Carpal tunnel syndrome historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2]

Overview

Carpal tunnel syndrome (CTS) is the most common and a well–recognized mononeuropathy in medicine. Historical evaluations showed that it took more than 100 years from the initial reports and observations to describe the pathophysiology of this problem as a median nerve compression of wrist.

Historical Perspective

According to the available pieces of evidences about the Carpal tunnel syndrome (CTS) are interesting. The first description of median nerve illness in the carpal tunnel originates from 1854 and almost 100 years later this problem with its specific sign and symptoms called Carpal tunnel syndrome (CTS). Prior to this event, patients having these sign and symptoms were diagnosed as having acroparaesthesia or even the motor branch of the median nerve compression or the brachial plexus compression. Meanwhile, the "acroparesthesia" was used to describe a chronic and early morning and nocturnal paresthesias, numbness, pain, and weakness in hand with a slight decrease of sensibility of fingers; which was more common in female population. Nowadays, we can call this condition as Carpal tunnel syndrome (CTS). Here we can find the historical perspective of CTS in clinical practice [1][2][3][4][5][6][7][8][9]:

In 1854, Paget J had the first clinical description of CTS in his two cases diagnosed with the median nerve compression within the carpal tunnel: one case was post-traumatic and another one was idiopathic

In 1880, Putnam JJ had reported the first case series of 37 patients which most of them were female with the age of 35 years old, suffering from the same problems: "the subjective sensibility impairment of the skin (which nowadays we call it as "numbness"), with repeatedly occurrence at nights or very early in the mornings and in some cases it’s been reported that shaking bit or hang out of the bed would decrease the symptoms. Which we can conclude that these previously mentioned symptoms nowadays are considered as symptoms of CTS.

In 1893, Friedrich Schultze confirmed the Putnam's sensory findings about the median nerve compression. and he "Schultz" used the word acroparesthesia" for the sensory symptoms description .

In 1895, considering the recent discoveries of X-rays, Doctors had this opportunity to observe both motor and sensory conversions of the hand among their patients.

In 1909, Hunt have published a series of reports about the thenar muscle atrophy as a disease process different than the sensory findings reported by Putnam (in 1880). Hunt with total exclusion of sensory pathology had been emphased on motor pathology caused by median nerve compression.

In 1913, Marie and Foix published an article entitled “Atrophie isolée de l’éminence thenar d’origine névritique: rôle du ligament annulaire antérieur du carpe dans la pathogénie de la lésion”, which was an anatomopathological descriptions of the structural conversion affecting the median nerve due to the  carpal tunnel compression.

In 1914, Hunt JR, described the pathological evaluation of the thenar eminence atrophy. Which in his opinion it happened due to the motor branch compression of the median nerve within the carpal tunnel.

In 1988, Pfeffer GB hypothesised that the cervical rib is responsible for the compression of the brachial plexus at the level of thoracic outlet. And because of this conclusion the cervical rib removal was considered as the main therapy for CTS during the first 40 years of the 20th century.

In 1922, Lewis D, Miller EM reported the possible role of fracture of the distal epiphysis of the radius on chronic compression of the median nerve.

In 1924 Galloway described the surgical method of the carpal tunnel treatment “…marked wasting of the thenar eminence and trophic changes in the nails of the index finger and thumb… an exploration from the flexor crease at the wrist downward for an inch and upward for 2 inches was performed…immediately following the operation, sensation in the index finger improved”

In 1929, Watson JR reported the possible role of arthritic deformities of the carpal bones on chronic compression of the median nerve.

In 1933, Abbott LC, Saunders M reported the possible role of dislocation of the carpus on chronic compression of the median nerve.

In 1933, Learmonth JR perforemd the first surgery to open the carpal tunnel in a post-traumatic case suffering from the compression of the median nerve.

In 1938, Moersch published described the median nerve compression within the carpal tunnel without previous history of trauma.

In 1992, Amadio PC Mayo Clinic, published a letter by Galloway dated 1924.

In 1946, Cannon BW, Love JG performed and described of a surgery of idiopathic CTS.

In 1947, Russell Brain described acroparesthesia and neuritis of thenar area as a result of median neuropathy due to the flexor retinaculum compression.

In 1947, Brain, Wright, and Wilkinson described idiopathic CTS from both clinical and anatomopathological aspects.

In 1949, McArdle described the possible relationship between acroparesthesias and median nerve compression within the carpal tunnel.

In 1950 – 1966 Phalen GS worked on the pathophysiology of idiopathic CTS.

In 1953, Gilliatt and Wilson described the tourniquet test for diagnosis of CTS.

In 1950s CTS reached its final characterization.

In 1960, CTS became an easily diagnosed disease with well defined treatment options. It was known as the most frequent peripheral entrapment neuropathy with an incidence of 99 cases per 100,000 population.

In 1989, Chow JC described the endoscopic intervention method of CTS

In 1988, Le Loet X concluded that the CTS was the most comon nerve compression syndrome.

In 1996, Kerwin described different underlying causes of CTS. He concluded that increasing the carpal tunnel volume (for example due to the inflammation, edema, and tumor) would increase pressure within the canal, causing the mechanical changes or even ischemia of the median nerve.

References

  1. Aroori S, Spence RA (January 2008). "Carpal tunnel syndrome". Ulster Med J. 77 (1): 6–17. PMC 2397020. PMID 18269111.
  2. Herbert R, Gerr F, Dropkin J (January 2000). "Clinical evaluation and management of work-related carpal tunnel syndrome". Am. J. Ind. Med. 37 (1): 62–74. PMID 10573597.
  3. de Krom MC, van Croonenborg JJ, Blaauw G, Scholten RJ, Spaans F (January 2008). "[Guideline 'Diagnosis and treatment of carpal tunnel syndrome']". Ned Tijdschr Geneeskd (in Dutch; Flemish). 152 (2): 76–81. PMID 18265795.
  4. Banach M, Gryz EA, Szczudlik A (2004). "[Carpal tunnel syndrome]". Prz. Lek. (in Polish). 61 (2): 120–5. PMID 15230155.
  5. McDonagh C, Alexander M, Kane D (January 2015). "The role of ultrasound in the diagnosis and management of carpal tunnel syndrome: a new paradigm". Rheumatology (Oxford). 54 (1): 9–19. doi:10.1093/rheumatology/keu275. PMID 25118315.
  6. Kohara N (November 2007). "[Clinical and electrophysiological findings in carpal tunnel syndrome]". Brain Nerve (in Japanese). 59 (11): 1229–38. PMID 18044199.
  7. Van Meir N, De Smet L (October 2003). "Carpal tunnel syndrome in children". Acta Orthop Belg. 69 (5): 387–95. PMID 14648946.
  8. Wilder-Smith EP, Seet RC, Lim EC (July 2006). "Diagnosing carpal tunnel syndrome--clinical criteria and ancillary tests". Nat Clin Pract Neurol. 2 (7): 366–74. doi:10.1038/ncpneuro0216. PMID 16932587.
  9. Newington L, Harris EC, Walker-Bone K (June 2015). "Carpal tunnel syndrome and work". Best Pract Res Clin Rheumatol. 29 (3): 440–53. doi:10.1016/j.berh.2015.04.026. PMC 4759938. PMID 26612240.