Nerve Root Compression

Nerve root compression is the original chiropractic definition of nervous interference. Early chiropractors
hypothesized that vertebral subluxations could impinge a nerve, causing an increase or decrease in its function.
Since those early days, research has shown that actual nerve impingement by a subluxated vertebra occurs very
rarely (Leach '86). If bony impingement is rare, then how can nerve root compression occur at all?

Evidence has shown that postural deviations which cause abnormal strains on the spinal column and soft tissues,
create histopathologic changes in the structures surrounding the nerve roots, such as spondylosis, disc protrusion,
posterior joint osteoarthritis, and ligamentum flavum hypertrophy. These changes are not due to the aging process,
but are initiated by alterations in spinal biomechanics resulting in a cascade of positive feedback loops (Bland '83).
These degenerative or hypertrophic changes are the true causes of nerve root compression. To better understand
the pathological implications of nerve root compression, we must take a close look at its anatomy.

Nerve roots are the transitory junction between the central nervous system (CNS) and periferal nervous system
(PNS), possessing histological characteristics of both. They are formed by the union of the anterior (motor) and
posterior (sensory) roots emerging from the spinal cord. This union can occur in the vertebral canal, at or above the
corresponding segment, or in the IVF. From the union, the nerve root extends through the IVF where it exits the spinal
column, becoming the peripheral nerve.

Nerve roots are more susceptible to compressive and tensile forces than peripheral nerves because they lack the
same amount of protective connective tissue. The perineurium which forms fascicles in peripheral nerves, providing
the most tensile strength, is completely absent in the nerve root (McCabe '69) (figure 7). This is fundamental, since
many of the situations regarded as compressive, such as a protruded disc, actually result in tension and only rarely in
true compression (Breig '63).

The blood supply to the nerve root comes from the vasa corona and the intermediate branch of the segmental artery.
This blood supply is critical to the survival of the Schwann cells, oligodendrocytes, and the axon itself. The schwann
cells and oligodendrocytes not only provide insulation for conduction purposes, but also function to produce
neurotrophic factors vital to the neuron's survival. Axonal transport is also vital, being the main mechanism for
distribution of nutrients and trophic factors and for removal of metabolic wastes within the axon. If either the blood
supply or the axonal transport mechanism is decreased, pathophysiology will occur to the nerve root and its
peripheral nerve continuation.

The effects of nerve root compression can be categorized as: a) those due to circulation impairment in the nerve
root, or b) those due to the mechanical deformation of the nerve root (Dahlin '92). In other words, nerve functions can
fail secondarily to ischemia (low pressure compression) or they can fail primarily to mechanical deformation (high
pressure compression). Most nerve root compressions are probably of the low pressure type, maintained over a
long period or over multiple short periods such as that which only occurs in certain spinal positions.

Circulatory impairment is one of the earliest consequences of nerve root compression. Pressures of only 5-10
mmHg are required to initiate venous stasis of the nerve root in humans (Olmarker '89). For comparison, the lightest
touch of a fingertip is estimated to be around 5 mmHg. These findings show that minute pressure on the vasculature
can lead to ischemia. It is widely accepted that hypoxia, or lack of oxygen, is the ultimate cause of cellular disease.
This seems to be true in the nerve root due to the fact that a reduction in the oxygen supply will cause demyelination,
or death to the Schwann cells/oligodendrocytes. This demyelination causes a decrease in the rate of conductivity of
the nerve root leading to altered target organ physiology. Sudden, repeated compression of the neural tissue and
vasculature will cause microdamage to the neurons leading to edema and fibrosis. Intraneural edema can severely
effect the conduction, axonal transport, and blood supply to the neuron.

It is important to understand that many of these effects will occur without any pain or symptomology. Pain seems to
have a strong correlation only when there is inflammation, especially when the dorsal root ganglion is involved. If no
inflammation occurs with compression, then it could very well go unnoticed. Cases which present with most of the
classic signs and symptoms of nerve root compression may involve no nerve root pressure whatsoever (Mooney
'76), and asymptomatic or mildly symptomatic patients may have profound nerve root compression (Watanabe '86).
Estimates of the percentage of spine related symptoms caused by nerve compression range from only 1-3%
(Troyonavich) to at least 10-15% (Flesia '89). Three studies using various imaging mediums suggest that from
24-35% of asymptomatic persons have at least mild nerve root compression (Powell '86, Wiesel '84, Hitselberger
'88). It appears that nerve root compression is more common than we suspect, and may have a 30% or higher
occurrence in the general population.

If nerve root compression cannot be effectively diagnosed due to the lack of symptomology, then how can it be dealt
with? Since the cause of compression results from histological changes in the structures surrounding the nerve root
secondary to postural deviations which alter the biomechanics of the spine, then the answer is obvious. Maintenance
of an ideal spinal configuration with normal biomechanical function is the only answer.

Spinal Cord and Brain Stem Tension   Bone Deformation
Restricted Blood Flow   Nerve Root Compression