This is a Chapter 3 summary of “Clinical Neurodynamics” by Michael Shacklock.
Table of Contents
What it is
General neuropathodynamics are abnormalities consistent throughout the nervous system, with specific referring to local abnormalities. These changes may lead to a neurogenic pain experience, in which pain is initiated by a primary lesion, dysfunction, or transitory perturbation in the nervous system. This definition means that dysfunction in the nervous system, it’s surrounding tissues, and innervated tissues can all be related to neurogenic pain.
Definitions of Clinical Problems
When discussing dysfunction, there are several descriptors:
1) Optimal/desirable: When the neuromusculoskeletal system behaves well and does not create symptoms in situations of high stress.
2) Suboptimal: Imperfect neuromusculoskeletal behavior which results in potential symptom increasing if an adequate trigger occurs.
3) Normal: Function of neuromusculoskeletal system is within normal values.
4) Abnormal: Neuromusculoskeletal system is outside of the normal range.
5) Relevant: When pathodynamics are linked to the clinical problem.
6) Irrelevant: When pathodynamics are not linked to the clinical problem.
You will oftentimes have multiple of these components in a clinical situation.
Mechanical Interface Dysfunction
These dysfunctions deal with abnormal or undesirable forces on the nervous system. There are two main categories with their own subcategories.
1) Closing dysfunctions – Altered closing mechanisms of the movement complex. Can be reduced (protective response) or excessive (hypermobility/instability).
2) Opening dysfunctions – Altered opening mechanisms of the movement complex. Can be reduced which creates impaired pressure reduction, or excessive leading to tissue traction.
This type of dysfunction is when interfacing structures of abnormal shape or size exerts undesirable pressure on neural structures. These cases typically have poor responses to therapeutic interventions, simply because clinicians are unable to directly alter pathology. Neurodynamic techniques are often contraindicated in these folk.
These dysfunctions occur when physiological changes in interfaces lead to pathodynamics in the nervous system. These processes include inflammation, swelling, or bulging disks to name a few.
There are five types of neural dysfunctions:
1) Sliding – reduced nerve excursion. Often relieving positions worsen symptoms.
2) Tensioning – abnormal elongation mechanics or sensitivity.
3) Hypermobility – Excessive neural excursion.
4) Pathoanatomical – Neural symptoms created by nervous system pathology.
5) Pathophysiological – Abnormal neural physiology leads to pathophysiological dysfunction. Blood pressure changes are an example of this, based on magnitude and time.
Other irritants can influence neural responses. Mechanical irritation can play a role based on C fiber innervation. These fibers can lead to inflammation due to efferent activity. These nociceptors can responds to mechanical movements because they innervate the epineurium and dura.
The way the nervous system can become a symptom source with movements and postures is by mechanosensitivity. When a nerve becomes mechanosensitive from a force, increased afferent firing travels to the central nervous system. This signal can potentially create a pain experience.
All nerve have some mechanosensitivity, but the amount varies depending on the mechanical trigger magnitude and the nervous system’s health. This aspect can be tested by performing tapping along a nerve tract or performing a neurodynamic test. In abnormal situations, nerve impulses more readily fire leading to potential symptoms. Altered mechanosensitivity can occur in peripheral nerves, nerve roots, the dorsal root ganglion, and the spinal cord.
Mechanosensitivity can also occur from chemical and cytoskeletal influences. Neurofilaments can accumulate in unmyelinated areas. This adaptation occurs to protect neural structures.
Suboptimal musculoskeletal activity can also play a role in nervous system sensitivity. If motor control is altered via hyper or hypoactivity, neural tissue can be exposed to danger or overprotected. Motor control can be altered many ways, to include trigger points, muscle imbalance, and paralysis to name a few.
There are two inflammatory dysfunctions – neurogenic and reduced. Neurogenic inflammation involves substance P and calcitonin gene-related peptide (CGRP) release from C fibers in the dorsal root ganglion. These substances travel to the peripheral nerve’s distal terminals to affect vasodilation and inflammation. This inflammation occurs with increased efferent activity.
Reduced inflammation is when there is a decreased inflammatory response due to decreased efferent nerve activity. You see this dysfunction in those with denervation and hypoactivity, which can lead to poor healing.
The sympathetic nervous system can also play a role in inflammation. This act happens by releasing prostaglandins, adrenaline, and noradrenaline. These changes occur when there is excessive pressure on the nervous system.