Vertebrae, the structural units of the spine are stacked together to form the entire vertebral column. Discs are cushion-like structures acting as shock absorbers between two vertebrae.

They also permit some movement between the vertebral bodies and the transmission of weight.

Each vertebra consists of an anterior body which is attached to a posterior ring called posterior neural arch [pedicle and laminae together].

Two struts of bones called pedicles arise from body and join two converging struts called laminae. Pedicles, laminae and posterior surface of body forms boundaries of spinal canal, which is the space for passage of spinal canal.

This spinal canal is the space where spinal cord passes. There is a transverse process on either side of the arch which serves as attachment to various muscles and ligaments. Posteriorly is the posterior spinous process that also serves as an attachment to ligaments and muscles of the spine.

The neural foramen is the opening where the nerve roots exit the spine and travel to the rest of the body. There are two neural foramina located between each pair of vertebrae, one on each side.

Muscles and Ligaments

Various muscles and ligaments attach to the spine. They help the spine to stabilize and allow it to carry various movements.

Pathology of Tuberculosis of Spine

The bacteriae reach the site of infection via bloodstream. The focus of infection usually begins in the cancellous bone of the vertebral body. Occasionally, it is in the posterior neural arch, transverse process, or subperiosteally deep to the anterior longitudinal ligament in front of the vertebral body. Up to 5% of spinal tuberculosis has been reported in posterior elements.

As the disease progresses, the area of infection gradually enlarges and spreads to involve two or more adjacent vertebrae by extension beneath the anterior longitudinal ligament or directly across the intervertebral disc.

Sometimes there may be multiple vertebrae may be involved which are separated by normal vertebrae termed as skip lesions. The infection may be disseminated to distant vertebrae via the paravertebral abscess.

As the tuberculosis of spine progresses, vertebral bodies lose their mechanical strength due to progressive destruction under the force of body weight. Extreme weakening leads to angular kyphotic deformity.

The severity of the deformity depends upon the extent of destruction, the level of the lesion, and the number of vertebrae involved.

Kyphosis is most marked in the thoracic area because of the normal dorsal curvature. In the lumbar area, it is less because of the normal lumbar lordosis because of which the body weight is transmitted posteriorly and collapse is partial.

The collapse is minimal in the cervical spine because most of the body weight is borne through the articular processes.

Healing takes place by gradual fibrosis and calcification of the granulomatous tuberculous tissue. Eventually, the fibrous tissue is ossified, with resulting bony ankylosis of the collapsed vertebrae.

Paravertebral abscess [abscess around vertebra – literal meaning], formation occurs in almost every case. With the collapse of the vertebral body, tuberculous granulation tissue, caseous matter, and necrotic bone and bone marrow are extruded through the bony cortex and accumulate beneath the anterior longitudinal ligament.

These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion.

In the lumbar region, the abscess gravitates along the psoas fascial sheath and usually points into the groin just below the inguinal ligament.

In the thoracic region, the longitudinal ligaments limit the abscess, which is seen in the radiogram as a fusiform radiopaque shadow at or just below the level of the involved vertebra.

Thoracic abscess may reach the anterior chest wall in the parasternal area by tracking via the intercostal vessels.

Neural Deficit in Spine Tuberculosis

Neurological complications may arise due to compression of the cord by the abscess, caseating or granulating mass, intervertebral disc or edge of bone c. Other contributory factors may be thrombosis of the local vessels and edema of the cord.

The neural deficit can be paraparesis, to begin with, and eventually, lead to paraplegia. It occurs most often in the mid-or upper-thoracic region, where the kyphosis is most acute, the spinal canal is narrow, and the spinal cord is relatively large.

The neural deficit in TB spine occurs due to pressure on the tissues of the cord, as follows. Other factors are cord edema and inflammation.

Following can contribute to the pressure on the spinal cord.

Extradural Mass formed by tubercular abscess [fluid pus, granulation tissue or caseous material.
Extradural Granuloma and Tuberculoma
Sequestra [dead bone] from avascular diseased vertebral bodies or intervertebral disc
Granulation tissue on the with peridural fibrosis [cicatrization or scar formation]
Infarction of the cord by thrombosis or arteritis.
Cord atrophy

Paraplegia due to tuberculosis of the spine can be early onset or late onset.

Early onset paraplegia occurs during the active phase of the vertebral disease usually within first 2 years of the onset.

Late-onset paraplegia occurs many more than 2 years after the disease has persisted and could be due to recrudescence of the disease or mechanical pressure on the cord.

It is also called paraplegia associated with the healed disease.

Types of Lesions in Spinal Tuberculosis

Four types of the lesion are known in spinal tuberculosis

Paradiscal type – On either side of the disc
Central type – central part of the vertebral body
Anterior type – anterior surface of the vertebral body
Appendiceal type (involving pedicles, laminae, spinous process or transverse processes).

Paradiscal Lesion

In this type, the infection is on either side of the disc, involving two vertebrae. This is the most common type of presentation. The narrowing of the disc space is often the earliest radiological finding, often associated with a fuzziness of The narrowing of the disc space may either be due to either atrophy of the disc tissue or prolapsed.

Central Type of Lesion

The infection starts from the center of the vertebral body, where it reaches through Batson’s venous plexus or through the branches of the posterior vertebral artery.

On x-ray, the diseased vertebral body loses the normal bony trabeculae and many show areas of destruction or the body may be expanded or ballooned out like a tumor and finally collapse like vertebra plana.

Loss of disc space is minimal.

Anterior Lesion

The infection starts beneath the anterior longitudinal ligament and the periosteum.

On x-ray, the peripheral portion of the vertebral body shows erosion as shallow excavations. Vertebral collapse and a decrease in the disc space is usually minimal and occurs late.

Appendiceal Lesion

This involves isolated infection of the pedicles, transverse processes, laminae, and the spinous process does occur.

These lesions are not generally visible on routine x-rays.

CT or MRI is better at detecting these lesions.

Presentation of Tuberculosis of Spine

The onset of is usually insidious. Initial symptoms are vague, consisting of generalized malaise, easy fatiguability, loss of appetite and weight, and loss of desire to play outdoors in children. There may be an afternoon or evening fever.

However, the acute presentation of tuberculosis is known.

A backache is usually minimal and may be referred segmentally.

Muscle spasm makes the back rigid. The motion of the spine is limited in all direction. The patient may complain of inability to flex spine when picking an object up from the floor. For doing this, the patient flexes his hips and knees, keeping the spine in extension.

On examination, the spine is stiff and painful on movement. The stiffness of the spine is noticed by an increase of depth of spinal midline gutter as paraspinal muscle spasm makes them prominent.

There may be a localized kyphotic deformity which would be tender on palpation.

A cold abscess may be noticed. The abscesses may be palpated as fluctuant swellings in the groin, iliac fossa, retropharynx, or on the side of the neck, depending upon the level of the lesion.

In spite of the vast spectrum of the disease, the early cases may not have any clinical finding except for tenderness in the region of the complaint. Several of these symptoms and sign may be absent even in cases of the active vertebral disease.

A history of contact with a known case of tuberculosis or a recent visit to an endemic area should be asked.

A kyphus in the thoracic region may be the first noticeable sign. As the kyphosis increases, the ribs will crowd together and a barrel chest deformity may develop.

When the lesion is situated in the cervical or lumbar spine, a flattening of the normal lordosis is the initial finding.

The gait of the person with Pott’s disease is peculiar, reflecting the protective rigidity of the spine. His steps are short, as he is trying to avoid any jarring of his back. In tuberculosis of the cervical spine, he holds his neck is in extension and supports his head with one hand under the chin and the other over the occiput.

Neural Deficit in TB Spine

The compression of neural structures leads to signs of neurological deficit. The compression of neural structures is indicated by

Spasticity of the limbs [uper and lower limbs in case of the cervical spine and lower limbs in case of dorsal and lumbar spines]
Hyperactive deep tendon reflexes
Spastic gait
Motor weakness
Disturbances of the bladder and anorectal function.

A neural deficit in tuberculosis could be caused by the following factors

Inflammatory

Inflammatory edema – recovers by rest and drug therapy
Tuberculous granulation tissue – mostly recovers by rest and drug therapy
Tuberculous abscess – recovers by conservative therapy, rarely requires evacuation and decompression
Tuberculous caseous tissue – May subside by conservative therapy, sometimes requires evacuation and decompression

Mechanical

Tubercular debris- Solid debris requires removal and decompression
Sequestra from vertebral body and disc – Require operative removal and decompression
Constriction of cord due to stenosis of vertebral canal- Requires operative decompression
Localized pressure due to internal gibbus along anterior wall of the vertebral canal – Requires operative decompression

Intrinsic

Prolonged stretching of the cord over a severe deformity – Decompression, release of cord, and anterior transposition may lead to recovery
Atrophy of cord – Does not recover completely
Infective thrombosis/endarteritis of spinal vessels – Does not recover appreciably
Pathological dislocation of spine – Rare complication, causes irreparable severance of cord
Tuberculous meningomyelitis – Does not recover completely
Syringomyelic changes – poor recovery
Spinal Tumor syndrome – Poor recovery
Diffuse extradural granuloma or tuberculoma or peridural fibrosis -Present as spinal tumor syndrome

Neural deficit in spine TB is classified as follows

Stage 1

Patient walks normally and is not aware of any deficit
Extensor plantar response
Ankle clonus
May be accompanied by brisk tendon reflexes

Stage 2

Clumsy gait
Incoordinated jumpy gait
Weakness, walks with support

Stage 3

Severe weakness
Patient bedridden and cannot walk because
<50% sensory deficit

Stage 4

The patient has paraplegia with flexor spasms or paraplegia in flexion.
Paraplegia in extension with spontaneous flexor spasms
Sphincter disturbances
Flaccid paralysis [ occurs due to very severe cord compression]

Neural deficit in tuberculosis is of slow onset.

The earliest symptom may be twitching of muscles in the lower limbs and clumsiness while walking.

Motor functions are almost always affected before and to a greater extent than the sensory functions due to anterior site because the disease is mostly in the anterior part [motor tracts are anterior too] and probably the motor tracts are more sensitive to compression of the cord.

The paralysis as noted above may pass from spastic motor paraparesis to spastic paraplegia in extension and then on spastic paraplegia in flexion.

In severe compression of the cord, flexor spasms may occur which refers to involuntary flexions of the lower limb. This indicates complete loss of conductivity in the pyramidal and extrapyramidal neural tracts.

Bladder and anal sphincters may be involved.

There may be a sensory deficit. The sense of position and vibration are the last to disappear.

In severe cases all spasticity disappears and the paralysis becomes flaccid (areflexic paraplegia) with anesthesia and loss of sphincter control.

Sometimes, the insult to the cord is sudden [such as ischemia] and the patient may present with flaccid paralysis ”spinal shock” and later gradually change into spasticity.

Rarely, the disease may present like a ”spinal tumor syndrome” due to a localized tuberculoma or a diffuse granuloma or due to peridural fibrosis.

Differential Diagnosis of Tuberculosis of Spine

Mostly the diagnosis of tuberculosis can be made by clinical and radiological examination by its characteristic findings.

Doubtful cases need to be confirmed by biopsy and/or culture.

The differential diagnoses vary with age of presentation. Congenital defects of the spine, Calve’s disease are common d/ds in young patients. Schmorl’s disease and Scheuermann’s disease may sometimes cause confusion in adolescent patients.

Tuberculosis is suggested by the presence of constitutional symptoms [fever, malaise etc], characteristic radiological appearance and disc space is well maintained. Local signs like pain, spasm, and tenderness are less pronounced in other diseases than TB spine.

In adults, malignancy is major d/d.

Following is a list of main differentials of the tuberculous spine.

Infections

Bacterial Spondylitis

This may follow infection or surgery of urogenital tract, or postabortal or postpartum infections. Also called pyogenic osteomyelitis, it presents as sudden onset disease with severe localized pain, spasm and high-grade fever with chills and rigors.

Bone destruction is eventually followed by sclerosis and new bone formation and even bony ankylosis.

Typhoid Spine

This is a rare complication of enteric fever. Most of the cases present at the time intervals of 4 weeks to a few months after the episode of typhoid fever.

Excruciating pain and muscle spasm. The radiological picture resembles that of tuberculosis and low-grade pyogenic spondylitis. Confirmation can be obtained by agglutination tests, therapeutic trial or by biopsy.

Brucella Spondylitis

This can produce changes in the spine which can be very similar to those seen in tuberculosis of the spine. The diagnosis is best established by identification of the causative organisms, agglutination tests or by biopsy.

Fungal Spondylitis

Actinomyces group or blastomycosis group can be responsible for the infection of vertebrae.

In blastomycosis, paravertebral abscess formation is a common feature. In actinomycosis sclerosis and destruction of bone proceed hand in hand.

A collapse of the vertebra is rare, sometimes the involved vertebrae may produce an appearance described as ”honeycomb” or ”lattice-like” and the condition is usually accompanied by multiple sinus formations and involvement of the subcutaneous tissues.

Diagnosis can be confirmed by a demonstration on the mycotic organism from the discharging sinuses, pus or from the diseased bone.

It is quite rare.

Syphilis

The commonest site of involvement is thoracolumbar and lumbar spine though it is of rare occurrence after modern antibiotics which cure syphilis much earlier.

Three types are known

Arthralgic type of syphilitic spondylitis
Gummatous type of syphilitic spondylitis
Charcot’s disease of the spine.

Xrays show gross disorganization and destruction of the involved vertebrae along with proliferative new bone formation extending into the adjacent paraspinal tissues. It is extremely difficult to differentiate this condition on x-rays alone.

Diagnosis is confirmed by serological tests, tissue biopsy or by the response to antisyphilitic treatment.

Hydatid Disease

Hydatid disease of the spine is a very rare condition

Tumors

Benign Tumor

Following benign tumorous conditions may clinically and radiologically have some resemblance with spinal tuberculosis.

Hemangioma
Giant-cell-tumor
aneurysmal bone cyst

Malignant Tumor

Ewing’s sarcoma

Osteogenic sarcoma
Fibrosarcomas
chondrosarcomas
Multiple Myeloma
Lymphomas
Metastases

Histiocytosis-X

eosinophilic granuloma (spine-Calve’s disease)
Hand-Schuller-Christan disease
Letterer-Siwe disease

Spinal Deformities

Hemivertebrae
Block Vertebrae [Fusion of two or more vertebral bodies]
Neural arch defects

Spinal Osteochondrosis

It is an ischemic lesion of the apophysis of several vertebrae occurring in early adolescence. A rounded kyphosis develops because of fragmentation, and mild wedging of several vertebral bodies.

The absence of any constitutional reaction, spasm or any radiological paravertebral shadows and bony destruction, together with minimal local symptoms distinguishes this condition from infective lesions of the spine.

Spondylolisthesis

It is a forward displacement of one vertebra on another. The commonest sites are between L5 and S1, and L4 and L5.

Destruction of posterior articular elements or destruction of pars interarticularis with or without the involvement of paradisical regions due to tuberculous process or other infective lesions may result in spondylolisthesis.

Imaging in Tuberculosis of Spine

Xrays

In addition to the lesion-specific appearance of the disease [ radiolucent lesion, fuzzy vertebral margins, reduced disc space, vertebral collapse – refer to types of the lesions], the following findings may be noted.

Findings are suggestive, but not pathognomonic. Routine views are anteroposterior and lateral views of the spine. Chest radiograms are taken to rule out outer foci of systemic disease in case of a suspected person.

Paravertebral shadows

Paravertebral shadows in TB of the spine is produced by extension of tuberculous granulation tissue and the collection of an abscess in the paravertebral region.

In the cervical region, this presents as increased prevertebral space.

Prevertebral space is soft tissue shadow between the vertebral bodies and pharynx and trachea. On an average, the normal space between the pharynx and spine above the level of cricoid cartilage is 0.5 cm and below this, it is 1.5 cm.

An increased space suggests collection in the prevertebral space.

In the upper thoracic spine, abscess appears V-shaped shadow stripping the lung apices laterally and downwards.

It may also show as squaring of borders of superior mediastinum.

Shifting of tracheal shadow to one side may be present on AP view.

Normal tracheal shadow is concave anteriorly in lateral view of the thoracic spine. Any change in the contour should raise the suspicion of the disease from C7 to D4 vertebrae.

Below that region [D4 vertebra is watershed], a typical fusiform-shape (bird nest appearance) shadow suggests paravertebral abscess.

Abscesses below the diaphragm tend to extend along the course of psoas muscle which may be noted as the bilateral widening of the psoas shadow but is less common.

Kyphus

This occurs in typical para discal lesion due to the collapse of two vertebral bodies.

Lateral Shift and Scoliosis

A lateral curvature and deviation have been recognized as one of the rare deformities of Pott’s disease.

CT and MRI

CT and MRI provide cross-sectional imaging which describes the extent of involvement better and are good at showing the presence of an epidural component and cord compression. MRI is the investigation of choice for this, with CT with contrast being a distant second.

In addition to this, MRI also reveals the status of the spinal cord health.

These show vertebral destruction and paraspinal collections.

Lab Studies

Most of the times, especially in endemic regions, the diagnosis of tuberculosis is clinicoradiological but lab tests are called for help when a clear diagnosis cannot be reached out at.

Routine lab investigations done in Pott’s spine are complete blood count, ESR, and CRP. Liver and kidney functions should also be assessed during treatment.

CBC might show lymphocytosis but could be normal as well.

ESR and CRP are generally elevated but in some cases, the increase is not seen.

ESR is deemed to be inflammation marker and some authors recommend serial ESR levels to assess the decrease in activity of the tubercular disease.

Tuberculin skin test is found positive in most of the patients with spine TB who are not infected with HIV

Microbiological Studies

The tissue for microbiological studies can be obtained through CT guided biopsy. This is more useful in cases with an equivocal diagnosis.

AFB staining of the tissue
Culture and sensitivity.

Treatment of Tuberculosis of Spine

The treatment of spinal tuberculosis is mainly by chemotherapy. Presence of neurological deficit complicates the matters and for sake of simplicity, I have divided the treatment into two groups

Treatment of Spine Tuberculosis Without Neural Deficit

The prevention of neural deficit in tuberculous disease of the spine is of paramount importance, it can be largely achieved by early diagnosis of spinal caries and its prompt and suitable treatment.

These patients are treated with antitubercular chemotherapy which consists of isoniazid, rifampicin, pyrazinamide, and ethambutol as the first line of drugs. However, depending upon the patient profile, drugs may be added or replaced.

Gradual mobilization of the patient is encouraged in the absence of neural deficit with the help of suitable spinal braces. After 3 to 9 weeks of starting of treatment, the patient is put on back extension exercises. Spinal brace is continued for about 18 months to 2 years.

Surface cold abscesses may be aspirated, deeper collections may not be required to drain.

Open drainage of the abscess is performed if aspiration fails to clear the collection.

Sinuses in a large majority of cases heal within 6 weeks to 12 weeks from the onset of the treatment

Periodic evaluation of the patient with X-rays and ESR is done to assess the activity of the disease and decreasing ESR is deemed to be a sign of reducing bacterial activity.

Treatment of Spine Tuberculosis With Neural Deficit

Patients with neural deficit require a more aggressive approach. Classical approach was to put all the patients on chemotherapy and strict bed rest.

Some authors in the recent past suggested a radical approach which advocated operating almost every tubercular lesion with [or even without] neural deficit to debride the tissue and relieve the pressure on neural structures.

While the first approach produced less than desirable results, the second one is associated with an increased surgical burden and associated mortality.

Middle path regime solves this problem to a great extent by taking the best of both approaches.

It puts the patient on chemotherapy and rest and observes for a response. The premise of the treatment is that, as the drugs act on the bacteriae, the reduced destruction and pus production leads to lesser pressure on the neural structures which tend to recover once milieu gets better by use of medicine.

This regime advocates surgery for the patients of TB of the spine who do not get better with the initial treatment or are not candidates for conservative treatment.

The surgery is indicated in the following situations

Every patient with neural complications will not be cured by antitubercular drugs and rest alone, however, all patients do not need surgical decompression.

An absolutely conservative approach to Pott’s paraplegia is considered unjustifiable as one might be losing very valuable time. Irreparable damage of the cord may take place if the deterioration progresses to complete loss of motor and sensory function.

Indications for surgery in presence of neural deficit are

Neurological complications which do not start showing signs of progressive recovery to a satisfactory level after a fair trial of conservative therapy (3 to 4weeks).
Patients with spinal caries in whom neurological complications develop during the conservative treatment
Patients with neurological complications which become worse while they are undergoing therapy with antituberculous drugs and bedrest
Patients who have a recurrence of neurological complication
Patients with prevertebral cervical abscesses, neurological signs, and difficulty in deglutition and respiration
Advanced cases of neurological involvement such as marked sensory and sphincter [bladder/bowel] disturbances, flaccid paralysis or severe flexor spasms.

In the cases who started showing progressive recovery complications on triple-drug therapy between 3 to 4 weeks and progressed to complete recovery surgical decompression was considered unnecessary.

Surgery in Spinal Tuberculosis

Surgery in the spinal tuberculosis is required mostly for decompression of the neural structures or drainage of abscesses.

Surgery is also done for deformity correction in severe kyphus.

In children, posterior spinal fusion is done so as to correct the deformity with growth.

Operative Procedures for Decompression of Neural Tissues

Decompression and debridement with or without bone grafting
- Cervical spine and cervicodorsal junction- anterior approach
- Dorsal spine and dorsolumbar junction – anterolateral approach or transpleural approach
- Lumbar spine and lumbosacral junction – extraperitoneal approach.
Laminectomy for posterior spinal disease, extradural granuloma or tuberculoma
Anterior transposition of the cord through the anterolateral in severe kyphotic deformity causing paraplegia.

Recovery after surgery has been observed after 24 hours to 12 weeks after the decompression. Most of the patients showed the first evidence of objective recovery within 3 weeks of the decompression, however, others took a longer time to recover. The time taken for near complete recovery varied between 3 to 6 months and in few cases more than a year.

Extensor plantar response, a sign of pyramidal tract involvement, lasts for a very long time.

Patients who recover are able to return to their full activity within 6 to 12 months of the treatment. Brace is recommended for about 2 years.

Prognosis

The prognosis of the disease is determined by the severity and duration of the disease.

If diagnosed and treated in very early stages, before bony destruction and deformity have occurred, the patient usually recovers completely without any residual problem.

After, vertebral collapse, the deformity occurs. This deformity would persist after the treatment as well when tubercular activity has finished.

If this deformity is severe, it could cause mechanical back pain in later years.

With the neural deficit, the prognosis is better if there is

partial cord involvement
Neural complications are of short duration
Early onset neural deficit
Slow progression of neural complications
Young patient
Good general condition of the patient

The prognosis is relatively poor if there is

Complete cord involvement
- Severe flexor spasms
- Flaccid paralysis
- Gross sensory loss
Long-standing neural complication
Late-onset neural deficit
Rapid development of neural complications
Patient is of older age
Poor general condition of the patient. Irrespective of the mode of treatment the patients who show neural recovery various modalities generally recover in the following order. Vibration and joint sensation; temperature, touch, pain, voluntary motor activity, sphincter functions and wasting of muscles.

Recurrence or relapse of a tuberculous lesion [ Also called recrudescence of the Disease] poses a special problem. The commonest cause is grumbling activity of infection caused by resistance strain of acid-fast bacilli.

Surgery may be required in these cases.

Atypical Presentation of the Tuberculosis of Spine

The classical form of tuberculosis is usually easy to recognize. However, atypical forms of the disease may occur involving other parts of the vertebra or also in the form of the extraosseous involvement of the neural and perineural tissue.

These are relatively uncommon and more difficult to diagnose.

Posterior Complex Tuberculosis

Posterior spinal tuberculosis is the lesion caused by Mycobacterium tuberculi in the posterior elements of the vertebral arch. The location is

It has been reported with patients suffering from HIV infection.

The lesion commonly arises in the dorsal, dorsolumbar and lumbar vertebrae. Cervical lesions involving the posterior complex are extremely rare.

The clinical picture is often similar to that of typical spinal tuberculosis. However, posterior abscesses may present earlier while the typical radiographic changes will not be present.

In fact, a conventional x-ray is not of much use in early diagnosis and one must have a high index of suspicion and get a CT Scan or an MRI done early to avoid delay in diagnosis.

CT Scan or MRI can determine the site and extent of the lesion, the presence of any vertebral body involvement or encroachment of the spinal canal. These are able to pick up the diagnosis at an earlier stage.

The lesion may occur in elements of the vertebral arch including the laminae, pedicles, transverse or spinous processes. Rarely the apophyseal joints may be involved.

The lesions may be in isolation or in combination with each other.

Classification

Lesions involving the vertebral arch – lamina and pedicles
Lesions involving the processes of the vertebral arch i.e. the transverse articular and spinous process.
A combination of both

The primary mode of treatment is anti-tuberculosis chemotherapy. Neurological involvement may warrant surgical treatment.

Intraspinal Tuberculous Granuloma (Tuberculoma)

Tuberculosis can involve neural and perineural tissue directly invading the spinal cord or meninges.

Spinal tiberculoma could be

Extra dural
Sub dural
Sub dural and extra dural
Arachnoidal [no dural involvement
Intramedullary

Extradural Granuloma

These typically present with compression of the cord. MRI or CT myelography is required to localize these lesions.

Where an extra dural granuloma is present surgery is advocated as there is a risk of healing with scar tissue on drug treatment only.

If there is anterior body disease is present then the anterior or antero-lateral decompression is recommended.

If there are associated neural arch lesions or when no osseous lesion is present, laminectomy and excision of the extra dural granuloma is recommended.

Subdural Granuloma

Presents with compressive myelopathy with no radiological localization of lesions. Myelography, myelo CT or MRi is required to localize the lesion.

Laminectomy at the level of the lesion is recommended. Where the dura is tense it needs to be opened to remove the sub dural granuloma.

Intramedullary Tuberculoma

These are very rare and patients present with a picture of severe spinal cord compression with a rapidly progressive course.

The presence of a tuberculous lesion elsewhere or in the past may be a clue to the diagnosis. MRI is the most useful investigation sequential.

Anti-tubercular chemotherapy is the mainstay of the disease.

Single Vertebral Disease

Single vertebral disease without involvement of the disc spaces is also considered as atypical spinal tuberculosis.

It may present as a cystic lesion involving the body or as vertebra plana simulating lesions such as eosinophillic granuloma.

Here the diseased vertebral body is weakened by the permeation of granulation tissue and collapses. It protrudes radially and may cause the neurological deficit.

Plain radiograph will slow collapse of a singe vertebral body with preservation of adjoining disk spaces.

CT Scan and MRI may help in differentiating it from other lesions such as eosinophillic granuloma, solitary plasmacytoma, metastatic disease.

However, the histological evidence is required in these atypical lesions and all efforts should be made to establish a tissue diagnosis.

In the event of neurological deficit anterior decompression is recommended as laminectomy may worsen the neurological deficit.

Other forms of Atypical Tuberculosis

These may include

Multiple vertebral skip lesions
- 2 – 7% of cases
Giant Tuberculous Abscess with little or no demonstrable bony focus.
- May present as cold abscess in the thigh, loins or as a psoas abscess.
Sclerotic Vertebrae with intervertebral bony bridging.
- Seen occasionally in healthy individuals with good immunity.
- On x-ray, lateral osteophytes with little evidence of erosion or destruction can be seen.
Pan Vertebral Disease
- concomitant involvement of anterior and posterior elements.
- Have severe instability

Intervertebral Disc Anatomy and Biomechanics

By Arun Pal Singh

Intervertebral disc is kind of cushion between two vertebrae. The discs absorb the forces across the vertebra and provide cushion during motion of vertebrae, thus preventing grinding of vertebrae against each other.

Discs are avascular structures, and in fact largest structure of the body without blood supply.

They receive nutrition via osmosis from surrounding structures. Discs are attached to vertebral bodies by hyaline cartilage.

On x-ray, the disc is not visible but a gross idea about its height can be made by looking at intervertebral space, which is space between two vertebrae.

Structure of Intervertebral Disc

Each disc is made up of two parts: the annulus fibrosus and the nucleus pulposus.

Annulus Fibrosis

Annulus or anulus is the word derived from the Latin word anus which means ring. The annulus is a ring-like tough structure that surrounds and encases the other structure of the intervertebral disc, called nucleus pulposus.

The annulus provides rotational stability and resists compressive stress.

The annulus is made of water and type I collagen fibers which are oriented at different angles horizontally to create the strength. Water and proteoglycans are other constituents.

Multiple layers or lamellae of collagen fibers arranged in a unique circumferential orientation along the disc periphery.

Each lamella is oriented at a 30-degree angle to the horizontal axis of the disc, and this pattern alternates in successive lamellae. The outer collagen fibers attach to the ring apophysis, and the inner layers attach to the end plate surround the nucleus.

High collagen/ low proteoglycan ratio makes the disc flexible enough.

Fibroblast-like cells are responsible for producing type I collagen and proteoglycans.

Nucleus Pulposus

It is gel-like elastic substance within the annulus fibrous and is composed of the same material as annulus fibrosis – water, collagen, and proteoglycans but in different concentration and structural arrangements.

nucleus pulposus is composed of type II collagen, water, and proteoglycans. Nucleus pulposus contains approximately 88% water.

This hydrophilic matrix provides the height of the intervertebral disc and makes it compressible enough.

Viscoelastic matrix makes annulus fibrous elastic and enables distribution of the forces smoothly to the annulus and the endplates.

In contrast to annulus fibrous nucleus pulposus as low collagen / high proteoglycan ratio.

It contains chondrocyte-like cells which are responsible for producing type II collagen and proteoglycans and allows to tolerate hypoxic conditions.

Blood Supply of Intervertebral disc

The intervertebral disc is avascular because the capillaries terminate at the vertebral endplates. The nutrition reaches nucleus pulposus through diffusion through pores in the endplates

Nerve Supply of Intervertebral Disc

Sinuvertebral nerve originates from the dorsal root ganglion gives rise to the innervates the superficial fibers of the annulus.

The disc is not innervated beyond the superficial fibers

Vertebral End Plate

The vertebral endplates that are in direct contact with the disc, consisting of cortical bone in the periphery, which in adolescence is referred to as the ring apophysis, and compressed cancellous bone in the central disc area, which covers nearly 70% of the disk.

The outer 30% consists of dense cortical margin and is the strongest area of the end plate.

Nutrition of Intervertebral Disc

The nutrition of these cells is derived from diffusion across the hyaline cartilage and subcortical end plates.

The cells in the central part of the disc lie closest to the end plate. By virtue of their position they lie nearest to vascular supply and are responsible primarily for nutrient and waste product exchange. The ultrastructure of the bony endplate comprises numerous sinusoids with specialized loops of capillaries that come into close contact with the underlying cartilaginous layer.

Simple diffusion of molecules across the cartilage occur depending on the size of small nutrients. As there is anaerobic metabolism due to anaerobic avascular nature of the disc, the latent pH within the disc under normal conditions is acidic.

Microscopic Constitution of Disc

Collagen

Collagen provides strength to the intervertebral disc and is most abundant in the outer annulus, making almost 70% of dry weight of annulus. [In contrast, collagen forms only 20% of the dry weight of nucleus pulposus]

The type of collagen is type I collagen, which is highly cross-linked for increased strength, and small amounts of types II, III, V, VI, and XI collagen.

Fibroblasts that diminish in a number closer to the disc center are interspersed.

The inner annulus contains a relatively greater proportion of chondrocytes and varying amounts of type II collagen fibrils in a loose, nonorganized manner. The central nucleus is a gelatinous core containing chondrocyte-like cells and nearly 85% of type II collagen.

Proteoglycans

Proteoglycans consist of a protein core covalently attached to a glycosaminoglycan subunit. The glycosaminoglycan units are hydrophilic in nature and retain water in its normal state.

Chondroitin sulfate and keratan sulfate are the most common glycosaminoglycans found in the disc, the former more prevalent in the normal. Multiple proteoglycan subunits are attached to a central hyaluronate filament by a link protein, a kind of glycoprotein.

The entire structure forms aggregate molecules, of which aggrecan is the largest found in the annulus, Others are versican, decorin, biglycan, and fibromodulin. Fibroblasts and chondrocytes are suspected within this mesh framework along with remnants of notochordal-like cells.

Gradient

The gradient of the cellular and extracellular matrix components from the fibrous well-organized periphery to the randomly organized gelatinous center.

The gradient progresses through four less distinct zones of the disc

Outer annulus
Inner annulus
Transition zone
Central nucleus

Production and Remodeling of Disc

Chondrocytes and fibroblastic cells are within an extensive, intricate extracellular matrix.

These cells are responsible for homeostasis of the extracellular matrix, including matrix formation, maintenance, and remodeling.

The cells are responsible for production and constant remodeling of the principal components of the extracellular matrix collagen and proteoglycans.

Biomechanics of Intervertebral Disc

Highly hydrated amorphous central disc structure that in the normal state is constantly under expansible stress.

The nucleus retains water and expands, providing stiffness and resistance to compressive forces. This mechanism effectively transfers compressive load on the nucleus to a radially directed force with tensile stress to the annulus.

Constant load on the disc applies pressure to the nucleus, reducing the ability of the proteoglycans and, thus, the nucleus to hold water, causing creep of the disc.

After pressure is relieved, the time-dependent viscoelastic properties of the disc nucleus allow it to retain water.

The annular fiber orientation within the lamellae allows for resistance to tension. Because lamellae are oblique, it results in tension or relaxation of the fibers in different areas within the disk and with different forces. The phenomenon is called anisotropy.

In the anterior or posterior translation of a vertebral body and disc along the horizontal axis, all of the fibers of the annulus are stretched in the direction of the applied force.

However, fibers aligned in the direction of the force will undergo stain while the remaining fibers actually will be brought closer to one another and will relax.

Annulus fibrosus has highest tensile stresses and nucleus pulposus has highest compressive stress.

This alternating tension and relaxation with translation and axial rotation maintain the stability of the intervertebral segment.

In axial compression, the nucleus expands radially toward the inner aspect of the annulus fibers; the annulus fibers also expand circumferentially.

Anterior flexion of sagittal plane rotation causes the anterior annulus compression. The nucleus also is compressed eccentrically over its anterior aspect, after which it deforms and migrates posteriorly. The posterior annular fibers expand radially the shifting nucleus, and the fibers stretched in line with these forces resist further motion.

As rotation occurs, the weight of the upper body and trunk lead to shear strain forces at the disc and slight translation, which is resisted by the active and passive constraints of the posterior column, may occur.

Lumbar range of motion varies between vertebral levels and individuals.

The instantaneous axis of rotation continually changes throughout the range of motion and typically is located posterior toe the midvertebral body and below the superior endplate of the inferior vertebral body except at L5-S1, where it is located posterior to the disc space.

Function of Intervertebral Disc

It allows spinal motion and provides stability
It serves as a link to attach adjacent vertebral bodies together
The disc is responsible for 25% of spinal column height

Changes in Intervertebral Disc with Aging and Disease

Aging of disc leads to an overall loss of water content and there is conversion to fibrocartilage.

There is a decrease in nutritional transport along with a decrease in water content. The pH becomes acidic and there is a reduction in the number of viable cells and proteoglycans.

Along with that, there is an increase in keratin sulfate to chondroitin sulfate ratio, lactate. the activity of enzymes causing degradation decreases.

In disc herniation, there is increased production of osteoprotegerin, interleukin-1 beta, receptor activator of nuclear factor-kB ligand (RANKL) and parathyroid hormone.

Clinical Significance of Intervertebral Disc

Disc Prolapse

Also called disc herniation or slipped disc. In this condition, the nucleus pulposus along with protrudes out from a weakness in the annulus fibrosus and indents on the nerve root in the vicinity.

This condition can lead to radiating pain in the lower limb, commonly known as sciatica.

The bulge is usually posterior, especially in the lateral area.

Schmorl nodes are another kind of herniation, where the nucleus pulposus, herniates on vertebral endplates.

This is referred to as vertical disc herniation.

Degeneration of Disc

The disc degenerates with age. Before age 40 approximately 25% of people show evidence of disc degeneration at one or more levels. Beyond age 40, more than 60% of people have it.

In degeneration, the nucleus pulposus begins to dehydrate and the concentration of proteoglycans in the matrix decreases. This limits the ability of the disc to absorb shock. The annulus fibrosus also becomes weaker with age and has an increased risk of tearing.

Sclerosis of the bones underlying the end plates also occur.

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