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The College of Animal Physiotherapy

Diploma in Animal Physiotherapy

Module 5

Neurology

Copyright: The College of Animal Physiotherapy Ltd 2011

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AIMS

To extend the students knowledge of the structure and function of the nervous

system.

To familiarise students with some of the key neurological disorders.

To enable students to identify the role of physiotherapy in the treatment of

neurological disorders.

OBJECTIVES

At the end of this module you should be able to;

Describe the key features of nerves and synapses.

Describe the basic mechanism of nerve conduction.

Identify the main features of the brain and spinal cord.

Identify the composition of the parasympathetic nervous system.

Identify key nerves of the horse and dog and their relative skeletal muscles.

Identify physiotherapy options suitable for neurological conditions.

Outline the main features of the neurological conditions and their symptoms.

CONTENTS

INTRODUCTION 3

SECTION 1 – The ‘brains’ of the nervous system 4

Neurons 4

Synapses 10

Ions 13

Action potential 16

Impulse conduction 19

SECTION 2 – The systems 22

THE Central Nervous System 22

The Spinal Cord 22

The brain 23

The Peripheral Nervous System 30

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The Autonomic Nervous System 31

The Sympathetic Nervous System 32

The Parasympathetic Nervous System 32

The Enteric Nervous System 30

SECTION 3 – Pain 34

Synapses blocking pain signals 34

Pain and why it hurts 34

The Gate Control theory 36

Pain Relief 38

Pain Receptors 38

SECTION 4 – Physiotherapy options 41

Neurological Examination 41

Physiotherapy Treatment 41

Motor Muscle Points 44

SECTION 5 – Neurological conditions 45

Equine Conditions 45

Canine Conditions 46

Toxicity and poisoning 47

APPENDIX 1 – KEY TERMINOLOGY 48

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APPENDIX 2– CASE STUDY 49

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INTRODUCTION You have studied the scaffolding of the animal, his skeleton. You have studied the

prime mover of the animal, his muscles. Now you will study his control centre, the

Neurological system. The Neurological system has a complex anatomy. It provides

instructions for all movement and function of the body. Damage to any part will have an

undesired effect on the normal function of the animal. This can be as little as an

atrophied muscle through to severe paralysis and death.

Neurological disease is dynamic. Often the signs are masked by other conditions.

Equally some conditions can present with neurological signs even though no disease is

present. The deterioration of an animal with a degenerative condition can be heart

wrenching. For an owner to see their much loved companion becoming depressed and

functionally compromised brings both distress and frustration as they are unable to do

anything about it . This change in the owner will add to the distress of the animal who is

already suffering with the progressive effects of the disease. The role of physiotherapy

in these cases will not only slow the deterioration and increase the comfort of the animal

but will increase the quality of life for both the animal and their owner.

Physiotherapy treatment of neurological disease is usually supportive rather than

curative. However, where there is a possibility of repair, much can be done to aid

healing and return normal function. Excellent results have been achieved in treating

damaged muscles and their nerve supply, returning them to normal function. Many of

these cases would have otherwise deteriorated, usually ending the animals‘ working

career (if they have one) and possibly leading to euthanasia.

To have a good understanding of the control network of the animals‘ body is a prime

requirement in the successful treatment of neurological disease.

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SECTION 1

THE “BRAINS” OF THE NERVOUS SYSTEM

Neurons and Neurotransmitters: The "Brains" of the Nervous System

Introduction

The nervous system serves three functions:-

The nervous system is the body's control and communication network, this system:

* Senses changes both in and outside the body (the sensory function).

* Interprets and explains the changes (the integrative function).

* Responds to the interpretation by making muscles interact and glands secrete

hormones or other chemicals into the bloodstream (the motor function).

The nervous system itself has two main parts: The central nervous system includes

the brain and spinal cord, acts as a "control centre." The peripheral nervous system

includes all other nerve elements. These elements connect the brain and spinal cord to

muscles and glands.

Neurons "power" these functions

To serve its three functions, the nervous system includes vast circuits of delicate cells

that are elaborately interconnected. In fact, the brain, spinal cord, and nerves

throughout the body are all made up of one kind of cell. These are nerve cells, also

called neurons. The brain includes billions of neurons; so does the spinal cord and all

the nerves that fan out from the spinal cord to the glands, organs, and muscles.

Neurons are specialised. Their specific function is to allow the brain to learn, reason, and

remember. Through the activity of neurons, the body responds and adjusts to changes in

the environment. These changes, called stimuli, set off impulses in our sense organs:

the eye, ear, organs of taste and smell, and sensory receptors located in the skin, joints,

muscles, and other parts of the body.

Every time you feel something, including the effects of a drug, millions of neurons are

"firing" messages to and from one another. Those messages consist of chemicals and

electrical impulses.

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Neurons

What is inside of a neuron? A neuron has many of the same "organelles," such as

mitochondria, cytoplasm and a nucleus, as other cells in the body.

* Nucleus - contains genetic material (chromosomes) including information for cell

development and synthesis of proteins necessary for cell maintenance and survival.

Covered by a membrane.

* Nucleolus - produces ribosomes necessary for translation of genetic information

into proteins

* Nissl Bodies - groups of ribosomes used for protein synthesis.

* Endoplasmic reticulum (ER) - system of tubes for transport of materials within

cytoplasm. Can have ribosomes (rough ER) or no ribosomes (smooth ER). With

ribosomes, the ER is important for protein synthesis.

* Golgi Apparatus - membrane-bound structure important in packaging peptides

and proteins (including neurotransmitters) into vesicles.

* Microfilaments/Neurotubules - system of transport for materials within a neuron

and may be used for structural support.

* Mitochondria - produce energy to fuel cellular activities.

The nucleus of a neuron is located in the cell body. Extending out from the cell body are

processes called dendrites and axons. These processes vary in number & relative length

but always serve to conduct impulses (with dendrites conducting impulses toward the

cell body and axons conducting impulses away from the cell body).

Structure of a nerve cell

A neuron is a cell specialised to conduct electrochemical impulses called nerve impulses

or action potentials. All neurons outside the central nervous system (and many within it)

conduct impulses along hairlike cytoplasmic extensions, the nerve fibres or axons. The

axons connecting your spinal cord to your foot can be as much as 1 m long (although

only a few micrometers in diameter) and contain microtubules, intermediate filaments

and vesicles.

The cell body, which is also called the perikaryon, contains the nucleus and the usual

cytoplasmic organelles. The nucleolus is large, reflecting a high rate of ribosome

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production. The cytoplasm is rich in ribosomes, many of which are attached to the

endoplasmic reticulum. The rate of protein synthesis is also high, in part because the

cell body supplies proteins to the axon which lacks the machinery for protein synthesis.

Therefore neurons are similar to other cells in the body because:

1. Neurons are surrounded by a cell membrane.

2. Neurons have a nucleus that contains genes.

3. Neurons contain cytoplasm, mitochondria and other "organelles".

4. Neurons carry out basic cellular processes such as protein synthesis and energy

production.

However, neurons differ from other cells in the body because:

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1. Neurons have specialised extensions called dendrites and axons. Dendrites

bring information to the cell body and axons take information away from the cell body.

2. Neurons communicate with each other through an electrochemical process.

3. Neurons contain some specialised structures (for example, synapses) and

chemicals (for example, neurotransmitters).

One way to classify neurons is by the number of extensions that extend from the

neuron's cell body (soma).

Unipolar neuron

Unipolar neurons have only one process from the cell body. However, that single, very

short, process splits into longer processes (a dendrite plus an axon). Unipolar neurons

are sensory neurons - conducting impulses into the central nervous system.

Bipolar neurons have two processes extending from the cell body - one axon & one

dendrite. These neurons are also sensory. For example, biopolar neurons can be found

in the retina of the eye (examples: retinal cells, olfactory epithelium cells).

Pseudounipolar cells (example: dorsal root ganglion cells). Actually, these cells have 2

axons rather than an axon and dendrite. One axon extends centrally toward the spinal

cord, the other axon extends toward the skin or muscle.

Multipolar neurons have many processes that extend from the cell body. However, each

neuron has only one axon (examples: spinal motor neurons, pyramidal neurons, Purkinje

cells). Functionally, these neurons are either motor (conducting impulses that will cause

activity such as the contraction of muscles) or association (conducting impulses and

permitting 'communication' between neurons within the central nervous system).

Neurons can also be classified by the direction that they send information.

Sensory (or afferent) neurons: send information from sensory receptors (e.g., in skin,

eyes, nose, tongue, ears) TOWARD the central nervous system.

1. Sensory neurons run from the various types of stimulus receptors, e.g.,

* touch

* odour

* taste

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* sound

* vision

to the central nervous system (CNS), the brain and spinal cord. The cell bodies of the

sensory neurons leading to the spinal cord are located in clusters, called ganglia, next to

the spinal cord. The axons usually terminate at interneurons.

Motor (or efferent) neurons: send information AWAY from the central nervous system to

muscles or glands.

Motor neurons transmit impulses from the central nervous system to the

* muscles and

* glands

that carry out the response.

Most motor neurons are stimulated by interneurons, although some are stimulated

directly by sensory neurons.

Excitable Cells

Excitable cells are those that can be stimulated to create a tiny electric current. Links to

* muscle fibres

* types of neurons

* Muscle cells and

* nerve cells (neurons) are excitable.

The electric current in neurons is used to rapidly transmit signals through the animal.

However, in muscles it is used to initiate contraction.

Interneurons: transmit information between sensory neurons and motor neurons.

Most interneurons are located in the central nervous system.

These are found exclusively within the spinal cord and brain. They are stimulated by

signals reaching them from

* sensory neurons

* other interneurons or

* both.

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Axons

Axons grow out of the cell body, which houses the nucleus as well as other organelles

such as the endoplasmic reticulum. The length of some axons is so great that it is

difficult to see how the cell body can control them. Nevertheless, there is a steady

transport of materials (e.g., vesicles, mitochondria) from the cell body along the entire

length of the axon. This flow is driven by kinesins moving along the many microtubules

in the cytoplasm within the axon.

In many neurons, nerve impulses are generated in short, branched fibres called

dendrites and also in the cell body. The impulses are then conducted along the axon,

which usually branches several times close to its end.

Myelinated Neurons

Many axons are covered with a fatty sheath, the myelin sheath. It is the greatly-

expanded plasma membrane of an accessory cell, the Schwann cell, Neuroglial, or

glial, cell, whose general functions include:-

1 - forming myelin sheaths

2 - protecting neurons (via phagocytosis)

3 - regulating the internal environment of neurons in the central nervous system

Schwann cells are spaced at regular intervals along the axon. Their plasma membrane

is wrapped around and around the axon forming the myelin sheath.

Where the sheath of one Schwann cell meets the next, the axon is unprotected. The

voltage-gated sodium channels of myelinated neurons are confined to these spots called

nodes of Ranvier.

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The in-rush of sodium ions at one node creates just enough depolarisation to reach the

threshold of the next. In this way, the action potential (explained later) jumps from one

node to the next. This results in much faster propagation of the nerve impulse than is

possible in non-myelinated neurons.

Synapse

This is the point of impulse transmission between neurons; impulses are transmitted

from pre-synaptic neurons to post-synaptic neurons

At first, it was thought that axons and dendrites simply ran through the body

continuously, like wires. Then it was discovered that a space exists between each axon

and dendrite:- a synaptic gap, or synapse. The synapse is the space between the

axon of one neuron and the dendrites of the next neuron in a nerve pathway. That gap is

extremely small-about one-millionth of an inch.

Synapses usually occur between the axon of a pre-synaptic neuron and a dendrite or

cell body of a post-synaptic neuron. At a synapse, the end of the axon is 'swollen' and

referred to as an end bulb or synaptic knob.

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An impulse travelling down an axon is transmitted by means of the synapse to the

dendritic processes of another neuron. From the dendritic processes of the second

neuron the impulse is propagated by the plasma membrane down its axon to another

neuron and so on…….

Synapses made by sensory neurons and by interconnecting neurons are always of the

neuron to neuron type. However the axons of effector neurons transmit impulses to

other target cells, usually striated muscles and the smooth muscle cells surrounding

glands. At the synapse the signal is passed from cell to cell by chemical means. The

membrane of the transmitting cell (presynaptic cell) is separated by a gap, called the

synaptic cleft, from the membrane of the receiving cell (post synaptic cell).

Types of neurotransmitters:

1- Excitatory - neurotransmitters that make membrane potential less negative (via

increased permeability of the membrane to sodium) &, therefore, tend to 'excite' or

stimulate the postsynaptic membrane

2 - Inhibitory - neurotransmitters that make membrane potential more negative (via

increased permeability of the membrane to potassium) &, therefore, tend to 'inhibit' (or

make less likely) the transmission of an impulse.

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Neurotransmitter Mobilisation and Release

At the synaptic terminal (the presynaptic ending), an electrical impulse will trigger the

migration of vesicles containing neurotransmitters toward the presynaptic membrane.

The vesicle membrane will fuse with the presynaptic membrane releasing the

neurotransmitters into the synaptic cleft. Until recently, it was thought that a neuron

produced and released only one type of neurotransmitter. However, there is now

evidence that neurons can contain and release more than one kind of neurotransmitter.

Diffusion of Neurotransmitters Across the Synaptic Cleft

The neurotransmitter molecules then diffuse across the synaptic cleft where they can

bind with receptor sites on the postsynaptic ending to influence the electrical response in

the postsynaptic neuron. In the figure on the right, the postsynaptic ending is a dendrite

(axodendritic synapse), but synapses can occur on axons (axoaxonic synapse) and cell

bodies (axosomatic synapse).

When a neurotransmitter binds to a receptor on the postsynaptic side of the synapse, it

changes the postsynaptic cell's excitability: it makes the postsynaptic cell either more or

less likely to fire an action potential. If the number of excitatory postsynaptic events is

large enough, they will add to cause an action potential in the postsynaptic cell and a

continuation of the "message."

Turning Synapses Off

Once its job is done, the neurotransmitter must be removed from the synaptic cleft to

prepare the synapse for the arrival of the next action potential. Two methods are used:

* Reuptake. The neurotransmitter is taken back into the synaptic knob of the

presynaptic neuron by active transport. All the neurotransmitters except acetylcholine

use this method.

* Acetylcholine is removed from the synapse by enzymatic breakdown into

inactive fragments. The enzyme used is acetylcholinesterase.

Nerve gases used in warfare (e.g., sarin) and the organophosphate insecticides (e.g.,

parathion) achieve their effects by inhibiting acetylcholinesterase thus allowing ACh to

remain active. Atropine is used as an antidote because it blocks ACh muscarinic

receptors.

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Synapses:- how they fit in?

The co-ordination of cellular activities in animals is usually considered to involve

* an endocrine system: where the response is to hormones: chemicals secreted

into the blood by endocrine glands and carried by the blood to the responding cell.

* a nervous system: response to electrical impulses passing from the central

nervous system to muscles and glands.

But, in fact, co-ordination by the nervous system is also chemical. Most neurons achieve

their effect by releasing chemicals, the neurotransmitters, on a receiving cell:

* another neuron (a "postsynaptic" neuron)

* a muscle cell

* a gland cell

So the real distinction between nervous and endocrine co-ordination is that nervous co-

ordination is

* faster and

* more localised

(Neurotransmitters are chemicals that act in a paracrine fashion.)

The junction between the axon terminals of a neuron and the receiving cell is called a

synapse. (Synapses at muscle fibres are also called neuromuscular junctions or

myoneural junctions.)

Ion Channels

Channel proteins form hydrophilic (water loving) pores across (water hating)

membranes. These channel proteins in the bi-lipid plasma membrane of animal cells

connect the cytosol (cytoplasm) to the cell exterior and have narrow highly selective

pores. These protein channels are specifically concerned with inorganic ion transport

e.g. Na +, Ca 2+, K +, and Cl – and are called ion channels.

These channels cannot be coupled with energy sources to carry out active transport and

therefore their transport mediation is always passive. Thus, the function of the ion

channel is to allow specific inorganic ions to diffuse rapidly down their electrochemical

gradients across the cell membrane (lipid bi-layer). As the concentration of ions

increases, the flux of ions through the channel increases proportionally but then levels

off (saturates) at a maximum rate. Although transport of ions is passive the ion channels

themselves can still be controlled, and in turn, ion fluxes can also be controlled, which is

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an important control mechanism of cell function, especially in nerve cells when they are

receiving, conducting and transmitting signals.

Ion channels are not continuously open. Instead they have gates which open briefly

and then close again. In most cases the gates open in response to a specific stimulus.

The main types of stimuli that are known to cause ion channels to open and close are a

change in the voltage across the membrane (voltage gated channels), a mechanical

stress (mechanically gated channels) or the binding of a ligand (ligand gated ion

channels). The ligand can either be an extracellular mediator, specifically, a

neurotransmitter; or an intracellular mediator, such as an ion or a nucleotide

Gated Ion Channels Closed

Open

Voltage-Gated Ligand-Gated Extracellular

Ligand-gated Intracellular

Mechanically-Gated

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Nervous System Physiology

Neurons can respond to stimuli and conduct impulses because a membrane potential is

established across the cell membrane. In other words, there is an unequal distribution of

ions (charged atoms) on the two sides of a nerve cell membrane.

Establishment of the Resting Membrane Potential

Membranes are polarised or, in other words, exhibit a RESTING MEMBRANE

POTENTIAL. This means that there is an unequal distribution of ions (atoms with a

positive or negative charge) on the two sides of the nerve cell membrane. This

POTENTIAL generally measures about 70 millivolts (with the INSIDE of the membrane

negative with respect to the outside). So, the RESTING MEMBRANE POTENTIAL is

expressed as -70 mV, and the minus means that the inside is negative relative to (or

compared to) the outside. It is called a RESTING potential because it occurs when a

membrane is not being stimulated or conducting impulses (in other words, it's resting).

Ionic Relations in the Cell

The sodium/potassium ATP produces a concentration of Na+ outside the cell that is

some 10 times greater than that inside the cell and a concentration of K+ inside the cell

some 20 times greater than that outside the cell.

The concentrations of chloride ions (Cl-) and calcium ions (Ca2+) are also maintained at

greater levels outside the cell EXCEPT that some intracellular membrane-bounded

compartments may also have high concentrations of Ca2+.

What factors contribute to membrane potential?

Two ions are responsible: sodium (Na+) and potassium (K+). An unequal distribution of

these two ions occurs on the two sides of a nerve cell membrane because carriers

actively transport these two ions: sodium from the inside to the outside and potassium

from the outside to the inside. AS A RESULT of this active transport mechanism

(commonly referred to as the SODIUM - POTASSIUM PUMP), there is a higher

concentration of sodium on the outside than the inside and a higher concentration of

potassium on the inside than the outside.

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The nerve cell membrane also contains special passageways for these two ions that are

commonly referred to as GATES or CHANNELS. Thus, there are SODIUM GATES and

POTASSIUM GATES. These gates represent the only way that these ions can pass

through the nerve cell membrane. IN A RESTING NERVE CELL MEMBRANE, all the

sodium gates are closed and some of the potassium gates are open. AS A RESULT,

sodium cannot diffuse through the membrane & largely remains outside the membrane.

HOWEVER, some potassium ions are able to diffuse out.

OVERALL, THEREFORE, there are lots of positively charged potassium ions just inside

the membrane and lots of positively charged sodium ions PLUS some potassium ions on

the outside. THIS MEANS THAT THERE ARE MORE POSITIVE CHARGES ON THE

OUTSIDE THAN ON THE INSIDE. In other words, there is an unequal distribution of

ions or a resting membrane potential. This potential will be maintained until the

membrane is disturbed or stimulated. Then, if it's a sufficiently strong stimulus, an action

potential will occur.

Action Potential

The action potential is all-or-nothing. It is a very rapid change in membrane potential that

occurs when a nerve cell membrane is stimulated. The strength of the action potential is

an intrinsic property of the cell. So long as they can reach the threshold of the cell,

strong stimuli produce no stronger action potentials than weak ones. However, the

strength of the stimulus is encoded in the frequency of the action potentials that it

generates.

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Specifically, the membrane potential goes from the resting potential (typically -70 mV) to

some positive value (typically about +30 mV) in a very short period of time (just a few

milliseconds).

What causes this change in potential to occur? The stimulus causes the sodium gates

(or channels) to open and, because there's more sodium on the outside than the inside

of the membrane, sodium then diffuses rapidly into the nerve cell. All these positively-

charged sodium ions rushing in cause the membrane potential to become positive (the

inside of the membrane is now positive relative to the outside). The sodium channels

open only briefly, then close again.

The potassium channels then open, and, because there is more potassium inside the

membrane than outside, positively-charged potassium ions diffuse out. As these positive

ions go out, the inside of the membrane once again becomes negative with respect to

the outside.

Threshold stimulus & potential

* Action potentials occur only when the membrane is stimulated (depolarised)

enough so that sodium channels open completely. The minimum stimulus needed to

achieve an action potential is called the threshold stimulus.

* The threshold stimulus causes the membrane potential to become less negative

(because a stimulus, no matter how small, causes a few sodium channels to open and

allows some positively-charged sodium ions to diffuse in).

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* If the membrane potential reaches the threshold potential (generally 5 - 15 mV

less negative than the resting potential), the voltage-regulated sodium channels all open.

Sodium ions rapidly diffuse inward, & depolarisation occurs.

All-or-Nothing Law - action potentials occur maximally or not at all. In other words,

there's no such thing as a partial or weak action potential. Either the threshold potential

is reached and an action potential occurs, or it isn't reached and no action potential

occurs.

Depolarisation

Certain external stimuli reduce the charge across the plasma membrane.

* mechanical stimuli (e.g., stretching, sound waves) activate mechanically-gated

sodium channels

* certain neurotransmitters (e.g., acetylcholine) open ligand-gated sodium

channels.

In each case, the facilitated diffusion of sodium into the cell reduces the resting potential

at that spot on the cell creating an excitatory postsynaptic potential or EPSP.

If the potential is reduced to the threshold voltage (about -50 mV in mammalian

neurons), an action potential is generated in the cell.

This depolarisation causes the membrane to open up hundreds of voltage-gated

sodium channels in that portion . During the millisecond that the channels remain open,

some 7000 Na+ rush into the cell. The sudden complete depolarisation of the membrane

opens up more of the voltage-gated sodium channels in adjacent portions of the

membrane. In this way, a wave of depolarisation sweeps along the cell. This is the

action potential (In neurons, the action potential is also called the nerve impulse.)

The Refractory Period

A second stimulus applied to a neuron (or muscle fibre) less than 0.001 second after the

first will not trigger another impulse. The membrane is depolarised and the neuron is in

its refractory period. Not until the -70 mV polarity is re-established will the neuron be

ready to fire again.

Repolarisation is first established by the facilitated diffusion of potassium ions out of the

cell. Only when the neuron is finally rested are the sodium ions that came in at each

impulse actively transported back out of the cell.

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In some neurons, the refractory period lasts only 0.001-0.002 seconds. This means that

the neuron can transmit 500-1000 impulses per second.

ABSOLUTE REFRACTORY PERIOD –

* During an action potential, a second stimulus will not produce a second action

potential (no matter how strong that stimulus is)

* corresponds to the period when the sodium channels are open (typically just a

millisecond or less)

RELATIVE REFRACTORY PERIOD-

* Another action potential can be produced, but only if the stimulus is greater than

the threshold stimulus

* corresponds to the period when the potassium channels are open (several

milliseconds)

* the nerve cell membrane becomes progressively more ‘sensitive’ (easier to

stimulate) as the relative refractory period proceeds. So, it takes a very strong stimulus

to cause an action potential at the beginning of the relative refractory period, but only a

slightly above threshold stimulus to cause an action potential near the end of the relative

refractory period.

Hyperpolarisation

Despite their name, some neurotransmitters inhibit the transmission of nerve impulses.

They do this by opening

* chloride channels and/or

* potassium channels in the plasma membrane.

In each case, opening of the channels increases the membrane potential by

* letting negatively-charged chloride ions (Cl-) IN and

* positively-charged potassium ions (K+) OUT

This hyperpolarisation is called an inhibitory postsynaptic potential (IPSP).

Although the threshold voltage of the cell is unchanged, it now requires a stronger

excitatory stimulus to reach threshold.

Impulse conduction

An impulse is simply the movement of action potentials along a nerve cell. Action

potentials are localised (only affect a small area of nerve cell membrane). So, when one

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occurs, only a small area of membrane depolarises (or ‘reverses’ potential). As a result,

for a split second, areas of membrane adjacent to each other have opposite charges

(the depolarised membrane is negative on the outside & positive on the inside, while the

adjacent areas are still positive on the outside and negative on the inside). An electrical

circuit (or ‘mini-circuit’) develops between these oppositely-charged areas (or, in other

words, electrons flow between these areas). This ‘mini-circuit’ stimulates the adjacent

area and, therefore, an action potential occurs. This process repeats itself and action

potentials move down the nerve cell membrane. This ‘movement’ of action potentials is

called an impulse.

Conduction Velocity

* impulses typically travel along neurons at a speed of anywhere from 1 to 120

meters per second

* the speed of conduction can be influenced by:

* the diameter of a fibre

* temperature

* the presence or absence of myelin

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Speed of conduction relative to fibre type

This is not related to impulse strength, but to diameter, to presence / absence of

myelin sheath and, to a lesser degree, to temperature. Impulse speeds vary

according to the type of nerve fibre.

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* A type fibres (fast). These are the largest, 5 to 20m in diameter, and all

myelinated. Nerves relaying impulses related to touch, pressure, position of joints

and temperature as well as those connecting to skeletal muscle are all A type.

* B type fibres (fast). Have a diameter of 3m or less and are found in

nerves transmitting impulses from viscera to brain and spinal cord. They also

make up axons of efferent neurons of viscera that extend from the brain and

spinal cord to autonomic ganglia. B type are also myelinated.

C type fibres (slower). The smallest, 0.5 t0 1.5m, these are

unmyelinated. They conduct some impulses for pain, touch etc from the

skin and viscera. Motor functions include functions of the autonomic

nervous system.

Therefore we can see that neurons with myelin (or myelinated neurons) conduct

impulses much faster than those without myelin. Impulses ‘jump’ over the areas of

myelin – going from node to node in a process called salutatory conduction (with

the word salutatory meaning ‘jumping’):

When an impulse arrives at the end bulb, the end bulb membrane becomes more

permeable to calcium. Calcium diffuses into the end bulb & activates enzymes that

cause the synaptic vesicles to move toward the synaptic cleft. Some vesicles fuse with

the membrane and release their neurotransmitter (a good example of exocytosis). The

neurotransmitter molecules diffuse across the cleft and fit into receptor sites in the

postsynaptic membrane. When these sites are filled, sodium channels open & permit an

inward diffusion of sodium ions. This, of course, causes the membrane potential to

become less negative (or, in other words, to approach the threshold potential). If enough

neurotransmitter is released, and enough sodium channels are opened, then the

membrane potential will reach threshold. If so, an action potential occurs and spreads

along the membrane of the post-synaptic neuron (in other words, the impulse will be

transmitted). If insufficient neurotransmitter is released, the impulse will not be

transmitted.

This describes what happens when an ‘excitatory’ neurotransmitter is released at a

synapse. However, not all neurotransmitters are ‘excitatory’, as discussed earlier.

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SECTION 2

THE SYSTEMS

THE CENTRAL NERVOUS SYSTEM

The central nervous system is divided into two parts: the brain and the spinal cord. The

brain contains about 100 billion nerve cells (neurons) and many more "support cells"

called glia. The spinal cord is much shorter than the vertebral column (the collection of

bones, back bone, that houses the spinal cord).

The spinal cord

* conducts sensory information from the peripheral nervous system (both somatic

and autonomic) to the brain

* conducts motor information from the brain to our various effectors

* skeletal muscles

* cardiac muscle

* smooth muscle

* glands

* serves as a minor reflex centre

Approximately 42 pairs of spinal nerves arise along the spinal cord in the horse and

approximately 36 in the Dog. These are "mixed" nerves because each contains both

sensory and motor axons. However, within the spinal column,

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* all the sensory axons pass into the dorsal root ganglion where their cell bodies

are located and then on into the spinal cord itself.

* all the motor axons pass into the ventral roots before uniting with the sensory

axons to form the mixed nerves.

The spinal cord carries out two main functions:

* It connects a large part of the peripheral nervous system to the brain. Information

(nerve impulses) reaching the spinal cord through sensory neurons is transmitted up

into the brain. Signals arising in the motor areas of the brain travel back down the cord

and leave in the motor neurons.

* The spinal cord also acts as a minor co-ordinating centre responsible for some

simple reflexes like the withdrawal reflex.

The interneurons carrying impulses to and from specific receptors and effectors are

grouped together in spinal tracts.

The brain

* receives sensory input from the spinal cord as well as from its own nerves (e.g.,

olfactory and optic nerves)

* devotes most of its volume (and computational power) to processing its various

sensory inputs and initiating appropriate — and co-ordinated — motor outputs.

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The brain of all vertebrates develops from three swellings at the anterior end of the

neural canal of the embryo. From front to back these develop into the

* forebrain (also known as the prosencephalon)

* midbrain (mesencephalon)

* hindbrain (rhombencephalon)

The brain receives nerve impulses from the spinal cord and pairs of cranial nerves.

Some of the cranial nerves are "mixed", containing both sensory and motor axons.

Some, e.g., the optic and olfactory nerves contain sensory axons only. Some, e.g. ones

that control eyeball muscles, contain motor axons only.

The Hindbrain

The main structures of the hindbrain are the

* medulla oblongata

* pons and

* cerebellum

Medulla oblongata

The medulla looks like a swollen tip to the spinal cord. Nerve impulses arising here

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rhythmically stimulate the intercostal muscles and diaphragm making breathing

possible; regulate heartbeat; regulate the diameter of arterioles thus adjusting blood

flow. The neurons controlling breathing have mu (µ) receptors, the receptors to which

opiates, like heroin, bind. This accounts for the suppressive effect of opiates on

breathing. Destruction of the medulla causes instant death.

Pons

The pons seems to serve as a relay station carrying signals from various parts of the

cerebral cortex to the cerebellum. Nerve impulses coming from the eyes, ears, and

touch receptors are sent to the cerebellum. The pons also participates in the reflexes

that regulate breathing.

The reticular formation is a region running through the middle of the hindbrain (and on

into the midbrain). It receives sensory input (e.g., sound) from higher in the brain and

passes these back up to the thalamus. The reticular formation is involved in sleep and

arousal.

Cerebellum

The cerebellum consists of two deeply-convoluted hemispheres. Although it represents

only 10% of the weight of the brain, it contains as many neurons as all the rest of the

brain combined.

Its most clearly understood function is to co-ordinate body movements. Animals with

damage to their cerebellum are able to perceive the world as before and to contract their

muscles, but their motions are jerky and uncoordinated.

So the cerebellum appears to be a centre for learning motor skills (implicit memory).

Laboratory studies have demonstrated both long-term potentiation (LTP) and long-term

depression (LTD) in the cerebellum.

The Midbrain

The midbrain occupies only a small region, however it is relatively much large in "lower"

vertebrates.

* the reticular formation: collects input from higher brain centres and passes it on

to motor neurons.

* the substantia nigra: helps "smooth" out body movements; in humans it is

damage to the substantia nigra that causes Parkinson's disease.

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* the ventral tegmental area (VTA): packed with dopamine-releasing neurons that

synapse deep within the forebrain. The VTA seems to be involved in pleasure.

The Forebrain

The forebrain is made up of a pair of large cerebral hemispheres, called the

telencephalon. Because of crossing over of the spinal tracts, the left hemisphere of the

forebrain deals with the right side of the body and vice versa. A group of unpaired

structures located deep within the cerebrum, called the diencephalon.

Diencephalon

Thalamus.

* All sensory input (except for olfaction) passes through it on the way up to the

somatic-sensory regions of the cerebral cortex and then returns to it from there.

* signals from the cerebellum pass through it on the way to the motor areas of the

cerebral cortex.

Lateral geniculate nucleus (LGN). All signals entering the brain from the optic

nerves enter the LGN and undergo some processing before moving on the

various visual areas of the cerebral cortex.

* Hypothalamus.

* The seat of the autonomic nervous system. Damage to the hypothalamus is

quickly fatal as the normal homeostasis of body temperature, blood chemistry, etc. goes

out of control.

* The source of 8 hormones, two of which pass into the posterior lobe of the

pituitary gland.

* Posterior lobe of the pituitary receives

* antidiuretic hormone (ADH) and

* oxytocin

from the hypothalamus and releases them into the blood.

The Cerebral Hemispheres

Each hemisphere of the cerebrum is subdivided into four lobes visible from the outside:

* frontal

* parietal

* occipital

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* temporal

Hidden beneath these regions of cerebral cortex are the olfactory bulbs; they receive

input from the olfactory epithelia. Striatum; it receives input from the frontal lobes and

also from the limbic system (below). At its base is the nucleus accumbens (NA).

The pleasurable (and addictive) effects of amphetamines, cocaine, and perhaps other

psychoactive drugs seem to depend on their producing increasing levels of dopamine at

the synapses in the nucleus accumbens (as well as the VTA).

The limbic system; receives input from various association areas in the cerebral cortex

and passes signals on to the nucleus accumbens. The limbic system is made up of the:

* hippocampus. It is essential for the formation of long-term memories.

* amygdala The amygdala appears to be a centre of emotions (e.g., fear). The

amygdala receives a rich supply of signals from the olfactory system and this may

account for the powerful effect that odour has on emotions (and evoking memories).

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White Matter vs. Grey Matter

Both the spinal cord and the brain consist of

* white matter = bundles of axons each coated with a sheath of myelin

* grey matter = masses of the cell bodies and dendrites — each covered with

synapses.

In the spinal cord, the white matter is at the surface, the grey matter inside.

In the brain of mammals, this pattern is reversed. However, the brains of "lower"

vertebrates like fishes and amphibians have their white matter on the outside of their

brain as well as their spinal cord.

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The Meninges

Both the spinal cord and brain are covered in three continuous sheets of connective

tissue, the meninges. From outside in, these are the:-

* dura mater — pressed against the bony surface of the interior of the vertebrae

and the cranium

* the arachnoid

* the pia mater

The region between the arachnoid and pia mater is filled with cerebrospinal fluid (CSF).

The Extracellular Fluid (ECF) of the Central Nervous System

The cells of the central nervous system are bathed in a fluid that differs from that serving

as the ECF of the cells in the rest of the body.

* The fluid that leaves the capillaries in the brain contains far less protein than

"normal" because of the blood-brain barrier, a system of tight junctions between the

endothelial cells of the capillaries. This barrier creates problems in medicine as it

prevents many therapeutic drugs from reaching the brain.

* cerebrospinal fluid (CSF), a secretion of the choroid plexus. CSF flows

uninterrupted throughout the central nervous system

* through the central cerebrospinal canal of the spinal cord and

* through an interconnected system of four ventricles in the brain.

CSF returns to the blood through veins draining the brain.

Damage to the Brain

Many cases of brain damage from, for example,

* strokes (interruption of blood flow to a part of the brain)

* tumours in the brain

* mechanical damage (e.g., bullet wounds)

have provided important insights into the functions of various parts of the brain.

The area of motor cortex controlling a body part is not proportional to the size of that part

but is proportional to the number of motor neurons running to it. The more motor

neurons that activate a structure, the more precisely it can be controlled.

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The Blood Brain Barrier (BBB)

The blood brain barrier (BBB) keeps many substances out of the brain, but it also must

let nutrients into the brain. You might think of the BBB as a wall between the

bloodstream and neurons. A substance must cross through this wall from the blood to

reach neurons. The BBB can be crossed in three ways:

1. Some materials can fit through "holes" in the BBB.

2. Substances can be transported through the BBB by special carriers.

3. Some materials can break down the BBB.

THE PERIPHERAL NERVOUS SYSTEM

The peripheral nervous system is divided into two major parts: the somatic nervous

system and the autonomic nervous system.

1. Somatic Nervous System

The somatic nervous system consists of peripheral nerve fibres that send sensory

information to the central nervous system AND motor nerve fibres that project to skeletal

muscle.

2. Autonomic Nervous System

The autonomic nervous system is divided into three parts: the sympathetic nervous

system, the parasympathetic nervous system and the enteric nervous system. The

autonomic nervous system controls smooth muscle of the viscera (internal organs) and

glands.

The enteric nervous system is the third division of the autonomic nervous system that

you do not hear much about. The enteric nervous system is a meshwork of nerve

fibres that innervate the viscera (gastrointestinal tract, pancreas, gall bladder).

Some differences between the Peripheral Nervous System (PNS) and the Central

Nervous System (CNS):

1. In the CNS, collections of neurons are called nuclei.

In the PNS, collections of neurons are called ganglia.

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2. In the CNS, collections of axons are called tracts.

In the PNS, collections of axons are called nerves.

In the Peripheral Nervous System, neurons can be functionally divided in 3 ways:

A. Sensory (afferent) - carry information INTO the central nervous system from sense

organs OR Motor (efferent) - carry information away from the central nervous system (for

muscle control).

B. Cranial - connects the brain with the periphery OR Spinal - connects the spinal cord

with the periphery.

C. Somatic - connects the skin or muscle with the central nervous system. OR

Visceral - connects the internal organs with the central nervous system.

Electrical Trigger for Neurotransmission

For communication between neurons to occur, an electrical impulse must travel down an

axon to the synaptic terminal.

The Autonomic Nervous System

The organs (the "viscera") of the body, such as the heart, stomach and intestines, are

regulated by a part of the nervous system called the autonomic nervous system (ANS).

The ANS is part of the peripheral nervous system and it controls many organs and

muscles within the body. In most situations, we are unaware of the workings of the ANS

because it functions in an involuntary, reflexive manner. For example, we do not notice

when blood vessels change size or when our heart beats faster.

The ANS is most important in two situations:

1. In emergencies that cause stress and require us to

"fight" or take "flight" (run away)

and

2. In non-emergencies that allow us to "rest" and "digest.".

The ANS regulates:

* Muscles

* in the skin (around hair follicles; smooth muscle)

* around blood vessels (smooth muscle)

* in the eye (the iris; smooth muscle)

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* in the stomach, intestines and bladder (smooth muscle)

* of the heart (cardiac muscle)

* Glands

The ANS is divided into three parts:

* The sympathetic nervous system

* The parasympathetic nervous system

* The enteric nervous system.

The Sympathetic Nervous System

It is a nice, sunny day...you are on a nice leisurely hack on your horse. Suddenly, an

angry bear appears in your path. Your horses‘ "Fight or Flight" responses will be

initiated. In this type of situation, his sympathetic nervous system is called into action - it

uses energy - his blood pressure increases, his heart beats faster, and digestion slows

down.

The sympathetic nervous system originates in the spinal cord. Specifically, the cell

bodies of the first neuron (the preganglionic neuron) are located in the thoracic and

lumbar spinal cord. Axons from these neurons project to a chain of ganglia located near

the spinal cord. In most cases, this neuron makes a synapse with another neuron (post-

ganglionic neuron) in the ganglion. A few preganglionic neurons go to other ganglia

outside of the sympathetic chain and synapse there. The post-ganglionic neuron then

projects to the "target" - either a muscle or a gland.

Two more facts about the sympathetic nervous system: the synapse in the sympathetic

ganglion uses acetylcholine as a neurotransmitter; the synapse of the post-ganglionic

neuron with the target organ uses the neurotransmitter called noradrenaline or

norepinephrine. (Of course, there is one exception: the sympathetic post-ganglionic

neuron that terminates on the sweat glands uses acetylcholine.)

The Parasympathetic Nervous System

It is a nice, sunny day...you are on a nice leisurely hack on your horse. This time,

however, you decide to hop off and let him have a graze in the sun. This calls for "Rest

and Digest" responses. Now is the time for the parasympathetic nervous to work to save

energy - his blood pressure decreases, his heart beats slower, and digestion can start.

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The cell bodies of the parasympathetic nervous system are located in the spinal cord

(sacral region) and in the medulla. In the medulla, the cranial nerves III, VII, IX and X

form the preganglionic parasympathetic fibres. The preganglionic fiber from the medulla

or spinal cord projects to ganglia very close to the target organ and makes a synapse.

This synapse uses the neurotransmitter called acetylcholine. From this ganglion, the

post-ganglionic neuron projects to the target organ and uses acetylcholine again at its

terminal.

Here is a summary of some of the effects of sympathetic and parasympathetic

stimulation. Notice that effects are generally in opposition to each other.

The Autonomic Nervous System

Structure Sympathetic Stimulation Parasympathetic Stimulation

Iris (eye muscle) Pupil dilation Pupil constriction

Salivary Glands Saliva production reduced Saliva production increased

Oral/Nasal Mucosa Mucus production reduced Mucus production increased

Heart Heart rate and force increase Heart rate and force

decrease

Lung Bronchial muscle relaxed Bronchial muscle contracted

Stomach Peristalsis reduced Gastric juice secreted;

motility

increased

Small Intestine Motility reduced Digestion increased

Large Intestine Motility reduced Secretions/motility increased

It should be noted that the autonomic nervous system is always working. It is NOT only

active during "fight or flight" or "rest and digest" situations. Rather, the autonomic

nervous system acts to maintain normal internal functions and works with the somatic

nervous system.

The enteric nervous system is a third division of the autonomic nervous system that you

do not hear much about. The enteric nervous system is a meshwork of nerve fibres that

innervate the viscera (gastrointestinal tract, pancreas, and gall bladder).

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SECTION 3

PAIN

Pain Stimulation

Synapses blocking pain signals

The two enkephalins are released at synapses on neurons involved in transmitting pain

signals back to the brain. The enkephalins hyperpolarise the postsynaptic membrane

thus inhibiting it from transmitting these pain signals.

The ability to perceive pain is vital. However, faced with massive, chronic, intractable

pain, it makes sense to have a system that decreases its own sensitivity. Enkephalin

synapses provide this intrinsic pain suppressing system.

Opiates such as morphine bind these same receptors. This makes them excellent

painkillers. However, they are also highly addictive.

* By binding to enkephalin receptors, they enhance the pain-killing effects of the

enkephalins.

* A homeostatic reduction in the sensitivity of these synapses compensates for

continued exposure to opiates.

* This produces tolerance, the need for higher doses to achieve the prior effect.

If use of the drug ceases, the now relatively insensitive synapses respond less well to

the soothing effects of the enkephalins, and the painful symptoms of withdrawal are

produced.

Pain and Why It Hurts

You may not like it, but we need pain. Pain acts as a warning system that protects you.

Pain says, "Warning, Warning....stop what you doing and do something else". For

example, if you have your hand on a hot stove, pain tells you to stop touching the stove

and remove your hand. In this way, pain protects your body from injury (or further injury

if you have already hurt yourself). Pain also helps healing because an injury hurts so

you rest.

There are some people who are born WITHOUT the sense of pain. These people have a

rare condition called "congenital insensitivity to pain". Their nervous systems are not

equipped to detect painful information. You may think this is a good thing....it is NOT.

Without the ability to detect painful events, you would continue to cause injury to

38

yourself. For example, if you broke a bone in your arm, you might continue using the arm

because it did not hurt. You could cause further injury to your arm. People with

congenital insensitivity to pain usually have many injuries like pressure sores, damaged

joints and even missing or damaged fingers!

So, what kind of things in the outside world can cause pain? Events that cause reactions

are called stimuli. Stimuli are painful when they damage tissues or threaten to damage

tissue. Pain is nature's way of telling the brain about injury to the body. Painful stimuli

can be divided into several types:

Painful Stimuli

Energy Example Everyday Example Possible result

if untreated

Mechanical Strong Pressure

Thermal

(Temperature) Hot

Pinch

Squeeze

Twist Animal bite

Knife cut

Falling off a bike Bruises

Broken Bones

Cuts

Cold Fire

Hot Chocolate

Ice Burns

Frostbite

Electrical -- Electric Shock Burns

Chemical -- Acid

Chilli Peppers Chemical burns

Broken Skin

Visceral

(Inside the Body) -- Heart Attack

Inflamed appendix Condition gets worse

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Now we know some of the "stimuli" that may cause pain. How do these stimuli activate

the nervous system? There are specialised "receptors" in the skin and internal organs

that are sensitive to stimuli that are painful. These receptors are called "nociceptors" and

are free nerve endings connected to small diameter myelinated A and unmyelinated C

nerve fibres - these are the nerve fibres that are LACKING in people with congenital

insensitivity to pain. Nociception, then, is the response of the nervous system to painful

stimulation. When the nociceptors detect a nociceptive stimulus, they send a message to

the spinal cord.

A famous theory concerning how pain works is called the Gate Control Theory devised

by Patrick Wall and Ronald Melzack in 1965. This theory states that pain is a function of

the balance between the information travelling into the spinal cord through large nerve

fibres and information travelling into the spinal cord through small nerve fibres.

Remember, large nerve fibres carry non-nociceptive information and small nerve fibres

carry nociceptive information. If the relative amount of activity is greater in large nerve

fibres, there should be little or no pain. However, if there is more activity in small nerve

fibres, then there will be pain. Here is what the gate control theory looks like:

Gate Control Theory

PAIN

I = "Inhibitory Interneuron"; P = "Projection Neuron"

- = inhibition (blocking); + = excitation (activation)

Large Fibres

P I

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The theory step by step:

1. Without any stimulation, both large and small nerve fibres are quiet and the

inhibitory interneuron (I) blocks the signal in the projection neuron (P) that connects to

the brain. The "gate is closed" and therefore NO PAIN.

2. With non-painful stimulation, large nerve fibres are activated primarily. This

activates the projection neuron (P), BUT it ALSO activates the inhibitory interneuron (I)

which then BLOCKS the signal in the projection neuron (P) that connects to the brain.

The "gate is closed" and therefore NO PAIN.

2. With pain stimulation, small nerve fibres become active. They activate the projection

neurons (P) and BLOCK the inhibitory interneuron (I). Because activity of the

inhibitory interneuron is blocked, it CANNOT block the output of the projection

neuron that connects with the brain. The "gate is open", therefore, PAIN!!

Although the gate control theory has support from some experiments and does explain

some observations seen in pain patients during therapy, it does not explain everything.

However, think of this...what is one of the first things you do after you bump your head or

pinch a finger by accident? You probably rub it and it feels better. Could this be

explained by the gate control theory? Rubbing your bumped head or pinched finger

would activate non-nociceptive touch signals carried into the spinal cord by large nerve

fibres. According to the theory, the activity in the large nerve fibres would activate the

inhibitory interneuron that would then block the projection neuron and therefore block the

pain.

From the spinal cord, the messages go directly to several places in the brain including

the thalamus, midbrain and reticular formation.

Some brain regions that receive nociceptive information are involved in perception and

emotion. Also, some areas of the brain connect back to the spinal cord - these

connections can change or modify information that is coming into the brain. In fact, this

is one way that the brain can REDUCE pain. Two areas of the brain that are involved in

reducing pain are the periaqueductal grey (PAG) and the nucleus raphe magnus.

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Other ways that pain can be controlled:

Method Possible Mechanism(s) Uses/Examples

Aspirin Acts mostly in peripheral nervous system. Reduces inflammation.

Headache

musculoskeletal pain

Morphine Acts in central nervous system

(brain and spinal cord) to block pain

messages. Activates pain-modulating

systems in the brain that project to the

spinal cord. Post-operative pain;

other pain conditions

Other pain

reducing drugs Act on a variety of neurotransmitter

systems. Variety of pain conditions

Acupuncture

1. Stimulation of large diameter nerve fibres that inhibit pain ("close the gate").

2. Could be placebo effect, however this is absent in animals. Causes release of

endorphins ("the body's own morphine-like substances").

3. Some types of acupuncture may stimulate small diameter nerve fibres and inhibit

spinal cord pain mechanisms (this would not agree with the gate control theory) - Back

pain, minor surgical operations.

Electrostimulation

1. Stimulation of large diameter nerve fibres which "close the gate" and reduce

pain.

2. Could be placebo effect, however this is absent in animals. Post-operative pain,

arthritis, cancer pain.

Electromagnetic field

Please refer to your module on physiotherapy equipment.

Pain Receptors

Brain tissue is not sensitive to pain! The brain itself does not have any receptors for pain.

In fact, most brain surgery is performed using a local anaesthetic only. The meninges

(coverings of the brain), however, are very sensitive to pain.

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The Skin and pain receptors

The epidermis is the outside layer of skin. The dermis is the inside layer of skin. The

skin, is a washable, stretchable, tough, water-proof sensory apparatus covering your

whole body. It keeps your insides in!

There are four different types of skin:

1. Mucocutaneous: at the junction of the mucous membrane, hairy skin, lips, and

tongue.

2. Mucous membrane: lining the inside of body orifices.

3. Glabrous: skin without hair.

4. Hairy: skin with hair.

Glabrous skin has an epidermal layer of about 1.5 mm in thickness and a dermis of

about 3 mm. Hairy skin has an epidermal layer of 0.07 mm in thickness and a dermis of

about 1-2 mm.

Skin Receptors

Receptor Ending

Nerve Fibre

Function

Location

Hair Follicle Ending

A-beta

Responds to hair displacement

Wraps around

hair follicle in,

hairy skin.

Ruffini Endings

A-beta

Responds to pressure on skin.

Dermis of both

hairy and

glabrous skin.

Krause corpuscle

A-beta

Responds to pressure. Lips, tongue,

and genitals.

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Pacinian corpuscle A-beta Responds to vibration. Most sensitive

in 150-300 Hz

range Deep

layers of

dermis in both

hairy and

glabrous skin.

Meissner corpuscle A-beta Responds to vibration. Most sensitive

in 20-40 Hz

range Dermis

of glabrous

skin.

Free nerve endings A-delta and C Different types of free

nerve endings that

respond to mechanical,

thermal or noxious

stimulation.

Merkel Cells A-beta Responds to pressure

of the skin.

Various types

are found

throughout the

skin.

Epidermis of

glabrous skin.

Nerve fibres that are attached to different types of skin receptors either continue to

discharge during a stimulus ("slowly-adapting") or respond only when the stimulus starts

and sometimes when a stimulus ends ("rapidly-adapting"). In other words, slowly-

adapting nerve fibres send information about ongoing stimulation; rapidly-adapting nerve

fibres send information related to changing stimuli.

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SECTION 4

PHYSIOTHERAPY OPTIONS

Neurological examination

As a physiotherapist you will often be required to undertake a neurological examination,

especially on small animals. It is essential that you can recognise when a patient has

deteriorated between visits or since the initial Veterinary diagnosis was given. You will

learn how to carry out a neurological assessment on your practical days. An animal

with any signs of ataxia, paresis, paralysis or any other signs of neurological distress,

which has not been previously noted, must be referred back to the Vet as a matter of

urgency.

Physiotherapy Treatment

Much can be done using the application physiotherapy to aid repair and improve the

quality of life in patients with neurological problems.

Ultrasound and pulse magnetic therapy can be used over the muscles affected by

nerve depravation. These therapies can be used to improve blood flow and nutrients to

the muscle and encourage removal of waste products. Ultrasound will also help to

reduce adhesions. Treatment to damaged areas will provide the nerve and surrounding

tissues with the optimum conditions in which to repair.

Heat therapy can also be beneficial to affected muscles, and cryotherapy and magnetic

field therapy for vasoconstriction can help to reduce inflammation to and around

damaged nerves. Great care must be taken to avoid damage when applying heat or

cold therapy due to decreased sensation to the injured area.

Soft tissue and joint mobilisation will optimise nutrition to muscles and joints and help

maintain strength and comfort. This will also help reduce adhesions and promote

wellbeing.

Placing bands around the limbs of a dog before a walk can help the animal be more

aware of his limbs. Other props can be used to create similar effects such as using

massage balls on the paws of dogs and cats or bandages around horses‘ legs.

45

Hydrotherapy can also help to increase proprioception and maintain muscle strength, as

can exercises such as weight shifting and pole weaving (you will learn about these in a

later module). Swimming is an excellent tool for encouraging early motor function.

Many patients, who make minimal efforts to move when on dry ground, will often make

some small motor movements whilst in water. Further reading on body awareness

can be found in a selection of books written by Linda Tellington-Jones.

Other muscles often become sore due to having to compensate for dysfunction of

affected muscles. Massage, phototherapy and stretches can be used to treat these

muscles along with pulsed magnetic therapy and ultrasound. Phototherapy can also be

used to treat any bed sores or associated wounds such as grazed paws of dogs

caused by paresis. Special boots are available to help protect vulnerable paws.

A muscle deprived of its nerve will degenerate. Electrostimulation is used for muscle

strengthening. Atrophy of muscles may be caused by a number of reasons;

Lack of nerve conduction

Destruction of muscle structure ie: strain, bruising, tearing or presence of

chemical toxins.

Ischemia – loss of blood supply due to disruption of circulatory flow ie; due to a

poorly fitting saddle.

Excessive exercise – due to lack of fuel muscle breaks down. The reduction or better still the prevention of muscle atrophy is a key aim in the

physiotherapy treatment of neurological conditions. Wastage of muscles will contribute

to the deterioration of the condition and the unhappiness of the animal. Therefore

maintaining as much strength and movement as possible should be a primary

consideration.

Motor muscle points

When using electrostimulation you will get the best response from the muscle if you

place the electrodes over the motor points. The motor point is where a major motor

nerve enters the muscle. Being aware of the points of motor innervation of the skeletal

46

muscles will enable you to analyse which nerve has been damaged (by which muscles

have atrophied) or, if you know which nerve is damaged then you will know which

muscles are likely to be affected.

PROJECT: Make a table for your records listing the major muscles and the nerves

which supply them.

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48

SECTION 5 NEUROLOGICAL

CONDITIONS

Many neurological diseases have similar symptoms. Conditions that originate in the CNS

could be neoplastic (tumour) or could equally be caused by trauma, toxins, congenital

defects or inflammation. Below are some of the most common neurological diseases

found in the Horse and the Dog.

EQUINE

Spondylitis (Kissing spines) is Inflammation and new bone of the vertebrae of the

thoracic and lumbar spine. New bone formation is thought to be due to longstanding

inflammation of the interosseus ligament joining the dorsal spines, which can lead to

touching and grating of the dorsal spinous processes. Ankylosing spondylitis can

develop when bone spurs form on the underside of the vertebrae eventually touching and

fusing. Both of these conditions are very painful when forming, but become less so when

formed.

Typical signs of back pain including objection to being tacked up and mounted are

among the first signs of spinal problems. Progressive signs of ataxia or clumsiness and

a reduction in athleticism usually follow. Ataxia is not a sign associated with kissing

spines.

Wobbler disease a condition most commonly found in young Thoroughbred and

warmblood horses. This disease is characterised by gradually increasing ataxia of the

hindlimbs and, in its more severe forms, the forelimbs will also be affected. This

conditionis caused by compression of the spinal cord due to malformation of the cervical

vertebrae and a narrowing of the spinal canal in the neck. This condition is most

noticeable at walk and whilst turning, this condition may reach a level where the horse

loses the ability to remain upright. Severe cases can be a danger to themselves and their

handlers as they thrash about knocking into anything in their path. Mild cases can be

confused with conditions of the hock and stifle. Other conditions such as equine

protozoal myeoencephalitis can cause very similar symptoms and should be eliminated

as a cause before a diagnosis of wobbler disease is made. Wobbler disease can be

treated with a surgical procedure, but this surgery is highly invasive and not always

successful. Sadly, the majority of horses with wobbler disease will not be rideable and are

49

not candidates with the surgery. As it is believed to have a heritable component, affected

horses should not be bred from.

Equine protozoal myeoencephalitis is a disease affecting the brain and spinal cord.

The carrier of the protozoal organism sarcocyystis neurona is believed to be the possum

and this disease is found in horses throughout North and South America. Cases have also

been found in other countries, including the UK, in horses which were imported from the USA.

Paralysis of the ears, lips and eyelids can be a result of the effect on the cranial nerves, as can

difficulty in swallowing and chewing. Muscle wastage often occurs and serious cases can result

in complete paralysis. EPM causes a whole range of neurological signs and should be considered in

horses that have spent time in the USA.

Shivering, with a few exceptions, affects the hind end only. Characterised by the

exaggerated flexion and shivering of a limb seemingly initiated when the limb is touched

or the horse is startled. The horse leans on the weight bearing leg, sometimes so much

so that he falls over. There is no known cause.

Stringhalt is characterised by the exaggerated movement of a hind limb during action.

The degree of movement varies from case to case. Sometimes this is so exaggerated

that the fetlock hits the belly. Some horses exhibit stringhalt with every stride others only

show it when backed or turned. Australian stringhalt, found in Australia, New Zealand and

the USA is believed to be related to the continual ingestion of dandelion weeds.

Some of the above conditions such as spondylosis and wobblers are also found in

smaller animals. Below are some of the most recognised diseases found in Dogs.

CANINE

Radiculomylopathy (RM) previously known as Chronic degenerative RM (CDRM) is

usually found in German shepherds over eight years of age, however it has been

recorded in other large breeds and of varying ages. Affected dogs show slowly

progressive hind limb ataxia and paresis. An early sign is knuckling of the hind paws,

especially when turning corners. The lesions are restricted to the thoracic spinal cord

and the dorsal nerve roots, both grey and white matter undergo degeneration.

Degenerative diseases of the nervous system may also involve the peripheral nerves. This

is now known to be an inherited condition, and the gene has been identified. The diagnosis

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can therefore be confirmed by a simple genetic test. Unfortunately the disease is not

curable, but its progression may be slowed by exercises and treatments aimed at

maintaining hindlimb muscle strength.

Fibrocartilaginous Embolism is a syndrome of acute obstruction of the blood supply to

a segment of the spinal cord thought to be caused by sudden obstruction of spinal cord

blood vessels by fragments of intervertebral disc. This disease is characterised by a

sudden onset of ataxia, paresis or total paralysis on one or both sides. It is a non-painful

condition and dogs may go on to have a complete or partial recovey. Affected dogs can be

any age, from a puppy to a senior dog, and diagnosis can only be confirmed via a MRI

scan.

Intervertebral disc disease causes protrusion of the intervertebral disc into the spinal

column compressing the spinal cord. The thoracolumbar junction is the most common

place for disc protrusion but cervical disc protrusions also occur frequently. A disc

protrusion can either be a sudden explosive prolapse of disc material or a slower bulging

of the disc, therefore the clinical signs can be of varying degrees. Paresis, paralysis, loss

or exaggeration of reflexes and incidence of local pain are all clinical signs of this

disease. Complete loss of pain sensation below the lesion indicates the need for urgent

surgical decompression.

Canine distemper is a virus which commonly causes inflammation of the brain

(encephalitis) and/or the spinal cord (myelitis). Paresis, axatia, disorientation,

depression and seizures are the neurological signs associated with the virus. Affected

dogs usually develop rhythmical muscle spasms in either the face or the limbs.

Toxicity and poisoning (bacterial, chemical or plant based) can cause neurological

distress. Botulism is an example of this. Botulism is caused by the bacterium

Clostridium botulinum. Horses can ingest this with soiled forage and dogs by eating

contaminated carcasses, typically dead seabirds. This toxin blocks transmission of

impulses of nerves to muscles.

Injuries to specific nerves can also occur, such as brachial plexus injuries, radial nerve

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paralysis and obturator nerve paralysis. Using your anatomy texts, consider how trauma

to specific nerves might present clinically. The treatments you can apply would be

focusing on decreasing inflammation and preventing/treating muscle atrophy.

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APPENDIX 1

KEY TERMINOLOGY

ANS - Autonomic nervous system

Ataxia - Lack of co-ordination. There are three types; Sensory, Vestibular and

cerebellar.

Atrophy (muscle) – Muscle wastage

CNS – The central nervous system

Deep pain – Type C fibres transmit deep pain. Absence of deep pain indicates a poor

prognosis.

Differential diagnosis – Identification of a range of possible causes.

Dysmetria – The inability to regulate the rate, range and force of movements.

Herniated disc – The protrusion of one of the spinal discs into an opening in the spinal

cord, thereby compressing the nerve root.

Hytrophy – Opposite to muscle atrophy

Lower Motor Neuron – The final motor neurons that innervate the skeletal muscles.

Motor (efferent) neuron – Send information away from the CNS to muscles or glands.

Myopathy – Any disease of muscles.

Neoplasm – Abnormal growth of tissue. Tumour.

Nerve root compression – squeezing of one or two bundles of nerve fibre emerging

from the spine; frequently caused by a herniated disc.

Nociception – The response of the Nervous System to painful stimulation. The

perception of pain.

Paralysis – The loss of the ability to move part or most of the body.

Paresis – Reduced ability to voluntarily move a limb or body part. Weakness rather

than paralysis.

PNS – Peripheral nervous system

Proprioception – The ability to sense the position, orientation and movement of a limb

or body part.

Reflex – A reaction which occurs automatically and predictably to a particular stimulus.

Sensory (afferent) neurons – Send info from receptors ie; skin toward the CNS.

Spinal Plexus – A network of nerves. Connections of fibres joining the peripheral

nerves.

Upper Motor Neuron – Motor neurons of the motor cortex. Initiates and maintains

normal motor activity.

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APPENDIX 2

CASE STUDY

Max an eight-year-old event horse, thoroughbred type, suffered a fall xc and hit his near

side quarters on the fence. The next day the horse was 6/10ths lame on Vets Px and

presented with paresis of the left hind limb. After thorough investigation the Veterinary

Dx was - Extensive bruising to muscles of the left hind limb particularly to the

quadriceps femoris muscle and the location of the femoral nerve. No fractures. Most

likely cause of Paresis of the limb is pressure on the sciatic nerve, due to bruising.

Without Physiotherapy - The horse was prescribed box rest for 1 week and cold

hosing to the area twice a day. Then field rest for four weeks.

When the horse was brought in five weeks later severe atrophy to the quadriceps

femoris muscle had occurred. The horse was mechanically unsound and some bruising

was still present. There was still slight paresis of the limb. The owner decided more

field rest was required. The physiotherapist was eventually called in 10 weeks after the

initial injury. There was still some bruising present. This was successfully dispersed

with Ultrasound and pulsed magnetic field therapy. The quadriceps muscle responded

poorly to electrostimulation due to the time lapse. The horse was made comfortable but

was mechanically unsound and weakened. Max‘s ridden career was over.

Max lived happily in the field for the next 7 years but during this time DJD had developed

in his hips and near side stifle. Max was put down at 15-years of age.

With Physiotherapy – Max‘s treatment started the day after injury.

Day 1 > 3 – Max was treated with PEMF on settings of base 50Hz and pulse 5Hz three

times a day for 10 minutes, over the injured muscles. Gentle massage to the

surrounding muscles was carried out twice a day and gentle PROM was carried out on

the left limb. He was box rested but was walked in hand for 5 minutes 3 times a day.

Day 4 – The area was treated with Ultrasound on mode 6 for 5 minutes followed by a

walk in hand for 5 minutes. He was then treated with PEMF on a setting of Base 50Hz

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and pulse 17.5Hz for 10 minutes, three times a day. This was followed by PROM

exercises. He was treated on day 6 and 8 with Ultrasound.

This treatment continued for 4 weeks. During this time he was treated once a week with

Ultrasound. His exercise was slowly increased and by week 3 he was sound and being

gently ridden. Paresis had almost gone and was only noticeable to he trained eye. He

was also turned out all day but the nights were cold so he was in and rugged up. Pulsed

Magnetic Therapy was continued twice a day until week 6.

Max was treated for 1 week – twice a day – for 10 minutes with electrostimulation during

week 3. This was because some slight muscle atrophy of the quadriceps femoris was

noticed at this point.

Week 7 – Max was seen by the Vet. He was sound and there was no sign of paresis.

The muscles were bilaterally symmetrical even although he had lost tone all over. His

work load was gradually increased and he was back eventing 12 weeks after the initial

fall.

Max went on to have a successful career. He retired from eventing at eighteen years of

age and continued to hack for the rest of his life.