Cervical Spine Scapegoats

CERVICAL SPINE

Headaches, shoulder pain, pins and needles in your hand might sound like very separate injuries but in fact can all potentially be traced back to dysfunction at the cervical spine. In this post we’ll look at some of the pathologies, signs and symptoms that can be attributed to problems occurring at the neck.

Cervical headaches

Cervical headaches or cervicogenic headaches are tricky to differentiate from migraines or regular headaches but are defined as being caused by dysfunction and resultant inflammation of the upper cervical spine (Jull, 1994) and usually feel like a dull aching pain spreading up into the head and predominantly on one side (Sjaastand and Fredriksen, 2000). These can arise suddenly after a traumatic injury such as whiplash or gradually from poor head posture sustained for long periods (e.g. at work working at the computer too far ahead of you). Other causes for cervical headaches include compression or entrapment of the greater occipital nerve as it runs through the neck muscles such as semispinalis and the upper fibres of trapezius. (Rosenholtz et al, 2003.)

A forward head or “pokey chin” posture is one of the common correlates with cervical headaches. (Griegel-Morris et al, 1992; Haughie et al, 1995). This can arise from tightness in certain muscle groups placing excessive stress on the joints of the upper cervical spine. Muscles that are commonly tight are: sternocleidomastoid, suboccipitals, upper traps, pecs and weakness in the deep neck flexors lower and middle fibre traps (Janda, 1994).

Referred pain into shoulder, arm or hand

Inflammation, disc protrusions or degenerative changes in the cervical spine such as narrowing of joint space or the formation of small bony growths called osteophytes can impinge on nerves resulting in: pain (often described as shooting or burning), sensory disruption (e.g. tingling, numbness, altered sensation, pins and needles), and in more severe cases motor dysfunction (muscle weakness, reduced reflexes).

Dermatomes are areas of skin innervated by predominantly one nerve root. While there is invariably some overlap of these areas, pain in a certain dermatomal region can indicate the corresponding level of the cervical spine where the dysfunction is originating from.

C2 - Posterior occipital headaches, temporal pain
C3 - Occipital headache (back of head), retro-orbital (behind eyes) or retroauricular (behind ears) pain
C4 - Base of neck, trapezial (upper shoulder) pain
C5 - Side of upper arm pain
C6 - Thumb side forearm pain, pain in the thumb and index fingers
C7 - Middle finger pain
C8 - Pain in the ring and little fingers
T1 - Little finger side forearm pain

Source: www.necksolutions.com

In conclusion don’t be too quick to assume that where you’re experiencing symptoms is necessarily where the source of problem is. Your physiotherapist through a comprehensive assessment of your history and physical examination will be able to determine the most likely cause of referred pain and discuss the most appropriate treatment approach.

J.Glover BSc Physiotherapist MCSP

What is quad dominance and does it actually exist?

WHAT IS QUAD DOMINANCE? DOES IT ACTUALLY EXIST?

Just an informal article guys and gals on a topic that was brought to my attention and thought I'd have a look into. As always your thoughts, opinions and questions are always welcome. 

Suggested definitions

“Defining an exercise as a being hip or quad dominant is determined by the joint at which the main action of the movement occurs and on which group of muscles are most active” Precision Nutrition

This website uses the example of a step-up exercise to demonstrate how altering the parameters will change the emphasis on certain muscle groups, making it supposedly hip or quad dominant.

For example, step-ups at a low step height will be more quad or ‘knee’ dominant, whereas raising the height of the step increases the activation of the glutes and hamstrings, making it more of a hip dominant exercise.

 

Livestrong also define quad dominance as a category for movements rather than a condition i.e. exercises that involve more motion at the knee compared to other joints of the lower limb. The example they use is the squat.

These pictures show variations of the squat with the bar (or load) in different positions (front, high bar and low bar squat). The ‘elephant in the room’ here is the trunk angle variance, the front squat maintaining a fairly upright torso compared to the low bar squat where there’s  so much forward lean that the guy has almost folded in half.

Now full range of motion of the hip into flexion is supposed to be 120 degrees and at the knee about 140 degrees. If we’re talking about a ‘CrossFit squat’ in which the hip must go below parallel then by that definition hip flexion must be more than 90 degrees flexion.

In this picture hip and knee are both in full flexion so you could argue that neither joint is being overly emphasised by this exercise, performed to this depth.

You can tell Jim Wendler dislikes the term ‘quad dominance’ from this subtle description: “unless your quads hang over your kneecaps like an elephant’s testicles, you’re not quad dominant. You’re hamstring weak.” But what’s interesting, apart from comparing quads to an elephant’s balls, is that his example has nothing to do with a category of movements placing more emphasis on the quadriceps but rather an imbalance between agonist and antagonist muscle groups.

Still confused? The lack of consensus in terms of a clear definition for quad dominance makes the whole concept pretty ambiguous. So perhaps breaking down what’s going on with the use of another example can shed some light.

The quadriceps are primarily knee extensors. In a non-weight bearing position e.g. sitting on a chair and you straighten your knee, your quads work concentrically to overcome gravity and achieve this motion. Their action changes somewhat in function though, for example when you’re running the quads act eccentrically to decelerate knee flexion as you land on your lead leg.

NB: In the interest of keeping this fairly short I’m only going to be talking about the hip and knee flexors and extensors but there are a LOT of other muscles working during these activities.

If you perform a forward lunge the lead leg during the downward phase undergoes the most muscle activity. The body weight comes forward and the quads have a massive eccentric demand as the knee moves into flexion. Distally the hamstrings reciprocally shorten at the knee end while being eccentrically loaded at the hip end along with the glute max.

During the upward phase the knee drives into extension from the concentric contraction the quads while the hip is extended concentrically by the glute max and hamstrings. 

If you’re performing the classic 90/90 lunge in which your knee and hip are kept at 90 degrees then no one joint moves more than the other, so regardless if it’s a forward or reverse lunge, the above definition can’t call this a quad dominant exercise. But if you get up now and try a forward lunge chances are you’ll probably feel it working the quads in the lead leg a lot more than the hamstrings. But why is this? A reverse lunge for people with knee pain can be more comfortable due to less potential shear force from excessive anterior translation of the tibia and less eccentric demand on the quads putting stress through the patella tendon. You don’t have to ‘catch’ the weight of your body in a reverse lunge compared to a forward one and it’s a lot easier to maintain a vertical shin position.

But what if the angles were altered? A longer stride forward may eccentrically load the posterior chain more by decreasing the amount of knee flexion compared to hip flexion. The point of load on the foot can change the emphasis as well. Have a go at performing a forward lunge and moving the weight around your foot (heel, mid-foot, fore-foot etc) and you’ll feel certain muscles fire more than others.  

So in conclusion does quad dominance actually exist? It depends on which definition you use. If you’re talking about a category of movements that emphasise the quads then sure, that exists.  If you’re talking about an athlete with an agonist-antagonist muscle imbalance between quads and hamstrings I’d agree that this is quite a common condition. A lot of the athletes that I’ve treated have presented with this type of imbalance and it seems increasingly rare to find someone with over-active hamstrings and weak quads. Why is this? Perhaps for a lot of the population who spend several hours a day in a chair with the hip and knee flexed (quads and hip flexors in a shortened position) this can create long and weak hamstrings, altering the length-tension relationship. What do you need to do about it? If you were at my awesome mobility class last week we went over exercises to help increase glute and hamstring activation and this is the first port of call that I’d suggest.

Sources/References

http://www.precisionnutrition.com/

http://www.livestrong.com/

How To Solve Your Tennis Elbow

HOW TO SOLVE YOUR TENNIS ELBOW

It’s ironic that the number of tennis players that suffer from tennis elbow are said to account for 5% of all cases (Peterson and Renström, 2001). In fact those most at risk of developing this condition are people in manual trades (carpenters, builders, electricians, painters etc) that involve repetitive wrist flexion and extension (imagine painting a wall) and also pro and supination (think of turning a screwdriver). I guess ‘Painter’s Elbow’ didn’t catch on but the terms you will commonly here used to describe this injury are: lateral elbow tendinosis, lateral epicondylitis and lateral epicondylalgia. Each of these is an attempt to describe the underlying pathological process, but what is actually going on inside that elbow of yours? 

“What causes it?” Aetiology/Pathophysiology

Ljung et al (1999) conducted biopsies on patients with tennis elbow and found no evidence of inflammatory markers while Nirschl et al (1989) and Regan et al (1992) discovered degenerative changes in the wrist common extensor tendon, synonymous with other chronic tendiopathies (achilles, and patella etc). There are still several hypotheses as to what the main cause of the pain is: raised glutamate levels (Alfredson et al, 2000); secondary hyperalgesia (Wright et al, 1992) or my favourite ‘angiofibroblastic hyperplasia’ (Brukner and Khan, 2000). 

This basically suggests that in response to the micro-damage to the tendon, the body deploys cells called fibroblasts that begin to lay down repair tissue (granulation tissue) which contain a lot of painful nerve endings (potentially accounting for the pain).

So what does all this mean and what’s important for you to know? Tennis elbow is essentially an overuse injury where the wrist extensor tendon (mainly extensor carpi radialis brevis) undergoes microscopic tears. The tendon has a poor blood supply leading to a continuous failed healing response as the tissue healing struggles to keep up with the demands placed upon it. 

“How do I know I’ve got it?” Signs & Symptoms 

•   Gradual onset of pain (24-72 hours after training or manual work) 
•  History of overuse or return to training after a prolonged break
•  Pain over lateral aspect of elbow (+ or – radiating pain down forearm
•  Pain shaking hands or opening doors (turning door handle) 

"Who's most likely to get it?" Predisposing Factors 

• Age 35-50
• Tennis player: overtraining or sudden increased frequency of play
• Faulty technique (poor back hand)
•  Manual work involving repetitive wrist motions

(Peterson and Renström, 2001)

“What else could it be?” Differential Diagnosis

Before commencing on any treatment regime, it’s important to confirm that the injury is actually tennis elbow by ruling out other potential conditions first. Other causes of lateral elbow pain are:

·        

•     Referred pain from cervical or upper thoracic spine  Radial nerve tension
•      Radiohumeral bursitis
•      Synovitis of the radiohumeral joint 
•     Posterior interosseous nerve entrapment 
•         Osteochondritis dissecans (flaking of the articular cartilage and subchondral bone) of the captiellum or radius

Brukner and Khan (2000)

“How can I avoid it?” Prevention

If you’re a tennis player correcting/adapting technique will definitely play an important preventative role in reducing abnormal stresses placed on the wrist extensor muscles (e.g. adopting a double handed back hand rather than single arm), along with ensuring adequate recovery between training sessions. 

Other preventative measures include checking the grip width of your racket (should be equal to the distance from the middle of your palm to the top of your middle finger) and replacing tennis balls on a regular basis.

If you’re in a manual trade, factory worker or in any job that involves repetitive stress on the forearm muscles I’d advise taking breaks when able and to regularly alternate arms i.e. not relying purely on dominant side to do all your work. 

“How do I get rid of it?” Treatment

Once a diagnosis of tennis elbow (lateral epicondylitis) has been confirmed your physiotherapist can talk you through a range of treatment options available to you, offer advice and education as to what movements and activities to avoid and inform you when it’s safe to return to activity. Which ones are most appropriate will depend on the severity and stage of the injury. 

Treatment options include:

• Graduated therapeutic strengthening and stretching programme
• Mobilisations with movement (MWM)
•  Sports taping / Counterforce bracing
• DTF (Deep Transverse Frictional Massage

Non-Conservative Measures 

If your symptoms persist for more than 6-12 months and you’re unable to return to your activity/sport despite rehabilitation from a registered physiotherapist then surgery may be indicated. The surgery is an arthroscopic debridement of the extensor carpi radialis brevis tendon that is generally uncomplicated and completed within 30 minutes. 80-85% of patients regain full strength and complete relief of pain although the surgery is always followed by a post-operative rehabilitation programme on week 3. Steroid injections are also another option prior to surgery if conservative measures fail to reduce pain. 

References/Sources

·         

·         Images sourced from www.orthogate.org, www.optimumtennis.net, www.sportstek.net, www.prolotherapy.org

·         Brukner, P., Khan, K (2000) Clinical Sports Medicine, Australia, McGraw-Hill

·         Greene, J (1992) Cost-conscious prescribing of nonsteroidal anti-inflammatory drugs for adults with arthritis, Archives of Internal Medicine, 152:1995-2002

·         Peterson, L., Renström, P (2001) Sports Injuries: Their Prevention and Treatment (3^rd Ed), United Kingdom, Taylor and Francis.

·         Ljung, BO., Forsgren S., Friden, J., (1999) Substance P and calcitonin gene-related peptide expression at the extensor carpi radialis brevis muscle origin: implications for the etiology of tennis elbow, Journal of Orthopaedic Research, 17: 554-559.

·         Nirschl, R (1989) Patterns of failed healing in tendon injury. In: Leadbetter W., Buckwalter, J, Gordon S (eds) Sports-induced Inflammation, American Academy of Orthopaedic Surgeons, Illinois, pp 577-585.

·         Regan, W., Wold, LE., Coonrad, R., Morrey., BF (1992) Microscopic histopathology of chronic refractory lateral epicondylitis, American Journal of Sports Medicine, 20: 746-749. 

Frozen Shoulder

Mainy stiff and painful shouders can be mis-takingly diagnosed as frozen shoulders. Painful shoulder impingements and pain referred from the cervical spine can have presentations in common with a frozen shoulder but respond very poorly to treatment directed at a frozen shoulder. A mis-diagnosis can lead to a delay in appropriate physiotherapy intervention  and a prolonged period of discomfort for the patient.

Frozen Shoulder

So what is a frozen shoulder?  Adherent bursitis, adhesive capsulitis, pericapsulitis are just some of the terms used to define the condition of a ‘stiffening or frozen shoulder’, each is a description of
the potential underlying disease process (Siegel et al, 1999). The term ‘Frozen
shoulder’, first used by Codman in 1934, describes a gradual onset of shoulder
pain, progressive reduction of range of motion and discomfort sleeping on the
affected side (Pearsall and Speer, 1998).

The exact cause of frozen shoulder remains unclear. Some theorized that the disease results from a thickening and tightening of the normally flexible and elastic joint capsule leading to a contracture (Neviaser and Neviaser, 1987) while other suggest the cause
originating from an inflammatory response leading to scar tissue formation (Hanafin
and Chiaig, 2000).

Frozen shoulder usually occurs with no prior injury or notable cause but can follow traumatic injuries such as fractures where the arm is immobilised for a prolonged period of time. You may be more likely to develop the condition if you have one or more of the
following risk factors:

3:1 female to male ratio (Walker et al, 1997)

Most presenting cases 40-60 years of age

History of diabetes, thyroid or heart disease (Walker et al, 1997)

Dupuytren’s contracture (Schaer et al, 1936; Smith et al, 2001)

The two types of frozen shoulder are defined by whether the
cause is known or unknown:

Primary (insidious)

Primary adhesive capsulitis is
characterised by an insidious progressive painful loss of active and passive
glenohumeral joint motion (Hannafin and Chiaia, 2000).

Secondary (traumatic)

Secondary adhesive capsulitis presents
in the same way as primary but stems from a known underlying illness or extrinsic
cause (Hannafin and Chiaia, 2000)

STAGES OF FROZEN SHOULDER

Freezing ‘Painful’ Phase: Pain increases with movement, often worse at night, progressive loss of motion with increasing pain (Duration approx: 2 to 9 months)

Frozen ‘Stiff’ Phase: Pain begins to diminish,significantly reduced range of motion (as much as 50% less than in the other arm) (Duration approx: 4 to 12 months)

Thawing ‘Recovery’ Phase: Condition may begin to spontaneously resolve, most patients experience a gradual restoration of motionover the next 12 to 42 months
Apply heat or cold packs to help reduce and manage the pain
Consult your GP for advice regarding pain medication/anti-inflammatories
See your physiotherapist for advice and treatment

Physiotherapy treatment for frozen shoulder aims to restore normal range of motion to the joint, increase tissue extensibility and improve strength of the muscles around the shoulder:
Pain management
Graduated stretching programme
Passive joint mobilisations
Ultrasound/Soft tissue massage
Specific home exercise programme
Postural re-education

Some evidence suggests that physiotherapy intervention can have a more profound impact on the condition in the earlier stages (Mao et al, 1997). However most patients do not seek help until pain and loss of range of motion begin to affect day to day tasks. If you begin to notice any symptoms, seek advice from your physiotherapist or local health care professional.

Hannafin.,
JA., Chiaia, TA (2000) Adhesive capsulitis: A treatment approach, Clinical Orthopaedics and Related Research,
372, 95-109.

Mao,. CY.,
Ja., WC., Cheng., HC (1997) Frozen shoulder: Correlation between response
to physical therapy and follow-up shoulder arthrography, Archives of Physical Medicine and Rehabilitation, 78: 857-859.

Neviaser , RJ.,
Neviaser  TJ (1987)  The frozen shoulder: Diagnosis and management.
Clinical Orthopaedics,
233:59–64.

Pearsall., AW.,
Speer., K P (1998) Frozen shoulder syndrome: Diagnostic and treatment strategies in
the primary care setting, Medicine
and Science in Sports and Exercise,
30: 33-39.

Schaer, H (1936) Die aetiologie der
periarthiritis humeroscapularis, Ergebn Chir Orthop, 29: 11.

Siegel, L., Cohen, N., Gall, E (1999)
Adhesive Capsulitis: A Sticky Issue’, American Family Physician,
59(7):1843-1850.

Smith et al (reference in Watson’s shoulder manual)

Walker, K., Gabard, D., Bietsch, E., Masek-VanArsdale,
D., Robinson, B (1997) A profile of patients with adhesive capsulitis, Journal
of Hand Therapy, 222-228.

Image sourced from www.shoulderdoc.co.uk