Defining Scapular Dyskinesis and Its Causes

In previous articles, we’ve looked at the scapula’s complex anatomy, the scapula’s rotations, and the scapula’s translations.

In this article, we’ll cover scapular dyskinesis and its causes.

Defining Scapular Dyskinesis

We can better understand what is meant by dyskinesia by breaking it down into its parts—“Dys,” meaning alteration of, and “kinesis,” meaning motion.

Scapular dyskinesia is a general term used to describe loss of control of normal scapular physiology, mechanics, and motion. Dyskinesia describes motions that were once voluntary and have transitioned to involuntary. Scapular motions are primarily accessory meaning they are not voluntary to begin with. As such, the term dyskinesia should not always be utilized as the primary term to described altered scapular motion or mechanics.

Dyskinesis, by itself, is not an injury, a guarantee of an injury, or directly related to a specific injury. It is an impairment that results from one or more sources such as muscle tightness, weakness, loss or impediment of motor control, global movement dysfunction, and/or pathoanatomical injury. In other words, something has to cause the dyskinesis.

It can be clinically characterized by medial or inferior medial border prominence, early scapular elevation or shrugging upon arm elevation, and rapid downward rotation upon arm lowering.¹

The alteration of motion reduces the efficiency of shoulder function in several ways, including changes in:

• Three-dimensional glenohumeral (GH) angulation
• Acromioclavicular (AC) joint strain
• Subacromial space dimensions
• Maximal muscle activation
• Optimal arm position and motion

These scapular components can create symptoms by themselves or may interact with other shoulder pathology to increase the dysfunctional problems, affect treatment direction, and affect outcomes.

Causes of Dyskinesis

There are four main categories of scapular dyskinesis or SICK scapula syndrome:

Neurological

The most common perception of the “winged” scapula, with prominence of the medial scapular border, is that all cases occur as a result of damage to the nerves supplying the scapular stabilizing muscles. However, although neurological injury is possible (i.e., long thoracic nerve palsy, spinal accessory nerve palsy, etc.), the term “winging” is reserved specifically for the neurologically verified injuries rather than all cases of medial border prominence. This is because the injured nerve(s) inhibit muscle function, which creates scenarios where the prominent medial border or inferior angle are visibly pronounced throughout a complete arm range of motion–both elevation and descent. Therefore, it is recommended the term “winging” be used to describe scapular dysfunction with a verified neurological injury.

The exact frequency of neurologically based winging is poorly defined, and the clinical interpretation requires careful history and examination. Injury may be traumatic, iatrogenic, or idiopathic. The three nerves most often involved include the long thoracic, spinal accessory, and dorsal scapular nerves.^2-10

The long thoracic nerve is a purely motor nerve that innervates the serratus anterior muscle and originates from the ventral rami of C5, C6, and C7.

The course of the nerve predisposes it to frequent injury. After passing through the middle scalene, the nerve crosses under the clavicle and remains superficial along the lateral chest wall. Here, it can be subject to blunt trauma, diverse athletic injuries, or traction.

Numerous reports of compressive neuropathy exist from lateral positioning or prolonged convalescence. Patients can also receive an iatrogenic injury following lateral thoracic surgery such as radical mastectomy or axillary lymph node dissection. Finally, patients with a viral infection can be diagnosed with Parsonage-Turner type neuritis, which can cause neurologic symptoms in patients experiencing significant pain.

A patient typically recovers from idiopathic causes in one year, but it may take longer. Chronic thoracic nerve injury creates loss of the serratus anterior muscle function, which results in translation of the scapula superiorly and medially, and disruption of normal scapulohumeral kinematics. Clinically, this rotation causes the inferior angle to become notably prominent in both static and dynamic examination.

Scapular winging can also be the product of injury to the spinal accessory nerve (cranial nerve eleven). Upon loss of the trapezius activation, the scapula assumes a more inferior and lateral, or “drooping,” posture. Winging is often less prominent than serratus anterior palsy; however, the atrophy in the upper trapezius, loss of muscle tone, and inability to shrug are easily discernible. Inability of the lower trapezius to achieve and maintain the retracted “functional” position of the scapula leads patients to report pain and weakness with forward elevation and abduction.

Less commonly, weakness of the major and minor rhomboid muscles is encountered in deficits of the dorsal scapular nerve. The nerve is a branch of the C5 nerve root and may be involved in radiculopathy. With loss of the rhomboids, unopposed pull of the serratus anterior results in lateral rotation of the inferior angle of the scapula. Atrophy of the rhomboids may be observed.

Bony Disruption

The AC joint—stabilized by both the coracoclavicular (CC) and AC ligaments—represents the critical link in coordinated scapuloclavicular kinematics and scapulohumeral rhythm.

The AC joint disruption or injury may disrupt the synchronicity of motion of the clavicle, scapula and, ultimately, the arm in multiple planes by altering the screw axis of the coordinated motion. This alteration may be clinically manifested as scapular dyskinesis and associated with the spectrum of subsequent shoulder symptoms.

In a study to evaluate the scapula, 34 patients with Rockwood type III injuries, i.e., complete disruption of the AC joint, were followed and evaluated by defined measures at a mean follow-up of 28 months. A total of 71 percent of patients exhibited scapular dyskinesis. Of these, 58 percent met criteria for scapula malposition, inferior medial border prominence, coracoid pain and malposition, and dyskinesis. Patients with dyskinesis achieved significantly lower constant and simple shoulder scores, suggesting they needed AC joint reconstruction to increase their functional capabilities.¹¹

Malunited or non-united clavicle fractures can alter normal scapular position and motion. The scapula moves as the distal clavicle fragment moves because they are connected through the intact AC joint. The alteration in clavicle anatomy may be:

• Medial/lateral overlap and shortening
• Excessive angulation with shortening
• Malrotation

All three positions alter scapular resting position, producing the winged scapula, and altering scapular motion and kinematics, which results in altered arm function.

Fracture patterns that disrupt normal clavicle mechanics and function and create the resulting altered scapular position and shoulder motion should be addressed by restoring the bony anatomy via surgery. Most frequently, this is best accomplished by operative fixation. Identification of scapular dyskinesis as part of the exam of the injured shoulder can help clinicians correctly recognize fractures that need this open reduction internal fixation approach.

Muscle Disruption

Scapular muscle detachment is a relatively rare and poorly characterized injury, and the diagnosis is often delayed or missed.^{1, 5} The pathoanatomy appears to be detachment of the lower trapezius and rhomboids from the spine and medial border of the scapula. The scapula usually presents in a position of protraction and lateral translation.

The majority of cases present after an acute traumatic tensile load, such as:

• Seat belt-restrained motor vehicle accidents
• Catching or lifting a heavy object with the arm at full extension
• Pulling against a heavy object

The presenting symptom cluster is very uniform with early post-traumatic onset of localized and intense pain along the medial scapular border. There is a weakness of the rhomboids and lower trapezius with difficulty in retracting the scapula and resulting major limitations of arm use away from the body in forward flexion or overhead positions.

Increased upper trapezius activity and spasm, resulting from lack of lower trapezius activity, create migraine-like headaches. Neck and shoulder joint symptoms may be present due to dyskinesis and will often become the focus of treatment, including surgery, which may not properly address the underlying pathology.

Soft Tissue Impairment

Kinetic-Chain-Based Scapular Dyskinesis

The kinetic chain is a coordinated sequencing of activation, mobilization, and stabilization of body segments to produce an athletic activity. Dysfunction within a particular segment in the chain can result in either altered performance or injury to a more distal segment.

The scapula is the link within the kinetic chain that connects the energy-producing core with the energy-transferring arm and the energy-delivering hand. Therefore, scapular stability is essential to proper kinetic chain function. Deficits at or around the scapula, such as muscle weakness and/or tightness, can negatively impact the desired biomechanical output during arm-specific tasks.

Weakness or tightness within proximal kinetic chain segments can create a dysfunctional scapula. Deficits at the hip or knee can create scapular dyskinesis by altering force generation, decreasing proximal kinetic chain motion, or placing the scapula in a biomechanically disadvantaged position. Muscle imbalances within different segments can exist in many sports and activities and suggest that these deficits may play a role in the dysfunction of the kinetic chain and facilitation of scapular function.^12-30

This type of scapular dyskinesis is a nonspecific response to the loss of proximal activation and facilitation rather than a specific response to specific pathology and has multiple kinetic chain causative factors, including:

• Previous leg or hip injury
• Muscle weakness/imbalance
• Nerve injury
• Poor mechanics

The medial border prominence seen on observation appears to be the result of abnormal muscle activations, either directly due to muscle involvement or because of inflexibility, weakness, fatigue, or nerve injury, and is usually treated by rehabilitation.

Muscle Tightness/Inflexibility-Based Scapular Dyskinesis

Muscle tightness is a common factor in scapular dyskinesis and can include:

• Inflexibility of the muscles that insert on the coracoid process, the pectoralis minor, and the short head of the biceps
• Tightness of the posterior rotator cuff and latissimus dorsi muscles

This tightness leads to:

• Scapular protraction at rest or with arm motion
• Decrease in scapular posterior tilt
• Decrease in the subacromial space height
• Loss of scapular external rotation
• External impingement
• Decreased rotator cuff strength
• Internal impingement

The discovery of dyskinesis with physical impairments but without obvious pathology should prompt an evaluation for kinetic chain or muscle inflexibility causative factors.