The evolving field of functional neurology demands training and examination procedures that consider the neurologic health of neuron pools integral to stability and movement.

A colleague recently told me that she spent 90% of her time in veterinary school learning how to treat problems that are seen only 10% of the time. This was a doctor with many years of practice experience. What she was referring to was the emphasis placed on pathological problems, when most of what we see are functional problems. While a mastery of disease processes and pathology is important, there seems to be a lack of appreciation for functional issues, for tissues that are not functioning at optimal levels.

When an animal is injured or recovering from a neuromusculoskeletal condition, the first question before treatment should be, “Why did the injury happen?” To answer this question, a thorough understanding of the neurological systems involved in joint stabilization is necessary. Evolution has provided a means to stabilize joints against gravity and other vector forces. This creates a ballet of activity involving pools of neurons within the central nervous system. An understanding of those pools and their central integrative state explain, in the absence of direct trauma, why joints fail. These joints may be in the extremities or spinal structures, allowing damage to soft tissues and neurological structures.

To a large degree, the stability of a joint depends on the firing frequency of the muscle-tendon units that cross the joint. This frequency depends in turn on the firing frequency of the presynaptic pool of neurons. These are the alpha and gamma motor neurons living in the spinal ventral horn and motor nuclei of the brainstem. Further, the firing frequency of these neurons depends on the firing frequency of their integrative presynaptic pool. There are 10,000 to 12,000 pre-synaptic integers coming from spinal cord circuits and descending brain structures.¹ Some of these neurons are excitatory and some
inhibitory, all with different firing rates.

This is the motor ballet that keeps the animal safe and stable during his lifetime. Any aberrancy in one or more of these presynaptic pools increases the probability of injury. If, when rehabbing an animal, those pools of neurons are not evaluated and corrected, an increased probability of re-injury occurs. This also may be why, even with the best rehabilitative intervention, an animal fails to totally recover.

Evolution of a new frontier — functional neurology

The field of functional neurology has evolved as our understanding of neurophysiological processes grew. The explosion of research and knowledge surrounding these processes in the 1990s have made terms like “neuroplasticity” and “long-term potentiation” common in the national lexicon. Application of this knowledge in practice is an exciting and very practical new frontier in neurology and rehabilitation.

This article describes how the brain and the rest of the neurologic system, along with the synapses with muscles, affect movement and stability. This knowledge enables a trained practitioner to know where to most effectively manipulate the musculoskeletal system to return animals to normal function.

Motor ballet and joint stability

For efficient motor control of posture and volitional activity, we are looking for the most effective expression of motor output from ventral horn cells. In addition, the peripheral nervous system must be free to carry those messages to the muscles.

The ventral horn cells of the spinal cord and the brainstem motor neurons to the muscles of mastication and facial expression can be identified as alpha and gamma motor neurons. The alpha motor neurons provide the axons that excite muscles at the motor end plate. The gamma motor neurons dictate the sensitivity of the muscle spindle cells that share sensory information about the length and rate of change in muscle length to the central nervous system.^{1,3,4,5,6,7,8}

As mentioned earlier, the firing frequency of alpha and gamma motor neurons depends on the firing frequency of their integrated pre-synaptic pools of neurons coming from
a multitude of areas within the CNS, as well as incoming sensory data from sensory receptors.¹

The systems involved

A multitude of systems must coordinate for successful stability and movement. Cortically, there is a decision to move. This decision is shared with many areas of the nervous system even before the motor act begins. This sharing of information is known as efferent copy.^6,7 Some of these areas include the basal ganglia (nuclei), the cerebellum, and many structures in the brain stem.

The basal ganglion is a deep cortical organ that gates motor activity. It is a very complex structure but can be described simply as a “brake” to cortical output. Once a motor command is made the foot is taken off the brake for that specific activity.^{1,3,4,5,6,7,8}

The cerebellum can be thought of as a “comparer”. It receives sensory feedback about the actual performance of a motor act. It compares the desired outcome with the actual outcome. It then sends messages about the mismatch back to the cortex and other brain structures so that corrections can be made. In addition, the cerebellum creates neural networks within itself about the motor act. This eventually leads to learning the motor act so that the cerebellum can initiate future expression of the activity.^{1,3,4,5,6,7,8} This is an important aspect of learning new, novel motor programs, such as dressage movements for horses or the navigation of weave poles for agility dogs.

Within the brainstem are important regions and structures that contribute to motor activity of the head, eyes and body. A few are discussed here:

• The red nucleus is in the mesencephalon. Some of the output from the red nucleus will fire down the rubrospinal pathways to control mostly volitional flexor muscles. This pathway is highly developed in our animal patients.^{1,3,4,5,6,7,8}

• The vestibular nuclei are in the floor of the fourth ventricle in the medulla. They receive information regarding head position from the vestibular apparatus in the temporal bones. In addition, they receive information from the visual system, neck proprioceptors, and from the feet/paws/hooves. They also receive sensory data from proprioceptors located throughout the body. The vestibular nuclei are known as “neural integrators” as they are comparing different sources of sensory input. When a “sensory mismatch” occurs, clumsiness, dizziness and sometimes vertigo can take place.^{1,3,4,5,6,7,8} Dysautonomia is also a common result of sensory mismatch. The vestibular nuclei send their flow of information to numerous brain structures, including the cerebellum, the extra-ocular eye muscles, and to ventral horn cells responsible for posture and core muscle tone.^{1,3,4,5,6,7,8}

• Reticular neurons of the brainstem reticular formation also receive information from the cortex, basal nuclei, cerebellum and vestibular nuclei. They receive sensory data from all sensory systems but especially from those concerned with gravitational forces. The reticular system has broad influences on the nervous system, including brain arousal, pain inhibition and autonomic regulation. Our interest at this point is in its influence on postural muscles, mostly extensor, as it provides a foundation for volitional activity. This activity occurs through reticulo-spinal pathway influences, directly and indirectly, on ventral horn cells.^{1,3,4,5,6,7,8}

Reflexes

A reflex can be defined as an involuntary and nearly instantaneous movement in response to a stimulus. A reflex is hardwired. Animals are born with their reflexes intact. Examples include the “withdrawal reflex”, the “tonic stretch reflex” and the “crossed extensor reflex”. Reflexes are the simplest of neurological motor expressions. Although reflexes are simple in nature, their impact is profound. The tonic stretch reflex initiated by the muscle spindle
cell maintains an appropriate muscle tone in postural muscles as well as muscles involved in movement, preventing moments of instability and injury.

Central pattern generators (CPGS)

I describe CPGs as being like small computer chips with wiring commands for different stereotypical movements. Rather than the brain coordinating all movements via direct ventral horn modulation of the trunk and extremities, it delegates those responsibilities to packets of interneuronal pools. These pools or CPGs send commands to specific alpha and gamma motor neurons to orchestrate a particular stereotypical movement. We know that chewing, breathing and gaiting are all under the control of specific central pattern generators.^1-8

The hierarchy of motor control

I believe the evolutionary job of the brain is to be vigilant for survival. To that end, sensory systems monitor the external world and the body’s own internal environment. Integration of this incoming sensory information, and the filtering through the lens of past experience and memory, should lead to efficient output systems that serve and keep the body safe. These output systems go to the muscles and the autonomic nervous system (endocrine, enteric and immune systems). Our animal patients need to stand and move in response to a constantly changing demand for movement and postural stability against gravity. This activity must be supported with food and oxygen provided by the autonomic system. Although this article is essentially about joint stability, it must be recognized that the central nervous system must also simultaneously provide for the autonomic support of movement.

When considering the neurology of joint stability the two different motor systems must be considered – postural and volitional.

1. Postural control

We know that gravity was the most significant contributor to the evolution of the mammalian nervous system. To overcome the force of gravity, a neuromuscular system evolved that supported the animal, providing stability and a foundation for volitional movement.

Ventral horn cells to postural muscles receive pre-synaptic input primarily from descending reticulospinal and vestibulospinal pathways. These cells also receive input from muscle spindle cells, golgi tendon organs, joint mechanoreceptors and other proprioceptors in the muscle, or in the tissues surrounding the joints that the involved muscles support. Chiropractors and osteopaths describe dysafferentation syndromes in which faulty joint mechanics send aberrant sensory data into the central nervous system. This dysafferentation affects spinal cord circuitry and has suprasegmental consequences.³

In addition to supporting the animal against gravity, the postural control muscles are also intimately linked to stereotypical movements controlled by central pattern generators (CPG) and volitional activity from the sensorimotor cortices.

2. Volitional control

Volitional control of movement starts at the motor cortex. The cortex contains sensory and motor maps of our environment so that it is aware of where we are in space. It also contains body maps so it knows the relationship of one body part to another. The cortex
also integrates past experience and the consequences of a motor act.^{1,3,4,5,6,7,8}

“Neural representation” and “internal model” are terms used almost synonymously with “motor program”. Are large movements made up of stereotypical smaller movements? Do motor circuits such as central pattern generators make movement almost robotic? What effects do “hard-wired” reflexes have on movement? Probably all are involved in movement, with sensory feedback from the environment having a large impact on the modulation of ongoing movements. Changes in terrain, wind resistance, available light
and sound all alter motor acts while in process.

Volitional motor activity

It appears that volitional motor activity begins in the motor cortex, with flavoring from all other areas of the brain.

• The motor command leaves through the motor cortex, and cycles through the basal ganglion and thalamus before returning to the cortex. This circuitry primes specific neuronal pools in the motor cortex to refine a particular motor act or movement.

• As mentioned earlier, these signals travel to many different brain and spinal centers as efferent copies.

• The brainstem, receiving the motor command from the cortex, sends signals to postural muscles to provide the postural base of support for the motor act involving the extremities.

• Sensory signals from the environment are integrated into the somatomotor system, keeping the motor cortex abreast of constantly changing contexts of external conditions and moving body part data.

• Feedback from the cerebellum is a flow of information describing the differences of what was expected from the motor act as compared to what actually occurred. Thus the motor cortex can constantly fine tune its commands to elicit the most efficient muscle response to the motor commands.

• For novel motor acts as well as frequently used motor operations, neuroplastic strengthening of neuro-networks occur. Gene expression-driven feed-forward and feedback mechanisms build neurological networks that might be defined as new motor programs.

• It is believed that neuroplastic changes occur along the entire length of connections within all neuroanatomical areas participating in motor acts.

Methods of evaluation

To maximize our clinical approach to treatment, we need a methodology to access the different neurological mechanisms involved in normal movement and stability. Technology provides tools that can access information about the external expression of central and peripheral nervous system health, but do not allow direct access to those neurological systems directing the movement. Force plates, treadmills, electromyography, etc. are useful tools for evaluating normal from abnormal, and are certainly very valuable research tools. Imaging devices are helpful in localizing pathology but are not valuable for evaluating the functional health of different neuroanatomical areas involved in motor activity.²

Manual muscle testing as in applied kinesiology, in combination with history and neurological exam procedures, have proven to be very helpful in localizing the longitudinal level of pathological and functional lesions of the nervous system. Although limited in their application, these hands-on diagnostic tools can provide valuable localizing information about the status of neuron pools in specific parts of the nervous system.

It is important to approach each patient with the following goals and considerations:

• Diagnosing the longitudinal level of the physiological or pathological lesion should always be our primary goal. Without this information, our treatment will be arbitrary
with a lower probability of success.

• Our second serious consideration is whether the lesion is pathological or physiological (i.e. functional). We can greatly benefit animals with frank pathology, but we must also keep in mind that changes in motor activity can be secondary to aberrancies in the firing frequency of pools of neurons.

• Once we have addressed the above two aims, we can proceed with integrative therapies that address those pools of neurons.

• Prescribed owner-administered therapy, rehabilitation therapy and other modalities will now be more effective as they are directed more specifically to the affected neuromuscular anatomy.

Conclusion

Animals presenting for veterinary care deserve the best “state of the art” acute care and rehabilitation. In addition, the veterinary neurological exam and applied kinesiology may be used as tools to evaluate functional lesions of the central and peripheral nervous system. These are pools of neurons that are not functioning properly due to injury or a loss of a pre-synaptic frequency of firing. This demands a different kind of training and examination procedures that consider the neurologic health of neuron pools integral to stability and movement. This is the evolving field of functional neurology.

References

¹Hall, J. E. 1. (2016). Guyton and Hall textbook of medical physiology (13th edition.). Philadelphia,
PA: Elsevier.
²Back W, Clayton HM. Equine Locomotion, W.B. Saunders. 2001.
³Beck RW. Functional Neurology for Practitioners of Manual Therapy, Churchill-Livingstone, 2008.
⁴Binder MD, ed. “Peripheral and Spinal Mechanisms in the Neural Control of Movement”. Progress in
Brain Research, Vol.123; Elselvier, 1999.
⁵Haines DE, ed. Fundamental Neuroscience for Basic and Clinical Applications, 3rd edition Churchill-
Livingstone, 2006.
⁶Kandel ER, Schwartz JH, Jessell TM, Siegelbaum SA, Hudspeth AJ. Principles of Neural Science, 5th
edition, McGraw-Hill. 2013.
⁷Latash ML, Zatsiorsky VM. Biomechanics and Motor Control. Elselvier, 2016.
⁸Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia A, McNamara JO, Williams SM. Neuroscience, Sinauer Associates. 2004.
Henneman, K., Recognizing Soft Tissue Injuries in the Dog from and Integrative Perspective, Part 1,
Innovative Veterinary Care, vol.8, Issue 4, 2018.