Chapter 95Osteopathic Treatment of the Axial Skeleton of the Horse
Osteopathy originated in the United States with a Kansas physician, Andrew Taylor Still. He envisaged a system of healing that placed emphasis on the structural integrity of the body as being vital to the well-being of the organism. As knowledge of physiology and anatomy advanced, a concept evolved of the nervous system as an information network constantly changing and adapting in response to sensory information from the body and the environment. This knowledge allows a move away from the idea of pathological dysfunction as the only cause of illness to a concept of physiological (or somatic) dysfunction.1 To use a computer analogy, the body may suffer from software failure (physiological malfunction) and hardware failure (pathological malfunction). To extend the analogy, osteopathy may be thought of as a form of reprogramming.
Chiropractic treatment evolved at around the same time as osteopathy and is similar but subtly different. The differences are largely philosophical; both forms of treatment rely on mobilization of joints. Chiropractors in equine practice tend to look primarily for positional changes associated with skeletal dysfunction. Treatment is directed principally at restoring joint mobility, with manipulation directed to the local site of dysfunction.
The osteopathic approach considers local tissue dysfunction as the direct result of trauma or the breakdown of compensatory mechanisms consequent to past trauma. The diagnostic approach is based on identifying patterns of dysfunction, with minimal reliance on positional factors and emphasis on the interactions of the entire spine. Treatment is aimed not only at restoring local function but also at identifying and removing factors that predispose to acute relapse. Therefore treatment frequently involves tissues distant to the perceived area of local dysfunction.
It is not uncommon in clinical practice to encounter horses that exhibit musculoskeletal signs for which no pathological cause can be established. The osteopathic philosophy accommodates these horses with the concept of somatic dysfunction. This concept is fundamental to osteopathy and describes a disturbance in the neurological networks that affects the function of the body (software failure). In other words, somewhere in the course of entering information from the environment and body, processing the information in the central nervous system, and then generating a motor response, something has gone wrong. Clinically this presents as a horse with signs such as stiffness, loss of performance, poor coordination, or gait abnormality for which no pathological process can be identified. Osteopathic treatment is directed at changing the signals to the neural network to modify the way sensory information is processed and thus to correct the motor response generated in the central nervous system.
To explore this concept, it is necessary to appreciate aspects of neurological activity not only under normal circumstances and as part of the protective response to injury, but also when long-term and inappropriate changes occur that adversely affect function of the body.
The peripheral sensory system has two categories of neurons that provide information to the central nervous system. The division is made based on fiber size. The fast, low-threshold large fibers carry the sensation of touch and proprioception, and the high-threshold small fiber system (C and Aδ fibers) conveys potentially painful nociceptive and temperature modalities. In the spinal cord, these neurons synapse on interneurons where the first stage in information processing occurs. How the signals from the periphery are modified and sent onward to cortical areas for interpretation relies in part on the balance between large fiber input and small fiber nociceptor activity. This balance forms the basis of the pain gate theory where small fiber input, which may potentially be decoded as pain, can be held in check by large fiber activity. Under normal circumstances, much of the nociceptive input is screened out at the spinal cord level and never progresses to register as a painful sensation.
The basic motor pattern is one of mutual inhibition of flexor and extensor neurons,2 providing a balance between agonist and antagonist muscles. To refine the movements, proprioceptive information is sent constantly from muscle spindles and joint receptors back to the spinal cord. As sensory nerves enter the spinal cord, they send off sprays of ascending and descending collateral fibers, which synapse on interneurons that have connections within the spinal cord segment, with other spinal segments up and down the cord, and with tract cells up to the brainstem. The result is a network of neurons processing information from the body and environment. These generate flexible patterns of motor activity (sometimes referred to as central pattern generators [CPGs]). Thus a pattern of nerve activity is generated where the primary function is to move a limb, but simultaneously vital secondary functions are engendered—for example, changing the tone in the central musculature to counteract the changing load on the axial skeleton.
CPGs can cause many different routine patterns by virtue of the number and variety of interconnections, whose characteristics are determined by cellular and synaptic connections of the neurons. These patterns develop over time by a process of repetition and learning. Thus the inconsistent swing of a learner golfer becomes a confident, automatic swing after many hours of repetitive practice. This involves a process of chemical changes within a neuron and new synaptic connections with other neurons, which speed up or “fast track” a particular response and result in a consistent and reproducible pattern of motor activity.
In response to injury, a number of events occur, which involve not only the sensory and motor pathways but also the autonomic system. A painful stimulus is conveyed from the periphery along small caliber nociceptors to the spinal cord. If the stimulus is of sufficient intensity, it will pass on to the brain to register pain. It will stimulate motor neurons in the ventral horn, resulting in paravertebral and peripheral muscle spasm,3 and stimulate sympathetic activity in the lateral horn, causing reduced blood flow to the skin.4 These neurophysiological changes represent a protective response against further injury and will, in the short term, affect the function of the body.
Once these defensive measures are activated, a control mechanism exists at the level of the spinal cord to modify this activity to prevent constant discomfort. Mediated by the large fiber system input of discriminatory touch and proprioception and by descending inhibitory cortical activity, the pain gate can be closed to painful stimuli. This can be demonstrated by rubbing an injured area to ease pain. It is the balance between large and small fiber stimulation and higher center input that determines the activity of the interneurons and therefore sensory, motor, and autonomic responses.
It is tempting to consider the reactions of the neurons to injury as hard wired, with a certain level of stimulus giving a corresponding magnitude of response. In fact, these neuronal networks are plastic, and the sensitivity of neurons to stimuli can be altered at any point in the pathway. In some circumstances, this process of sensitization or facilitation, as it is sometimes called, can be useful, for example, patterns of motor neuron firing during the acquisition of a new skill. However, when pain circuits are involved, a lower firing threshold may result in neurophysiological changes that affect function of the body long after the original injury has resolved. This is the basis of the somatic dysfunction concept that encompasses distortion in sensory, motor, and autonomic activity in the absence of any obvious pathology.
A lowered threshold for firing may occur at any point in the sensory system extending from peripheral receptors through to the spinal cord and brain. In response to injury, nociceptor nerve endings produce neurochemicals such as substance P.5 Combined with other inflammatory mediators such as prostaglandins and serotonin, the firing threshold is lowered, and the intensity at which the nociceptors will fire is increased. This local sensitization is generally responsive to treatment with antiinflammatory medication.
If nociceptor activity is intense or prolonged, changes can occur in the chemistry and structure of the interneurons of the spinal cord.6 These can be traced 3 to 7 days after only 45 minutes of moderate nociceptive stimulation.7 These changes lower the threshold for interneuron firing in a process called facilitation or “wind-up.” They become supersensitive to afferent input and internal network activity within the spinal cord and will activate a pain circuit at an inappropriately low level of nociceptive input. This is the mechanism underlying hyperesthesia.
A further stage in this central sensitization of interneuron pools is the development of allodynia, where even an innocuous stimulus such as a light touch results in a pain response. The clinical manifestation may be a “cold-backed” horse or one with sensitivity around the poll. Furthermore, the central pain pathways may be driven without any peripheral input at all. In experiments when afferent activity was blocked by sectioning the dorsal (sensory) root, a sensation of pain accompanied by autonomic and motor responses may still be present, driven by the output of the sensitized interneurons. This means that pain persists long after the original injury has resolved. Even when pain is no longer felt, the neuronal pool remains sensitive, and relatively low levels of nociceptive activity will produce a pain response inappropriate to the magnitude of the stimulus. This may account for horses with recurrent injuries that occur with minimal physical provocation.
Another characteristic of central sensitization is the development of antidromic activity in the sensory nerves. Although under normal circumstances a sensory neuron is stimulated at the periphery and transmits a signal back toward the spinal cord, it is in fact capable of firing from the center outward to the receptor, in what is termed the dorsal root reflex.8 On reaching the periphery, depolarization of the nerve endings has the same effect as depolarization as a result of a noxious stimulus from an injury. Proinflammatory neurochemicals are released from the nerve into the surrounding area and trigger an inflammatory cascade. This centrally driven inflammatory response may explain those cases of intermittent limb swellings and dysfunction for which no pathological cause can be identified.6
Part of the response to injury is contraction of muscle, which protects the area from further harm. In the short term, this is a helpful emergency measure. However, persistent muscular changes are not desirable. There are a number of biomechanical, neurophysiological, and biochemical consequences arising from a muscle that remains in a contracted state.
From a biomechanical perspective, muscle spasm causes asymmetry of and restriction in joint movement. This not only has a local effect but also causes adaptation of movement by other parts to accommodate this loss of function. These distant sites may themselves become symptomatic in the long term.
On a neurophysiological level, persistent contraction reduces joint movement and results in length changes in muscle fibers. This diminishes the amount of large fiber input from muscle spindles and joint receptors into central interneuron pools and shifts the balance in favor of small fiber nociceptor activity and stimulation of pain circuits.