In early stages of closing dysfunctions, symptoms present as aches and pains. This presentation is due to the musculoskeletal tissues being more affected than the neural tissue. As severity increases, neurological symptoms such as pins and needles, tingling, and burning are more likely to occur. The severest end of the spectrum includes numbness and weakness; indicating further compromise to the neurovascular structures.
Interface dysfunctions behave with changes in posture and movement. Oftentimes cardinal signs of inflammation can be present, along with night pain/morning stiffness. Typically you will see a painful arc throughout movement.
During the physical exam, patients will show an inability to move in opening or closing directions. You can also find altered pain production, soft tissue thickening, or hypermobility/instability. Neurological changes will usually be present only in severe interface dysfunction.
There are four basic types of interface dysfunctions
1) Reduced closing
2) Excessive closing
3) Reduced opening
4) Excessive opening
In reduced closing dysfunction, closing movements such as squeezing or cervical extension provoke symptoms. Assessment may show a protective deformity developing in the opening direction so pressure is reduced on the nervous system. Symptoms will often not be reproduced unless neurodynamic testing is combined with interface testing.
Excessive closing is when, well, interfaces are closing too much. An example of this dysfunction is excessive lumbar lordosis present with low back pain that increases with standing, walking, and running. A patient’s history will often show habitual use of the body or postural imperfection. There may also be localized tenderness and increased tone at dysfunctional segments. Neurodynamic tests are often okay because there is usually only transient mechanical irritation.
In reduced opening dysfunctions, there are local aches and pains with potential for referred pain. Opening movements provoke symptoms and are restricted. There is often an associated trauma that occurred in which the patient has been forced into an opening position. The patient can present with an ipsilateral listing deformity in order to reduce tension in involved neural tissues. Palpatory exam may show local tenderness, muscle tightness, and local thickening. Neurodynamic tests will often be more sensitive than other dysfunctions.
Excessive opening presents with aches in pains both locally and often referred. Opening movement provoke symptoms due to increased tension in both musculoskeletal and neural tissues. There are often signs of hypermobility and excessive postures present along with these complaints. The patient may complain of abnormal response to touch, pins and needles, and numbness can occur with this dysfunction. Symptoms occur intermittently with a subtle neurodynamic component.
History for excessive opening dysfunctions includes traumatic stretching events or habitual hypermobility/instability usage. The examination will show localized tenderness with subtle neurodynamic changes. Often contraction of interface structures in a neurodynamic position helps guide diagnostics.
Interface Pathoanatomical Dysfunction
Sometimes you will have patients that you simply cannot help. This is where pathological knowledge comes in. The pathology problem is that symptoms have a wide variety. However, you can see diffuse neurological change in certain processes. Patients will state histories of insidious and progressive symptom onset with no mechanical trigger. If the patients are not improving, then one ought to refer.
Interface Pathophysiological Dysfunction
These dysfunction types include inflammatory behaviors such as diurnal pain patterns. In degenerative conditions, movement and sustained postures may evoke symptoms; with rest as a relieving factor. Neurodynamic tests may deceptively be positive, as inflammatory responses can lead to central sensitization and therefore false positive responses.
There are five neural dysfunctions:
Sliding dysfunctions can occur at the problem site and along the nerve tract that are mechanically evoked. Dysesthesia and Paresthesia can occur as well. Neurodynamic test may reveal that adding differentiating movements may reduce symptoms.
Tension dysfunctions have a wide variety of symptoms including aches, pains, dysesthesia, and pins and needles. Stretching based movements often create problems, and range of motion is often decreased as nerves tense. The neural structures will often be tender.
Hypermobility is seen as a dull, clicking nerve throughout the movement range. Often the patient only hears the sound. There can be local pain or discomfort, and pins and needles may occur as well. Neurodynamic responses can be variable, though sometimes the nerve can be seen jumping underneath the skin.
Pathoanatomical symptoms include pain, dysesthesia, paresthesia, and neurological impairment. Neurodynamic responses can vary, and palpation is unlikely to reveal a pathology unless the nerve is very accessible.
Pathophysiological dysfunctions are similar to the interface pathophysiology, only the nervous system physiology is what is compromised.
Innervated Tissue Dysfunctions
There are two main categories of innervated tissue dysfunction:
1) Motor Control
The first motor control dysfunction includes protective dysfunction. With this type, muscle activity changes in order to protect neural structures.
The second type of motor control dysfunction is muscle imbalance. Shacklock does not go into detail on these problems, but the large association is to find if neurodynamics and muscle imbalances are related. An example would be lower trap weakness during a neurodynamic test.
Trigger points are another dysfunction that often occurs via neuropathodynamics. Hypoactivity can be another relevant issue.
Increased inflammation involves localized pain and swelling unless there is not a specific structure involved. This change would implicate neurogenic inflammation, especially if there is local sensation loss. The history may involve current or past neural problems. Active motion may reproduce symptoms, but not apply tissue stress. Neurodynamic responses can be variable. Palpatory exam can assess swelling and abnormal sensitivity.
Reduced inflammation occurs in neural loss, and often results and poor healing.
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.
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.