Scott F. M. Duncan and Ryosuke Kakinoki (eds.)Carpal Tunnel Syndrome and Related Median Neuropathies10.1007/978-3-319-57010-5_2

2. History of Carpal Tunnel Syndrome

Margaret E. Cooke¹ and Scott F. M. Duncan²

(1)

Orhtopaedic Surgery, Boston Medical Center, 850 Harrison Avenue, Boston, MA 02118, USA

(2)

Department of Orthopedic Surgery, Boston University/Boston Medical Center, Boston, MA, USA

Margaret E. Cooke

Email: Margaret.Cooke2@bmc.org

Keywords

Carpal tunnel syndromeNeuropathyMedian nervePost-traumaticAcroparesthesia

General Outline

Before carpal tunnel syndrome was well understood, there was significant confusion as to pathophysiology that caused the classic sensory (paresthesias) and motor (thenar atrophy) symptoms. Three main ideas are developed to provide an explanation:
- 1 = “post-traumatic” median nerve injury, usually seen in distal radius fractures with entrapment of the median nerve at the fracture site.
- 2 = “acroparesthesia” attempted to explain only the sensory aspect of the syndrome with a lesion at the brachial plexus caused by compression of the plexus by cervical ribs.
- 3 = “thenar neuritis” attempted to explain only the motor findings of thenar atrophy with a lesion at the motor branch of the median nerve at the border of the carpal tunnel.
Finally, median nerve injury at the site of the carpal tunnel was determined to be the culprit, and surgical techniques emerged to increase the volume of the canal to relieve pressure on the nerve.

Carpal tunnel syndrome is a now relatively well-understood clinical phenomenon in which neuropathic symptoms are secondary to median nerve compression within the carpal tunnel. However it was not until the mid-1900s that the pathophysiology was sufficiently understood to provide a strong foundation for clinical care. Prior to this understanding, the symptoms of carpal tunnel syndrome were attributed to several different etiologies resulting in several different diagnoses. Three mechanisms were proposed to explain the symptomatology and physical findings : (1) entrapment of the median nerve at the site of an injury, such as the post-traumatic median neuropathy described in distal radius fractures; (2) compression of the lower trunk of the brachial plexus which was invoked to explain the sensory aspect of the syndrome, i.e., acroparesthesia ; and (3) a lesion of the motor branch of the median nerve (e.g., thenar neuritis) as it passed beneath the anterior annular ligament of the wrist, which would explain the motor findings of thenar atrophy. It was only after understanding that the pathophysiology was related to compression of the median nerve at the level of the carpal tunnel that effective operative management emerged. The primary goal of operative treatment is to increase the volume of the carpal tunnel by releasing the transverse carpal ligament.

Post-traumatic

One of the earliest reports of post-traumatic median neuropathy was described by Gensoul in 1836 [1]. He reported a case of direct injury to the median nerve by entrapment in an open distal radius fracture in an autopsy of a young girl who died of tetanus. Gensoul’s description was followed by several others who described median nerve injury following distal radius fracture.

In 1854, Sir James Paget came very close to anticipating our current understanding of carpal tunnel pathophysiology in his Lectures on Surgical Pathology [2]. He described a case of median neuropathy that developed after a compression injury at the wrist. He noted that a “cord had been drawn very tight round this man’s wrist seven years before the amputation of the arm. At this time it is probable the median and other nerves suffered injury.” The second case that Paget described was a median neuropathy that developed after a distal radius fracture and resulted in ulcerations of his radial digits. He reports that these ulcers were “cured only by so binding the wrist that the parts on the palmar aspect being relaxed, the pressure on the nerve was removed. So long as this was done, the ulcers became and remained well; but as soon as the man was allowed to use his hand, the pressure on the nerves was renewed, and the ulceration of the parts supplied by them returned.” It is clear through these descriptions that Paget recognized the pathologic effect of compression of the nerve at the wrist, as well as the therapeutic effect of relieving the pressure on the nerve.

In 1933, Abbott and Saunders published their classic cadaveric study that supported the notion that neuropathic symptoms may be due to increased pressure in the carpal tunnel [3, 4]. In this study, they injected dye into the forearm with the wrist held at different positions and described increased fluid resistance with acute flexion and ulnar deviation. The ability to manipulate the volume of the carpal canal and compression of the median nerve with varying wrist positions was an important discovery. This led to their recommendation to immobilize distal radius fractures with a neutral wrist position after fracture reduction, rather than the established Cotton-Loder position , which maintained the wrist in a flexed position.

This change in treatment was adopted and supported in the following years as more evidence mounted against immobilization with wrist flexion. In 1949, Meadoff recommended prevention of median neuritis after distal radius fracture with closed fracture reduction, neutral wrist immobilization, and surgical exploration of the median nerve with release of the transverse carpal ligament only after 4 months of failed conservative treatment [5].

Lynch and Lipscomb provided further support for this approach in their retrospective review of 600 patients with distal radius fractures followed for 10 years at the Mayo Clinic. In this cohort they found a 3.3% rate of associated carpal tunnel syndrome [6]. The majority of patients that developed carpal tunnel syndrome did so within 3 months of the inciting trauma. Two patients that were initially immobilized in full wrist flexion and ulnar deviation (Cotton-Loder position ) immediately developed carpal tunnel syndrome requiring re-manipulation of the wrist to a neutral position. Based upon their retrospective review and their surgical experience, these authors recommended conservative management with observation and neutral wrist positioning to treat median nerve symptoms, with surgical decompression reserved for severely symptomatic patients. As an alternative to incising the transverse carpal ligament, they noted the benefit of nonoperative treatment with steroid injections to decrease swelling. In their work, they were undoubtedly influenced by their Mayo colleagues P. S. Hench and E. C. Kendall who were awarded the Nobel Prize in Physiology or Medicine in 1950 for discovering the anti-inflammatory effects of corticosteroids [7].

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