Chiropractic & Central Afferent Inhibition:
A Chiropractic Care Path & Mechanism for Chronic Pain, Tremors, Spatial and Inhibitory Distortion
By Mark Studin
William J. Owens
A report on the scientific literature
Although it is unusual in the literature to place a disclaimer in the beginning of an article, we want to ensure that our reporting is not inflammatory since the foundation of this article was written with the following limitation in our primary literary source, Haavik, Niazi, Holt and Murphy (2017) reported:
This study was not designed to test the efficacy of chiropractic care for treating chronic pain; therefore, conclusions about efficacy cannot be drawn from our findings. The study did not include randomization with an adequate control group, thus limiting the interpretations that can be made about the changes in pain observed in the trial. Causation cannot be claimed. (pg. 135)
Although Haavik, et al. reported limitations in their study, the results cannot be overlooked or minimized, particularly when those results match what doctors working within a “Best Practice Model” (the patient and doctor feedback component) have been reporting for decades. Additionally, in the clinical setting, this information provides direction to practitioners searching for answers although the mechanisms are not yet fully understood. Results often don’t mandate detailed knowledge of the mechanism and that is the primary reason why both “evidenced based” and “best practice” models must be embraced and combined (pure literature results with doctor and patient feedback or experiences) as a matter of public health.
When we consider central afferent neurological input, the inability to inhibit those signals leads to sensorimotor disturbances that are found in the chronicity of many chronic pain conditions, essential tremors, dystonia and other central spatial and temporal mismatches. In addition, we must consider to the long-term negative sequalae of those conditions, such as brain shrinkage.
Baliki, Geha, Apkarian and Chialvo (2008) reported:
Recent studies have demonstrated that chronic pain harms cortical areas unrelated to pain, long-term pain alters the functional connectivity of cortical regions known to be active at rest, i.e., the components of the “default mode network” (DMN). This DMN is marked by balanced positive and negative correlations between activity in component brain regions. In several disorders, however this balance is disrupted. Studying with fMRI [functional MRI] a group of chronic back pain patients and healthy controls while executing a simple visual attention task, we discovered that chronic back pain patients, despite performing the task equally well as controls, displayed reduced deactivation in several key default mode network regions. These findings demonstrate that chronic pain has a widespread impact on overall brain function, and suggest that disruptions of the default mode network may underlie the cognitive and behavioral impairments accompanying chronic pain.” (pg. 1398)
“The existence of a resting state in which the brain remained active in an organized manner, is called the ‘default mode of brain function. The regions exhibiting a decrease in activity during task performance are the component members of the “default-mode network” (DMN), which in concerted action maintain the brain resting state. Recent studies have already demonstrated that the brain default mode network is disrupted in autism, Alzheimer’ disease, depression, schizophrenia and attention deficit hyperactivity disorder, suggesting that the study of brain resting activity can be useful to understand disease states as well as potentially provide diagnostic information.” (pg. 1398)
This is important since for the first time we are starting to see a published correlation between spinal function, chronic pain and central nervous system changes. This is what our founders have observed yet were unable to prove.
“Thus, the alterations in the patient’s brain at ‘rest’ can result in a different default mode network organization. In turn, potential changes in the default-mode network activity could be related to symptoms (other than pain) commonly exhibited by chronic pain patients, including depression and anxiety, sleep disturbances, and decision-making abnormalities, which also significantly diminish their quality of life… chronic pain patients display a dramatic alteration in several key default-mode network regions, suggesting that chronic pain has a widespread impact on overall brain function” (pg. 1398)
This information is pointing to the fact that a doctor of chiropractic should be involved in the triage and treatment of these patients and part of a long-term spinal care program.
Baliki Et. Al (2008) continued “Consistent with extensive earlier work examining visuospatial attention tasks, dominant activations were located in posterior parietal and lateral prefrontal cortices, whereas deactivations occurred mainly within Pre-Frontal Cortex and Posterior Cingulate/Cuneate Cortexes. Although activations in chronic back pain patients’ and controls’ brains were similar, chronic back pain patients exhibited significantly less deactivations than healthy subjects in Pre-Frontal Cortex, amygdala, and Posterior Cingulate/Cuneate Cortexes. The focus was on identifying differences in the way chronic back pain patients’ brains process information not related to pain. This is the first study demonstrating that chronic back pain patients exhibit severe alterations in the functional connectivity between brain regions implicated in the default mode network. It seems that enduring pain for a long time affects brain function in response to even minimally demanding attention tasks completely unrelated to pain. Furthermore, the fact that the observed task performance, compared with healthy subjects, is unaffected, whereas the brain activity is dramatically different, raises the question of how other behaviors are impaired by the altered brain activity” (pg. 1399).
“However, the disruption of functional connectivity observed here with increased chronic back pain duration may be related to the earlier observation of brain atrophy increasing with pain duration also in chronic back pain patients. Patient’s exhibit increased pre-frontal cortex activity in relation to spontaneous pain, in addition to dorsolateral prefrontal cortex atrophy. Therefore, the decreased deactivations described here may be related to the dorsolateral pre-frontal cortex /pre-frontal cortex mutual inhibitory interactions perturbed with time. If that is the case, it will support the idea of a plastic, time-dependent, reorganization of the brain as patients continue to suffer from chronic back pain. Mechanistically, the early stages of this cortical reorganization may be driven by peripheral and spinal cord events, such as those that have been documented in animal models of chronic pain, whereas later events may be related to coping strategies necessary for living with unrelenting pain. It is important to recognize that transient but repetitive functional alterations can lead to more permanent changes. Accordingly, long term interference with normal activity may eventually initiate plastic changes that could alter irreversibly the stability and subsequently the conformation of the resting state networks” (pg. 1401).
Essential Tremors which, according to Wikipedia
Essential tremor (ET, also referred to as benign tremor, familial tremor, or idiopathic tremor) is the most common movement disorder; its cause is unknown. It typically involves a tremor of the arms, hands or fingers but sometimes involving the head, vocal cords or other body parts during voluntary movements such as eating and writing. It is distinct from Parkinson's disease—and often misdiagnosed as such—although some individuals have both conditions. Essential tremor is commonly described as an action tremor (i.e., it intensifies when one tries to use the affected muscles) or postural tremor (i.e., present with sustained muscle tone) rather than a resting tremor, such as is seen in Parkinson’s, which is usually not included among its symptoms. (https://en.wikipedia.org/wiki/Essential_tremor)
Restuccia, Valeriani, Barba, Le Pera, Bentivoglio, Albanese and Tonali (2003) reported:
...our present data seem to indicate that somatomotor cortical areas play an important role in generating ET. This finding can be important in the future understanding of its pathophysiologic mechanisms, as well as in its management. (pg. 127)
This study suggests that somatosensory cortical areas plays an important role, therefore the afferents “feeding” that region is critical in normalizing function of the cortex a that region. Another negative sequela of aberrant input.
When we consider one potential etiology of maladaptive plastic changes in the brain that can cause chronic pain, essential tremors, brain shrinkage and a host of other maladies, regulatory control of the impulses must be considered and interfered with. The lack of gating (inhibition) will lead to an overflow of impulses and crate a negative cascade that can lead to chronic and often permanent changes. Haavik, Niazi, Holt and Murphy (2017) reported:
Thus, distorted sensory information is thought to disturb SMI (sensorimotor integration) and impair accurate motor control. In normal circumstances, 2 inputs that engage the sensory system have a reciprocally inhibitory action that gates the total amount of signal at all central levels, spatially and temporally limiting the amount of input engaging the CNS. This is thought to prevent sensory “overflow.” The defective gating may cause an input-output mismatch in specific motor programs, and such mismatches in motor programs may in themselves lead to production of distorted sensory information and issue of less than ideal motor commands. In this way, the chronicity of the problem can be maintained via a self-perpetuating mechanism. The reduced frontal N30 SEP (somatosensory evoked potential) peak ratio observed in the current study after 12 weeks of chiropractic care may reflect a normalization of pain-induced central maladaptive plastic changes and may reflect one mechanism for the improvement of functional ability reported following chiropractic adjustment or manipulation. (pg. 134)
The N30 ratio change represented on average a 37.4% decrease following the 12 weeks of chiropractic care. The N30 MU (median-ulnar) amplitude changes following chiropractic care represented an 18.0% decrease in amplitude compared with baseline (pg. 131) Alongside this change in the N30 SEP ratio, the subjects reported a decrease in both current pain and average pain over the last week. A control period of 2 weeks of no intervention resulted in no significant changes in any SEP peak ratio. (pg. 134)
When considering care paths for this population of patients, the following was reported by Haavik, Niazi, Holt and Murphy (2017) reported:
The 2-week control period, during which no intervention was applied, was followed by a 12-week chiropractic care intervention. During the 12 weeks of chiropractic care, the chiropractor assessed and treated the subject as she would any other chronic pain patient. The participating chiropractor (H.H., with 7 years clinical experience) assessed the spine for segmental dysfunction using tenderness on palpation and passive intervertebral and global motion of the spine. Other treatments included as part of chiropractic care were exercises, peripheral joint adjustments/manipulations, soft tissue therapy, and pain education if deemed by the chiropractor to be appropriate based on history and examination. The chiropractic adjustment/manipulation was the delivery of a high-velocity, low-amplitude thrust to dysfunctional spinal segments. (pgs. 129-130)
The changes observed conclude (with the aforementioned disclaimer that more research is needed) that chiropractic is a verifiable treatment option. Haavik, Niazi, Holt and Murphy (2017) continued:
The changes observed in dual SEP ratios after several weeks of chiropractic care in a chronic pain population suggest that this treatment option may improve gating of peripheral afferent input to the brain, thus improving impaired SMI in cortical motor areas and improving processing of motor programs. Impaired SMI and defective motor programming is known to be present in various chronic pain populations and is implicated in the clinical symptomatology. We know from the literature that in normal circumstances, afferent input to the motor system leads to finely tuned activation of neural elements and ultimately results in the correct execution of movement. Multiple experimental and clinical studies have confirmed the importance of sensory feedback to the motor system. Thus, distorted sensory information is thought to disturb SMI and impair accurate motor control. In normal circumstances, 2 inputs that engage the sensory system have a reciprocally inhibitory action that gates the total amount of signal at all central levels, spatially and temporally limiting the amount of input engaging the CNS. This is thought to prevent sensory “overflow.” The defective gating may cause an input-output mismatch in specific motor programs, and such mismatches in motor programs may in themselves lead to production of distorted sensory information and issue of less than ideal motor commands. In this way, the chronicity of the problem can be maintained via a self-perpetuating mechanism. The reduced frontal N30 SEP peak ratio observed in the current study after 12 weeks of chiropractic care may reflect a normalization of pain-induced central maladaptive plastic changes and may reflect one mechanism for the improvement of functional ability reported following chiropractic adjustment or manipulation. (pgs. 134-135)
Haavik, Niazi, Holt and Murphy (2017) concluded:
After the 12 weeks of chiropractic care, when he was also feeling better symptomatically, this was reversed, and all of his MU traces for all SEP peak complexes were smaller in amplitude than his M + U trace, indicating a greater level of central reciprocal inhibition was occurring… Thus, if sensory “overflow” occurs, then incomplete processing of this incoming signal may occur in the brain, resulting in its perceiving not only excessive, but also spatially distorted information. (pg. 135)
The N9 SEP peak (the “N” is a location for electrodes) reflects the afferent signal over the brachial plexus before it enters the CNS, and thus can be used to ensure that the incoming signal is consistent before and after an intervention. Furthermore, these experiments demonstrated that the subjects' N30 SEP peak ratios decreased significantly after a single chiropractic manipulation of the cervical spine. As the N30 SEP peak is thought to reflect early cortical SMI, the authors argued that their results suggest that the subject's SMI networks' ability to suppress the dual input after the adjustment was increased. The N30 SEP peak ratios remained decreased even after repeating the 20-minute repetitive thumb abduction task. This suggested that the treatment effects appear to have altered the way in which each subject's CNS responded to the repetitive thumb typing task.
When considering treating chronic pain, dystonia, essential tremor or any other type of patient where there are spatial (distorted or excessive afferent) input issues, the above care path (treatment plan) should be considered. By not completed a complete treatment protocol might expose your patient to a chronic issue that may become permanent if the maladaptive cortical changes persist over time. Since there are no timetables for how long a patient can withstand for the issue to become permanent and there is an indexed peer reviewed suggestion of correction, that must be adhered as a minimum until further evidence suggests otherwise. In addition, no two patients are alike and the treatment plan should be guided with a full clinical reevaluation and consider performing that examination every 30 days of active care considering all facets, both history and clinical.