The Pain Game: A Very Basic Anatomical and Physiological Process Review


Pain is an integral part of life. It is an everyday neural process which has the potential to teach individuals and groups. It has be understood, misunderstood and misinterpreted for years. Business, Professions and Religions have been influenced and in some cases built on the concept of pain. In this article we review the anatomical and physiological changes which occur in the body when pain is occurring to get a better understanding of the issues surrounding pain, before next month’s follow-up article looking at the overall concepts surrounding pain, pain management and the cognitive interpretation of individuals.
The imposition of stimuli upon the body from internal or external influences has the capacity it to generate the sensation of pain. The stimuli are carried through from the place of concern via the Peripheral Nervous System to the Central and Autonomic Nervous Systems; this process of tissue damage being communicated to the brain is known nociception and is assisted via nociceptors attached to mylinated axon and unmylinated C fibres. There are a number of strong stimuli which can activate nociceptors through inflammatory or biomecular stimulation within a localized environment.
The instigation of nociception may not necessarily cause the sensation of pain but in most circumstances it will. A comparison can be drawn to the circumstance of those who undergo significant trauma, such as a car accident, who may appear to be in a stoic painless state. Alternatively those individuals with functional pain syndromes may exhibit strong pain symptoms despite the presence of very little, if any tissue damage.
Perception of pain will occur when axon fibres are stimulated creating a sharp or prickling sensation, furthermore if strong enough the pain can elicit a burning pain which may last after the stimuli has stop due to the activation of C fibres. The areas of the brain associated with subjective cognition of pain experienced include regions of the cerebral and cingulated cortex which process somatosensory input and relay neural impulses which influence pain perception and nociception.
Pain processing can be divided into two phases;
The First Phase is known as “fast pain” which is immediate and less intense than that of the second phase.
The Second Phase or Slow Pain is a less localized, more unpleasant and communication delayed pain.

All nociceptors send information via a excitatory neurotransmitter known at glutamate and can be activated by either mechanical, chemical or thermal stimuli, with the addition of an “inflammatory brew” being secreted at the initial site of injury. The Inflammatory Brew comprises of a number of neurotransmitters, neurotrophins, lipids and peptides which has the potential to increase or decrease nociceptors activation thresholds; and initiate neurogenic inflammation as a result of afferent signal transmission to the dorsal horn of the spinal cord.
Neurogenic Inflammation is responsible for vasodilation, leaking proteins and fluids into the extracellular area in close proximity to the inflammatory brew and stimulating immune cells which may contribute to said inflammatory brew. This process is activated via nociceptor neurotransmitter release from peripheral terminals. As a result the local environment changes due to neurochemical presentation and both Axon and C fibres increase creating peripheral sensitisation.
Following this occurrence nociceptive signal transduction occurs along the spinothalamic tract resulting in an increased release of noreponephrine, which is projected to the thalamus and thus, nociceptive information is relayed to the hypothalamus, hippocampus and somatosensory cortex.
At the same time, pain processing may be inhibited as a result of opiod receptor stimulation by endorphins, dynorphins or enkephalin causing analgesia; this process is controlled via the Descending Central Modulation of Pain.

The Descending Central Modulation System influences nociceptive input from the spinal cord. The brain structures involved with this process coordinate activity and changed nociceptive signals via descending projections to the spinal dorsal horn, by coordinating this process the central nervous system has the ability to selectively control signal transmission from specific areas of the body.
It is believed that central modulation may have been preserved within the human evolution because of its potential adaptive effects for survival. This can be seen in traumatic events such as war where an extremely injured soldier may benefit from pain suppression in order to remove themselves from danger. However, neurobiological bonding between a number of vital structures develop a physiological pathway which can allow negative emotions or stressors to amplify or increase pain duration lending to functional deficit or suffering.

Conclusion
Pain is a very complicated, intricate and still misinterpreted phenomenon which is difficult and dare I say impossible to objectively measure. That which is measured in pain associated studies is more commonly the amount of tissue damage present or change in chemical compounds of the tissue. However, this rarely is correlated with the pain felt by an individual. The anatomical and physiological processes in an otherwise health human will be somewhat identical but, the way in which that individual interprets and therefore reacts to the stimuli may be complete over the top or under-welling leading to further injury. This is where real interest develops and can be used to explain why treatments, preventions and interventions need to be individualized to each patient rather than a stock standard protocol which can be used broadly.

In the next article we delve further into the concepts of pain, including a link to one of the most influential academics in the field of pain explanation and pain procession Dr. Lorimier Mosely.

Jackson McCosker
Director /Chief Editor

References

Garland, E. L. (2012). Pain Processing in the Human Nervous System. Primary Care Clinic and Practical .

BREAKING BONE: An Overview of Stress Fractures and Subsequent Management


It happens to everyone, you get a sudden urge to get fit, you increase a training load to reach that desired Personal Best, and you start a new job where you change from office desk jockey to trekking the pavement in shoes which were made for being a desk jockey. At first it’s a feeling of fatigue, your body, legs hurt, a couple of sharp pains here and here but hey, once you get home kick off the shoes, maybe walk on the carpet or put the feet up that pain subsides and you forget about it for another day.
Unfortunately, over the next 3-4 weeks that pain which once disappeared at the end of a long day is still around, the use of voltarin or ice packs are working less and less; the pain has finally come to a stage where you think “maybe it is time I see a professional about this”.

Pathophysiology
A stress fracture can be defined as a complete or partial continuity of bone. Stress fractures develop due to an overloading of a particular hard tissue structure where; increased shear forces lead to the stimulation of osteoclast activity and eventual bone resorption which outweighs the bone’s strengthening and adaption to stress by way of osteoblasts remodelling. This can occur due to a number of both intrinsic and extrinsic factors. Biomechanical abnormality is commonly the first assessed area of risk, however it has been proposed by (Diehl, Best, & Kaeding, 2005) that soft tissue overuse and fatigue may lead to focal bending beyond the physiological and structural tolerance of a bone creating micro fracture initiation.
Stress fractures do not heal via the formation of callus similar to traditional traumatic breaks but by way of direct remodelling spanning the fracture line, this in turn leads to a much slower healing time comparable to that of a non-unionized fracture.

Risks (intrinsic/extrinsic)
The risk factors which can contribute to a stress fracture can be categorized into intrinsic and extrinsic. Quite commonly it is indicated to be a combination of both categories which lead to the onset of pain associated with stress fractures.  Below is a table which separates the potential risk factors into their specific categories;

Stress Fracture / Stress Reaction Risk Factors
Intrinsic Extrinsic
– Nutrition

– Hormonal Deviation

– Gender

– Age

– Race

– Bone Density

– Sleep

– Collegen Disease
– Autoimmune Disease

– Female Triad
     +Disorder Eating
+Low Bone Density
+Menstrual Disturbances

– Type, Duration, Intensity, Rhythm of Training

– Poor Footwear Choices

– Sporting Equipment

– Poor Physical Conditioning

– Training Location

– Environment and Surface

– Temperature/Climate

– Recovery Time

– Previous Injury

Populations
Although still widely debated it is believed to be the female sex who is more likely to experience stress fractures than their male counter parts. This may be due to the existence of the Female Triad outlined in Intrinsic Risks which suggests that a combination of Disordered Eating, Menstrual Disturbance (hormone changes) and Low Bone Density create a significant structural deficit within the bone (Iwamoto & Takeda, 2003). Additionally, a female athlete who competes or trains with male counter-parts also have an increased risk due to physical differences such as appropriate stride length.
Goodwillie, Nussbaum and Gatt, found in a study of adolescent athletes that lower limb stress fractures were by far the most common, with the following numbers published in regard to area of fracture and sports where stress fractures are likely to occur:

Stress Fracture Male Female
48% Tibia

19% Metatarsals

10% Fibula
6% Spine

6% Pelvis

4% Rearfoot

4% Femur

26% Track & Field

23% American Football
19% Cross Country

28% Track & Field

23% Cross Country

In note with the figures shown t (Weel, Opdam, & Kerkhoffs, 2014) found that Endurance athletes were more like to suffer stress reaction or stress fracture injuries. Alternatively, children were found to be less likely to develop these conditions, which may be due to the anatomical differences in bone structure at a cellular level creating increase flexibility within the hard tissue

Clinical Findings
Clinically, a patient will most likely have an active lifestyle (not necessarily sporting) which has been reduced recently with the gradual worsening of a pain which had an insidious onset and now is chronic in character. Alternatively, it is not uncommon to have a client speak of a moment of intense pain, which quickly reduced but has remained a chronic low grade pain for some time now.
A change in lifestyle through; activity level, diets, type of activity or footwear all contribute, as seen in the risk factors above.
Typically the client will be at least of adolescent age or begun maturation.
Local tenderness is present, there is pain during facilitated movement and there is palpable swelling.

The navicular stress fracture is known as a high risk fracture (discussed later) and can display a number of different clinical findings given its physical and physiological structure.  The bone is a boat shaped keystone of the medial arch which is positioned between the three cuneiforms and the talus. Given its keystone status the navicular becomes impinged between the previously discussed bones during foot strike with maximum force focused at the central third of the navicular itself. Although the navicular is supplied with blood from both the anterior and posterior arteries, they unfortunately only feed the medial and lateral thirds of the bone, leaving it avascular and with significantly poor ability to heal efficiently (Khan, Fuller, Brukner, Kearney, & Burry, 1992).
Coris & Lombardo, found that in 81% of clients who were diagnosed with a navicular stress fracture, were found to be tender at the “N” Spot – the dorsally central region of the navicular bone. Additionally, patient would have increased pain with closed-chain plantarflexion and hopping.

Imaging
Medical imaging for stress reaction and stress fractures is an area of interest for a number of reasons. Each form of appropriate imaging has pros and cons which largely rotated around the following points; Cost, Availability, Sensitivity, Specificity and Radiation Exposure. As discussed in a previous article in 2014, I believe as practitioners we are not the patient’s financial adviser – we are present to provide the best possible options available, educate the patient on the pros and cons and suggest our most preferred option for them to pursue – therefore cost is not a point of concern when referring a patient unless specifically objected too.
Sensitivity is of importance, being made aware of an issue and ruling in/out pathologies of concern is of great use to a practitioner and can have a direct impact on treatment of the area of complaint. The modality of X-Ray has not been found to be reliably sensitive to the presence of stress reactions or stress fractures, especially within the first 2-4weeks of symptoms presenting. According to a study by (Weel, Opdam, & Kerkhoffs, 2014) X-ray has only been found to show 30% of stress fractures of the Tibia and 15% of the calcaneal, with the fibula based injuries not being visible for at least four weeks post symptoms and sesamoid stress fractures being unable to identify between a fracture and bipartite/tripartite sesamoid.
Alternatively the use of CT scan has increased sensitivity which can make it difficult to distinguish between than which is a stress reaction and a stress fracture – this can be of the utmost importance when assessing fractures believed to be High Risk.
Magnetic Resonance Image (MRI) is both sensitive to stress related injury and specific in diagnosing the condition, by far it provides the most amount of information to a practitioner of all the modalities used for stress injury investigation and there is little to no exposure of radiation to a patient. This type of imaging has been promoted when a practitioner suspects stress fractures/reactions of the tibia, talus, calcaneus or navicular (Duarte Jr & Silva, 2014).
There are downsides to this particular modality including; small confined area being involved (claustrophobia), those with metal plates or aneurism clip being contraindicated and availability of MRI within some districts – particularly those of regional or rural existence.

Categorizing and Risk Status
By classifying and categorizing stress fractures it allows for practitioners to decide on the most appropriate form of treatment. The New Classification System by Kaeding & Miller (2013) looks to classify stress fractures into one of five categories based on both objective and subjective findings when assessing a patient. The classification identifies the following grades of a stress fracture:
Grade I: Asymptomatic stress reaction on imaging.
Grade II: Pain but no fracture line on imaging.
Grade III: Non-displaced fracture
Grade IV: Displaced fracture
Grade V: Fracture with non union.

Additionally, the two categories of High and Low Risk are based on the anatomical and physiological issues associated with the area of complaint. Just because a stress fracture may been seen as Low Risk does not necessary mean that the injury has no risk and this should be taken into consideration during treatment planning with the patient; discussing both the benefits and deficits of continued athletic participation against partial or complete rest. Gradual progression into activity should be done so at approximately 10% per week.
Those who are unfortunate enough to sustain a stress fracture of High Risk are not recommended to complete activity until such time as complete treatment and healing of injury has been achieved.

Treatment
The prompt diagnosis and treatment of an athlete with a stress fracture which is believed to be of High Risk is significantly important in minimizing the impact upon the athlete’s career (Diehl, Best, & Kaeding, 2005). General theory and protocol for stress reactions and fractures; is the use of rest or activity modification to allow for remodelling of bone which is under stress. Additionally, education relating to the patient’s increased workload contributing to the incidence, nutritional intake and hormonal state may also play a key role in general consultation (Weel, Opdam, & Kerkhoffs, 2014).
More specifically treatment options advocated for stress fractures of the following structures, as well as, their risk status and specific populations have been tabled below.

Structure Risk Status Conservative Tx Surgical Tx Population
Tibia High 4-8 weeks in a non-weight bearing cast Advocated for complete or displaced fracture- usually associated with internal fixation with compression screws Long distance runners, Jumper and gymnasts
Fibula Low 3-6weeks rest or weight bearing CAM Boot Only advocated in non-union occurs Runners and Footballers (All Codes)
Talus High 6+weeks in non-weight bearing cast Advocated for athletes, however healing time still significant Very Rare Condition but will not return to previous level of play
Calcaneus Low Reduction in activity and offloading of area
6weeks+
If conservative treatment does not work Long Distance Runners and Military Recruits
Navicular High 6weeks in a well molded non-weight bearing cast.
If pain no longer present at N spot rehab can begin.Orthotics should be prescribed for biomechanical issues.
Screw fixation with possibility of bone graft Running Sports, primarily associated with poor mechanics.
Metatarsal I-IV Low CAM Boot 4-8weeks with gradual activity increase after. If conservative treatment fails, followed by 6-8weeks in a CAM boot Dancers, Sprinters, Military Recruits  and short distance runners
Metatarsal V High Non weight bearing cast for minimum of 6weeks Srew fixation recommended in athletes Football(All Codes) and Basketball
Sesamoids High Modification to activity, partial weight bearing with use of CAM BOOT. Prevention of dorsiflexion for 6weeks. If conservative treatment is not successful Plantarflexed first ray patients with poor windlass mechanism

Finally, before the implementation of a rehabilitation program it is important that any risk factor which was identified as a potential cause or contributor to the development of a stress fracture is addressed. Obviously, this is much easier to achieve in regards to extrinsic contributors than intrinsic however, ensuring the client has a more efficient personal awareness of limitations without encouraging fear avoidance is an achievable goal for a practitioner.

Rehabilitation
Rehabilitation should be focused on returning the client to their previous state of athletic ability. The achievement of this process is not something to be rushed and each stress fracture may have a number of different methods in completing this goal.
Rehabilitation or at a minimum body maintenance may begin very early within the treatment of a client. Programming exercise regimes which are inclusive of non-weight bearing activities allow for cardio and strength maintenance. Cycling, Swimming, Water Running and machines such as the Elliptical Trainer can be utilized to reduce conditioning deficit as a result of injury.
Although much of the time for clients of non-elite level, measures of pre-injury flexibility, range of motion, strength, agility, speed and power are not recorded and do not allow for specific recognition of pre-injury ability. However, it is important that the practitioner in combination with the client develop a number of goals within these areas to insure that a return to sport strategy can be scheduled.

Return To Sport
Non-weight bearing bones such as the fibula and Low Risk stress fractures have a much faster return to sport expectation than bones associated with weight bearing or of High Risk. By over treating patients with Low Risk stress fractures by way of unnecessary surgery issues such as body deconditioning and decreasing competition fitness can increase the time it takes a client to return to sport. Approaches of conservative measures allow for activity and maintenance of body conditioning while minimizing significant complications. Alternatively, stress fractures of particular anatomical sites which are subject to non-union, poor healing times and significant complications should be treated with the best available treatment and invasively is deemed necessary as soon as possible (Diehl, Best, & Kaeding, 2005).

Conclusion
This topic has been a large one, and in all honesty much bigger than I had anticipated. The scary thing about it is that it could be completed in further detail and in the future may just be done.
At the end of the day, diagnosing a patient with a stress fracture as early as possible has a significant influence on their return to sport or activity. For this reason by-passing a plain radiography would be considered plausible in placement of CT or MRI.
Setting goals with your patient to be reached and establishing realistic time frames for rehabilitation when considering the stress fractures risk level is also necessary. If advocated, at the very least it does not hurt to refer for surgical opinion and for that matter should the same treatment you would suggest for an elite athlete not be at least discussed with your average client, being best practice?

That’s a question to ponder on and I’ll leave this conclusion on the short side.
FootNotes next article will be on Pain, because in many cases, the treatment of such a complex physiological response is the reason many patient approach us in the first place.

Until next time.

Jackson McCosker
Director /Chief Editor

 

References

Coris, E. E., & Lombardo, J. A. (2003). Tarsal Navicular Stress Fractures. American Family Physician , 85-90.

Diehl, J. J., Best, T. M., & Kaeding, C. C. (2005). Classification and Return to Play Considerations for Stress Fractures. Clinics In Sports Medicine , 17-27.

Duarte Jr, A., & Silva, A. (2014). Stress Fractures in the Foot and Ankle of Athletes. Rev Assoc Med Bras , 512-517.

Goodwille, A. G., Nussbaum, E., & Gatt Jr, C. (2010). Stress Fractures in Adolescent Athletes. New Jersey, United States of America: Robert Wood Johnson Medical School.

Handoll, R. H., & Ashford, R. (2005). Interventions for Preventing and Treating Stress Fractures and Stress Reactions of Bone of the Lower Limbs in Young Adults (Review). The Cochrane Collaboration , 1-66.

Iwamoto, J., & Takeda, T. (2003). Stress Fractures in Athletes: Review f 196 Cases. Journal of Orthopaedic Science , 273-278.

Kaeding, C., & Miller, T. (2013). The Comprehensive Description of Stress Fractures: A New Classification System. Journal of Bone Joint Surgery of America , 1214.

Khan, K. M., Fuller, P. J., Brukner, P. D., Kearney, C., & Burry, H. C. (1992). Outcome of conservative and Surgical Management of Navicular Stress Fracture in Athletes. The American Journal of Sports Medicine , 657-666.

OrthopaedicsOne Articles. (2010). Base of 5th Metatarsal Fracture.

Weel, H., Opdam, K., & Kerkhoffs, G. (2014). Stress Fractures of the Foot and Ankle in Athletes, an Overview. Clinical Research on Foot and Ankle .