Neuroplasticity and Chronic Pain

2021-05-13 02:08:08
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Aage Moller, a professor at The University of Texas, describes neuroplasticity as peoples ability to pronounce an unfamiliar word in their native language is always available to us. That is due to a tiny bit of neuroplasticity. In other words, neuroplasticity does not describe brain items easily forgotten such as the memory of a specific word. Instead, the ability to be plastic, in a sensed brainflexibility, includes the innate ability to learning to learn new words. This paper provides a basic understanding of neuroplasticity with a focus on chronic pain including central sensitization, short-term synaptic plasticity and visceral/mixed neuroplasticity in chronic pancreatitis.

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Neuroplasticity is typified by generating and continuing functional and structural changes in the brain which lead to the feeling of pain by the patient. This is not acute pain produced by pain nerves (nociceptors). This is pain that happens with no firing or chemical exchange of the nociceptors but due to altering functions in the brain. The neuroplasticity term is often used to describe pathological processes in the brain that accidentally create other problems than the ones they were meant to fix. Moller (2008) reports that some examples of conditions with pathological changes in the brain are tinnitus (ringing in the ear), spasm, spasticity, low back pain, fibromyalgia, and (probably) chronic fatigue syndrome. According to Moller, (2014, p. 201) even chronic neuropathic pain is a plasticity disorder.

A basic understanding of neuroplasticity process with a focus on chronic pain reveals a five-step progression beginning with neurogenic inflammation. First, chronic pain pathology usually starts developing from the aftermath of acute pain where the body is trying to answer a perceived noxious stimulus. For example, in inflammation, there is an increase in the prostanoid build-up at the injured area in the body. This is protected so that the injured area does not receive even more injury (such as using it or banging it). It brings about the human or other animals to cover or protect the area from further hurt resulting in allodyna (lowered pain threshold) and hyperalgesia (increased sensitivity). These continue unnecessarily in chronic pain, long after the original wound has healed. Next in the progression of acute pain to chronic pain, there may be damage to the nerves themselves, which then misfire and continue to send to the brain an alarm which does not shut off. The third step is the notorious sensitization/WINDUP. May (2008) referred to WINDUP as, under conditions of persistent injury, C fibers fire repetitively and the response of dorsal horn neurons increases, p. 62). For WINDUP to even begin, glutamate (a learning neurotransmitter that is excitatory) must be at large and act in several receptors. Fourth, at this point, the patient begins paying excessive attention to the area where all of this is occurring. These make the pain feel stronger and creates a sense of or even memory of the pain, bringing on a neurochemical link between the pain situation in the body and the memory.

Some reports hypothesize that changes in the brain create a changed functional state and chronic pain that is functionally altered state of the brain. Changes occur in the neurotransmitters and neuropeptides. These changes can be found in the peripheral receptor/ion-channel; reorganization; and also the neurotransmitters change. Other changes include the nervous cerebral system (functional changes of representational field) including the spinal cord (sensitization and dis-inhibition of the shut-off message) and the alterations in the messaging between these systems within themselves, with higher cognitive functions and the immune system. Lastly, the kindling idea of Goddard is significant. Goddard, called neuroplasticity kindling because he could train the brain over time, to change due to a current sent to the amygdala, which eventually brought on a seizure (Moller, 2014).

Besides changes relating to function, neuroplasticity also includes structural changes during the processing of pain in the brain. Brain changes due to changes in the environment such as chronic pain input are called central plasticity. The known modifications in the brain are either the result of or caused by the changes in excitability, changes in the routing of information, and changes in functional mapping of the body on many neural structures in the spinal cord and the brain (Moller, 2014, p. 201). Another structural change in the brain during neuroplasticity is between excitation and inhibition in input. It can become unbalanced as there is the elimination of entire cells through programmed cell death. Another example of structural changes occur neurons fire at the same time, often dubbed, neurons that fire together, wire together (Moller, 2014, p. 369).

Central Nervous System

The outcomes of neuroplasticity in the central nervous system include syndromes like neuropathic pain, spasticity after spinal cord trauma, including surgery, and phantom limb symptoms, which will be mentioned further on in the paper. The activation of neuroplasticity due to central sensitization in pain brings about changes, for example, in grey matter in cortical and subcortical parts of the brain (Rodriguez-Raecke, Niemeier, Ihle, Ruether & May 2009). Three more specific changes can be found in the peripheral receptor/ion-channel, reorganization of the brain and neurotransmitter changes.

Cohen, Quintner, and Buchanan (2013) also reported that substantial functional, anatomical and neurochemical evidence that chronic pain patients have abnormal brains (Cohen et al., 2013, p. 1286). However, this leads to the question, the chicken, and egg idea. Scientists ask, were the changes in the brain before or after the pain? Cohen et.al ruled out that the brain changes are due to the disease process of pain in the brain. Cohen et al. (2013) report, it is simply not clear whether the change described reflect changes due to pain (nociceptive input) or changes due to the consequences of pain or both (p. 1287).

Also, it appears that there are brain activities at the synaptic level in the cerebral cortex that are considered neuronal plasticities, especially in the thalamoscingulate pathway. This type of neuroplasticity may be among the first to occur with eventual chronic pain. The potentiation of ACC neuronal activity induced by thalamic bursting suggests that short-term synaptic plasticities enable the processing of nocioceptive information from the medial thalamus and this temporal response variability is particularly important in pain because temporal maintenance of the response supports cortical integration and memory formation related to noxious events (Shyu and Vogt, 2009, p. 51).

Apkarian et.al (May, 2008, p. 9) studies chronic back pain and brain atrophy. They concluded that the thalamocortical process of the pathophysiology of chronic pain is crucial as involves a decrease in grey matter in the right thalamus and the dorsolater prefrontal cortices. May (2008) discusses the difference between the role of neurodegeneration and tissue shrinkage without huge challenges on the rest of the brain/spinal functioning.

Both ascending and descending pain signals occur in pathological pain. The spine and thalamus (spinothalamic) tract carry to other brain sites and descending inhibitory pathways (noradrenergic and serotonergic) attempt to stop the release of substance P in the lamina II layer of the dorsal horn (part of the spinal column). They also bring about the release of natural opioids. Descending pathways input use the medulla and specifically the rostroventral medulla (which is involved in hyperalgesia) and its nucleus raphes magnus. Descend can also help to increase the transmission in the spinal cord. The rostroventral medulla is thought to maintain sensitization by increasing the firing of on-cells and by keeping the glutamatergic system engaged.

Incredibly, no signals coming from the periphery can create neuroplasticity to cause complete or partial interruption of afferent nerve impulses (called deafferentated pain). For example, a clinical example of this is when amputees report the same pain after it has been amputated as the pain prior to amputation. Other reasons some patients experience phantom limb pain is a result of neuro system change and include the cerebral nervous system (functional changes of representational field), the spinal cord (sensitization and disinhibition) as well as the changes in the interaction between these systems and the local immune system. In fact, one model described as, representational fields of adjacent areas (from the limb area in the brain) move into the representation zone of the deafferented limb (May, 2008, p. 7). A study by May (2008) revealed that this situation could be reversed. In this study, the correlation was negative as cortical reorganization reversed coincidently with clinical improvement (May, 2008, p.7). Hence, this relationship represents a negative correlation which is a relationship between two variables in which one variable increases (clinical improvement) as the other decreases (plasticity reverses and brain re-organizes back to a more normal state). According to Moller (2014, p. 202), chronic neuropathic pain has no apparent objective signs, and it is, therefore, a phantom sensation.

Short-term synaptic plasticity

Nocicpetive evoked responses can bring on central sensitization, which a type of pain neuroplasticity. Another interesting type is short-term plasticity. Obviously, nerves message each other with communication via short lasting processes mostly through chemical synapses which have some variability in terms of strength and duration and so on. However, even at that level in the anterior cingulated and probably in the cerebral cortex, short-term plasticities have been described in several forms, such as paired-pulse facilitation (PPF), augmentation, post-tetanic potentiation and synaptic depression which are each distinguished by their decay kinetics (Shyu and Vogt, 2009, p. 51)

Visceral/mixed example

One of the commonly known painful human chronic pain conditions is pancreatitis. It is an example of visceral pain (deep, achy, poorly localized pain). However, as science progresses, the complex situation of chronic pancreatitis appears to be a unique example of neuroplasticity, visceral hyper sensitivity with sensitization of the central nervous system and reorganization of brain areas involved in visceral pain processing (Brondum, Schou, Drewes, 2013, p 1554). Chronic neuropathic pain is typified by generating and continuing functional changes in the brain which lead to the feeling of pain by the patient. However, one type of pain does not exclude the other, and chronic pancreatitis appears to be a mixed type of chronic pain. Chronic neuropathic pain can also happen alongside nociceptive real pain that is caused by traditional nociceptors going off. Prior to looking at the complexities of a visceral/mixed neuroplasticity pain, a thorough understanding of the complex nature of neuroplasticy is imperative. Seifert and Maihofner (2011) formally define the process of neuroplasticity in pain as the following:

First, peripheral or central sensitization may result in increased nociceptive input to the brain and also changes the processing of nociceptive information within the brain. Second, chronic nociceptive input from the periphery or lesions within the central nervous system may result in cortical reorganization and maladaptive neuroplasticity within somatosensory and motor systems. Thirdly, there is evidence for pain-induced changes in large-scale neuronal network connectivity. Fourth,...

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