Over the last few years I have found that nothing ceases to amaze me when it comes to the human body. As it becomes possible to dissect systems and assess interactions of specific stimulus, observing the input/output relationship between stimulus and body.
Pain is observed to be chemical, thermal or mechanical in nature. Please bear with the technicalities before I explain the simplified mechanisms or skip to the last part of the blog, if you get bored!
There are many factors that contribute to a patient’s perception and physical feeling of pain. Pain is the central nervous systems response to an event that has the capacity to injure the tissues of the body. Nociception or pain can be qualified from the following pathways.
The ‘First’ pain is usually a withdrawal mechanism (Nociceptive Withdrawal Reflex or NRA) mediated by the neurotransmitter glutamate and utilises the neospinalthalmic (new pain) tract in the anterolateral system or ALS. This typically lasts less than 0.1 of a second and the signal, suggested to be dampened in the substantia gelatinosa, an area found in the dorsal aspect of the spinal cord. Think about that sharp initial pain experienced causing you to move away from a stimulus, which has been detected by free nerve endings.
The ‘Second’ pain is also part of the ALS but is part of the paleospinalthalmic tract (old pain). It typically takes over from the initial first pain/neo. It is mediated by the compound substance P and can be associated with that long, lingering pain experienced from an injury.
In addition to pain, we have the capacity to assess many other features of mechanical distortion such as pressure, stretch and touch. The Dorsal Column Medial Lemniscus or DCML, allows the nervous system to provide adequate feedback to tasks and environmental stimulus.
Another part of the pain detection system is the trigeminal chemosensory system, which has nociceptive/pain and temperature pathways that feedback to cranial nerve five, called the Trigeminal nerve (CNV). When a noxious or toxic substance is processed by the neurons in the mucosal areas of the nose, mouth, eyes and lips it is relayed into the thalamus. The VPMN (or ventral posterior medial nucleus) relays signals to the sensory cortex and provides responses, such as watery eyes, sneezing and withdrawal
When we inspire air with small particles of pollutants, they pass from the lungs into the blood stream. Although the blood brain barrier is supposed to prevent any unwanted chemicals, crossing from the blood to the brain; the Circumventricular organs present an area that does not have the capacity to restrict compounds that can create dis-organisation of neurological signals entering and leaving the brain. The area postrema, also has a chemosensory role to initiate vomiting to deal with exposure to harmful compounds
So let’s have something a little easier on the eyes and brain to read now. For example:
Perhaps you are walking across the road in heavy traffic. Sucking up all the pollutants such as benzene, carbon monoxide and other waste products of burning fossil fuels into your lungs as you find your way from one side of the road to another.
For a few seconds your brain, exposed to the onslaught of pollution, has a hard time processing the compounds that have made their way into areas such as the pineal gland or chemoreceptors that can induce vomiting in response to a noxious stimulus.
You are in a rush and bump into someone, his or her shoulder hitting you firmly in the chest. It was slightly painful but you don’t really notice it, the pain pathway, along with pressure, stretch and touch receptors provided some form of feedback. The brain, perhaps still not capable of processing this feedback due to the short exposure of increased pollutants, is just trying to get on with the milieu of everything else that your body demands of it.
Meanwhile the pectoralis muscle, which is being used with each step that you take, has been exposed to increased pressure, a state of contraction or small window of pain that necessitated a withdrawal reflex. The intrafusal muscle fiber that monitor both stretch and contraction now have increased signal towards sustained contraction due to the chaos of external compounds that entered areas of the brain.
So now we might have some level of muscle dysfunction. We probably don’t even know about it. That level of muscle dysfunction now increases and decreases tension demands to receptors found in the ligaments and tendons. The joint mechanoreceptors have a different signal. The skin exteroreceptors perhaps have a different signal. There’s no pain to remind us of the event. In fact we have now gone to the gym and started doing a bunch of push-ups or gone shopping for food and simply carrying the bag home with that hand and shoulder. This doesn’t create pain, but simply sets the foundation for increased areas of dysfunction from distorted neurological signalling.
The concept of this neurological/chemical chaos is often referred to as ‘brain fog’. It seems to be in the literature for many reasons, blood sugar issues, gluten, estrogen (PMS and menopausal females are particularly susceptible) and other factors. It’s also possible that brain fog can be created from specific food stressors, once again eliciting the same response, proposed in the heavy traffic.
Some might say, how can the body be so fragile? Surely we are more robust than that? But it is possible to create these specific dysfunctions but they can be unravelled. Understanding specific stimulus can give us a solution to what dysfunction exits. We might never find out how it came about but a thorough history taking can help to influence where we assess and how to treat it. This is where a technique like P-DTR or Proprioceptive Deep Tendon Reflex, developed by Dr Jose Palomar is unique and effective at uncovering specific neurological dysfunction.
If emotions, visual, auditory, mechanical, chemical and pain factors perpetuate dysfunction, then using those stimulus can pose an effective form of assessment and treatment.
- Palomar, J. Proprioceptive Deep Tendon Reflex: Course Notes.
- Purves D et al Neuroscience 5th edition. Sinauer Associates 2012