Differential onset patterns and causes of carpal tunnel syndrome after distal radius fracture: a retrospective study of 105 wrists.

23:51 EDT 3rd September 2015 | BioPortfolio

Summary of "Differential onset patterns and causes of carpal tunnel syndrome after distal radius fracture: a retrospective study of 105 wrists."

It is well known that carpal tunnel syndrome (CTS) can occur in a wide range of time periods after distal radius fracture (DRF). Few studies have evaluated in detail the relationship between fracture and electrophysiological finding characteristics and time to onset of CTS after DRF. To clarify the characteristics of CTS after DRF, we classified a large number of clinical cases based on the period from the injury to onset of CTS. These cases were analyzed retrospectively.
We reviewed 105 wrists with CTS following DRF. Patients' ages ranged from 13 to 89 years. These 105 wrists were divided into three groups according to the period of post-fracture onset of CTS. Twenty-eight wrists were classified into the acute onset group (when the symptoms of CTS occurred within 1 week after fracture). Forty-seven wrists were classified into the subacute onset group (when symptoms of CTS occurred from 1 to 12 weeks after fracture). The remaining 30 wrists were classified into the delayed onset group (when symptoms of CTS occurred more than 12 weeks after fracture). Deformity of the distal radius on X-ray films was evaluated and distal motor latency (DML) of the median nerve was recorded to compare values among these three groups.
In the acute onset group, 68% had an AO C-type fracture and 46% were caused by a high-energy injury. The percentage of this fracture pattern and mechanism was significantly higher in the acute onset group than in the other groups (P < 0.05; Kruskal-Wallis test). In the subacute onset and delayed onset groups, 79% and 63% had an A-type fracture and more than 90% were caused by a low-energy injury. In the delayed onset group, the incidence of prolonged DML in the contralateral wrists was 71%, which was significantly higher than in the other two onset groups (P < 0.05; Kruskal- Wallis test).
There were three onset patterns of CTS after DRF, and each CTS onset pattern had different etiologic mechanisms and different clinical features of CTS. In the acute onset group, a high-energy fracture pattern was associated with CTS. In the subacute and the delayed onset groups, lowenergy injury in elderly women was associated with CTS. Both deformity of the fracture and preexisting median nerve dysfunction were suggested as predisposing factor for CTS.


Department of Orthopaedic Surgery, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan.

Journal Details

This article was published in the following journal.

Name: Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
ISSN: 1436-2023
Pages: 518-23


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Medical and Biotech [MESH] Definitions

Entrapment of the MEDIAN NERVE in the carpal tunnel, which is formed by the flexor retinaculum and the CARPAL BONES. This syndrome may be associated with repetitive occupational trauma (CUMULATIVE TRAUMA DISORDERS); wrist injuries; AMYLOID NEUROPATHIES; rheumatoid arthritis (see ARTHRITIS, RHEUMATOID); ACROMEGALY; PREGNANCY; and other conditions. Symptoms include burning pain and paresthesias involving the ventral surface of the hand and fingers which may radiate proximally. Impairment of sensation in the distribution of the median nerve and thenar muscle atrophy may occur. (Joynt, Clinical Neurology, 1995, Ch51, p45)

Disease involving the median nerve, from its origin at the BRACHIAL PLEXUS to its termination in the hand. Clinical features include weakness of wrist and finger flexion, forearm pronation, thenar abduction, and loss of sensation over the lateral palm, first three fingers, and radial half of the ring finger. Common sites of injury include the elbow, where the nerve passes through the two heads of the pronator teres muscle (pronator syndrome) and in the carpal tunnel (CARPAL TUNNEL SYNDROME).

Syndromes of bone destruction where the cause is not obvious such as neoplasia, infection, or trauma. The destruction follows various patterns: massive (Gorham disease), multicentric (HAJDU-CHENEY SYNDROME), or carpal/tarsal.

Disorders of the peripheral nervous system associated with the deposition of AMYLOID in nerve tissue. Familial, primary (nonfamilial), and secondary forms have been described. Some familial subtypes demonstrate an autosomal dominant pattern of inheritance. Clinical manifestations include sensory loss, mild weakness, autonomic dysfunction, and CARPAL TUNNEL SYNDROME. (Adams et al., Principles of Neurology, 6th ed, p1349)

A syndrome characterized by multiple system abnormalities including DWARFISM; PHOTOSENSITIVITY DISORDERS; PREMATURE AGING; and HEARING LOSS. It is caused by mutations of a number of autosomal recessive genes encoding proteins that involve transcriptional-coupled DNA REPAIR processes. Cockayne syndrome is classified by the severity and age of onset. Type I (classical; CSA) is early childhood onset in the second year of life; type II (congenital; CSB) is early onset at birth with severe symptoms; type III (xeroderma pigmentosum; XP) is late childhood onset with mild symptoms.


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