Carpal Tunnel Syndrome (CTS) is the most common compression neuropathy. It is the reason for pain and functional impairment. On the picture we see in yellow the median nerve, being compressed under a ligament in the wrist. This gives rise to chronic pain. Pain normally can be reduced with oral neuropathic analgesics. However, the side effects of most of the NSAIDS limit its use.  

Palmitoylethanolamide (PEA), a fatty acid occuring naturally in our body, has also neuropathic pain reducing properties. Furthermore, it stabilizes mast cells, present in the carpal tunnel. Besides the pain reducing effect, PEA has also neuroprotective properties. To evaluate the clinical effects of PEA in CTS, Italian researchers randomised 28 diabetic patients with CTS, in two groups: one group received PEA twice daily 600mg and the other group received placebo.It has been administered in clinical trials in around 2800 patients.

Carpal Tunnel Syndrome and cytokines 

Many cytokines are involved, for instance the expression of leukemia Inhibitory Factor in human nerves following Injury is increased. This expression of leukemia Inhibitory Factor is rapidly increased in nerves at the injury site and promotes both sensory and motor neuron survival.  LIF is seen as a peripheral nerve trauma factor. LIF expression is increased in nerves within hours of injury and can be found in Schwann cells, in peripheral nerve axons, and also in neutrophils, mast cells, macrophages, and blood vessel walls. Continued expression of LIF is in chronically irritated nerve tissue continues to activate the inflammatory cascade, and activate cells such as the mastcell. ^[1] LIF also regulates expression of both neuropeptide Y (NPY) and galanin following peripheral nerve injury. ^[2] 

Carpal Tunnel Syndrome and pressure 

Chronic pressure in a compartment such as the Carpal Tunnel gives rise to many histological changes. The epineurium of the median nerve in the carpal tunnel syndrome due to pressure is also considerably thickened, with solid attachment. This leads to the median nerve becoming relatively immobile and constricted. Apart from fibroblasts, the outer layer of the epineurium in the CTS contains mast cells and vasa nervorum as well as myelinated nervi nervorum. The mast cells play a define rol in the pathogenesis of chronic pain in CTS. ^[3] 

Treatment of Carpal Tunnel Syndrome with palmitoylethanolamide 

Patients were evaluated on the following parameters: painintensity on the Visual Analog Scale (VAS), symptoms and functions on the "BostonCarpal Tunnel Questionnaire", sensory conduction velocity (SCV), sensorynerve action potential (SAP) amplitude, and nerve distal motor latency of themedian nerve.^[4]

Already after one month of treatment, significant differences between groups were seen in favour of the PEA group. These differences were even more robust after two months of treatment. In the PEA group, the pain intensity mean scores were 81.1±3.74 and 66.6±3.36 after one month (T1) and 2 months (T2) of treatment respectively. In the control group the pain increased: 75.9±3.74 at T1 and 88.7±2.33 at T2. The functional status of the patients in the PEA group improved on the BostonCarpal Tunnel Questionnaire, though in the control group the patients showed a worsening in function.

Also the SCV improved in the PEA group (T0 = 38.1±7.07 and T2 = 44.8±6.52), where as in he control group the SCV worsened (T0 = 41.5±4.65 and T2 = 36.1±5.38).De SAP amplitude improved in the patients using PEA (T0 = 6.7±0.76 and T2 = 9.4±0.85), though in the control group the SAP amplitude worsened (T0 = 7.4±0.76 and T2 = 5.8±0.85)

These results were all significant.(p≤0.0001)

These data suggest that PEA is a viable treatment option for patients with mild to moderate degrees of pain due to the CTS.

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