REPETITIVE STRAIN INJURIES
To ensure full recovery, it is imperative that:
• As a patient: RSI symptoms are recognized in the early stages of the condition.
• As a doctor: the cause is identified so that correct treatment can be administered.
Long-term neglect of symptoms and an inability to correctly diagnose the condition results in a
high number of permanent disabilities.
There is a lack of understanding regarding repetitive strain injuries throughout the medical
community and the insurance industry.
The etiology of RSIs are multifactorial.
Tendonitis as the primary versus secondary/tertiary:
• Conventional medical treatments have focused on anti-inflammatory agents.
• Often a patient is diagnosed following a cursory examination.
• Evidence shows that tendonitis is merely one manifestation of RSI but clearly not the
SEVERAL DIFFERENT CAUSES OF RSI:
NERVE ENTRAPMENT SYNDROMES
• Entrapped nerve → irritability of pain fibers → increased sympathetic tone
atrophy of muscles → increased load on the tendon → TENDONITIS
Thoracic Outlet Syndrome: compression of brachial plexus and associated vasculature between
• Hypertonicity/dystonia of anterior neck muscles
• Reflex inhibition/weakness of musculature
• Congenital anatomical structures
Common sites of peripheral nerve entrapments in upper extremity:
• Axillary nerve – quadrangular space of axilla (posterior shoulder)
• Radial nerve – axilla/rotator cuff, supinator muscle
• Musculocutaneous nerve – in coracobrachialis muscle
• Ulnar nerve – medial elbow
• Median nerve – elbow, pronator teres muscle, carpal tunnel
rib, and anterior neck musculature due to postural abnormalities.
Sergio F. Azzolino, DC, DACNB
• Ischemia to muscles → dystonic muscles → increased load on tendon → tendonitis
Causes of sympathetic hyperactivity:
• Wind-up of sympathetic nerves by continuous firing of pain pathways
• Poor inhibition of sympathetic nerves due to decreased brain function
• Plastic deformity of ligaments and tendons
• Hypertonicity of certain muscle groups with resultant reciprocal inhibition
(e.g., when an individual contracts his biceps, his triceps – the antagonistic muscle –
must be neurologically inhibited to allow the contraction of the biceps. Performed over
long periods, this contraction results in the efficiency of the pathway causing biceps
contraction and the inefficiency of the pathway contracting the triceps.)
• Subluxations/altered mechanics of joint
• A small portion of our postural control is volitional
• Posture is reflexogenically controlled by the cerebellum
• The cerebellum is constantly bombarded by receptors from our joint and muscles
• Correct movement of joints, and the appropriate load on joints, results in increased
• Decreased firing of the cerebellum as a result of joint subluxation, and decreased receptor
stimulation, results in reflexogenic inhibition/weakness of muscle groups
THE CHIROPRACTIC NEUROLOGIST’S APPROACH TO A PATIENT WITH
It is imperative that any person with symptoms of RSI be evaluated for all of the following:
• Reflex sympathetic dysfunction
• Reflex muscle weakness/inhibition
• Functional imbalances of the nervous system predisposing the patient to dystonic muscles
• Remove any peripheral nerve entrapments
• Address central relay centers to restore functional integrity of the nervous system
• Address rib mechanics to maximize chest wall excursion
• Address postural integrity reflexogenically and volitionally
• Rehabilitate central relay centers dealing with pain inhibition, sympathetic control, and
muscle control through neuromuscular reeducation exercises
• Rehabilitate muscles once the central relays are plasticized