Introduction: with consideration for causes, symptoms and signs.

Introduction:

Patients are never just like a textbook.  They always have differences, underlying
problems and usually have more than one condition (previous or current). As a
healthcare professional, specifically a physiotherapist, these need to be
considered when treatment or diagnosis occurs. In this case, a 57 year old male
has already been diagnosed with a Cardiovascular problem, Atrial Fibrillation
and suspected Cervical Spondylosis. The Pathophysiologies of each condition
will be discussed with consideration for causes, symptoms and signs.

Cervical
Spondylosis Pathophysiology:

Cervical Spondylosis is a degenerative form of arthritis
which occurs within the cervical spine or neck. 
It is a common age related disorder which develops from wear, tear and
deterioration of the cartilage and bones within the cervical joints.  This condition can cause extreme, chronic
pain, discomfort and stiffness of the neck. 
However, in some cases, there are no notable symptoms so the condition remains
untreated. (1-2) Cervical Spondylosis is very common and affects around 85% of
people aged over 60. The treatment for this condition is usually medication and
physiotherapy but, occasionally requires surgery. (1)

The symptoms of this condition are pain in the cervical
spine that is aggravated by movement, referred pain (e.g. in the back of the
head or occipital, in upper limbs and in between the shoulder blades), pain in
the temporal and retro-orbital regions between the C1 and C2 vertebrae,
dizziness/vertigo, poor balance, vague numbness in upper limbs, tingling in
upper limbs, weakness in upper limbs, migraines and cervical stiffness (whether
this is reversible or irreversible). The signs of this disease are a limited
range of movement in forward flexion, backward extension, lateral flexion and
rotation of the neck; small neurological changes (e.g. inverted Supinator jerks
(reverse reflex)) and poorly localised tenderness. Poorly localised tenderness
is when the pain or tenderness cannot be pinpointed. The inverted Supinator
jerks only occur if the patient doesn’t have myelopathy or radiculopathy. (3)

Cervical Spondylosis is caused by the lack of elasticity and
dehydration of the Intervertebral disks within the cervical spine and can occur
in people as young as 40. The water, collagen, and proteoglycans within the
nucleus pulposus dries out over time and causes a narrowing in the space
between the cervical vertebrae, also known as the spinal canal, and cracks or
breaks in the nucleus pulposus.  The change
in disk position causes a strain on the surrounding ligaments which cause the
elasticity to lessen and traction spurs to occur. Therefore, with no support,
the Intervertebral disks collapse and the weight of the individuals head is
placed on the vertebrae. The roots of the cervical nerves then become stretched
or compressed and this could allow the vertebrae to be forced out of proper
alignment. The narrowing of the spinal canal causes the ring of annulus
fibrosus within the Intervertebral disk to bulge and the facets to override,
allowing increased motion of the bones within the cervical spine. This
increased motion causes the more damage to occur at an increased pace. The
bulge in the annulus fibrosis could break causing a herniation or annulus
fissures to occur.  As the bulge gets
bigger, the spinal canal narrows.  This
condition becomes more obvious in the elderly because of the increase in thickness
above normal of the Ligamentum Flavum and the posterior degeneration/
enlargement (hypertrophy) of the facet joints. (4-5) Also, it could become more
obvious, because during extension of the neck, the ligaments fold inward which
reduce the anteroposterior diameter of the spinal canal. The hypertrophies and
degeneration of the disk causes the uncinate process to override.

The vertebral uncinate process, that is hook-shaped, is situated
on the posterolateral borders of the superior surface of the vertebral bodies
of C3 to C7 and T1. The uncinate process acts as reinforcement for the disk,
prevents lateral hyperflexion and prevents abnormal movements (posterior,
linear and translation) of the vertebral bodies. (4,6) The uncinate process
adapts the ventrolateral and decreases the dorsolateral aspect of the foramen.
This variation contributes to the Cervical Spondylosis associated radiculopathy
and marginal osteophytes (small bone spurs) begin to develop. (4,7-8)
Additional trauma or stress can make this process worse. These small bone spurs
grow to act as stabilisation for the vertebral bodies and increase the
weight-bearing aspect of the endplates of the vertebrae. This decreases the
overall effective forces on the cervical spine. These bone spurs can press on
nerves and/or the spinal cord which can be a source of pain.

The degeneration of the joint surfaces and ligaments causes
a decrease in the available motion which can act as a limiting mechanism
preventing further declination.  The
ossification, hardening and thickening of the posterior longitudinal ligament
also shrinks the canal diameter. (4)

Other influences that may exacerbate and influence the cause
of Cervical Spondylosis include neck injuries (i.e. whiplash), genetics (i.e.
family history of Cervical Spondylosis), occupation (i.e. heavy lifting), neck
position (repetitive neck strain or stress), smoking, obesity, inactivity,
depression and anxiety. As injury speeds up the ageing process, bones will age before
their time meaning that individuals could get Cervical Spondylosis earlier. A
constant abnormal neck position and overuse (through sports, etc.), can cause
early aging and will cause ligament damage/strain. Smoking also influences this
condition because it affects the bone metabolism in the vertebrae. (2,9)

Associated dysfunctions for Cervical Spondylosis include
Cervical Spondylotic Myelopathy or spinal cord compression and Cervical Radiculopathy.
Cervical Radiculopathy occurs due to the affects of Cervical Spondylosis
compressing the nerve roots in C5 to C7. These nerves and radicular arteries,
which are located in the dural sleeves, have low endurance for compression and
repetitive minor trauma. The compression and trauma affect the blood supply to
the nerves and arteries which can lead to neurological features such as,
segmental distribution in the upper limb and other symptoms. These symptoms
include shooting pains, numbness, hyperaesthesia and weakness in the upper
limb. Reflexes are also diminished. 
Cervical Spondylotic Myelopathy is an injury to the spinal cord due to
spinal compression. In this case the spinal compression is caused by the Cervical
Spondylosis.  Therefore, spinal cord and
canal size are signs of the myelopathy. However, just a narrow canal doesn’t
necessarily mean that the individual has a myelopathy but the disease rarely
occurs in individuals that have a spinal canal larger than 13mm diameter. The
symptoms of this condition is muscle wastage in the upper limbs, increased
pronation of the wrists, increased tone in finger flexor muscles, bladder
dysfunction, hand clumsiness and gait interference/instability. The clumsiness
and instability is caused by having spastic paraparesis
in the lower limbs. (3-4,9-10)

Although a symptom of Cervical Spondylosis is pain, there
are different types and different pathways it follows within the brain. This
perception of pain starts at the pain receptors and these receptors are located
all over the body (skin, joint surfaces, arterial walls, certain structures in
the skull, etc.). These pain receptors are free nerve endings that are
sensitive to pain stimuli. Chemical, thermal and mechanical are the three types
of pain receptor stimuli.  Thermal
stimuli are released as a result of extreme hot or cold such as touching a hot
oven. Mechanical stimuli are secreted as a result of high pressure or
stretching the skin such as an injection under high pressure because as the
fluid enters the body at high pressure it damages a relatively large area of
soft tissue around the entry site. Chemical stimuli are the chemicals released
as a result of trauma or inflammation. 
Examples of these stimuli are lactic acid (causes muscle pain after
heavy exercise resulting from anaerobic respiration), potassium ions, serotonin
and bradykinins.

There is another type of chemical, prostaglandins, that is
released with the stimuli that makes the receptors more sensitive, it doesn’t
directly stimulate them. Certain drugs (paracetamol and non-steroidal
anti-inflammatory drugs) act to decrease these prostaglandins which stop the
pain receptors from being so sensitive thus reducing pain signals to the brain
and perceived pain. Paracetamol works within the central nervous system
whereas, the non-steroidal anti-inflammatory drugs work within the peripheral
nervous system. From these pain receptors, the stimulus is transported through
the peripheral nerves to the spinal cord and then to the brain. This occurs
through two different types of fibres and this is known as the pain gait. One
type transports ‘fast pain’ and the other type transports ‘slow pain’. The fast
pain is the initial response and it is perceived as sharp pain. The slow pain
the response that follows a few seconds later and this is usually a dull or
burning pain. This type of pain usually lasts for a few days or weeks. However,
if it is inappropriately processed by the body, it can last longer and become
chronic.

Fast pain fibres are alpha fibres and there are two types, alpha-beta
fibres (heat and touch) and alpha-delta fibres (sharp pain). Fast pain occurs
when a painful stimulus occurs such as touching a hot surface.  The transmission nerves are comparatively thick
for nerves, with a 0.002-0.005 millimetre diameter.  Due to their thickness, the pain stimulus can
be transmitted at speed, usually between 5 and 30 m/s and acts as a reflex
response allowing the body to quickly withdraw preventing further damage and
removing itself from danger. The patient can usually pin point the location of
this pain because the pain doesn’t radiate away from a certain point. This pain
is difficult to manage and can’t be overcome by normal painkillers. Therefore,
if surgery is needed as a treatment for the Cervical Spondylosis, the pain of
the insertion will require an anaesthetic injected into the nerve that removes
all sensation, which would include the sharp pain of the insertion.

The slow pain fibres are c-fibres, which are very thin,
between 0.0002 and 0.001 millimetre diameter. Due to the size, the transmission
is slow. Stimuli travel to the brain at less than 2m/s. The body’s response to
this pain is to guard the affected area by rendering it immobile so it can
heal. This type of pain is the only type of pain that occurs in organs. It
occurs in all apart from the brain as the brain has no pain receptors. Slow
pain can be described as radiating, is hard to pinpoint so, it is poorly
localised and it can be referred to other parts of the body from the source of
pain. Unlike fast pain, ophoids and paracetamol is an effective treatment for
this type of pain. Local anaesthetics can also be used.  With this information, Cervical Spondylosis
can be treated with paracetamol and ophoids because the pain is transmitted
through c-fibres.

The peripheral nerves, which are nerve outside the nervous
system, transmit the pain impulse to the spinal cord. Transmission requires an
action potential and occurs in the following way. Neurones have a stable
potential across the membrane until they receive an electro-chemical impulse.
Excitatory or inhibitory inputs enter through the dendrites causing
depolarisation and hyperpolarisation. An action potential (AP) occurs when the
summation of all the inputs exceed the threshold potential. Temporal and
spatial summation cause large enough inputs to activate the AP.  Once an AP has been produced it is conducted
down the axon.  The inside of the neuron
becomes more positive, the rising phase. There follows a rapid decline back to
the resting potential, the falling phase. The AP is an ‘all or nothing’ event
occurring over a few milliseconds. The AP occurs through the movement of ions
through protein channels called leak and voltage gated ion channels (Sodium
Potassium Pump). AP is initiated through the voltage gated ion channel. Gates
open when the threshold potential is exceeded. Electrical and diffusion forces,
force 3 Na+ ions into the neurone. Once the sodium ions go through the channel,
the increase in positive charge depolarises some of the membrane. This change
triggers the next voltage gated ion channel to open and so on so that they open
in a wave (the rising phase). Due to the electrical and diffusion forces,
potassium ions (K+) exit through the leak channels and hyperpolarisation occurs
(falling phase). Upon stability, the AP stops.

The different types of pain are carried through different
pathways to the brain via the spinal cord. The fast pain action potential
travels to the cortex in the brain and this area allows the pain to be easily
located or pin pointed. However, the slow pain action potential travels to
different areas of the brain, such as the ‘wake centre’, where it then
diffuses. Each area generates a different response and explains why some pain
can’t be localised with different symptoms occurring alongside the pain
(difficulties sleeping, a depressive mood, etc.).

The body can act to moderate localised pain.  Rubbing the area of localised pain provides
stimuli that are received by the brain in preference from those of the pain
site and during this pain process, the brain releases natural ophoids (enkephalin,
endorphin and dynorphin) which bind with the pain receptors making  the receptors less sensitive reducing  transmission and sensation. (11)

Cardiovascular
Pathophysiology of Atrial Fibrillation (AF):

The cardiovascular system contains the heart, veins,
arteries and the blood. It is the system within the body that transports
oxygen, hormones, nutrients and waste products, via the blood, to where it is
required. This movement of blood is called circulation. The heart is a pump
that consists of four chambers, the left atrium, the right atrium, the left
ventricle and the right ventricle. The atria are the superior chambers of the
heart and are the primary receivers of the blood. Blood contained within the
atria flows, it isn’t pumped. The ventricles are the inferior chambers of the
heart that contract pumping the blood to the needed tissues.

The right atrium receives the low oxygenated blood from the
body’s tissues which then flows into the right ventricle. The right ventricle
contracts to pump blood to the lungs to for oxygenation and offload carbon
dioxide (pulmonary circulation). The left atrium receives oxygenated blood from
the lungs and it flows into the left ventricle. The left ventricle contracts
and pumps the blood to the tissues of the body (Systemic circulation). These
chambers are separated by valves and the septum. The septum separates the left
and the right side of the heart allowing the heart to act as a double pump. The
valves separate the atria and the ventricles. These valves are called the
tricuspid (right atrium to right ventricle) and bicuspid (left atrium to left
ventricle) and prevent any back flow. The heart also contains the pulmonary and
aortic valves which prevent the back flow from the pulmonary and aortic
arteries into their respective ventricles. The contraction of the chambers, the
timing of the movement of blood and the operation of the valves within the
heart is controlled by electrical signals released from the Sinoatrial
node.  If the Sinoatrial node becomes
defective, cardiovascular diseases can occur. (12)

In this case, the problem is Atrial Fibrillation (AF) AF is
a common arrhythmia condition. AF is when the Sinoatrial node sends out
irregular impulses to the atrium and causes the atria to quiver out of
synchronisation with the ventricles. The uncoordinated atrium impulses cause
the ventricles to contract erratically and results in a less efficient heart
pump generally resulting in a fast irregular pulse. It can be detected by
Electrocardiogram. (13)

Symptoms of AF include palpations, tiredness, breathlessness
and dizziness. The symptoms can be linked to inefficiency in the circulation
providing lack of oxygen to the tissues. 
Blood can remain in the pulmonary vein and can pool in the atria due to
the insufficient contraction of the ventricles, increasing the risk of clotting
and stroke. Lack of oxygen occurs because fluid can build in the lungs and the
site of gaseous exchange becomes thicker. The diffusion pathway for the
transferral of oxygen extends resulting in shortness of breath. Insufficient
oxygen is transferred from the lungs to the haemoglobin in the blood resulting
in the brain, lungs and body tissues receiving an inadequate supply of oxygen.
(14)

The cause of
the defect to the Sinoatrial node is unknown but potential causes are high
blood pressure, heart attacks, coronary artery disease, abnormal heart valves,
congenital heart defects, an overactive thyroid gland, metabolic imbalance,
lung diseases, previous heart surgery, viral infections, sleep apnoea,
pneumonia stress, sick sinus syndrome, stimulant exposure and the most common
is abnormalities or damage to the structure of the heart. (15)

 

The associated dysfunction of AF is heart failure, stroke,
mortality and morbidity. Heart failure is when the heart isn’t pumping enough
blood around the body to meet demand. 
This is an associated dysfunction of AF because AF causes the heart to
beat so fast that it doesn’t fully fill with blood and therefore transportation
is inefficient. Heart failure symptoms develop because there can be a back flow
in the pulmonary veins because of insufficient pressure to move the blood away
leading to a fluid build up in the lungs which then causes fatigue and a
shortness of breath. With the inefficient supply there is not enough
oxygen-rich blood to meet the demand of the body and the brain causing both
physical and mental fatigue and reduced stamina. Fluid can also build up in the
lower limbs which will cause weight gain (morbidity) related to the heart
failure. 

AF can lead to a stroke and this occurs through the
fibrillation of the atria causing failed or inefficient contractions which
doesn’t allow all the blood to leave the atria before more blood starts flowing
into the atria again. Due to the pool of the blood, the risk of clotting goes
up. Therefore, if clots occur it can travel to the brain and cause blockages.
This blockage would cause an embolic stroke. Both heart failure and strokes have
a high risk of death or mortality. 
(13,16-18)

Normal atrial cells have normal atrial action potential and
therefore a normal atrial function, known as the ectopic activity. Normal
action potentials occur with normal voltage changes over time (sodium potassium
pump). AF is not a normal atrial function so individuals with this condition
have abnormal atrial cells and atrial action potentials.  This ectopic atrial activation occurs because
there is an abnormal diastolic leak of Ca2+ which causes the exterior
of the atrial cells to be more positive.

To produce automatic activity, a threshold potential has to
be exceeded for the cell to fire. However, because of the Ca2+ leak,
automatic firing occurs before the next normal Sinoatrial node rhythm and a
resulting ectopic atrial activation occurs. 
This ectopic atrial activation is what occurs during AF as the action
potentials occur before the atrial contraction has fully completed thus causing
a fibrillation. This atrial tachycardia leads to the remodelling of the atria
and multiple- circuit re-entry or multiple premature contractions. This ectopic
activity maintains AF and continually acts as the trigger. (13) In order for
this to possibly become normal again; a catheter ablation or cardioversion is
undertaken. Medication to control outcomes includes beta blockers that slow
heart rate and blood thinners to prevent clotting. (19-20)

Conclusion

Through the research completed and information gathered, a
greater understanding of each of the conditions has been established. This
understanding is essential for a healthcare professional because although you
may be treating one condition, the other condition always needs to be
considered and may impact on the treatment of the other. The professional is
treating the patient as a whole and not just a condition. In this case, even
though the treatment is for Cervical Spondylosis and the coinciding pain, their
other condition of AF can lead to severe consequences (stroke, heart failure
and even death).  Therefore, the
physiotherapist should look out for potential signs that other conditions or
severe symptoms that occur and referring them onto the relevant medical
professionals. In order for this referral to occur, the (above) gathered wide
and relevant knowledge is needed.