The autonomic and somatic nervous systems are the integral anatomical and physiological components of the spine. Due to the fact that the majority of the central and peripheral nervous system dysfunctions are somatic in nature, the autonomic nervous system has been over-shadowed and has received very little attention in regard to its role in spinal pathology.

In acute noxious injuries to the spine, usually the somatic sensory and motor dysfunctions originate as acute pain which is referred to as acute "nociceptive" or somatic pain (fig. 1). In occasional situations the pain may have a tendency to persist for months or several years after the original injury has healed. This type of persistent pain has been referred to as "neuropathic pain".

FIGURE 1

Proprioceptive input (right side of diagram) exerts inhibitory

effect on anterolateral (intermediolateral) pyramidal cells of the spinal cord with the resultant inhibition of A-beta and small C-fibers (left side of diagram), prevention of sensitization ("wind up") as well as deafferentation of the sensory input to the spinal cord and lack of inhibition of the anterolateral horn cells which leads to vasospasm and muscle spasm.

The chronic, neuropathic pain-e.g., nerve root contusion, neuralgia, stump neuroma pain and sympathetically maintained pain (SMP) - becomes persistent and has a tendency to affect the function of the sympathetic nervous system (SNS). The neuropathic pain has a tendency to cause referred pain, spasm, chronic tissue damage, and inflammation. It may be accompanied by vascular and trophic changes. These chronic autonomic dysfunctions and their relation to the spine are discussed below.

The autonomic nervous system (sympathetic and parasympathetic nervous system) is mainly responsible for the following functions:

1. Control of the vital signs (blood pressure, pulse, and respiration).

2. A balanced and stable homeostasis of the internal environment ("Milieu interne") Through the control of the body temperature, cell membrane exchange, and rate of metabolism.

3. Control of the immune system.

There are two major autonomic spinal structures.

1. Thoracolumbar autonomic system.

2. Craniocervical autonomic system.

These two divisions are under reciprocal and putative influence of the higher centers of the brain and brain stem in one extreme, and the peripheral neurovascular structures on the other. The neuronal structures in the autonomic nervous system are divided into supraspinal, preganglionic, and postganglionic neurons, The postganglionic fibers are poorly or myelinated (small c) fibers.

By virtue of the fact that the sympathetic ganglia have a close affinity to the spine, the pathologic spinal or autonomic changes are apt to affect the function of these two distinct structures.

Vertical and midline connections and plexi of sympathetic nervous system. This complex intermingling of the SNS fibers renders unilateral sympathectomy ineffective in the long run. The affinity of the sympathetic nervous system to the spine explains the involvement of the SNS in spinal injuries in the form of "neuropathic pain", SMP" and in other manifestations such as regular headaches and vertebral artery insufficiency (dizziness,

The supraspinal efferent nerves influencing the sympathetic system are mainly beta and alpha 2 receptors. They influence the sympathetic preganglionic cell bodies mainly in the intermediolateral grey columns of the thoracic and upper lumbar spinal cord regions. These preganglionic fibers traverse through the ventral root of the spinal nerve and synapse at the sympathetic ganglion. These preganglionic fibers synapse with the postganglionic nerves in a 1/20 ratio. The postganglionic sympathetic nerve fibers (alpha 1) (Table 1) end up in the target tissues such as arterioles with resultant peripheral vascular changes. On the other hand, the parasympathetic preganglionic nerves originate mainly from the brain stem and sacral portion of the spinal cord. The brain stem (cranial) portion of the parasympathetic nerves traverse through the 3rd, 7th, 9th, and 10th cranial nerves with 3/4 of the cranial parasympathetic nerves being represented in the 10th (vagus) nerve. Less the 10% of the sympathetic post ganglionic nerve fibers are cholinergic (responsible for sweating, and for vasodilation in the face and neck)

The craniocervical and thoracolumbar divisions of the sympathetic nervous system involvement in the spinal injuries result in referred pain, and other symptoms mistaken for different illnesses

1. CRANIOCERVICAL SYMPATHETIC DYSFUNCTION

Cervical spine pathology, usually cervical sprain or cervical spondylosis, is quite frequently accompanied by sympathetic dysfunction resulting in a series of symptoms (Table 3). As a result, the patient is exposed to ineffective and at times dangerous treatments such as occipital neurectomy or cryosurgery for treatment of occipital neuralgia, traumatic manipulation of the spine with resultant stroke, and unnecessary surgery and fusion. The spondylosis in and of itself is a natural development of osteophytes to stabilize the spine and to minimize damage to the nerve roots. The surgical removal of the osteophytes is throwing off the natural balance and can not be expected to provide any long standing relief. Simple physiotherapy in the form of traction, moist heat, along with treatment with muscle relaxant and nerve blocks are treatment of choice.

As is the case with the rest of the sympathetic system, the craniocervical sympathetic system follows the craniocervical arteries and arterioles closely to gauge the circulatory and temperature changes (fig. 3). The sympathetic nerves follow a thermatomal pattern-in contrast with somatic radicular dermatomal pattern (fig. 3). This results in erroneous diagnosis of "functional" or "malingering" sensory loss.

The sympathetic nerve fibers follow the arteries and arterioles. In sympathetic dysfunction, the sensory loss is more likely to be in the distribution of carotid, brachial, or femoral arteries in

the form of thermatomes rather than dermatomes that are involved in disc herniation. This causes a confusing picture of sensory loss mistaken for "functional" or "hysterical" sensory loss.

The sherrington-kerr phenomenon (fig. 4) (1) points to the overlapping afferent sensory pools in the cervical spine region. The substantia gelatinosa of the upper cervical C1 through C4 nerve roots region overlaps the nuclei of the ophthalmic branch of the trigeminal nerve.

The sherrington-kerr phenomenon refers to sherrington's overlapping afferent pools of sensory nerves in substantia gelatinosa. The C1 through C4 regions of substantia gelatinosa overlap with the ophthalmic nerve endings of the trigeminal nerve. This explains the high instance of vascular headaches, occipital headaches, retro-orbital pain, abd sharp frontal pain in cervical spine injuries.

Injury to the upper cervical sensosry nerve roots results in overlapping afferent pool of sherrington and referred pain to the retro-orbital region, frontal region, as well as to the shoulder and the occipital region. The end result is frontal, occipital, and retro-orbital vascular headaches (3,1) (fig. 5). Treatment with traction, moist heat, as well as occipital amd paravertebral blocks is most effective (1,3).

The craniocervical sympathetic nerves surround the carotid and vertebral arteries with resultant manifestations of chest pain, migraine or cluster headaches (involvement of SPG ganglion), ophthalmic pain, vertigo, tinnitu, and pain in the upper extremities mistaken for entrapment neuropathies. these manifestations are seen frequently in cervical spine injuries.

Reflex sympathetic dystrophy is a syndrome that may develop as a consequence of any noxious stimulus (trauma, ets.) chronically affecting the sympathetic system in the limbs, craniocervical region, thoracolumbar region, or visceral organs (stroke, heart attack, or cancer). The original injury is usually minor in nature. The lesion may be obvious on the surface or concealed. The syndrome is characterized by:

1. Allodynic pain (pain induced by a non-noxious stimulus), hyperpathic pain (over-reation with pain to stimulus which may persist after the stimulation has ceased). The pain is usually practically constant, burning, and/or stabbing in nature. In early stages of the disease the pain is abated with sympathetic nerve blocks (such as IV Phentolamine, and Bier block). In lare stages of the disease the sympathetic block may not effectively or completely control the pain (the pain is no longer sympathetically maintained pain-or SMP).

2. Efferent vascular, motor, and sudomotor response to the pain. This is in the form of vasoconstriction with cold extremity in the area surrounding the lesion, muscle spasms, tremor, dystonia, and abnormal sweating.

3. Edema, inflammation, and dystrophic changes due to the disturbance of sympathetic function which results in the extravastion of fluids, neurodermatitis, cell membrane and immune system disturbance with secondary inflammation.

4. Due to the fact that the sympathetic afferent input chronically stimulates the limbic (frontal temporal) system, the patient suffers from insomnia, agitation, depression, poor memory, and poor judgment (fig. 6).

The neuropathic and especially SMP afferent pain fibers (paleocortical) is more mutisynaptic and terminates in medial thalamic nuclei and bilateral limbic structures. The somesthetic (neocortical) afferent fibers undergo less synaptic relays. They terminate in the lateral nuclei of thalamus and in the contralateral neocortical somatosensory parietal region. The sympathetic input almost exclusively terminates in the limbic system (Benarroch, Mayo Clinic Proceedings, 10/93) and results in insomnia, agitation, depression, poor memory, and poor judgment.

In both craniocervical and thoracolumbar Rsds, efferent motor dysfunction quite frequently results in an accordion effect on the spine with secondary disc bulging or even disc herniation. This is an affect rather than a cause. The treatment should be aimed at treating RSD rather than surgery for this side effect of the disease.

The same efferent reflex manifestation of RSD quite frequently results in cervicogenic tremor, dystonia, and even Parkinsonian type of tremor (4). The movement disorder responds best to muscle relaxants such as Baclofen, or Skelaxin, and simultaneous treatment with nerve blocks, physical therapy, and ACTH (4,1). The movement disorder is due to the sympathetic dysfunction, and to quote Janokovic, "the negative or positive outcome of litigation rarely influences the course of the movement disorder" (4).

The inflammation of RSD results in entrapment neuropathies such as carpal tunnel and tarsal tunnel syndrome. Surgical treatment for such entrapment neuropathies invariably fails to relieve the condition, and only accelerates and aggravates the deterioration of RSD. Such entrapment neuropathies can be easily differentiated clinically by a careful neurologic examination (Table 4). The main features that differentiate the conditions are the Tinnel's Sign not being focalized to the area of nerve entrapment, allodynia being present over the entire distal portion of the extremity, and edema especially noted on MRI of the wrists or ankles showing joint extravasation as well as osteopenia in the small bones of the involved area (Table 4).

The best treatment for such entrapment neuropathies are nerve blocks, muscle relaxants, epsom salt and hot water, and physical therapy along with the use of newer antidepressants (as the analgesic of choice).

Surgical treatment, application of ice or assistive devices such as brace or cast aggravate the condition. The application of a cast is a high risk for the patient to develop cervicogenic Parkinsonian tremor (4).

The diagnostic and therapeutic difficulties in the thoracolumbar division are identical to the craniocervical division. The disc bulging and herniation due to paravertebral spasm secondary to RSD are more likely to confuse the diagnosis in the neuropathic pain and the spasm in the thorcolumbar region. Especially ladies who have had natural birth, the L5-S1 disc bulging is an incidental painless byproduct of the natural delivery.

The neuropathic referred pain from the lower extremity to the lumbar spine is mistaken for the problem of disc bulging and the patient undergoes unnecessary lumbar surgery with disastrous results.

RSD is not simply a reflection of a hyperactive sympathetic system, but a pathologic sympathetic system. Any operation in the distribution of the nerves involved with RSD results in flare-up of the disease and aggravation and spread of the RSD. The surgical procedures for disc bulging or herniation, and for relief of entrapment neuropathy, in RSD patients throw the patient from stage 1 or 2 into stages 3or 4 of RSD (stage 2 is the dystrophic stage, stage 3 is atrophic, and stage 4 is addition of complications such as stroke, heart attack, hypertension, suicidal attempts, and immune system dysfunction).

The dorsum of the hand, foot, knee, and elbow are the common sources of post traumatic RSD. Secondarily, the disease causes referred pain, spasm, and inflammation spreading to the paraspinal structures (fig. 7). The involvement of the paraspinal nerve and muscle results in muscle spasm, headache, back pain, dizziness, and movement disorder.

RSD commonly involves the extremities. However, the extremity involvement of RSD causes referred pain, spasm, and inflammatory changes in the paravertebral nerves and muscles (fig. 7). This has been mistaken for entrapment neuropathy (Table 4), or "myofascial syndrome". The pain in myofascial syndrome is truly a neuropathic and sympathetically driven pain (5) with a tendency for referred pain and inflammation in the trunk of the afferent nerves from the extremity to the paraspinal nerves and vice versa (5). Clinically, the areas of referred pain, nerve and triggerpoint irritation can easily be identified by careful examination of the paravertebral muscle and joints.

The "red spots" become apparent on application of pressure over the articular facets. The area of neuropathic referred pain shows the accumulation of substance P. The substance P which is an irritant is usually encapsulated and pressur on the area causes a release of the substance P. Massage therapy provides the same goals and eventual absorption of the dubstance P systemically. Application of paravertibral nerve blocks provides a longer lasting relief.

In SMP type of pain, pressure in these areas results in a reddish discoloration (fig 7). As the area of nerve and trigger point irritation is identified, this area should be treated with paravertebral nerve block with 4-5cc Lidocaine and 40-80mg Trimcinolone or Depo Medrol (3,1). This nerve block results in pain relief and improved circulation to the extremity lasting from a few weeks up to 2 months. In more acute patients, one set of treatment in usually enough to provide a successful nerve block and permanent pain relief.

The axial sympathetic dysfunction is far less common. In abdominal trauma and especially in post traumatic sympathic dysfunction secondary to repeated abdominal operations, the patient develops classical neuropathic pain which can be successfully blocked by coeliac ganglion block, combined paravertebral nerve blocks.

Approximately 1/3 of the patients with FAILED BACK SYNDROME suffer from neuropathic pain both referred to the extremity as well as in the paraspinal area. This is especially true if the patient has undergone the so-called esploration for conditions such as disc or nerve root contusion. In some patients a foraminotomy is done to release the pressure on the nerve root. These patients quite frequently suffer from severe neuropathic pain which has a strong sympathetic component to it (SMP). In such patients, the paravertebral nerve blocks as outlined above are quite helpful in alleviating the pain and counteracting the muscle spasm (which works as a vicious circle in aggravating the pain).

Axial sympathetic dysfunction in the thoracic area is quite rare. The usual forms are the intecostal diabetic neuropathy and malignancy involving the intercostal nerve roots. The patient does not develop the full blown picture of RSD. In such patients, systemic treatment with anti-viral medications (Zovirax) and sodium channel blockers (Carbamazepine, Phenytoin) or treatment with Neurontin may be helpful. Addition of newer antidepressants (Fluoxetin, or Trazodone) as analgesic of choice in the long run render the best relief. Tricyclics such as Elavil or Tofranil should be avoided due to their side effects of weight gain and aggravation of fatigue.

Multi-disciplinary treatment is the key to sucess:

1. Avoidance of ice application which aggravates the vasoconstriction and accelerates the sympathetic nerve damage. Moist heat and epsom salt are the treatments of choice.

2. Avoidance of braces, immobilization, application of casts Janovic has noted that 8 of 9 of the cervicogenic Parkinsonian tremors were among the patients that were treated with application of cast (4). The reason for avoidance of immobilization is the fact that immobilization deprives the spinal cord from the inhibitory effect of somatic proprioception on the intermediolateral horn cells with resultant aggravation of sympathetic dysfunction.

3. Nerve blocks: epidural, paravertebral, ganglionic, regional, and systemic such as the use of Clonidine patch or the use of oral alpha blockers ( Dibenzyline, Hytrin, Clonidine, or Yohimbine) (Table 1).

4. Avoidance of surgery, especially exploration of the area of nerve root contusion, exploration of the area of arachnoiditis, or exploration of entrapment neuropathies secondary to inflammation of RSD (avoidance of surgical procedures for carpal tunnel syndrone, tarsal tunnel syndrome, or "thoracic outlet syndrome").

5. Discontinuation of addicting narcotics and benzodiazepines, Non-addicting narcotics (which are not controlled substances) and newer antidepressants are the treatment of choice for chronic pain. The tricyclic antidrepressants should be avoided because they can cause obesity, inactivity, and fatigue.

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