This now well-established but generally under-appreciated principle of physiology is aptly known as ‘Cannon’s Law of Denervation Supersensitivity’. It describes the wide ranging effects of the complete loss of nerve inputs to a variety of bodily structures under experimental conditions. One of the many responses to nerves that are sick or dysfunctional (now termed Disuse Supersensitivity) is that the muscles that are supplied by these nerves shorten and tighten (due to the supersensitivity of both the muscle’s specialized stretch receptors and motor nerve-muscle junctions), resulting not only in muscle spasm and stiffness which limit flexibility, but a whole sequence of pain compounding reactions. The two earliest are that localized taut bands of muscle fibers begin to compress the small specialized pain sensing (and now extra-sensitive) nerve fibers within the muscle (known as myofascial tender or trigger points) causing type 1 pain, and the compressed muscles do not allow proper blood flow in, or waste products to be removed. This leads to a build up of lactic acid, which further enhances the perception of pain through type 2 pain mechanisms. Continued and prolonged muscle shortening or contracture gradually leads to increased mechanical tension on the muscle’s tendonous attachments to bone, causing all of the various tendonitis (types 1 & 2 pain) syndromes throughout the body. The end result is a truly vicious snowballing cycle of pain, with the muscle shortening further increasing pressure on the nerves.
Cannon’s law of denervation tells us that if a post-ganglionic neurone has it’s pre-ganglionic input removed, then it will become super-sensitive to the normal neurotransmitters that mediate that pre-ganglionic input. There is a variety of reasons for this, including up-regulation of receptors for the neurotransmitter(s), post-receptor effects, and impaired removal of neurotransmitters from the synapse
Most authors do not describe clinically significant capsular adhesions as a predominant finding in the chronic phase of this condition. Instead, pathologic data confirm an active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae). However, these findings were observed in surgical patients who had severe and late-phase disease and cannot be applied to early phases of the disease.
From the chromosomal, cytochemical, and histologic points of view, the soft-tissue contractures are identical to those seen in a Dupuytren contracture of the hand. These contractures result in the classic progressive loss of ROM of the glenohumeral joint, which affects external rotation and abduction, then flexion, adduction, and extension (in descending order of severity). Despite these histopathologic similarities, the favorable and regressive outcome of adhesive capsulitis differs from the unfavorable and progressive outcome of Dupuytren disease.