This is a summary of Chapter III of “The Sensitive Nervous System” by David Butler.
Table of Contents
When we discuss peripheral issues, we are not only talking about the pathoanatomical source, but pathobiological processes dominating the clinical picture. There are several instances in which the pathoanatomical model falls short:
- Phantom limb pain.
- Why pain persists post-healing.
- Why similar injuries heal faster in certain people.
- Why 10-14% of the world’s population have an ongoing pain state.
Tissues do get injured, but we must not forget the nervous system’s intricate link to injury. When tissues are hurt, they repair but are unlikely to ever be the same again. To protect against further threat, the CNS has the ability to increase nerve sensitivity. This change happens only if the person decides consciously or subconsciously that there is a need for it, and does not occur in everyone. There are two ways in which this sensitivity develops;
- Primary sensitivity: Increased sensitivity to input at the injury site.
- Secondary sensitivity: Increased sensitivity to uninjured tissues around the injury.
All pain is neurogenic, operates in a continuum, and has many components.
NOC is tissue pain that occurs at a neuron’s end that is excited by mechanical, thermal, or chemical stimuli. It does not always match up with tissue health status. A normal nerve ending has a very high firing threshold, and nearly 1/3 will never fire. These are called silent nociceptors.
Looking at a chemical process such as inflammation shows us how these nerves fire. When acute inflammation begins, a chemical soup with a swelling broth enters the area. Inflammatory chemicals flood the area, lowering the nerve’s firing threshold and increasing its firing rate. This process makes movements painful. In a chronic inflammatory case, the body becomes depleted of inflammatory mediators, thus potentially leading to change in the sensory neuron’s properties.
The nervous system is also involved with inflammation. C fibers begin neurogenic inflammation by releasing substance P and CGRP. These chemicals flatten capillaries, which further encourage swelling. The spinal cord uses antidromic impulses (firing in an opposite direction along a nerve) to mediate inflammation, thus suggesting a central influence.
The sympathetic nervous system can affect inflammation by releasing catecholamines, which maintain or enhance pain. This gives us clinicians a way to affect the inflammatory response by targeting stress reduction.
There are two ways to classify NOC based on inflammatory response. It is much easier to do this than it is to find a structure at fault.
- Fluids forced out of tissues.
- Evident in prolonged/unusual postures
- End of the day
- No trauma
- Rapid ease with posture change
- Poor anti-inflammatory response
- Acute pain / tissue damage
- Concordant signs (redness, swelling, temperature change, etc.)
- Diurnal pattern
- Hints of an unhealthy nervous system
- Neurogenic inflammation
- Anti-inflammatories help.
Peripheral Neuropathic Pain (PNP)
Butler lists several modern concepts of nerves.
1) Peripheral nerves are long, living, and responsive tissues.
2) The dorsal root ganglion is the peripheral nervous system’s brain.
3) Nerves are stable and take many mechanical forces during movement
4) Axons are highways that transmit pulses, which get modified but abnormal impulse generating sites (AIGS) in chronic pain.
5) A nerve’s connective tissue is innervated and capable of causing pain. Therefore healthy connective tissue = healthier nerve.
6) It is unlikely that nerve entrapment exists on its own. Stress response and central sensitization likely occur as well.
7) The immune system plays a role in PNP.
When a peripheral nerve segment becomes injured, it can begin to generate its own impulses. These sites can form just about anywhere in the nervous system, including the spinal cord and dorsal root ganglion. AIGS can only occur in sensory nerves, and are likely what neurodynamic tests affect. Here is a list of stimuli that can cause an AIGS to fire.
1) Temperature: Cool excites C fibers, heat excites A fibers.
2) Metabolic/chemical stimuli.
3) Ischemia, anoxia, blood gas change.
5) Muscle, nerve, bone.
6) Spontaneously: You’ll notice this when people cannot give an aggravating activity or likely an innocuous unperceived incident.
7) Mechanical: if nerves do not slide or glide well, more force is placed on the AIGS. Moreover, scar tissue formation highly correlates with nerve root mechanosensitivity.
One very important point to make, and this goes for all injuries is that pain does not equal injury. There have been several cadaveric studies that demonstrate nerve damage or compression in people who never complained of pain.
– Dermatomal or cutaneous innervation field. Can be a localized part.
– Pain along a nerve trunk.
– Minor spot pain (trigger point – an AIG in a cutaneous nerve struggling with relationship to myofascia).
– Motor involvement.
– Burning, especially in cutaneous nerves.
– Diffuse cramping if it is a nerve that innervates muscle.
– Paresthesia in a peripheral neural zone.
– Evoked by nerve movement or surrounding tissue change.
– Mechanosensitivity beginning, during, or at stimulus release.
– DRG – More spontaneous.
– Linked to stressed states or inflammation.
– Antalgic postures.
– AIGS give weird symptoms like strings pulling, ants, and/or electrical feelings.
– AIGS may be silent for a few days after injury.
Ultimately, the goals of treating these conditions follow a 3 step approach with the overall goal being turning a firing nerve off.
1) Alter sympathetic and immune inputs – explain pain, make goals, and decrease fear.
2) Increase circulation – simple exercise
3) Decrease mechanical forces – posture, nervous system health, and altering temperature.
This treatment must be done as soon as possible, for if AIGS continue to fire, the CNS may upregulate and lead to central sensitization.
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