Have you ever wondered why so many different interventions work for the same problem? A person with low back pain may respond very well to myofascial release, joint mobilization, exercise, craniosacral therapy, strain-counterstrain, SNAGs, NAGs or physical agents. How is that possible? The answer is in the brain. The brain simply does not care which technique you use. The brain does not have regions specifically labeled “myofascial nucleus” or “ strain-counterstrain laminae”. The brain cares about the sensory input parameters: intensity, frequency and duration.
The higher nervous system centers play a substantial role in inhibiting the sensation of pain. Pain can be abolished with anesthesia, hypnosis, acupuncture, certain pharmacologic agents or from sustained levels of mental concentration often seen in athletes or performers. The thalamus serves as the processing station for all tactile input to the brain with the exception of olfaction. The ventrobasal nucleus of the thalamus is the first processing point for information conveyed by the A-delta fiber pain pathway – the sensations of sharp and immediate pain. The C fiber pain pathway conveys burning and aching sensations frequently associated with deep tissue damage through the midline nucleus of the thalamus. All thalamic nuclei (except reticular), relay information to the cerebral cortex. In addition, these nuclei process emotional and memory information, integrate sensation, or regulate consciousness, arousal and attention. In other words, the thalamus processes your ticket to the higher centers of the brain and it remembers what ticket you used. Mechanoreceptors located in joints and soft tissues end with an inhibitory synapse on the substantia gelatinosa (SG) in the spinal cord. The balance of excitatory and inhibitory activity determines the nature of the impulses relayed through the spinothalamic tract. Many of these axons synapse in the periaqueductal gray region of the brain known for its activation of a descending inhibitory effect on pain. The projections form periquaductal gray then continue on to the thalamus for processing.
Okay, now that we know the anatomy – so what? Here is a creative interpretation of what happens. I trip and ram my naked toe directly into a giant rock – really hard. A family of Angry Impulses hop the pain train running on the Adelta fiber and ride directly to the spinal cord. Here they transfer to the spinothalamic tract bound for the thalamus and periaquaductal gray stations. They have a message to deliver and it is not going to be fun. The thalamus DECIDES, based on the passengers’ message, where the train goes next. It may go back down and unload in the spinal cord causing such a traffic jam that no more passengers can travel or it may decide to send the train on up to the cortex where the passengers can get off a do all sorts of creatively disruptive and nasty things. An hour or so after the first Adelta train departs, a hiking expedition along the C fiber trail begins. It is a long and arduous journey up to the thalamus and the cousins of Angry Impulses, the Really Ticked Receptors, are beginning to shout as they close in on the thalamus. “You think you know pain? Well, wait till we get there! We’ll show you pain all right! Today, tomorrow and forever !” By the time the Really Ticked Receptors arrive, they are livid. The show is convincing. The thalamus is just about to send them on when , suddenly, out of nowhere, a massive onslaught of anti-pain demonstrators arrive. Some from the joints, some from the skin and still more from muscles and tendons. These feel good crusaders are masters at persuading the thalamus to see things their way. They cajole, beg, yell, purr and whimper until finally the thalamus concedes. Ah, there goes the pain. We’re all just friends up here now. Just friends cruising through the cranium on a Golden Thread having a most enjoyable ride. Until the next pain train arrives.
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