Ross Hauser MD

Many people live with chronic pain, they have no choice. They have health conditions that cannot be helped beyond the prescription of medications and psychiatric counseling. Other people manage their chronic pain by just “living with it.” Should you be “just living with it?” Many researchers say no. In fact, “living with it” may affect your brain cells and future cognitive skills. The chronic sufferer, according to researchers, should explore ways to address their chronic pain situation. The purpose of this article is to demonstrate, through peer-reviewed scientific research, that chronic pain alters your brain function and accelerates neurological-like symptoms, memory, and cognitive function.

I have asked patients who have a complex medical history of ten, twenty, thirty even more disorders, “Do you really think it’s these numerous individual disorders separately causing your problems or do you think it may be one common source?  It is much more likely you have one condition causing all symptoms and disorders. That condition is usually cervical instability resulting in vagopathy, is called cervicovagopathy. The cause of cervicovagopathy is actually what I’ve termed cervical dysstructure (Hauser’s disease), the breakdown of the cervical spine supporting structures which ultimately leads to destruction of a person’s nervous system.

• Degenerative neurologic diseases, such as Parkinson’s disease, multiple-system atrophy, pure autonomic failure presenting or suffering from Orthostatic Hypotension (OH), fixed heart rate responses, etc.
• An immune-mediated attack, either idiopathic or paraneoplastic, can be a source of focal or generalized autonomic dysfunction, as in Guillain-Barre syndrome, or autoimmune autonomic ganglionopathy
• Metabolic and toxic damage, as in diabetes mellitus, amyloidosis and Fabry disease
• Genetic disorders, like in dopamine-beta-hydroxylase deficiency and familial dysautonomia
• Abnormal reflex responses in carotid sinus hypersensitivity, vasovagal syncope, and other neuro-meditated syncope; and probably in Postural Tachycardia Syndrome (POTS)
• Abnormal sweating responses, as in generalized or focal hyperhidrosis, related to an excessive activation
• Traumatic or tumor spinal cord injuries at different levels and presenting with the so-called autonomic dysreflexia
• Pharmacologic effects of several drugs that interfere with normal autonomic function and provoke symptoms include alpha- and beta-blocker-triggered OH

We see it all the time – chronic pain patients suffering from more than just pain. They are depressed, have trouble concentrating and struggle to remain positive in their pain. Current research shows why – chronic pain has an adverse effect on the brain, but it can be reversed with pain relief.

In March 2024, researchers writing in the journal Frontiers in neurology (1) had 45 patients with chronic low back pain and 45 healthy controls do an MRI scan of the brain. Afterwards, comparisons were made between the two groups in terms of the volumes of the amygdala sub regions.

Side note explanation: The central, basolateral and lateral nuclei of the amygdala are part of the brain that helps in processing, understanding and managing chronic pain.

Results of research: In comparison to healthy controls, patients with chronic low back pain exhibited a significant enlargement of the left central nucleus and left cortical nucleus. Furthermore, the increased volume of the left central nucleus was associated with a higher risk of chronic low back pain.

Increased volume is not a good thing. Many studies have demonstrated a possible cause of greater volume in left central nucleus and left cortical nucleus is major depressive disorder as well as chronic pain meaning more negative activity in those brain regions.

“Treating chronic pain can restore normal brain function in humans.”

This statement is the conclusion of an interesting study just released in the Journal of Neuroscience (2). Researchers at McGill University in Montreal studied 18 people that had been suffering for six or more months from chronic low back pain. When compared to people with no chronic pain, they found that these people had decreased brain gray matter and impaired cognitive ability. Using an MRI, researchers observed thinner tissue and abnormal brain activity while subjects performed a cognitive attention-requiring task. In other words, chronic pain affected areas of the brain that deal with depression and impaired concentration, memory, mood, and social judgment.

Pain Relief and the Brain

Now here’s the interesting part: when the pain was relieved there was a reverse in the deterioration of the brain – the area of the brain (known as the dorsolateral prefrontal cortex) was no longer thinner than the control group. Additionally, there was no abnormal activity observed by MRI when the chronic pain patients performed a cognitive task. In the three people that reported no pain relief from treatment, there was no regeneration of gray matter. This study suggests that chronic pain takes a toll on the brain, but with relief it can regenerate itself.

A June 2022 study in the publication Current rheumatology reports wrote: “Non-pharmacological therapeutics, such as vagus nerve stimulation, mindfulness-based meditation, and exercise, have shown promise in alleviating painful symptoms of joint diseases, and these interventions may be partially mediated through the autonomic nervous system. The autonomic nervous system appears be dysregulated in osteoarthritis progression (the way we handle stress may negatively impact the way we feel pain).

1 Gu SY, Shi FC, Wang S, Wang CY, Yao XX, Sun YF, Hu JB, Chen F, Pan PL, Li WH. Altered volume of the amygdala subregions in patients with chronic low back pain. Frontiers in Neurology. 2024 Mar 28;15:1351335. [Google Scholar]
2 Seminowicz DA, Wideman TH, Naso L, Hatami-Khoroushahi Z, Fallatah S, Ware MA, Jarzem P, Bushnell MC, Shir Y, Ouellet JA, Stone LS. Effective treatment of chronic low back pain in humans reverses abnormal brain anatomy and function. Journal of Neuroscience. 2011 May 18;31(20):7540-50. [Google Scholar]