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Equine Dry Needling

Andrea Schachinger · Cornelia Klarholz

Equine Dry Needling

Guide for the Schachinger Method


Table of Contents


Part 1: The Basics

1. The tissue

1.1 The muscles

1.1.1 Histological structure of the muscles
1.1.2 Action potential
1.1.3 Muscle contraction

1.2 The fascial body

1.2.1 Shape
1.2.2 Movement
1.2.3 Supply
1.2.4 Perception and communication
1.2.5 Components of the fasciae and matrix

2. The Myofascial Trigger Point

2.1 Explanatory models

2.1.1 End plate hypothesis
2.1.2 Energy crisis theory
2.1.3 Advanced integrated hypothesis

2.2 Myofascial pain syndrome

2.2.1 Referred pain
2.2.2 Myofibroblasts

2.3 Causal and perpetuating factors

2.3.1 Strain
2.3.2 Psychological factors
2.3.3 Nutrition
2.3.4 Cofactors

3. Dry Needling

3.1 Definition of the Schachinger Equine Dry Needling Method

3.1.1 Dry needling versus acupuncture

3.2 How dry needling works

3.2.1 Effects on the structure of the trigger point
3.2.2 Effects on blood flow to the tissue
3.2.3 The role of the “local twitch response” (LTR)
3.2.4 Effects on the neural structures
3.2.5 Effects on the state of tension in the trigger point
3.2.6 Biochemical effects
3.2.7 Comparing the effects of superficial (SDN) and deep dry needling (TDN)

3.3 Terminology

3.3.1 Basic treatment
3.3.2 Finetuning
3.3.3 Back line
3.3.4 Front line
3.3.5 Bony barrier
3.3.6 Bony landmarks
3.3.7 Referred Release
3.3.8 Pinching

3.4 The phenomenon of “referred release”

4. Needles and hygiene

4.1 Materials

4.1.1 The length of the needle
4.1.2 The quality of the needle

4.2 Hygiene

5. Legal Situation

Part 2: The Therapy

6. Treatment Procedure

6.1 Anamnesis

6.1.1 Vital signs

6.2 Adspection

6.3 Differential diagnosis

6.3.1 Primary diseases to be ruled out
6.3.2 Additional factors

6.4 Contraindications

6.4.1 Absolute contraindications
6.4.2 Relative contraindications

6.5 Palpation

6.5.1 Phase 1
6.5.2 Phase 2
6.5.3 Phase 3
6.5.4 Phase 4
6.5.5 Phase 5

6.6 Conducting a therapy session

6.6.1 Basic rules
6.6.2 Safety
6.6.3 Zone 1
6.6.4 Zone 2
6.6.5 Zone 3
6.6.6 Zone 4

6.7 Danger zones

7. Aftercare

7.1 Possible reactions to the dry needling treatment

7.1.1 “Educating and instructing” the horse owner

7.2 Physical exercises following treatment

7.3 Follow-up appointments

8. Treatment Zones

8.1 Zone 1 – cranial portion

8.1.1 Brachiocephalic muscle
8.1.2 Omotransversarius muscle

8.2 Zone 1 – caudal portion

8.2.1 Longissimus lumborum muscle
8.2.2 Iliocostalis muscle

8.3 Zone 2

8.3.1 Pectoralis descendens muscle
8.3.2 Biceps brachii muscle
8.3.3 Serratus ventralis muscle
8.3.4 Subclavian muscle
8.3.5 Infraspinatus muscle
8.3.6 Supraspinatus muscle
8.3.7 Deltoid muscle
8.3.8 Cervical portion of trapezius muscle
8.3.9 Rhomboid muscle
8.3.10 Triceps brachii muscle
8.3.11 Gluteus medius muscle
8.3.12 Superficial gluteal muscle
8.3.13 Semitendinosus muscle
8.3.14 Biceps femoris muscle

8.4 Zone 3

8.4.1 Semimembranosus muscle

8.5 Zone 4

8.5.1 Thoracic portion of trapezius muscle
8.5.2 Latissimus dorsi muscle
8.5.3 Longissimus thoracis and lumborum muscle

About the authors




In 1999, while I was studying at the university in Leiden, my “mettlesome” thoroughbred mare Jessyca tumbled over while trying on a saddle and landed with her nape on the tow-bar of the sales bus…

A wide range of different vets and therapists were unable to help the mare – that by now was not even able to bring her head to a horizontal position. By chance I heard of a man who allegedly worked with a special treatment technique, and he represented the final hope for Jessy and me.

Using needles, some of which were up to 12.5 cm long, he worked on the mare; watching it made me feel completely queasy, but after two treatments she actually began to get better. After a few months she was once more the “wild steed” that I knew all too well!

When I asked what kind of treatment technique this was, his answer was very clear: “It isn‘t acupuncture, anyhow! I learned this technique from a Japanese doctor in Hamburg. It’s designed for humans, but it seems to work really well on horses too!”

One year later, I found myself sitting next to this very man as an onlooker in a dry needling training course for professionals run by the Society for Myofascial Trigger Point Therapy (IMTT) in Switzerland. At that time, dry needling for humans was completely unknown in the Netherlands, and probably no one other than ourselves was yet thinking about using it to treat horses.

This experience was followed by six years of extremely intensive collaboration and a course of study in dry needling for my human patients. Becoming a member of the “International Myopain Society” and attending their international congresses brought the work to a completely new level.

Throughout these years, I have experienced real miracles. Patients who had already long exhausted the possibilities of conventional therapy methods and whose pain had been labelled a psychosomatic problem were given a new chance in life. Very often, I witnessed and initiated the complete relief of their pain. This period shaped my professional career forever.

As a horse-lover, it was not only an important but also a logical step to likewise build on the work with the horses and to ground it in sound scientific research. I went on to attend courses both at home and abroad and to enroll at the School of Animal Physiotherapy in the Netherlands, to have meetings with national and international horse trainers and to pursue every opportunity of developing my knowledge and skills further.

For six more years, I worked as a freelance collaborator at the “Beekvliet” horse clinic in the Netherlands, where (among other experience) I was supervised in my work by the orthopaedic surgeon there. What came out of this was an original method of dry needling for horses that is above all characterised by its efficiency and animal friendliness.

The relief or cure of pain in the equine musculoskeletal system is the driving motivation of all those of us who not only love but also work with these animals. Through my research over the past 15 years, I have elaborated this method to the point where it is now being taught by my team and me at the International Training Centre for Dry Needling, and can be passed on to therapists with the safe techniques that we have meanwhile developed.

This book is intended to support the work of those who want to help the equine species in a responsible and animal-friendly way.

Andrea Schachinger, Summer 2016

Part 1:

The Basics


1. The tissue

As a therapeutic approach to impaired movement and muscular problems in the horse, the Schachinger Dry Needling Method requires prior understanding of the complex interconnections between tissue structure, physiologically correct muscle function and neurological connectivity.

We need to know how the body regulates its movements in order to be able to recognise any dysfunction in this system. Healing can only occur if the body is empowered to heal itself. This requires the therapist to form a clear, inner picture of their perception and the necessary measures. The better you can visualise what your hand is feeling during palpation and the effect of your treatment, the better-focused your work will be.

1.1 The muscles

1.1.1 Histological structure of the muscles

The skeletal muscles are made up of individual muscle cells, which have a diameter of about 0.5 mm, but which can reach the considerable length of up to 40 cm. However, most muscle fibres are shorter than 10 cm. The outer membrane of the muscle cell is called a sarcolemma. A fine layer of connective tissue, the endomysium, surrounds several muscle cells, uniting them together in a bundle of muscle fibres. These muscle fibre bundles, also called fascicles, are in turn enclosed by a further connective-tissue – and therefore fascial – structure: the perimysium, which divides the fascicles and forms the boundary between them. The entire muscle fibre bundle located in the perimysium is surrounded by the outermost layers of the fascial structures, which are called the epimysium or muscle fascia. This layered embedding of the muscle cells in fascial tissue enables the fascicles to slide against one another and ensures not only the unhindered contraction of individual subzones of a muscle, but also the free mobility of different muscles next to one another.

The structure and function of the fascial connective tissue described here is going to be of decisive importance for the mobility of a body in this clinical overview of the phenomenon of trigger points and of myofascial pain syndrome.


Fig. 1: Muscle fibre bundle

The capacity of a muscle cell to contract becomes clear through examining its inner structure. A single muscle cell contains 1000 to 2000 myofibrils running parallel to one another. They are surrounded by sarcoplasm, which in addition contains three further structures which are necessary for the energy production of the cell as well as the contraction processes.

These are the mitochondria, the sarcoplasmic reticulum and what are called “T-tubules” (transversal tubules). The latter are, incidentally, integrated all the way deep into the cell structure through invaginations of the sarcolemma. The myofibrils consist of long chains of sarcomeres, whereby a single sarcomere reaches a length of just 1.5–2 μm. On the inside of the sarcomere we find the actual structures with the capacity to contract: two different, thread-shaped proteins interlock like interlaced fingers. Th is visual appearance is expressed in their name. What we are talking about here are the actin and myosin filaments.


Fig. 2: Microscopic structure of the myofibril

The sarcomere can be imagined as a small cylinder. Attached to both ends are actin filaments, which point to each other with their thin, thread-shaped molecule chains towards the centre of the sarcomere, but do not touch. Each sarcomere contains about 3000 of these actin filaments arranged parallel to one another. Positioned centrally between them lie the markedly thicker myosin filaments, with approx. 1500 filaments in each sarcomere. Each myosin filament is composed of several 100 myosin molecules arranged in a regular parallel pattern. The myosin molecules consist of two parts – a head and a shaft. The head parts of the myosin filaments are small, laterally positioned thickened bulges, which will play a decisive role in muscle contraction; their neck parts are mobile.

Although actin and myosin are the actual protein molecules which carry out the contraction of the muscle cell, this would not be possible without the help of the auxiliary proteins of the surrounding structures. What is called the Z-line forms the point of contact between one sarcomere and the next in the longitudinal course of the myofibril, and the protein α-actin holds the actin filaments in place here. Sarcomeres that lie next to each other are connected by the protein desmin. During a contraction, the elastic titin, as already mentioned, holds the myosin filaments in their place in the centre, between two Z-lines. In the middle of the myosin filaments is what is called the “M-line”, on which the myosin filaments are arranged in a regular pattern by further proteins such as myomesin and M-creatine kinase. The T-tubules, the fine invaginations of the sarcolemma, now come into play again: they sit on the Z and M-line of the sarcomere respectively. The T-tubules are important for muscle excitation, and we will be looking at them again later on.

1.1.2 Action potential

Every movement begins with the action potential – that is, the electrical stimulation that is passed on to the muscles in a nerve cell of the central nervous system. This nerve cell, the motoneuron, has a process called an “axon” on its end, which is located on the periphery of the body. This is enveloped by a sheath called Mauthner’s membrane, and together they form the actual nerve fibres. Their task consists of transporting the electrical nerve impulse from the cell body. For this purpose, the axon of the motoneuron has a special neuronal switchpoint – the motor end plate. It does not directly touch the muscle fibre, but is instead separated from it by the synaptic cleft. Small bulges on the axon, the synaptic boutons, contain secretion vesicles. These vesicles are filled with the neurotransmitter acetylcholine, the essential messenger substance. If the electrical stimulation reaches the axon, the change in electrical potential creates a situation in which positively charged calcium ions are attracted from the direct area of the motor end plate and migrate into the axion through voltage-controlled channels which open up. The vesicles start to move and when they have reached the outer membrane, they release acetylcholine into the synaptic cleft. Up to now, the entire process is still taking place inside the nerve fibre and is called “presynaptic”. Everything that is taking place on the other side of the synapse is the postsynaptic reaction.

This is where we encounter the sarcolemma again. On its surface is a specially structured area of membrane with multiple folds, which is known as a subneural folded apparatus. In the subneural folded apparatus, the released acetylcholine molecules make contact with receptors which have ion channels for sodium, potassium and calcium ions.

Even in a state of rest, a small amount of acetylcholine is constantly being released into the synaptic cleft. There is something called a miniature end-plate potential which does not produce a muscle contraction. Once a certain amount of acetylcholine has been released, the stimulus threshold is exceeded, at which point the contraction is then clearly triggered.

Due to the binding of the acetylcholine to its receptors on the surface of the sarcolemma, channels in turn open which initially allow sodium ions to enter, at first resulting in a change of electrical potential on the surface of the muscle cell, the sarcolemma. Th is depolarisation of the muscle cell does not yet represent new action potential, but instead remains below-threshold as a passive dispersal of electrical potential without a response. If a threshold level is exceeded, further ion channels open into the T-tubules of the sarcolemma and calcium ions flow into the intracellular space.