Neuropathic Pain: Difference between revisions
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The IASP defines neuropathic pain as pain that is caused by a lesion or disease of the somatosensory system. The pathophysiology involves a complex and redundant interplay of neural generators, circuits, and mediators. Neuroanatomical changes consist of both peripheral and central adaptive and maladaptive mechanisms. The adaptive processes include changes in pro-nociceptive and anti-nociceptive systems. | Neuropathic pain is pain that is caused by a lesion or disease of the somatosensory system | ||
== Definition == | |||
The IASP defines neuropathic pain as "''pain that is caused by a lesion or disease of the somatosensory system''". This definition deserves some discussion. Previously it was defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system." There are two key changes in the definition update. Dysfunction was replaced with disease, with disease referring to all types of abnormal conditions such as inflammation, autoimmune syndromes, and ion channel disorders. The term nervous system was replaced with somatosensory system in order to avoid confusion with other types of pain arising from the nervous system such as spasticity and rigidity of the muscles. | |||
Neuropathic pain is divided into two subtypes: peripheral and central, dependent on the anatomical location of the problem: i.e. whether it is a problem in the peripheral or central nervous system. | |||
== Epidemiology == | |||
The prevalence of neuropathic pain has been estimated at 7-10%, but with marked variations between countries ranging from 1-18%. With the aging population it is expected that the prevalence of neuropathic pain will increase.<ref>van Hecke et al, Neuropathic pain in the general population: A systematic review of epidemiological studies, Pain: April 2014 - Volume 155 - Issue 4 - p 654-662 doi: 10.1016/j.pain.2013.11.013</ref> | |||
== Aetiology == | |||
Neuropathic pain is triggered following a lesion within the somatosensory system, trauma, or from toxic effects of some medications. Causative conditions include metabolic diseases (e.g. diabetic neuropathy), infection (e.g. post-herpetic neuralgia), vascular disease (e.g. stroke), trauma (e.g. orofacial neuropathy), and cancer. | |||
== Pathophysiology == | |||
The pathophysiology involves a complex and redundant interplay of neural generators, circuits, and mediators. Neuroanatomical changes consist of both peripheral and central adaptive and maladaptive mechanisms. The adaptive processes include changes in pro-nociceptive and anti-nociceptive systems. | |||
There is an increase in excitatory neurotrasmitters and neuropeptides such as [[histamine]], [[bradykinin]], serotonin, and glutamate. Peripheral nerve fibres when injured bring about a intense and prolonged ectopic afferent activity to the central nervous system. This can induce secondary changes on second order neurons in the dorsal horn. | |||
In normal sensory experience, a noxious stimulus applied to nociceptive sensory endings is transmitted to the brain. Inflammation can lead to nociceptive endings becoming hypersensitive causing inflammatory pain. When an injury or disease affects the peripheral nerves (neuropathy), sensory ganglia (ganglionopathy), or sensory roots (radiculopathy), then pain signals can occur in areas ectopically away from the sensory ending. Abnormal impulse discharge can then lead to neuropathic pain. A range of inciting events can lead to ectopic impulse discharge, such as trauma, nerve entrapment, infection, inflammatory, metabolic disturbance, malnutrition, vascular disease, toxins, radiation, and genetic. Most commonly ectopic impulse generation arises from the site of injury and the associated dorsal root ganglion. This abnormal impulse discharge can not only drive pain sensation (spontaneous or evoked), but also induce and maintain [[Central Sensitisation|central nervous system pain amplification processes]]. | In normal sensory experience, a noxious stimulus applied to nociceptive sensory endings is transmitted to the brain. Inflammation can lead to nociceptive endings becoming hypersensitive causing inflammatory pain. When an injury or disease affects the peripheral nerves (neuropathy), sensory ganglia (ganglionopathy), or sensory roots (radiculopathy), then pain signals can occur in areas ectopically away from the sensory ending. Abnormal impulse discharge can then lead to neuropathic pain. A range of inciting events can lead to ectopic impulse discharge, such as trauma, nerve entrapment, infection, inflammatory, metabolic disturbance, malnutrition, vascular disease, toxins, radiation, and genetic. Most commonly ectopic impulse generation arises from the site of injury and the associated dorsal root ganglion. This abnormal impulse discharge can not only drive pain sensation (spontaneous or evoked), but also induce and maintain [[Central Sensitisation|central nervous system pain amplification processes]]. | ||
== Clinical Features == | |||
Neuropathic pain can be constant or periodic. There is often a significant difference between morning and evening in symptoms. The exact picture varies depending on aetiology. There is often a significant negative impact on quality of life, daily function, and psychological wellbeing. | |||
The morphological and functional nervous system changes lead to abnormal sensory signs. | |||
* Allodynia: pain due to a stimulus that does not normally activate the nociceptive system | |||
* Hyperalgesia: increased response to a stimulus that is not typically painful | |||
* Sensory loss | |||
The patient has evoked pain which may present as burning, tingling, prickling, shooting, electric shock-like, jabbing, squeezing, spasm, cold. | |||
== Treatment == | |||
The treatment options are often disappointing. There is no medication that exists that has been proven to have long-term efficacy or tolerability. The difference in aetiology and pathophysiology to nociceptive pain makes neuropathic pain particularly challenging to treat. | |||
==See Also== | ==See Also== | ||
Revision as of 09:48, 23 August 2021
Neuropathic pain is pain that is caused by a lesion or disease of the somatosensory system
Definition
The IASP defines neuropathic pain as "pain that is caused by a lesion or disease of the somatosensory system". This definition deserves some discussion. Previously it was defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system." There are two key changes in the definition update. Dysfunction was replaced with disease, with disease referring to all types of abnormal conditions such as inflammation, autoimmune syndromes, and ion channel disorders. The term nervous system was replaced with somatosensory system in order to avoid confusion with other types of pain arising from the nervous system such as spasticity and rigidity of the muscles.
Neuropathic pain is divided into two subtypes: peripheral and central, dependent on the anatomical location of the problem: i.e. whether it is a problem in the peripheral or central nervous system.
Epidemiology
The prevalence of neuropathic pain has been estimated at 7-10%, but with marked variations between countries ranging from 1-18%. With the aging population it is expected that the prevalence of neuropathic pain will increase.[1]
Aetiology
Neuropathic pain is triggered following a lesion within the somatosensory system, trauma, or from toxic effects of some medications. Causative conditions include metabolic diseases (e.g. diabetic neuropathy), infection (e.g. post-herpetic neuralgia), vascular disease (e.g. stroke), trauma (e.g. orofacial neuropathy), and cancer.
Pathophysiology
The pathophysiology involves a complex and redundant interplay of neural generators, circuits, and mediators. Neuroanatomical changes consist of both peripheral and central adaptive and maladaptive mechanisms. The adaptive processes include changes in pro-nociceptive and anti-nociceptive systems.
There is an increase in excitatory neurotrasmitters and neuropeptides such as histamine, bradykinin, serotonin, and glutamate. Peripheral nerve fibres when injured bring about a intense and prolonged ectopic afferent activity to the central nervous system. This can induce secondary changes on second order neurons in the dorsal horn.
In normal sensory experience, a noxious stimulus applied to nociceptive sensory endings is transmitted to the brain. Inflammation can lead to nociceptive endings becoming hypersensitive causing inflammatory pain. When an injury or disease affects the peripheral nerves (neuropathy), sensory ganglia (ganglionopathy), or sensory roots (radiculopathy), then pain signals can occur in areas ectopically away from the sensory ending. Abnormal impulse discharge can then lead to neuropathic pain. A range of inciting events can lead to ectopic impulse discharge, such as trauma, nerve entrapment, infection, inflammatory, metabolic disturbance, malnutrition, vascular disease, toxins, radiation, and genetic. Most commonly ectopic impulse generation arises from the site of injury and the associated dorsal root ganglion. This abnormal impulse discharge can not only drive pain sensation (spontaneous or evoked), but also induce and maintain central nervous system pain amplification processes.
Clinical Features
Neuropathic pain can be constant or periodic. There is often a significant difference between morning and evening in symptoms. The exact picture varies depending on aetiology. There is often a significant negative impact on quality of life, daily function, and psychological wellbeing.
The morphological and functional nervous system changes lead to abnormal sensory signs.
- Allodynia: pain due to a stimulus that does not normally activate the nociceptive system
- Hyperalgesia: increased response to a stimulus that is not typically painful
- Sensory loss
The patient has evoked pain which may present as burning, tingling, prickling, shooting, electric shock-like, jabbing, squeezing, spasm, cold.
Treatment
The treatment options are often disappointing. There is no medication that exists that has been proven to have long-term efficacy or tolerability. The difference in aetiology and pathophysiology to nociceptive pain makes neuropathic pain particularly challenging to treat.
See Also
References
- ↑ van Hecke et al, Neuropathic pain in the general population: A systematic review of epidemiological studies, Pain: April 2014 - Volume 155 - Issue 4 - p 654-662 doi: 10.1016/j.pain.2013.11.013
Literature Review
Literature Review
- Reviews from the last 7 years: review articles, free review articles, systematic reviews, meta-analyses, NCBI Bookshelf
- Articles from all years: PubMed search, Google Scholar search.
- TRIP Database: clinical publications about evidence-based medicine.
- Other Wikis: Radiopaedia, Wikipedia Search, Wikipedia I Feel Lucky, Orthobullets,
