THE REFLEX: MODULE 6

Dr. Kathleen Power, DC, DACNB

USF Course

Date of class: 02-96

A reflex is a pathway of synaptic connections which is shared by all humans. It is a phylogenetically determined maintained functional relationship which is stored in the DNA of the species. Although the relationship is maintained, 99.9% of all reflexogenic activity will never be visualized. The reflex system is segmentally presented in humans, but it is under suprasegmental control. Reflexogenic activity involves a wide range of nonvolitional activity and as such is not limited to muscle contraction; salivation, tearing, emotional responses and other physiologic events are associated with reflexogenic activities.The reflex pathways are pathways of neurons with specific synaptic connections, but the probability of summation and the presentation of any reflex depends upon the central integrated state (CIS) of the neurons in the canalized pathway as well as the frequencies of firing (FOF) and CIS of neurons in all presynaptic pools. To be clinically useful, reflexes need to involve large pools of neurons. These neurons in the reflex pathway therefore must haveaxon collaterals that would evoke synaptic activity at multiple postsynaptic neurons associated with a similar segmental function. They also have collaterals which synapse on pools of neurons which are associated with other functions, some segmental and some suprasegmental. Afferent neurons of reflexogenic pathways have collaterals which synapse on second order neurons in homologouspools (briefly discussed below) and these second order neurons synapse with increasing divergence on third order homologous neuronal pools, etc. Divergence in the system allows that the least amount of environmental stimulus will produce the greatest effect on the neuraxis. Also, the greater the activity of the pathway, the greater the plasticity of the pathway, so increased activity of first order neurons will produce increased plasticity of higher order pools.

 PICTURE

Refer to texts and class notes for schematic representation of divergence and convergence.

Comments: Because of this activity a greater frequency of firing of an afferent limb of the reflex arc will have a wider distribution and greater suprasegmental effect than one with less activity. The function of reflexogenic activity is to promote survivability. This is effected in part by facilitating plasticity and wind-up via divergence and convergence. We will also see that it allows for fuel delivery to be specifically directed by tissue need in a normally functioning neuraxis. It provides for the rapid removal of the individual from danger via the withdrawal reflex. It also helps to promote viability in neurons and target tissues allowing active inhibition of specific neuronal pools until such time that the inhibition needs to be itself inhibited.

 PICTURE

Refer to texts and class notes for pictures of a monosynaptic reflex arc between a Ia afferent and an alpha motor neuron.

Comments: The pathway is actually much more complex as it involves divergent and convergent synaptic connections, collaterals to many other pathways in addition to the alpha motor neuron, and modulating activity from higher structures and other segmental areas.

A simple reflex may be defined as a maintained pathway A to B such that A is the only input to B and the function B is a window of the FOF of A or the integrity of A and/or B. Simple reflexes do not exist in humans because the Ia afferent pathways involved in much of the reflex activity have multiple collaterals, only one of which is to the ventral horn cell. Our neuronal circuitry is such that these primary neurons fire through polysynaptic pathways to the brain which in turn exerts modulatory activity on the second order neurons in the pathways to affect the output of the system. For example, the brain may allow increased or decreased summation of reflexogenic activity by modulating spindle receptor potential or interneuronal synaptic activity involved with the reflex.

PICTURE

Refer to texts and class notes for cross sectional and longitudinal pictures of the spinal cord showing a Ia afferent entering the dorsal horn and its major collaterals at segmental and suprasegmental levels.

Comments:

The Ia afferent has numerous collaterals which synapse at segmental and suprasegmental areas. Each first synapse is monosynaptic and it is always excitatory. There are segmental and suprasegmental features of reflexogenic activity. First, we will look at the segmental reflexogenic activity associated with Ia afferent activity.

When a primary afferent enters the cord, it has collaterals which:

end monosynaptically on the alpha motor neuron of the muscle of which it is located to excite it;

end monosynaptically on alpha motor neurons of muscles which are synergistic to the muscle in which it is located, and of muscles in the same compartment to excite them (these normally do not summate due to inhibitory influences);

end monosynaptically at the IML (the primary neurons of the autonomic system), the IMM (the second order neurons of the decussating ventral spinocerebellar tract), and the IMI (an internuncial pool involved with many reflexogenic pathways) to excite them;

end at an interneuron on the ipsilateral side which inhibits the antagonist of the muscle which was stretched;

end at interneurons on the ipsilateral side which inhibits the alpha motor neurons of the muscles synergistic to the antagonist and the muscles of that compartment;

end at an interneuron on the contralateral side which inhibits its contralateral homologue and its synergists;

end at an interneuron on the contralateral side which excites the antagonist to the contralateral homologue and its synergists;

ends at interneurons which ascend or descend to have the opposite effects on the other extremity (the upper extremity effects are opposite to the lower extremity effects in a crossed type of pattern);

ascends in the dorsal column to synapse and decussate at the cervicomedullary junction to ascend to higher structures;

ascend in the ipsilateral dorsal spinocerebellar tract to end in the ipsilateral cerebellum;

end at the apical internuncial pool to excite an interneuron which presynaptically inhibits ascending nociceptive pathways; and

end at an interneuronal pool which presynaptically inhibits all other afferent pathways. When a Ib afferent from a golgi tendon organ enters the cord, it has the following major collaterals which:

end monosynaptically on an interneuron which inhibits the alpha motor neuron of the muscle in which it is located;

end monosynaptically at the IML to excite it;

end at an interneuron on the ipsilateral side which excite its antagonist;

end at an interneuron on the contralateral side which excites its contralateral homologue; and

end at an interneuron on the contralateral side which inhibits the antagonist to the contralateral homologue. When type II joint mechanoreceptors fire as a result of compression of joint structures, it has major collaterals which:

end at an interneuronal pool which presynaptically inhibits all other afferent pathways;

ends at the IML; and

ascend to synapse with higher order projections which summate at the contralateral cortex. All primary afferent neurons are monosynaptically excitatory to their postsynaptic neurons. All primary afferent neurons are monosynaptically excitatory to the IML. All primary afferent neurons are monosynaptically excitatory to interneurons which inhibit all other primary afferent pathways.

In addition to afferent input into the reflex system, there are modulating controls from suprasegmental structures. The contralateral paleocortex and mesencephalon send an excitatory barrage into motor neuronal pools, and also send inhibitory barrages to gate the excitation and promote smoothness of movement.

The ipsilateral neocortex inhibits the inhibition to allow function; this will be discussed in detail below. It is clinically useful to measure as many postsynaptic neuronal pools as possible to ascertain the meaning of information elicited during testing of a reflex. That is to say, tapping a tendon will give information, but that information will be useful only when compared to segmental IML effects, other segmental activities, etc. Because of the monosynaptic excitation of the IML, the segmental autonomic concomitants are often an excellent window to the interpretation of reflex function, to help localize where the lesion is, to dictate whether a "normal" reflex is normal or is merely compensated through other pathways. As discussed in prior modules, the function of the nervous system is to promote survivability by mediating its own fuel delivery and its own activation. To this end, the cortex must be greedy, creating activation of postsynaptic pools which, by their excitation or inhibition, subserve this end. In other words, the brain increases excitation of those synaptic activities which are needed for brain function.

Three primary functional activities by ipsilateral neocortex to effect its survivability are:

it actively inhibits inhibition to the ipsilateral alpha and gamma motor pools;

it actively inhibits the IML; and

it actively inhibits the ipsilateral anterior compartment muscles above T6 and post compartment below T6. Motor neurons must be actively inhibited to maintain viability in the absence of movement and to allow smoothness of movement when it does occur. Primary activation from the contralateral paleocortex is so excitatory that it must be inhibited. The inhibition occurs as a result of mesencephalic reticular activation of inhibitory interneurons (to be elaborated in future modules). The effects are seen in the integration of the alpha and gamma motor neuronal pools. At the time of volitional and reflexogenic activation, it is the ipsilateral neocortex which inhibits the inhibition and allows the motor neuronal pool an increased probability of summation.

These are functional, not anatomical, pathways. All neocortical activity is monosynaptically excitatory, so that when the neocortex inhibits function such as that of the IML or the inhibitory neurons to the alpha motor neuronal pool, it must do so through excitation of inhibitory interneurons.

We recall that the FOF of the cortex is dictated by the FOF of its presynaptic integrated neuronal pool. This is primarily dependent on the FOF of the Ia afferent pathways which respond to the amplitude of receptor potential in the earth's gravitational field, which the neocortex modulates via excitation of the gamma motor neuronal pool. The gamma motor neurons supply contractile proteins at the polar ends of the muscle spindle receptor and their contraction dictates the amount of distortion, preload, or gain of the spindle cell.

Let us review the anatomy and function of muscle spindle receptor in order to appreciate the cortical modulation of reflexogenic activity.

 PICTURE

Refer to tests and module 2 notes for a diagram of the muscle spindle receptor.

Comments:

The spindle receptor is the most complex receptor in the body. It is the only receptor (with one exception we will learn later) which has both an afferent and an efferent supply, the latter being modulated by neocortical function. The primary endings of the spindle fire through Ia afferents, the largest and fastest fibers of the nervous system.

 The spindle receptors fire through Ia afferents and the golgi tendon organs fire through 1b afferents. When a muscle is stretched the Ia afferents fire more than 1b afferents, unless that stretch is greater than the ability of the contractile elements to resist that stretch. When the muscle is contracted volitionally, the alpha and gamma motor neurons both fire. The gamma motor neurons allow the spindles to "keep pace" with the extrafusal fibers, allowing the higher motor centers to "know" the degree of tension in the muscle. There is a point when the increased tension allows the golgi tendon organ to reach threshold and fire, inhibiting the muscle.

The speed of a stretch dictates the probability of the contractile elements of stretched muscle being able to interdigitate and bond. In an individual with a high functioning cortex, a stretch will create stability of the system because the monosynaptic excitation of the alpha motor neuron of the stretched muscle promotes contraction. A slower stretch in a normal system allows more interdigitation of muscle contractile proteins at their binding sites and produces a greater probability of binding and contraction, whereas a faster stretch would allow a lesser probability.

When neocortical function is decreased, there is reduced inhibition of inhibition and therefore inhibition is allowed to occur. This reduces summation in the gamma motor neuronal pool, reducing its probability of firing and therefore increasing the probability that the spindle will be offloaded. As a consequence, more environmental stimulation is required to promote the probability of summation, such as a greater stretch or an increased force applied to a tendon during testing of the reflex. The Ia is less likely to summate at all of its ostsynaptic neuronal pools, including the alpha motor neuron. The alpha motor neuron moves farther from its excitation threshold as a result of the active inhibition from contralateral mesencephalic pathways as well as other segmental inhibitory pathways. The neuron, in other words, remains healthy, but because it does not summate, its postsynaptic cell (the muscle cell) suffers the consequences of decreased activation, which are the same as any other cell.

When muscle fibers suffer reduced protein replication as a result of the ventral horn cell shifting away from excitation threshold, there is less contractile protein. When the muscle is subsequently loaded by a force -- even a small one -- there is an increased probability that the load will not be resisted by the contractile elements and will be shifted to the series elastic element of the tendon. Normally, the muscle fibers should take 80% of the load of muscle activity and the tendons should take 20%, but when there is less protein there is greater vulnerability of tendons to inflammatory overuse syndromes, and joint structures to breakdown, as there is less contractile protein to resist stretch. This is a situation which may be brought about by disuse, by ipsilateral neocortical loss, contralateral paleocortical loss, excessive loading, etc., or any combination.

In summary, understanding the breadth of reflexogenic activity means understanding all aspects of integration: divergence and convergence, excitation and inhibition, summation and failure to summate, monosynaptic and polysynaptic pathways, segmental and suprasegmental influences, ipsilateral and contralateral controls. The "monosynaptic reflex" is in reality very complex; the Ia afferents have many collaterals and the ventral horn cells have a large presynaptic pool. Reflexogenic activity is due to the existence of the canalized pathways, but it is dictated by the frequency of activation of all of the associated neuronal pools and their states of integration. Most reflexogenic activity will never be perceived but it is required for survivability of the system. Inhibitory activity keeps neuronal pools viable and healthy, but it needs to be inhibited at appropriate times.

DEPTH

The chiropractor must first become fluent with the breadth of information on reflexogenic activity. Then he or she must perform an examination of each patient and interpret all observations in the context of the integration of the entire neuraxis rather than of the symptomatic segmental or regional areas. This is especially important when studying the reflexes because normal function of an end organ does not guarantee that the presynaptic pools were at appropriate integrated states. The chiropractor must ascertain the function of the neurons in the canalized pathways as well as the sum of suprasegmental excitatory or inhibitory effects that are acting upon the pathways -- the CIS of the presynaptic integrated pools. A reflex is not simple, but observing its activity yields clinically useful information when compared and contrasted to the functions of all other parts of the neuraxis.The chiropractor needs to know the segmental presentations of the reflexes such as the stretch and superficial reflexes and the anatomical locations of various synaptic relationships so that the examination may proceed with knowledge of possible areas of ablation as well as aberrant function. The chiropractor needs to know the locations of neuronal pools, where they synapse, where they decussate, etc. He or she needs to know the divergent and convergent pathways of reflexogenic activity so that observed function may be considered an end product of a olysynaptic system.

Some windows are more specific to localizing functional aberrancies and these include segmental and suprasegmental autonomic concomitants and summative effects of nonconstant sensory modalities. The chiropractor needs to appreciate the specific reflexogenic pathways associated with the stability of the vertebral column. That is, the intrinsic muscles on one side of the vertebral column are antagonistic to those on the other side. Activation of Ia afferent pathways of one side will promote contraction of the muscles if the postsynaptic pools are brought to summation. Failure of summation in Ia afferent pathways will allow a greater stretch to be caused on one side which will cause compression on the contralateral side; this compression activates type II pathways which decussate to the contralateral neocortex to increase the probability of descending inhibition of inhibition, reducing the compression by increasing contralateral contraction. These pathways subserve vertebral stability (when they are allowed to summate), but are phasic and do not contribute to plasticity in higher centers. The descending pathways to the intrinsic muscles of the vertebral column will be discussed in more detail in future modules, but the chiropractor needs to know that, while they are bilateral, their summation is dictated by ipsilateral neocortical activation. Unstable vertebral motion as a result of reflexogenic activity through pathways which are not summating will allow joint damage to occur, because joint structures will not be sufficiently protected from stretch by appropriate contraction. This type of damage is seen in all chiropractic offices. The chiropractor needs to know the condition of the structures and the integration of the pathways before giving an adjustment. The chiropractor then must develop skills in eliciting the reflex, because proper testing of available reflex activity will assist in locating lesions and planning therapy. Because the activity of pathways associated with nonconstant modalities is dictated by the activity of pathways associated with the constant modality, excellent windows of Ia afferent firing are seen in the activity of nonconstant modalities -- vision, smell, hearing, etc. The chiropractor needs to evoke potentials of these pathways by using graded stimuli and determining the integration of the neuronal pools by observing their ability to summate, their speed of summation and their fatiguability. Then the chiropractor must be able to interpret the response in the context of the integration of all measurable neuronal pools in the individual, realizing that any single observation will have different interpretations according tothe totality of findings in an ideographic examination. A given cell has three possible states of integration: at or above threshold (depolarized), close to threshold but below it, and further from threshold (hyperpolarized). Testing a reflex will allow observation of whether or not a response occurs, the amount of stimulation required to evoke the response, and how quickly the response fatigues (if it does). Some reflexes should be seen and some reflexes should usually not be seen. These latter are maintained in canalized pathways, but the pathways do not summate as a result of inhibition from other pathways. Some reflexes appear in neonates and disappear as cortical development takes place (the upgoing toe, for example), but they reappear following trauma or cortical damage.

Testing should involve the application of stimuli in a graded manner, tapping lightly on a tendon or applying a little light or sound, etc. If function is not elicited, then an increase in stimuli or the recruitment of homologous neurons (clench the fists, bite down, etc.) may allow summation. If function appears with very little stimulus, then it must be determined if this is due to metabolic activity with lots of protein and energy substrate or transneural degeneration with little protein and energy substrate. A reflex may thus be increased without fatigue, increased with fatigue, intact, decreased or absent. It must be compared to reflexes tested in the same segmental level, the same compartment, the same side of the body, etc. A reflex which may appear to be intact may be in a pathway A to B to C, where the function C appears intact, but B is down; perhaps another pathway D integrating into C and may increase its function to make it appear the same as A to B to C. This may confuse a clinician who does not perform a rostral to caudal examination. For example, when a reflex does not appear it does not necessarily mean there is a segmental or peripheral ablation as many of us have been taught. There could be ablation in the pathway such as compression axonopathy (which often occurs as a consequence of aberrant suprasegmental modulation as discussed in module 3) but there could also be a hyperpolarization of the neurons which reduces the probability of summation. The chiropractor needs to be able to differentiate these possibilities. In a compression axonopathy an absent reflex would be associated with motor loss as evidenced by atrophy and fibrillation or fasciculation. Other large diameter fiber loss would also occur, but this might be more difficult to observe since the sensory system is multimodally integrated and the patient may not perceive the loss. The chiropractor would, therefore, need to develop clinical skills to examine motor as well as sensory function in graded ways and be able to interpret the significance of these observations and also to exactly locate the compression. He or she might require additional electrodiagnostic modalities to monitor neuronal damage and the extent of regeneration. The greatest loss of motor reflexogenic activity is from ipsilateral neocortical loss of inhibition to the inhibitory centers of motor activity. If I fire my left paleocortex to move my right arm, the left neocortex also fires (areas of the cortex are homologous to each other) to change the gain on the spindle receptors of the left side which increases stability for movement of the right arm as well as increasing feedback to the right cortex to inhibit inhibition of the right side, allowing the right arm to work. This also allows for segmental summation of IML activity to provide fuel to the right arm muscles while inhibiting movement of excess fuel into other areas. Decreased neocortical activation can result in an actively hyperpolarized but stable neuronal pool with a loss of reflexes, but associated with global activation of the IML with its concomitant clinical presentations. Increased reflexogenic activity must also be appreciated in light of a complete examination. The target or end organ may be close to the sodium equilibrium potential as a result of metabolic disturbance (hypocalcemia, high pH, low O2, etc.), decreased activation or fuel supply, or similar conditions in presynaptic pools. Or perhaps it is close to threshold as a result of loss of inhibition such as ablation in pathways which are normally inhibitory (such as loss of antagonist function) or aberrancies in pathways which usually gate excitation (such as dysfunction in basal ganglionic loops). Only a full examination will provide the information to differentiate between the many possible etiologies. But the chiropractor must realize that "hyperreflexia" is not synonymous with upper motor neuron disease or damage, as we were taught in school. Neurologic examination is a skill which must be practiced. Its subtleties will be presented in a future module. The examination consists of observing target organ function, evoking changes in the environment, and again observing function in the patient. Here is a partial list of observations which may be made during an examination:

 PICTURE

Refer to class notes for drawing of a "generic" patient, so that a list reflexes can be placed in a rostral to caudal order.

1. Look at the top of the head, the scalp. One may observe aberrancies or attempt to evoke acapillary reaction, sweating, etc.

2. Look at the eyes and face.

a. Observe for ptosis of the lid and lid lag.

b. Observe the size and circumference of pupil and iris.

c. Apply light and look for the consensual reflex.

d. Look at the ophthalmic veins for ballottement,equality right and left.

3. Observe the general health of the skin, color, moisture,and inquire about healing time. Apply cutaneous stimulation to elicit capillary response, histamine reactions, etc.

4. Apply touch modalities such as pinwheel or tuning fork, comparing sides, and look for a withdrawal response.

5. Look at posture, for head tilt, angulations, TMJ deviation.

6. Check stretch and superficial reflexes, muscle tone and strength.

7. Examine the distal vascular system via the effects on nail beds, capillaries, temperature, etc.

8. Examine other functions of IML as we have described in the past.

Reflexogenic activity is an important part of the chiropractic examination. It is also important in determining the lesion and planning the therapy. The chiropractor must always be aware that the only constant environmental modality is gravity. As "change agents", chiropractors apply forces and evoke potentials to the body in such a way to effect permanent change by allowing a different response of the receptors from gravitational stresses. This then allows summation to increase in higher order neuronal structures and wind-up and plasticity may result, providing the metabolic activities of the involved pools will be accompanied with sufficient fuel delivery that the functions may be maintained. The chiropractor needs to have a full appreciation of the importance of assessing the state of integration of all neuronal pools for planning appropriate therapy. In earlier modules, we were introduced to the concept that to increase FOF of the cortex on one side we would possibly need to fire the contralateral cerebellum through activation of the spindle cells ipsilateral to the cerebellum, but not to exceed the metabolic rate of the postsynaptic integrated neuronal pools. Sometimes, the safest therapy for the patient may be to first stimulate pools which are functioning better and indirectly increase the firing of the decreased pools. Only a proper examination will dictate the best therapy.

If the cortex is not firing appropriately, then slow stretch of a muscle with decreased protein can produce 1b inhibition because the tendon has a greater probability of being loaded; a person's knee may give way as they are walking because the tendon was easily loaded, or an adjustment to an unprotected joint structure may inflict damage. A fast stretch, on the other hand, in a different individual with lots of contractile protein may allow the monosynaptic excitation of the muscle if the Ia fires higher thanthe 1b and so the adjustment needs to include activities which facilitate loading the tendon. The chiropractor needs to understand what the individual has in order to understand what the individual needs. Knowledge of the integrated state of neuronal pools and muscles is necessary to determining the manipulative and rehabilitative techniques best suited for the individual at any given time. The important depth of information on the reflex for the chiropractor is to evoke the potential and determine what it means by placing it in context of the entire examination. An increased reflex or a decreased reflex needs to be properly interpreted. The interneuronal pools involved in reflexogenic pathways have many presynaptic influences and their integration is often the most significant factor in the appearance and function of a reflex. The chiropractor will use the observations made during a complete examination to diagnose the lesion and determine the best treatment methodology for correction of the lesion, and then he or she may monitor reflexogenic activity as one window of efficacy of treatment when placed in context with all concomitants.

Reflexes are not simple. Human activity exists as a consequence of complexity and therefore there are many variables which need to be observed in the chiropractic examination. No two patients with the same symptomatology will have the same exact lesion or the same response to treatment and the treatment must be perfectly tailor-made to the individual's central state to prevent iatrogenesis and to maximize efficacy. The use of descending influences to reflexogenic pathways must be accomplished first to assure summation prior to treatment with cord reflexes. Any change in reflexogenic activity as a consequence of a chiropractic application also needs to be interpreted in light of the change of all aspects of neurologic function, especially autonomic and vital function as well as summation in pathways of nonconstant modalities.

APPLICATION

This is the case of a 32 year old female piano player, tuner and repair person, who stated that she fell and hit her head. She said that since that time she has experienced a number of symptoms. She said she has had problems using her arms; she gets tingling feelings in her hands and they cramp easily. She said she gets headaches, she can't think, and she gets tired easily. She has insomnia. She complained of spots before her eyes; she described the spots as "lines that go up and down", fortification spectra. She said she gets dizzy, but without a sensation of spinning. She said that her vision gets blurry. She denied numbness around her mouth or face. She said that her ears plug up at times as if she were in an airplane. She also described heaviness in her legs, and pain in her mid-scapular, upper thoracic and post cervical areas. An important part of taking a history is to begin to think of possible areas of the neuraxis which could have lesions that explain the symptoms and signs. The fatiguability could be related to a global disturbance, or perhaps an axonopathy with its segmental and suprasegmental effects; a brain lesion, a segmental lesion, or a compartment lesion could all possibly explain these effects. So we have to have an understanding of the interrelationships of the parts of the nervous system. Is the end organ beginning to fail and why is that? And what are the suprasegmental consequences of that? The spots before her eyes are related to possible focal anoxia, a posterior sympathetic migraine disorder, or floaters. Her dizziness needs to be differentiated between a cerebellar/labyrinthine type dizziness, which would give her a sensation of spinning, or a cerebral anoxia as an autonomicconcomitant, which would be a light-headed sensation, or both.

The extreme tiredness means that her metabolic rate exceeds the ability of her system to deliver fuel to the areas ofincreased metabolic activity. She could become tired if she has lost the ability of her IML to segmentally deliver fuel; that is, fuel delivery would be globally increased and not shunted preferentially to working tissues, as seen in cortical lesions. The blurry vision is usually due to an increase in the diameter of the pupil. People never get blurry with increased mesencephalic activity or a smaller pupil, but do get blurrywhen the pupils are dilated and they cannot focus the light rays, possibly from increased IML activity or mesencephalic failure.

The eyes were examined for their response to light. The vessels of the fundus were observed and compared for their diameter. The oral cavity was examined and a left palatal paresis was noted. As we examine the patient, we also begin to look at levels of lesion which could explain the findings. For example, a left palatal paresis could be as a consequence of a lesion in the brainstem, the vagal nucleus or pathway, the left glossopharyngeal nucleus, the jugular foramen, the vasculature to the brainstem, etc. We must be concerned because the left palatal paresis and the posterior fortification spectra from the same side of the cortex suggest a possible ischemia or infarct to parts of the brainstem or parts of the motor neuronal pool. With left palatal paresis, we can feel more secure because her palatal paresis is on the same side as her extremity symptoms, suggesting that the problem is one of descending modulation. This explains the autonomic concomitants on the side of pain. During examination of the auditory canal, the patient was asked to do a valsalva maneuver to increase pressure in her eustachian tube; her tympanic membranes failed to bulge out. Sensation was examined with a tuning fork and a pinwheel. She had increased pinwheel sensation and vibratory sensation in the hand on the right as compared to the left. The only two places where a lesion could be located, given these signs, would be above the cervicomedullary junction after both sensory pathways have decussated or an ablative lesion at the peripheral nerve; the former would more likely present symptoms such as palatal paresis on the right side whereas the latter would be associated with peripheral motor loss. The left palatal paresis makes a left cortical involvement more probable, associated with a compartment syndrome as a result of pyramidal paresis. The tuning fork was then applied to the elbows where it was perceived as equal. The area of compression was determined to be at the left carpal tunnel. A tap over the left flexor retinaculum evoked her symptoms. She showed percussion myotonia on the left. Her abductor pollicis brevis was atrophied. Examination of the peripheral vessels showed larger veins on the left. The pulse on her left side was thready, confirming autonomic disturbance. A carpal tunnel axonopathy can produce nociception perceived by the brain to be in the sclerotome. This means that she has been treated in the wrong area, in the area of pain, not the level of the lesion. The deep tendon (actually stretch) reflexes were tested. The biceps reflex was noted to be decreased on the right as a consequence of active inhibition from the increased biceps activity on the left. The increased biceps reflex on the left was increased as a consequence of loss of inhibition of inhibition of anterior musculature of left side above the level of T6. The chest was auscultated and showed a friction rub from ribs not moving. The use of accessory muscles such as the SCM during respiration was observed. Doorbell signs were elicited in her cervical spine. Palpation of her ribs was performed. She was asked about her use of a seatbelt during the automobile accident todifferentiate trauma from pyramidal paresis. While she was standing she was examined while her eyes were closed for her ability to touch her fingers to her nose; she had more difficulty on her right side. She was asked to "play the piano" and open and close her hands above her head rapidly, and fatiguability was observed. Her hands were palpated for temperature change following these activities. Her abdomen was auscultated for vagal activity and determined to be poor by the excessive amount of gas as well as her description of symptoms. Her lower extremities were tested for plantar and withdrawal reflexes, toe extensor strength, and straight leg raising. She had increased resistance to stretch on the left lower posterior muscles.

She has a lesion of the right cerebellum and the left neocortex, the latter associated with pyramidal paresis and an ablative lesion of the median nerve at the left carpal tunnel. She has increased activity of her left anterior compartment and decreased activity of her left posterior compartment. Her median nerve is closer to the flexor retinaculum. She has active fibrillation potentials in median innervated muscles. She has increased FOF of her IML. She's fatiguing. She's dyspraxic. She has an autonomic concomitant that is affectingthe calcarine area of her occipital lobe such that she is developing right sided fortification spectra associated withthe left side of her brain.

The treatment needs to promote survivability. It needs to increase the frequency of firing of the neuronal pools which are decreased at a rate not to exceed the metabolic rate. It needs to increase fuel delivery to the working tissues. It needs to prevent iatrogenesis by decompressing the carpal tunnel. Specifically it needs to increase the firing of the left neocortex, decrease thefiring of the IML on the left, and increase O2 delivery. It needs to provide appropriate rehabilitation to restore function to the muscles which have lost function. Her condition needs to be monitored and the program changed as determined by her progress orlack of it.

Her ribs and clavicle will be adjusted to restore appropriate O2 delivery; this will be monitored by listening for reduction in the friction rub. The carpal tunnel will be decompressed via an adjustment of the left hand and elbow with fast stretch modality in the left anterior compartment and slow stretch in the left posterior compartment. This will be monitored by re-examination for decrease in the percussion myotonia. The patient will be instructed to wear a cock-up splint at night. She will be instructed to exercise by performing protected and limited ROM activity but to visualize full ROM with the splint on.

This will create the maximum tissue response with the least tissue distortion. The cervical spine will be adjusted via coupled anipulative reduction. The left lower extremity will be adjusted to reduce resistance to stretch. We may want to actively decrease the left cortex to decrease the probability of exceeding threshold in the area of transneural degeneration. This can be done by plugging the ear or putting on blinders to decrease bombardment of Ia afferents into areas of transneural degeneration until we can evoke stability. We are unable in the beginning to fire the left cortex through direct cerebellothalamocortical pathways because of transneural degeneration, evidenced by her syncopal symptomatology. Increasing the frequency of firing of the right cortex will help the right cerebellum to fire the left cortex at a lesser, safer rate, through polysynaptic pathways. This will be done with:

a. providing left visual stimulation with mesencephalic eye fields, and using appropriate eye muscle exercises to stimulate the right cortex;

b. plugging the right ear;

c. decreasing anterior compartment activity and increasing posterior compartment activity volitionally to increase right brain by visualizing ROM of the wrist while it's in a splint to protect the joint and limit the actual ROM and/or watching someone else do it;

d. using left toe dorsiflexion exercises; and

e. fitting her for an orthotic device to promote increased Ia stretch to left anterior lower compartment muscles. These pathways will be used until her metabolic rate changes and she is able to tolerate more direct stimulation to the left cortex.

Following the adjustment, the percussion myotonia was decreased and the reflexes returned to 2+ and brisk. For the follow-up, I cannot state the prognosis due to lack of experience in cases such as this one. She will be constantly monitored for autonomic concomitants and other clinical signs and her treatment parameters will be changed as needed.