DIAGNOSIS: Synovial Seal of Gastrocnemius Tendon Sheath with Compensatory Sacroiliac Joint Inflammation
BACKGROUND: 3 months prior to treatment commencing, Norman experienced significant tarsal inflammation. The vet attended and did an ultrasound scan. No note of any pathology to tarsal joint, but was diagnosed with synovial seal of gastrocnemius tendon sheath. Norman was treated with steroid medication into his sacroiliac joint (2mo ago), and drained and steroid medicated tendon sheath 3.5 weeks prior to my visit. At this point, the tarsal joint had refilled back to its previous state prior to medication and draining and prognosis for repair was poor. The only option provided was for Norman to continue ridden work until a point whereby another treatment option may become suitable. Enter Vet Physio Phyle and INDIBA Radiofrequency!
I contacted Calli at Vet Physio Phyle following my horse (Norman) being diagnosed with a condition called Synovial Seal of the Gastrocnemious Tendon. Norman’s right hock had swollen to over double the size. I called my Vet who scanned the joint and recommended an initial period of field rest as he was sound, however after two weeks the swelling was still the same. His next option was to drain the joint and injected steroid into the area. The swelling immediately reduced however in just three weeks the swelling returned. Following a further consultation with my vet (who had also spoken with fellow colleagues and surgeons on the matter), he advised that due to Norman not being lame it would be safer to continue to ride and see what might happen, he wanted to avoid going down the surgery route straight away as the area was high risk and operating could have detrimental effect. I immediately started to look at alternative therapies.
I found Calli and INDIBA through a friend of mine that had great success when her horse that sustained an injury. I called Calli and left a message. She immediately called me back and we chatted everything through. She arranged an initial appointment/assessment where she started by watching Norman move and took comprehensive videos and pictures, she discussed at length a plan of action and also gave me ridden and in-hand exercises that would help to keep the joint mobile. Calli recommended an initial 6 week course of INDIBA treatment twice weekly and then we would review. By week 6 we were seeing consistent improvements. The original swelling which was rock hard had softened significantly and the swelling was also noticeably reducing. Calli continued to treat him twice weekly for a further 4 weeks and as each week went by we kept noticing improvements in the size of the swelling until it was almost back to its normal size.
As Norman was doing so well, Calli decided that it was time to reduce the frequency of the treatment to see how the hock faired. To be honest this absolutely petrified me as Norman was doing so well, the swelling was now minor and we were back enjoying hacking and light schooling, I was scared we would go backwards. Calli put my mind at rest completely, saying that all I needed to do was call and she would be back. We continued stretching out each appointment and he now has a treatment once every 8 weeks and we have started to alternate a physiotherapy session once a month and INDIBA the next month. Calli also helped me create a rehab/fitness plan for Norman which has helped to keep us on track, so we are now working at Novice/Elementary work at home.
INDIBA is AMAZING!! (Yes capital letters are required!), it has changed Norman’s life for the better. Calli also AMAZING!!, she is so wonderful with the horses, treating them with kindness and compassion. She has been my sounding board, an Agony Aunt, my therapist and a life coach! She will always be a part of Normans life and we am so blimmin lucky to have her.
It has been a real pleasure to be a part of Charlotte and Norman’s path to recovery, and to see them supersede the level of training they were previously at is just the icing on the already beautiful cake!
My chats with clients whilst I am treating their horse are often super eye opening. And there have been a few discussions this week in particular that have resonated with me. Unfortunately, it is fairly common practice to treat horses that have been taken advantage of and been pushed to do too much too soon. Where this may line the pockets of the producer or breeder at the the time of purchase, a few months into new ownership often results in the horses ridden career rapidly grinding to a halt. Many owners are left scratching their heads as their talented four year old jumping 1.30m courses is now refusing to even pick up canter.
Competitive Edge – one step too many?
Modern day equestrian concerns fundamentally revolve around the prevention of injury and maintenance of biological equilibrium in order to enhance performance (Hodgson et al., 2014). Yet, as performance boundaries are being constantly challenged and advanced, extensive gait characteristics and locomotive potential are becoming an omnipotent feature of the modern day sports horse. Attention now must be drawn to how we can create expressive gaits in a way that promotes the health of the musculoskeletal system. Upon reflection of this, the desynchronisation of the promotion of physical & psychological equine health and training (notably accelerated/incorrect) can be considered as a fundamental component of pathological developments.
Essentially, are we forfeiting musculoskeletal health in the name of competitive performance with incorrect, accelerated training? Training levels are aligned with competitive aims, and the goal posts are continually moving. In trying to achieve competitive success at a younger age for an unconditioned horse, detrimental chronic adaptations are made to their posture in addition to the repetitive overloading of joints. An example of this can be stifle weakness and instability due to poor conditioning of the quadriceps femoris muscle group.
Tunnel vision training approaches and management routines can play a part in building our horses to break as little attention is given to postural & proprioceptive strength and conditioning. Quite simply, our aim should be to lay the foundations for a strong and healthy musculoskeletal system to develop. Poor foundations lead to crumbling architecture, where fixing the problem now requires far more intervention and commitment than prevention.
Challenging our Role as Architects
The Tacoma Narrow Bridge can be referenced as an example. And you’re probably wondering why a wavy bridge is being mentioned on a veterinary physiotherapy blog!? Hear me out! Earmarked as an architectural failure, the bridge built in Washington was proud to be noted as being the third longest suspension bridge in the world. However, the foundations of the bridge were not at all strong or suitable as it severely oscillated even during its construction. A mere four months after its completion it collapsed due to high winds; its foundations were simply not strong enough to withstand environmental demands and so it was not able to fulfil its job. However, this engineering failure was an experience that was learnt from and has helped to develop future engineering techniques. This is analogous to our role as architects of our horses bodies; failure in our engineering techniques will result in damage, pathology, weakness and eventual collapse.
A systematic approach to identifying common injuries specific to the animal being treated, and then designing an appropriate series of exercises that work towards minimising their potential for occurrence. Essentially, it is like being one step ahead to prevent injury; prevention is better than cure!
Aims of Prehabilitation
Improve joint range of motion
Increased joint range of motion and flight arc is more desirable for preventing the incidence of injury. This is important for the activation of different muscles which improves the conditioning and performance of the horse. Additionally, joint ROM is essential for joint health through the production of synovial fluid.
Improve elasticity or flexibility ie. trunk mobility
Improvements to suppleness and flexibility through joint range of motion and muscle quality is essential for healthy biomechanics. Flexibility ensures movement is supple and not rigid through the extensibility and looseness of muscles and fascia. Rigid locomotion – which often occurs when the spinal column is placed into extension (hollow frame) – can mean that movement almost looks robotic and jarring. Parts of the musculoskeletal system should look and feel like they’re having a content chat with a cup of tea during movement, not like they are all arguing with one another.
Improve muscle strength, endurance and symmetry
Strong and symmetrical muscles that are able to correctly function for an extended period of time are able to support the body in a healthy posture successfully. This reduces the risk of injury as the body is evenly supported; atrophied and/or asymmetrical muscles cause areas of weakness in the body that are susceptible to injury.
This also draws a link to improving fitness as a way to prehabilitate. A fatigued muscle is more likely to become injured.
Improve coordination and proprioception
Weak proprioceptive abilities can mean an animal is more likely to trip or loose their footing for example, as they lack awareness of their body. Improving proprioception stimulates the neurological system to be conscious of the movements made by the body for more accurate and controlled movement.
Correct pre-existing problems
Whilst a poorly fitting saddle may not be making a horse acutely lame, or a incorrectly fitting collar may not cause immediate laryngeal problems… overtime the negative effects of such issues can amount to a larger dysfunction. Poor surface, nutrition, equipment fit and training are all examples of elements that can come together to create an injury later on in life. By correcting these at the beginning, the risk of a lameness occurring from one of these factors is minimised.
Examples of Different Exercises for Different Focuses
A spinal assessment involves applying pressure at varying levels and angles to the spinal column in order to determine joint health and mobility. It plays a crucial role in the static assessment of any animal as it aids in the identification of underlying pathology. Prior to a spinal assessment, active ROM of the animal should be conducted if possible to identify autonomous areas of restrictions. Also, a visual assessment should be done in order to identify any lumps/cuts. Communication with the owner is also essential to discuss history and current concerns.
Cervical to Coccygeal — ensure to include the tail!
This blog post will outline 5 key points to ensure are incorporated into a spinal assessment for both small and large animal patients.
Prior to manipulation and assessment, joint palpation is essential. Feeling for muscle changes (hypertrophy, atrophy), bony changes (thickening) and oedema/heat that will indicate injury and the stage at which it is occurring ie. active inflammatory stage (heat, swelling) versus chronic pathology (joint thickening and effusion with localised muscular changes).
Correct Angulation and Level of Pressure
Ensure that adequate pressure is used to cause movement to the vertebrae, but not so much firm pressure that it could cause pain or so much displacement that an accurate analysis of the ROM cannot be achieved. Practice the pressure on your own fingers so that you can feel what is the right amount to cause movement but not firm displacement.
Bear in mind how this will differ between species and breeds.
Ensure that you have an awareness of joint angulation and therefore range of motion. This requires an awareness of the angulation of each intervertebral joint and the range of motion it is biomechanically able to achieve. An example would be the anticlinal vertebrae of the horse (T15) whereby the angle of the dorsal spinous processes changes.
Analyse the Restrictions
When assessing each IVJ, ensure to note the degree of restriction and what the restriction feels like… not only that it feels restricted! This can be graded from mild to moderate to severe, and restriction types can vary from muscular to bony. Determine asymmetrical movement by comparing the left to the right side. Consider whether the restriction is present in lateral mobilisation, flexion or extension.
Ensure to monitor this at each visit to determine progress or regression.
Even though a spinal assessment is being conducted, the surrounding muscles cannot be omitted. For example, in the case where the thoracic spine of a horse is being assessed, the epaxial muscles should also be assessed simultaneously for localised trigger points, tonicity, pain response, temperature and mass.
Specific Orthopaedic and Neurological Tests
Where an area of restriction has been noted, ensure to correlate findings with potential pathological processes and conditions. This can be achieved with the use of special tests in order to aid a more specific analysis of the compromised area. For example, the conduction of a sacral pinch to analyse SI mobility in a horse, or the cutaneous trunci reflex in a dog with neurological deficits. Essentially, ensure to link findings to other MSK pathologies that may not only be occurring within the spine but as a primary condition elsewhere in the body.
Overall, the conduction of a spinal assessment has a fundamental role in the assessment of any animal that is being treated by a veterinary physiotherapist. Whether it is used the first time an animal is seen in clinic or weekly to assess progress in an intensive physiotherapy programme, it is a skill that is essential to have. Its method of conduction is a rather in-depth and separate topic, but I hope this blog post provides a quick read in covering some key elements that should be incorporated into a spinal assessment.
Trigger point: an area of lactic acid build up and motor nerve irritation located in the belly of the muscle. The presence of a trigger point will restrict muscle action.It is also known as an “energy crisis” within the muscle.
The term trigger point originates from the fact that when pressure is applied to a particular point, a pain signal will be sent to other parts of the body. It can be identified when the muscle is palpated perpendicular to the affected muscle fibres.
Clinical signs of a trigger point include:
Referred pain occurs as a result of the link between the sensitive loci located in the trigger point region and how they are integrated with the spinal cord. Trigger point can also be viewed as a “pathogenic pathway of muscle pain from different causes” (Hong, 1996).
a localised twitch response.
a localised twitch response is an involuntary spinal cord reflex.
An example of a clinical sign may be an adversion to girthing up, especially if a trigger point is located in the pectorals. Horses with an owner-reported history of girth-aversion behaviour had higher severity trigger point scores than horses without a history of girth-aversion behaviour. Based on this, a knowledge of the presence and location of trigger points could assist in the development of prevention and management strategies to improve comfort, optimise performance, and reduce girth-aversion behaviour (Bowen et al., 2017).
They can be located through palpation, but also through electromyographic needling. In a study by Macgregor and von Schweinitz (2006) all equid subjects demonstrated objective signs of spontaneous electrical activity, spike activity and local twitch responses at the myofascial trigger point sites within taut bands. The frequency of these signs was significantly greater at myofascial trigger points than at control sites (P<0.05).
Trigger points occur mostly in response to:
not enough stretching
not enough rest (leading to fatigue)
nervous system overexertion/stress
poor circulation — muscles of hypertonicity and hypotonicity most commonly can have decreased circulation and therefore decreased oxygen supply. This will result in a build up of toxins which can irritate the nerves.
compensatory movement patterns resulting from osteoarthritis
acute or chronic injury to a muscle, tendon, ligament, joint or nerve (Hong, 1996)
Trigger points vary in size and can feel like nodules. They are usually very tender, give easily under pressure and release fairly quickly. The surrounding muscle may remain supple, where the trigger point will feel like an intensely contracted sarcomere.
Different Types of Trigger Point
SILENT (LATENT) TRIGGER POINTS – triggered pain is of low intensity.
ACTIVE TRIGGER POINTS – triggered pain is of high intensity; very sensitive to palpation. A deep, dull, aching pain.
SPILLOVER TRIGGER POINT AREA – one trigger point that affects more than one area.
Types of Trigger Point Therapy
Trigger Point Technique
This technique is used to:
release trigger points
drain trigger points
(1) Hot hydrotherapy — application of heat to the trigger point will contribute to the effectiveness of TPRT. This is because it relaxes the muscle fibres by boosting microcirculation. This is most useful in cases of chronic trigger points.
(2) Effleurage — massage techniques to warm up the muscle and encourage muscle fibre relaxation longitudinally from origin to insertion.
(3) Pressure — light pressure at the location of maximum tenderness or over the nodule palpated. This should be held until you can feel the muscle relaxing and softening underneath your fingers. This may take a few seconds for acute trigger points, or 2-3 minutes for chronic trigger points. Every 30 seconds, intersperse the pressure with effleurage to boost circulation to the area and therefore promote toxin removal from the trigger point. When dealing with a silent trigger point, pressure may be increased with tolerance; depending on the muscle mass and horses reaction. When the trigger point begins to release, pressure should be gently released but maintained for a few seconds.
(3b) Pressure modifications — if pressure is not suitable for the location (ie. along venous or nervous tracks like in the brachiocephalic muscle), squeezing or pinching the trigger point between the thumb and first finger is an alternative. Depending on the horses tolerance, pressure may be continuous or varying.
(4) Observe — throughout treatment, continuously monitor the animals expression in order to determine the right amount of pressure. It should be a balance between pleasure and pain. Watch the eyes for softness, closing and slow blinking.
(5) Drainage — once the trigger point has been released, the area should be drained thoroughly with plenty of effleurage followed by light friction massage along the length of the muscle. This will aid in the long standing break up of toxins into the blood stream; this movement from the muscle into the circulation and thus lymphatic system is paramount for improved muscle health. As well as encouraging drainage, effleurage will also promote circulation to the area which will improve oxygen and nutrient supply essential for healing.
(6) Light movement — following TPRT, lightly exercising the animal in hand in walk can boost circulation and muscle movement further.
Trigger points can also be treated using dry needling by a veterinary surgeon only.
Cautions to the TPRT
Do not use more pressure than is necessary; trigger points can be over-treated!
Be gentle and do not rush; some trigger points may need up to 3 minutes to be released.
Avoid deep palpation or muscular exertion following TPRT. The area where the trigger point was located may be sore for a few hours to a day. Incases of chronic TPRT, avoiding intensive exercise to the area for a few days should be recommended in order to avoid a vicious cycle of the trigger point returning. However, the animal should not be isolated.
If there is inflammation present (indicative of heat and swelling), cold hydrotherapy applications can be useful post-treatment to calm nerve endings and stimulate circulation.
The Vicious Circle
Trigger points, if not treated or identified correctly, can either build up or return. It has been proposed that sustained low-level contractions (due to a trigger point spasm) cause a decrease in perfusion, hypoxia, and ischemia and that cellular responses occur due to stimulation of activating chemical substances, which affect neuropeptides. Specific neuropeptides, including calcitonin gene-related peptide and substance P, may facilitate an increased release of regulatory compounds, resulting in excessive acetylcholine (ACh). It is hypothesized that the excessive ACh release, sarcomere shortening, and inappropriate changes in receptor activity lead to development of a taut band and subsequent MTrPs. (ref)
The Link Between TP and Acupuncture Points
It has previously been claimed that there is a 71% correspondence between the location of trigger points and acupuncture points. A research article investigating the potential correlation between the location of trigger points and acupuncture points found that this was “conceptually not possible”. Only approximately 18%-19% correlate rather than the 71% that was previously claimed. However, this study found a probable correspondence of trigger points to a different class of acupuncture points, the a shi points, which appears to be an important finding (Birch, 2004).
Passive Stretching and TP
Jaeger and Reeves (1986) conducted research into effect of passive stretching on trigger point sensitivity and the referred symptoms of myofascial pain. The results showed that myofascial trigger point sensitivity decreases in response to passive stretch as assessed by the pressure algometer, and that trigger point sensitivity and intensity of referred pain are related.
Is Ischemic Pressure the Best?
Hou et al. (2002) – Ischemic compression therapy provides an alternative treatment to using either low pressure (within or at the pain threshold) and a long duration (90s) or high pressure (the average of pain threshold and pain tolerance) and short duration (30s) for immediate pain relief and trigger point sensitivity suppression. Results suggest that therapeutic combinations such as hot pack plus active ROM and stretch with spray, hot pack plus active ROM and stretch with spray as well as TENS, and hot pack plus active ROM and interferential current as well as myofascial release technique, are most effective for easing trigger point pain
Graff-Radford et al. (1989) No pain reductions were found in the 2 Hz, 250 msec TENS or the control. No significant alteration in myofascial trigger point sensitivity, assessed with the pressure algometer, was found between the groups. The results suggest that high frequency, high intensity TENS is effective in reducing myofascial pain, and that these pain reductions do not reflect changes in local trigger point sensitivity.
“Bone is a unique and fascinating material,” he began. “People often think of bone as being relatively inert, but I’d like to dispel that concept. Modeling and remodeling can be occurring in the same bone at the same time–bone is always in all stages of remodeling. Bone does not heal, incorporating the scar tissue as seen in most all other tissues–it regenerates itself. It changes its shape and structure based on its use, and if broken can resume 100% of its former strength and function.”
BROAD CLASSIFICATION OF FRACTURES IN THREE SEGMENTS =
Complete = loss of function of the limb.
Incomplete = lameness and localised signs; stress fracture.
Character = articular, non-articular, diaphysial, epiphyseal, Salter-Harris physeal, chip and slab (Nunamaker, 2002).
Single load = falls, collisions, impact
Accumulation load = continued fatigue damage from repeated loading beyond biomechanical limits.
Clinical Signs and Symptoms
Rapid inflammation of site
Immediate distress of animal
Leg hangs crooked
End of bone may penetrate skin
Attempted movement on three legs
Mild lameness usually
Methods of Diagnosis
Nuclear Scintigraphy – useful for detecting a hidden fracture
Stress fractures (also known as fatigue fractures) are most commonly found in the metacarpus, metatarsus, proximal sesamoid, tibia, humerus and pelvis.
Fractures of P3 (pedal bone) — commonly occur when a horse kicks out at a wall or lands on an irregular surface. If the fracture does not involve the joint (distal interphalangeal joint – DIP joint), most cases heal with box rest and bar shoes for support. If the fracture does involve the DIP joint, prognosis is lesser.
Fractures of P1 (pastern bone) — commonly longitudinal and extend down from the fetlock joint.
Sesamoid bone fracture — occur commonly in young foals, often presenting as avulsion fractures at the attachment of the suspensory ligament. Pain and lameness occur alongside fetlock inflammation, resulting in chronic or recurrent lameness.
Fracture of metacarpal/metatarsal bone — commonly occur due to a kick or fall, and extend into the fetlock joint.
Carpal fractures — most occur as chip and slab which can result in pain and joint distension.
Splint bone fracture
Olecranon fracture — usually the result of a kick, often compound or comminuted.
Pelvic fractures — most start as an incomplete stress fracture and will fully heal if given a prompt diagnosis, rest and adequate time. The wing of the illium is particularly predisposed to stress fractures.
In every horse that is presenting an acute onset non-weightbearing lameness, a fracture should be high on the differential diagnosis list (along with bone, joint or tendon sheath infection and hoof abscess).
Some fractures (ie. osteochondral chip fracture of a carpal bone) may only produce low grade lameness.
A cast might be changed as frequently as every 10 days for a foal, or as infrequently as every six weeks for an older horse. The duration depends on how healing progresses and how the horse’s skin and muscle react to the cast.
Bone fragment removal surgery via arthroscopy
Dependent on a variety of factors:
Poor prognosis = complete fractures of the radius and tibia in adult horses. This is because it becomes difficult to reconstruct and heal the fracture with enough stability to withstand weight bearing. Weight-bearing on the affected limb is essential, otherwise there is increased risk of laminitis in the contralateral limb. Areas that surround the fracture with a large muscle mass, ie. the pelvis, have a more positive prognosis via conservative therapy.
Fair prognosis = incomplete fracture with confinement.
Complications during Recovery
Laminitis in the contralateral limb
Osteoarthritis of adjacent joints
Flexural limb deformity
Increased joint laxity in young horses following immobility in a cast of affected limb; also, angular deformities in contralateral limb.
Joint stiffness = rare.
The Role of a Veterinary Physiotherapist in Recovery
The healing time of a fracture is dependent upon age, fracture type, every and site. An outline of the age and timescales for canine fractures is listed in the table below.
Younger than 3 months old
3-6 months old
4 weeks – 3 months
6-12 months old
5 weeks – 5 months
Over 1 year old
7 weeks – 12 months
An equine fracture can take between six to eight weeks to heal, with the rehabilitation extending to four to six months. Successful healing of a fracture is not solely determined by complete bony union presented on radiographs, but also the functional use of the limb. With this in mind, physiotherapy following veterinary management of a fracture can be beneficial to healing quality.
Physiotherapy can begin as soon as the area is accessible ie. when the cast is removed or immediately if internal fixation has been used.
Determine goals for the different stages of healing. Some used in this case would be:
avoidance of complications resulting from immobility
maintaining or improving muscle mass
retraining of functional activities
Ultrasound — low intensity, pulsed US (1MHz/1.5MHz/3.3MHz for 10-20 minutes daily beginning day 1 post-operative) has been shown to stimulate endochondral ossification. It also increases the positive stiffness and thus resilience of bone.
LASER — increases osteoblastic proliferation, collagen deposition, new bone formation, increased bone stiffness (by forming smaller and stronger callus with increased quantity of trabeculae).
Most effective when carried out in early stages where cell proliferation is occurring.
Pulsed Electromagnetic Field Therapy (PEMFT) — stimulate osteoblast and chondroblast production, although there are contradictory findings in literature.
Electrode placed 3cm proximal to fracture site and the other proximal to the first electrode, 25mA, pulse width = 50, 4Hz, 20s on:15s off for one hour daily beginning day four after surgery for 25 days.
Shockwave — effects bone by up regulating proteins critical for angiogenesis, boosting the release of growth factors which are needed for osteoblast formation.
Weight bearing and early mobillisation — avoidance of the disuse response, invariably leading to muscle atrophy and weakened bone tissue. Based on this response, the unloaded healing bone will repair in a weaker state due to decreased stress and strain placed upon it (Wolffs Law).
GRADUATED TREATMENT PROCESS = Hydrotherapy –> graduated weight-bearing exercise programme –> land treadmill –> strength, endurance and balance exercises.
With 60% of fatal racecourse injuries in the UK being associated with a fracture, hazard prevention is essential.
As racing injuries are “spontaneous”, preventing the hazard of fractures can be difficult as it is not caused by a specific traumatic event.
There is evidence that fractures that occur in racing are mostly stress fractures (57%), the end stage of a series of events relating to fatigue. Consequently, avoiding exercising a horse to an extreme fatigue level can decrease the risk of such injuries.
Stress fractures in racing occur in horses undergoing intense race training; a repetitive, high strain loading form of exercise. In order to reduce the incidence of stress fractures, avoiding repetitive and high strain training can be beneficial.
The fractures show a high degree of consistency in their morphology; they frequently share the same locations as incomplete cracks and they are often associated with pre-existing pathology.
Fatigue of bone is associated with progressive microdamage, which is important in the pathogenesis of stress fractures
Horses exercised before bone repair is complete are likely to be at significantly greater risk of sustaining a catastrophic stress fracture.
Rooney, J. (1982) → predicts that if the distances at which the horse became extremely fatigued were eliminated, lameness would be reduced about 14% and bone fracture-breakdown about 24%.
Mainwood and Renaud (1985) → found that H+ions are generated rapidly when muscles are maximally activated. This increases the acidity of the musclein combination with lactate increase. This can cause discomfortand mean the muscles will not work to the best of the ability to support bones and joints, allowing for the possibility of injury to occur.
Yoshikawa et al.(1994) → found (in an investigation using foxhounds) that muscle fatigue had an effect on bone strain, with peak principal strain on the tibia being increased by an average of 26–35% following muscular fatigue.
Hesse and Verheyen (2010) → found that the presence of pelvic bony asymmetry, muscle atrophy of the quarters, reduced reflex movements of dorsi- and/or ventroflexion and spasm or tenderness on palpation of the gluteal muscles were significantly associated with subsequent fracture diagnosis. Horses subsequently diagnosed with pelvic or hindlimb fracture were 11.1 times more likely to show pelvic bony asymmetry, 4.7 times more likely to display muscle atrophy of the quarters and 6.6 times more likely to have spasm or tenderness on palpation of the gluteal muscles than those that were not. This highlights the importance of the role of a veterinary physiotherapist in a racehorse training programme.
The peripheral nervous system consists of the nerves that arise from the central nervous system. The cranial nerves are part of the peripheral nervous system.
Cranial nerves originate from the brain (in comparison to the spine, like the spinal nerves) inside the cranium. They leave the cranial cavity via various foramina.
There are 12 pairs of cranial nerves. They are short in structure and supply the structures of the head. However, this is on the exception of the vagus nerve (CN10) which is the longest nerve of the body.
It is important to remember that cranial nerves are P A I R S. Anatomical diagrams tend to show you one side of the skull for illustrative purposes. However, remember that the nerves are also present on the other side of the skull.
What type of nerve fibres do cranial nerves have?
Cranial nerves can have:
ONLY sensory fibres — these nerves will relay messages TO the brain.
ONLY motor fibres — these muscles will create and control muscle movement.
BOTH sensory and motor fibres — these are mixed fibres with mixed function.
How to the cranial neves leave the cranium?
All of the cranial nerves (apart from CNIV Trochlear) exit the brain from the ventral surface and then pass through small foramina (openings) in the skull. CNIV Trochlear exits the brain from the dorsal surface but immediately follows down to the bottom of the brain to unite with the other cranial nerves.
CNI – Olfactory
CNII – Optic
CNIII – Oculomotor
CNIV – Trochlear
CNV – Trigeminal
CNVI – Abducens
CNVII – Facial
CNVIII – Vestibulocochlear
CNIX – Glossopharyngeal
CNX – Vagus
CNXI – Accessory
CNXII – Hypoglossal
There is a mention of CN0 in some textbooks. This is in reference to the Nerves Terminalis (a nerve associated with smelling pheromones and triggering mating behaviour).
CN ONE – OLFACTORY
Monocular vision means that horses rely more heavily on chemical signals. This nerve is responsible for smell. Its receptors (located in the mucous membranes in the upper portion of the nasal cavity) are elongated nerve cells, specifically designed to analyse smells. These elongated nerve cells all join together to form the axon of CNI.
It runs from the nasal cavity through to the olfactory bulb (located in the forebrain). On its path, it passes through the cribiform plate and is surrounded by meningeal sheets. For this reason, CNI is a potential site of infection that can track towards the brain. Injury of CNI can result in anosmia (loss of smell), hyposmia (decreased sense of smell) and parosmia (perversion of sense of smell).
The function of CNI is to relay sensory data about smells that enter the nasal cavity to the brain.
Olfaction in canines is very well developed as they use it to orientate themselves.
By sniffing, a horse can intensify the currents of air in the nasal passages, providing more contact between the odour molecules and receptor cells and therefore more time for analysis.
Why do horses sniff more when they smell something?
CNI contains sensory nerve fibres that are formed into bundles known as olfactory filaments.
Locate underneath the nasal cavity is a secondary olfactory system known as the Jacobson’s organs. It is innervated by the vomeronasa 1 nerve. It has a tubular and cartilaginous structure lined with mucous membranes, and is about 12 cm long. It connects to the nasal passages via a nasopalatin duct. The Jacobson’s organs expand and contract like a pump when stimulated with strong odours (these odours are specific and strong enough to have their own pathway to the brain!). The purpose of this system is to work alongside the CNI and detect and analyse pheromones. The flehmen response helps to trap these pheromones scents for the Jacobson organs to closer analyse; the curling of the lip temporarily closes the nasal passages and holds the particles inside.
The flehmen response and its link to olfaction.
P A T H W A Y = nasal cavity –> cribriform plate (via various foramina) –> olfactory bulb (forebrain)
Process of Stimulation (action potential generation):
Airborne chemicals and particles enter the nasal cavity and come into contact with the lipid and protein material of the mucous membrane.
They interact with small hairs protruding from the receptor cells.
Chemical substances are present and stimulate sensory neurones (these are the olfactory neurosensory cells that are found within the olfactory epithelium). This generates an action potential.
The nerve impulse travels to the brain via sensory nerve fibres. This fibres represent CNI.
When chemical substances interact with our bodies, they stimulate sensory neurones that are specific to that chemical. If no specific sensory cell exists for that chemical substance, it will go undetected.
THE OLFACTORY BULB — this is a distinct area of the brain that is responsible for analysing scents. It is located at the front of the cerebrum (one on each lobe). The two olfactory bulbs are connected to the receptors in the nasal passage by CNI. The olfactory bulbs are also one of the few brain structures that do not cross over – the left nostril is paired with the left olfactory bulb.
CN TWO – OPTIC
The optic nerve connects the receptor cells of the retina to the diencephalon (a region of the forebrain). It contains sensory nerve fibres.
CNII works with CNIII to cause CNVII to respond to blinking. It singularly functions to carry information about sight from the eyes to the brain.
The optic nerve is susceptible to shearing injury after a head trauma leading to prechiasmal blindness.
P A T H W A Y = optic disc of retina (bipolar cells) –> retinal ganglion cells bundle together to form optic nerve –> enters skull via optic canal –> brain (diencephalon; occipital cortex).
Some (85-88%) of optic nerve fibres decussate (cross over) at the optic chiasm in the horse and ox. It is 75% in the dog. The decussation of nerves at the optic chiasma ensures that both sides of the brain receives information from both eyes.
Optic nerve structure in canines versus equines
Indications of injury:
The pupils of the eye will point down and out during rest.
No response to bright light directed into the eye.
Paralysis of the oculomotor nerve results in a resting ventrolateral strabismus and an inability to rotate the eye upwards, downwards or inwards.
P A T H W A Y = synapse at ciliary ganglion of the eye –> orbital fissure –> pre-ganglionic nucleus in mesencephalon (ventral midbrain).
CN FOUR – TROCHLEAR
The trochlear nerve innervates the muscle of the head, especially the dorsal oblique muscle. It enables mastication by supplying nerve branches to the temporal and masseter muscles. It is comprised of motor nerves. It is the smallest of the cranial nerves, yet greatest in intracranial length. It is also the only cranial nerve that exits from the dorsal aspect of the brain stem
Indications of injury:
Loss of facial reflexes e.g. closure of the eyelid.
Headshaking (nerve can become damaged by a tumour or inflammation).
P A T H W A Y = orbit of the eye –> exits the orbit via superior orbital fissure –> along the lateral wall of the cavernous sinus –> orbital fissure dura matter –> subarachnoid space –> trochlear nucleus of the dorsal midbrain.
CN FIVE – TRIGEMINAL
The trigeminal nerve is responsible for innervating structures that originate from the brachial arches. It has three branches: the opthalmic nerve, the maxillary nerve and the mandibular nerve. It originates from the pons and medulla oblongata of the brain (location of trigeminal nerve nuclei).
a. OPTHALMIC NERVE — a sensory nerve that supplies sensory fibres to the orbit of the eye. It travels from the orbit of the eye (where it further splits into other nerves), through the orbital fissure to the brain.
b. MAXILLARY NERVE — a sensory nerve. It travels from the brain through the round foramen and rostral alar canal, entering the infraorbital canal via the maxillary foramen. Whilst in the infraorbital canal, the maxillary nerve then branches off to innervate the teeth (sensory). When the maxillary nerve exits the infraorbital canal, it branches again into two nerves that supply the horn (zygomatic nerve) and the palate (pterygopalatine nerve).
c. MANDIBULAR NERVE — a nerve with mixed fibres; both sensory and motor. It travels from the brain and passes through the oval foramen, dividing into motor nerve branches (masticatory nerve, masseteric nerve and temporal nerve) to innervate the muscles of mastication, ventral throat and muscles of the palate.
Indication of injury:
Reduced sensation in the sensory fibres results in loss of facial reflexes e.g. closure of the eyelid.
Headshaking – the nerve can be damaged by a tumor or inflammation.
CN SIX – ABDUCENS
The abducens nerve is a motor nerve that functions to control specific (lateral rectus & lateral portion of retractor bulbi) muscles of the eye. An indication that this nerve is damaged is that the affected eye is pulled medially.
P A T H W A Y = muscles of innervation –> orbital fissure –> medulla oblongata (brain)
CN SEVEN – FACIAL
The facial nerve is a mixed nerve. Motor nerve fibres innervate the ear canal, salivary glands (parasympathetic control), lacrimal glands, nasal cavity, muscles of facial expression and palate. Sensory nerve fibres innervate the rotary 2/3rds of the tongue.
Muscles of facial expression are superficial, flat and thin muscles that originate from bony landmarks of the skull and then radiate out around the skin.
Indications that this nerve is damaged include any facial paralysis, drooling or absence of blinding.
P A T H W A Y = variety of branches including palpebral nerve, internal auricular nerve, stylohyoid nerve… –> stylomastoid foramen (caudoventral aspect of skull) –> petrosal bone –> internal acoustic meatus, facial canal (here the nerve branches off), stylomastoid foramen–> medulla oblongata and second brachial arch.
CN EIGHT – VESTIBULOCOCHLEAR
The vestibulocochlear nerve is made of two components: the vestibular nerve and the cochlear nerve. It is a sensory nerve.
VESTIBULAR NERVE — this nerve is responsible for balance.
COCHLEAR NERVE — this nerve is responsible for hearing.
Indications that this nerve may be damaged include:
vomiting (canines, not equines)
ipsilateral ventrolateral strabismus (the visual axes of the eyes are not parallel and the eyes appear to be looking in different directions)
P A T H W A Y = inner ear (vestibular apparatus and cochlear) –> internal acoustic meatus –> petrosal bone (like facial nerve) –> brain.
CN NINE – GLOSSOPHARANGEAL
The glossopharyngeal nerve is part of the vagus group. It is a mixed nerve. It is responsible for swallowing and motor tongue movement and sensation.
P A T H W A Y = structures of the third brachial arch (carotid body, pharynx, stylopharyngess muscle, salivary glands, tongue…) –> a variety of nerve branches –> jugular foramen –> medulla oblongata.
Indication that this nerve may be damaged include:
Drooling out of one side of the mouth
Partial paralysis of the tongue.
The vagus group encompasses the vagus, glossopharangel and accessory nerves as they pass through the jugular foramen.
CN 10 – VAGUS
The vagus nerve is part of the aforementioned vagus group. It has mixed fibres. Motor fibres innervate muscles of the larynx, pharynx, palate, oesophagus, abdominal and thoracic viscera. Sensory fibres innervate the base & root of the tongue, pharynx, larynx, epiglottis (taste), palate, external ear and dura matter. The vagus nerve has many functions; from the heart to the pharynx.
Indications that the nerve is damaged include:
Any changes related to gag reflxes, blood pressure/heart rate, voice or inspiratory dyspnoea.
To test for vagus nerve dysfunction:
observe and palpate swallowing
nasal tube for testing gag reflex
P A T H W A Y — structures of the fourth brachial arch –> jugular foramen –> brain.
CN 11 – ACCESSORY
Also known as the spinal accessory nerve, the accessory nerve is part of the aforementioned vagus group. The cranial root of CNXI contributes to the vagus nerve and striated muscles of the pharynx, larynx, palate and oesophagus. The spinal root CNXI also contributes to the cervical spinal cord via the foramen magnum to innervate the muscles of the neck. After emergence from the foramen magnum, CNXI branches into the dorsal branch (innervates the brachiocephalic, trapezius and omotransversarius) and ventral branch (sternocephalic). It is a motor nerve fundamental for thoracoscapular function and scapulohumeral rhythm.
Indications that the nerve is not functioning correctly are:
Weakness and atrophy of the trapezius muscle.
Reduced shoulder abduction
CNXI is very vulnerable superficially and susceptible to injury (especially during surgery to the neck and lymph node biopsies).
P A T H W A Y — structures of the fourth brachial arch (this includes various structures of the neck from C5-C7) –> jugular foramen –> medulla oblongata
The accessory nerve starts off smaller and gets larger as more fibres are collected.
CN 12 – HYPOGLOSSAL
The hypoglossal nerve is responsible for movement of the muscles of the head. Due to its position (caudal location on the brain stem), it is partially considered as a cervical nerve. It is a motor nerve which controls the intrinsic and extrinsic muscles of the tongue. The muscular tone of the tongue is dependent on the function of CNXII.
Paralysis and atrophy of the tongue is indicative of malfunction of CNXII. This can be tested by grasping the tone and applying gentle traction. Inability to withdraw the tongue can suggest damage.
P A T H W A Y — muscles of the tongue –> hypoglossal canal –> medulla oblongata
CRANIAL NERVE EXAMINATION
Careful assessment of cranial nerve function is important since there are a number of diseases that may result in dysfunction of those nerves in addition to abnormalities found elsewhere. This can be found in particular with diseases such as polyneuritis equi and equine protozoal myeloencephalitis. Furthermore, if there are deficits noticed in multiple cranial nerves, there may be central disease for example in the area around the brainstem since that is where most cranial nerves originate. Deficits of the afferent pathways (sensory) would include reduced smell, taste, vision, hearing, or balance and specific proprioception. Deficits of the efferent pathways (motor) would include reduced ability to change pupil diameter, lesions of eyeball movement, reduced muscle of mastication mass, altered facial expression, reduced ear play, problems with swallowing, vocalization, and reduced tongue movement or tone. The most commonly seen deficits of cranial nerves in the horse include facial nerve paralysis, head tilt, laryngeal dysfunction, and dysphagia (Yvette and Not-Lomas).
Aspinal, M. and Cappello, M. (2015) Introduction to Veterinary Anatomy and Physiology Textbook.
In a sport where one pole down, one percentage mark, or one time fault can slip you down the rankings… every rider is looking for something to give their horse that competitive edge. With the therapeutic and holistic care of our horses becoming increasingly accepted and widespread, the question of “can I be doing something more for my horse?” is being prompted more often.
I remember the first time I saw The V.I.P.; it stuck out vividly in a market of sheepskin, gel and memory foam. As one of the most streamline, invisible and thin half-pads on the market, it drew my eye as it strongly differed from the thick sheepskin underlays.
The V.I.P is marketed as a pad like no other. Quite literally. After trawling the internet for an insight into the materials used for gel half-pads on the market… I was surprised to find very little. I found one page by Acavallo which described the materials that they use. Yet, it was difficult to find information about HOW the material actually worked, WHAT the material actually was and what (if any) research had been undertaken. Because of this, I was initially impressed with The V.I.P as scientific-based information based on clinical practice about its gel material Akton is easily accessible on their website.
The V.I.P is described as a half-pad made of a viscoelastic polymer Akton that sits between your saddle and your saddlepad, or can be applied directly onto your horses back. It isn’t to be confused with a gel pad, as gel and Atkon have very different properties. The V.I.P is laid bobble-side down, with the smooth surface facing upwards. Although self-explanatory, I found there to be no clear instructions on how to place and position the half-pad correctly and so a mixture of advice from their FAQ section of their website was used.
Akton is a viscoelastic polymer. A material that has viscoelasticity is able to exhibit both viscous and elastic characteristics in a response to deformation (pressure). An explanation as to why a viscoelastic material, such as Akton, is important in comparison to just a viscous or just an elastic material is below. Akton was founded by Dr. W.R. McElroy has been used for 40 years in the human medical field; specifically created to reduce the risk of skin and nerve damage caused by prolonged sitting, reclining or laying down.
WHY IS VISCOELASTIC IMPORTANT?
If a half-pad material was just viscous: over time, stress would be placed on the half-pad causing deformation and change in structure at a constant rate. When the stress is released, the material will remain in its deformed structure as it “forgets” its original shape. Over time, the shock absorbing properties of the half-pad will decrease.
If a half-pad was just elastic: over time, stress is placed on the half-pad. However, the half-pad has a solid memory of its original shape. And so when the stress is released, it returns back to its original structure.
If a half-pad is viscoelastic: over time, stress is placed on the half-pad. This causes deformation and change in structure, which then instantaneously returns back to its normal structure once the stress is released. Over time, the half-pad will acquire a “lasting memory” of the degree of deformation and the differing patterns of stress across the half-pad. Essentially, over time, the half-pad will become more adapted physically to your horse.
Bobbled – this increases the surface area of the half-pad, therefore increasing its shock absorbing capabilities and
Thin, film gullet – the gullet area across the horses spine should have no pressure, and the thin film used is enough to connect the two panels of gel but not cause unwanted pressure.
Seamless – adds no pressure points to underneath your saddle.
The V.I.P was relatively straight-forward to put on; I opted for placing it between the saddle and the saddlepad. It sat flush against the back, with minimal folds and provided a smooth surface for the saddle to sit on top of. It worked well with both a dressage and a jump saddle. The thin filmed gullet was generously wide enough to avoid the delicate spine. Once on, it did not slip or slide around… it stayed in the place that I put it under the saddle both statically and when the horse moved. I found The V.I.P to be a little heavier than other gel pads on the market, which I feel anchored the pad in place without adding a significant amount of weight to the horses back.
Once onboard, the only way I can describe the feeling of The V.I.P is having a thin layer of supportive but shock-absorbing material between you and the horse. It highlighted to me the amount of force transmitted from the rider to the horse just with the simple movement of the seat at a walk. I felt like the pressure was dispersed, even and reduced. In all honesty, I was unsure what to expect… but I didn’t expect to feel such a clear feeling of supportive safety underneath me. Yet, I didn’t feel lifted away from the back or sides of the horse, as the pad was so thin I still was able to have the close contact feeling.
I noticed the most difference in trot, with Junior’s confidence in lifting through the back growing over time. Whilst I did not experience and extraordinary change in his way of going, I did feel that The V.I.P was providing that extra layer of comfort to allow for the easier execution of movements and increased suppleness.
Aside from the horse, I feel like it benefitted my riding hugely! I felt much less discomfort in my lower back and hips and also more freedom in my seat because of this. A big thumbs up!
One of the most impressive features about The V.I.P was when squished together between two fingers I just could not make my fingers touch. In my opinion, this is where The V.I.P has the clear advantage over simple gel pads on the market. When two fingers are pushed together on gel, the gel will spread out and separate beneath the pressure to a point where you can feel your fingers touching. If this is simulated underneath the saddle with the pressure of the rider against the horse… it is clear to understand how in this instance shock absorption is minimal.
Overall I found The V.I.P to be a worthy addition to my equipment list. Although not completely transforming my horses way of going, I felt an added security under the saddle and more epaxial (back) muscle engagement and lift. I feel like with the use of this product over time, I would most definitely notice a positive development in Junior’s way of going. I would really like to see if longer front portions of the pad would improve its capabilities, as the edges of the pad did not quite end clear of the flocking panel of the saddle. Over time I could imagine this pad providing many horses with the additional help needed to develop epaxial musculature, confidence to be more supple through the back and elastic in their paces. I also feel The V.I.P would also be useful in horses being rehabilitated following an injury. As The V.I.P continues its successful journey in the equestrian world, I look forward to reading future research into its use.
Application to Equine Musculoskeletal Health
“Everything you learn becomes a shortcut for understanding something else” – Scott Adams. And this is very much true when it comes to any piece of equestrian equipment. I have learnt knowing the benefits of something is very different to understanding the benefits of something. So, based on this, I have added this section to explain how The V.I.P may be able to encourage positive musculoskeletal health for the horse with longevity in mind. A decrease in stress or pressure placed along the back will enable correct biomechanics of the thoracic vertebral column.
THE BOW AND STRING MODEL
This is a theory used to describe the correct biomechanics of the vertebral column during locomotion. It compares the animals back to an archers bow; the bow = vertebral column, associated ligaments, muscles, forelimb flexors, hind limb extensors; string = abdominal muscles, forelimb extensors, hindlimb flexors and sternum.
The horses spine is the bow, which is held in place by the engagement (not tension!) of the string. Contraction of the string (which translates to engagement of abdominal muscles) causes flexion and rounding of the bow (back).
The hyoid apparatus consists of a selection of small bones that articulate together. Its name means “shaped like the letter upsilon (Y)”, and it is situated at the base of the skull; between the cheeks of the horse. The hyoid apparatus connects to the skull via the temporohyoid joint. At this joint, the hyoid apparatus articulates with the skull. The hyoid apparatus gives biomechanical form and function to the larynx, pharynx and the tongue.
Every muscle in the horses body eventually connects to the hyoid.
The bones that make up the hyoid apparatus are the only bones in the body not to connect to another bone – they are held in place solely by ligaments.
Components of the Hyoid Apparatus:
Articulates with the petrous part of the temporal bone, allowing the stylohyoid bones to move cranially and then caudally like a pendulum.
Largest bones in the hyoid apparatus
Attaches to distal end of the stylohyoid via the epihyoid bone.
Articulation with the ceratohyoid to stylohyoid bone lengthens the stylohyoid-ceratohyoid unit.
The base of the tongue attaches to the lingual process of the basihyoid.
Can be argued to be the most important component.
Muscles are attached to the hyoid apparatus; their contraction determines its position and shape which in turn determines the shape of the larynx and nasopharynx.
Examples of muscles attached to the hyoid apparatus:
geniohyoideus – movement of the hyoid bone rostrally.
genioglossus – contraction = protracts the tongue and pulls the basihyoid bone rostrally (towards the nose).
styloglossus – contraction = retraction of the tongue
The tongue connects to the hyoid apparatus.
The hyoid apparatus has muscular connections from the throat to the forelimbs (omothyroid), shoulder (omohyoid) and sternum (sternohyoid).
Sternohyoid = hyoid to sternum; Omohyoid = basihyoid to medial scapula/subscapular fascia; these muscles provide a direct connection from the hyoid apparatus to the shoulder of the horse via the ventral neck. Tension within these muscles, along with sternothyroid, results in restricted shoulder movement and the development of hypertonicity. Contraction of these muscles can put strain on the temporomandibular joint (TMJ). Additionally, hypertrophy and hypertonicity of the sternocephalic muscle can occur when the horse strains against the bit as a result of negative pressure upsetting the hyoid apparatus.
The muscle chain continues ventrally, connecting the pectoral area to the abdominal muscles.
The abdominal muscles are connected to the pelvic muscles.
JUST A MUSCULAR CONNECTION?
“We connect all three main junctions of the horse through the bones of the hyoid in the horse’s jaw when we connect the muscles from the scapula and the sternum up to the hyoid; then from the hyoid to the occiput and finally from the poll to the nuchal ligament which then connects with the supraspinous ligament.”
“Dr. Ridgway presented it to us, muscle pathology of the long hyoid muscles ‘goes beyond just TMJ pain, it affects the entire balance of the body’. Specifically, he clarified for us that a contracted omohyoid muscle results in the following: it retracts the tongue back into the throat; interferes with the bit; locks the horse’s jaw; limits lateral flexion; interferes with shoulder freedom and range of motion; and interferes with balance and proprioception. When these long muscles are contracted, they mimic the body’s response to fear—they are a part of the Fright and Flight Muscle Groups. Dr. Ridgway reminded us that when humans react to emotional stress, we tighten our neck muscles, clench our teeth, and hunch our shoulders. It’s the same with horses.”
The Masterton Method
Connection to the TMJ
Small muscles of the hyoid apparatus connect to the TMJ and the poll. The TMJ has a dual purpose of mastication and registering of postural information. Therefore, it is an important anatomical location for nerves that control proprioception and balance; the highest concentration of mechanoreceptors (sensory nerves that report shape change) are found in the periphery of the disc and at the attachment site of local ligaments.The TMJ articulates with the hyoid apparatus.
The hyoid and cranial nerves are intricately connected with the jaw.
Function of the Hyoid Apparatus
The series of bones in the hyoid apparatus are responsible for the suspension of the larynx and tongue from the skull. The main function the hyoid is to support the tongue. It also places a role in balance.
BEAR IN MIND: Movement of the tongue by the equine dentist during a treatment can upset the balance of the hyoid.
Mouth health – due to the muscular connection from the tongue to the core, pectoral and pelvic muscles of the body… discomfort in the mouth from a poorly fitting/used/type of bit, harsh hands of the rider, poor dentition can influence whole body posture and locomotion. Also, a negative memory associated with the bit can cause the onset of “bridle lameness”. When the horse extends the cervical vertebrae longitudinally, stretches down and chews/licks softly this can indicate correct engagement and suppleness of the ventral chain. Engagement of both ventral and dorsal muscle chains is important as they work in synergy to produce correct dynamic posture and thus promote correct and healthy overall muscular development. This whole-body engagement is commonly referred to as the circle of muscles.
“A stiff poll and jaw, holding behind the vertical or a rider that hangs on to the reins can inhibit the engagement of the ventral muscle chain and therefore the hindlimb. This is why over-bending to the inside or pulling on the reins can inhibit hindlimb engagement.”
Susan E. Harris (2017) Horses Gaits, Balance and Movement: The natural mechanics of movement common to all breeds
Misalignment of the Hyoid.
Tension of the tonguecan result in tension within the muscles surrounding the sternum and the ventral neck (due to the muscular connections of the sternohyoid and omohyoid). Tension in the sternum means that the horse is unable to engage the pectoral muscles and lift through the back… an essential posture for healthy dynamic movement and collection.
Windsucking can also put stress on the hyoid apparatus and TMJ. Hypertonicity of the hyoid muscles can develop as a consequence.
Temporohyoid osteoarthopathy (THO) is also known as middle ear disease. This is a condition where the bone surrounding the temporohyoid joint is proliferated, leading to joint fusion and decreasing articulation. Aetiology is not clearly understood, but may be resultant from an inner ear/guttural pouch infection or degenerative. Fusion of the temporohyoid joint results in decreased range of motion and flexibility. This makes actions of swallowing and head/jaw/neck movement vulnerable to causing a fracture at the location where the hyoid bones attach the skull (Walker et al. 2002; Divers et al. 2006; Palus et al. 2012). The fracture commonly occurs in the stylohyoid bone. Clinical signs of a fracture include: rapid worsening of clinical signs associated with temporohyoid joint fusion, compression of the cranial nerves 7 & 8 (vestibulocochlear and facial) which are responsible for facial expression, eye lubrication and balance. Early clinical signs include: pain when pressure is applied at the base of the ear/throatlash area, tossing of the head, reluctance to accept the bit, reluctance to perform in specific head position. Once there is significant thickening of the bone there may be marked ataxia, lip and ear droop. Diganostics involve radiographs (to detect a thickening of the bone), upper airway endoscopy (to confirm diagnostics). The upper airway endoscopy involves placing the endoscope into the guttural pouch as this enables a view of the stylohyoid bone articulating with the skull. The endoscopy of a horse with THO will show enlargement of the stylohyoid bone. Checking both guttural pouches is essential as this disease can be bilateral. CT scans can provide a significantly more detailed image by detecting both bony and soft tissue changes to the hyoid apparatus, skull and inner ear. Treatment involves antibiotics, tarsorrhaphy (temporary surgical closure of the eyelids to protect the cornea), ceratohyoidectomy (removal of the ceratohyoid bone to decrease the pressure of the hyoid apparatus to the skull and thus decrease risk of fracture and incidence of pain). Prognosis is better for animals who have not suffered from pre-existing nerve damage prior to treatment; this can result in nerve deficits such as a head tilt or ear droop). Prognosis is also lower in cases where a fracture has already occurred. Further research into THO.
Tying down the Tongue
Before research into the hyoid apparatus, I was unaware of the morbid practice of tying a horses tongue to the mandible (jaw) or outside of the mouth to stop the horse from placing the tongue over the bit. Such measures are a poor attempt to improve airway function and therefore performance, along with decreasing airway noise.
Bottom line:research has shown these practices do not influence the position of the hyoid apparatus. The passive action of pulling the tongue from the mouth does differs dramatically from active muscle contraction. This is due to tying down of the tongue causing protrusion rather than depression of the tongue, and it is depression that causes the action of the extrinsic tongue muscles to dilate and stabilise the airways.
A horse MUST be able to confidently stretch over his back and down into a rider’s hands with his nose in front of the vertical, finding his full range of motion, while keeping his own free-flowing elastic balance. This is the starting point of relaxation, balance, and impulsion that builds to collection.
Assessment of Pain and Sensitivity:Application of digital pressure to 1cm below and cranial to the TMJ. There should be no reaction, yet sensitivity within this region is indicative of pain within the joint.
Assessment of Hyoid Imbalance:Hypertonicity of the hyoid musculature = often have lateral imbalances of the hyoid bones. When viewing the horses head from underneath, the tongue can be located in the depression between the two ramus of the mandibles. Applying gentle pressure underneath can identify a bony structure, which is the basihyoid bone. Lumps around this area are likely saliva glands. Feeling the location of this bone can determine deviation of the hyoid. Sliding the tips of the fingers along the inside curvature of the mandible upwards can move the hyoid gently to determine tension.
Sternocephalic muscle: assess this muscle for hypertonicity, hypertrophy. When moving, this muscle should be relaxed and swing gently from side to side.
Reaction to pain in the region of the hyoid can be adverse and quick; be cautious and slow.
Under-Scapula Release – Masterton Method (when applying this technique, the hyoid, TMJ and poll are all being assessed and treated too)
Light therapy on acupuncture points – further information linked here.
Tongue Release – this practice is controversial, as too much force on the tongue can easily place too much pressure on the hyoid bones. An article with more depth on this topic, accompanied by videos, is linked here. An example of the Tongue Release by the Masterton Method is linked here.
Hyoid Mobilisation:This practice involves placing the fingertips on the medial surface of the mandible, just to the side of the tongue. The fingers are slid upwards along the surface of the inner mandible. Starting on the looser side first, and then moving on to the stiffer side. Look out for signs of release. Hold the pressure; melt the tissue.
TARSAL BONE FUNCTION: undergo axial compression and tension alongside torsional loading during locomotion.
DISTAL TARSAL BONES: function to absorb shock and neutralise twisting forces.
Central tarsal bone absorbs most of the stresses.
The movement of the tarsus is linked to the movement of the stifle; they work in co-ordination due to the reciprocal mechanism (two opposing sets of muscles). Example: when the tarsus is flexed, the stifle also flexes simultaneously. This reciprocal mechanism is important for counteraction and absorption of concussive forces.
The tarsus is a ginglymus (capable of unidirectional movement) that is also able to absorb direct shock.
The trochlear (part of the talus bone) is important for the articulation of the tarsal joint. It articulates with the distal tibia (which is moulded so it sits over the trochlear ridges). When the joint is flexed, the distal limb is pulled slightly to one side as the trochlear ridges slant outwards. This is how the hindlimb hooves avoid hitting the abdomen; if the tarsus was a hinge joint, this would happen.
The rows of tarsal bones should have minimal movement (limited to slight gliding), and to ensure this there is a system of collateral and dorsal ligaments. The collateral ligaments are arranged in a fan shape to allow for the joint to return to its neutral position. The amount of ligaments means that fractures and laxations are not common.
The tibiotarsal joint is the joint of highest motion, accounting for 90% of the range of motion. The three lower joint below are responsible for the remaining 10% of the range of motion.
Smooth and without obvious swellings
Tarsus should be higher than the carpus
Left and right tarsal joints = symmetrical
Tarsal bones should be substantial; too light a structure increases the likelihood of injury.
When observing from behind, the whole limb should appear straight and the tarsus should lie in this straight line. There should be no major angulation inward and outwards.
Metatarsal bone should be near perpendicular to the ground when observing from the side.
Angle of the tarsal joint should not be too wide (post-legged/greater than 165 degrees) or too angled (sickle hocked/less than 155 degrees).
The range of hock angles is quite wide – a variety of angles can be present without causing lameness, it is the extreme ends of these angles that can pose a threat to soundness. Slight adaptations to angle can also benefit the horse; ie. increased tarsal angulation in dressage horses is beneficial to allow for collection potential.
The positioning of the pelvis, femur and tibia all require analysing as they can affect the location of the tarsus.
Deviation from the ideal conformation will place additional stress on tendons and ligaments.
Osteoarthritis ● Synovitis ● Osteochondrosis ● Osteitis ● Fractures (most commonly to exposed areas of tarsus such as sustentaculum tali/trochlear ridges) ● Luxation ● Ligament and tendon conditions ●Inflammation (capped hock, thorough pin, bog spavin)
The most common area for injury and damage (degeneration) is in the lower two rows of the flattened tarsal bones.
Tarsal dysfunction may cause or be resulting from a secondary or primary issue that is separate to the original issue.
Fluid in the tarsus joint; commonly on the medial aspect of the joint.
Clinical Signs: lameness (slight or absent), inflammation