Carpal Tunnel Syndrome
The carpal tunnel is a tight passageway comprised of bon e and connective tissue through which tendons and the median nerve pass. The carpal tunnel connects the forearm and the hand. Pressure within the carpal tunnel is normally between 2.5 and 15 mm Hg. Changes in nerve function begin at about 30 mm Hg, and nerve conduction is blocked when pressure exceeds 50 mm Hg. High pressure in the carpal tunnel region can cause reduced oxygen supply (hypoxia) to the median nerve and related structures. Mechanical and hypoxic stress can cause a number of harmful changes to the nerve that can lead to pain and numbness (Haase 2007; Khosrawi 2012). Many cases of CTS are related to occupations that involve forceful, repetitive use of the upper extremities. This is part of a spectrum of conditions called hand-arm vibration syndrome, in which nerves in the affected limb lose some of their protective sheath, a process known as demyelination. These structurally disturbed nerves no longer function normally (Dahlin 2014; Giersiepen 2011; Aroori 2008).
Several lines of evidence suggest that inflammation likely plays a role in the pathophysiology of CTS. For example, in one study, tenosynovial fluid samples from individuals with CTS were found to contain greater concentrations of inflammatory cells and elevated markers of oxidative stress compared to samples from people without CTS (Kim, Koh 2010; Buckley 2011). Other research shows the inflammatory enzyme cyclooxygenase-2 (COX-2), and one of its products, prostaglandin E2, may be higher in wrist tissue of CTS patients compared with those without CTS (Talmor 2003; Tucci 1997; Bland 2005a; Hirata 2004). Elevated levels of the inflammatory cytokine interleukin-6 (IL-6) have also been observed in tissue samples taken from individuals with CTS (Freeland 2002; Tucci 1997).
Cardiovascular Risk, Atherosclerosis, and Carpal Tunnel Syndrome – A Possible Connection?
A cross-sectional, observational study compared 40 patients with CTS to 40 healthy controls. The researchers rigorously excluded patients with other known health problems, including cardiovascular disease, in order to avoid confounding factors. A specialized test (carotid–femoral pulse wave velocity) that measures arterial stiffness was performed on patients and controls. Carotid intima-media thickness (CIMT), another sensitive indicator of cardiovascular risk, was also measured in both groups. Arterial stiffness and CIMT were significantly greater in CTS patients compared to controls, indicating that those with CTS had greater cardiovascular risk. In fact, CIMT was an independent predictor of CTS: each 0.1 mm increase in thickness of the lining of the carotid artery doubled the likelihood of having CTS (Durakoglugil 2013).
In another study, the CIMT of 58 females with CTS and no history of cardiovascular disease or stroke was compared to the CIMT of 53 healthy female controls. Maximum CIMT was significantly greater in CTS patients, and CTS was a stronger predictor of greater CIMT than age, high blood pressure, or systolic blood pressure (Park 2013).
An analysis of data collected during a Finnish national health survey provided additional correlational evidence for a link between cardiovascular health and CTS. This study examined cardiovascular risk factors in relation to CTS in 6254 subjects. A number of compelling associations were revealed, with obvious age-dependency. For those aged 30-44, obesity, elevated LDL cholesterol, high triglycerides, and high blood pressure all increased the risk of CTS 2-4 times; having a cardiac arrhythmia increased the risk of CTS over 10 times. Among subjects 60 or older, heart valve disease and coronary artery disease increased CTS risk by 2.3 and 1.9 times, respectively. Moreover, for subjects 60 or older, each 0.23 mm increase in carotid intima media thickness was associated with a 40% increased chance of having CTS, but this might have been due to chance. The researchers concluded that “CTS may either be a manifestation of atherosclerosis, or both conditions may share similar risk factors” (Shiri 2011).
For a detailed discussion about heart and vascular health, refer to the Atherosclerosis and Cardiovascular Disease protocol.