Pain is a significant adaptive mechanism. International Association for the Study of Pain, cited in Hazelgrove and Price (2000, pp. 27), defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”, however it is worth to notice, that pain is a very complex phenomenon and it is therefore difficult to define or identify pain interchangeably. Hazelgrove and Price (2000) classify pain into two types. First, nociceptive pain, refers to acute sensation triggered by stimulation of pain receptors, usually as a result of injury. It has a very useful, protective role. Second type, neuropathic pain, relates to nerve injury or dysfunction of the nervous system. This essay is going to explain mechanisms of central and peripheral neuropathic pain. It will describe causes and symptoms and provide some examples of common neuropathic syndromes. This piece will also discuss ways of treatment, including pharmacological and non-pharmacological methods.
Neuropathic pain originates from pathology of the nervous system due to alterations in neural input or processing, and could be divided into acute and chronic type. Chronic pain refers to the sensation that lasts even after healing process is completed and is mostly experienced by neuropathic pain sufferers (Dworkin, 2002). DeFriez and Huether (2008), classify neuropathic pain into central and peripheral, depending on the site, where abnormal processing of sensory messages takes place.
CENTRAL NEUROPATHIC PAIN
Central neuropathic pain results from the lesions or dysfunction in central nervous system. Central sensitisation is a major process in central neuropathic pain. It is caused by enhanced activity of the second order neurones, situated in the dorsal horn. This leads to increased transmission of nociceptive stimuli to higher cortical regions. Those mechanisms takes place as a result of peripheral nerve damage and secretion of neurotransmitters, and tachykinins. Long-lasting release of these substances leads to the activation of the N-methyl-D-aspartate receptor known as NMDA, which results in the rise of intracellular calcium concentration. A number of alterations occurs in dorsal horn neurones. The activation threshold is decreased, response to stimuli is increased as well as the size of nociceptive field. All those changes results in greater sensitivity and excitability of spinal cord neurons (Pasero, 2004). Disinhibition is another central mechanism involved in neuropathic pain. It occurs due to suppression of control mechanisms along the inhibitory pathways and leads to abnormal excitability of central neurones (Pasero, 2004).
PERIPHERAL NEUROPATHIC PAIN
Peripheral pain is caused by peripheral nerve damage or disease, such as nerve entrapment or diabetic neuropathy. Following nerve injury, inflammatory and damaged cells release cellular mediators that sensitize pain receptors to further neural input. This leads to alterations in ion channels, especially sodium channels, in damaged nerves and their dorsal root ganglia. Because of those changes, the depolarisation threshold is decreased and ectopic discharges could take place. Peripheral sensitisation occurs in nociceptors causing hyperalgesia (Pasero, 2004). Litwack (2009), classifies causes of peripheral neuropathic pain according to the level of nerve damage. Conditions causing damage to peripheral nerves in particular location, include nerve entrapment, nerve compression due to the presence of tumour and neuralgias. Diabetes mellitus, long-term alcohol use, hypothyroidisim and renal insufficiency are the examples of conditions that cause damage to peripheral nerves in broad areas. Nerve injury could also result in complex regional pain syndrome (CRPS). It is a group of chronic conditions that share several clinical features such as pain, hypersensitivity, autonomic and...
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