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CANALICULAR SYNDROMES
(NERVE ENTRAPMENT SYNDROMES)
- DEFINITION
- PATHOPHYSIOLOGY
- LESIONAL DYNAMICS
DEFINITION
The "canalicular syndromes" are compressive syndromes of the peripheral nervous system as they refer to the suffering of a nerve trunk as it passes from one anatomical compartment to another (e.g., the transition from the trunk to the limbs or from one segment of the limbs to another).
Compression can occur due to the narrowing of osteofibrous anatomical canals or structures formed by soft tissues.
The clinical symptoms may be irritative with pain, hypoesthesia (decreased skin sensitivity), or paresthesia (tingling, sensation of electric shock on the skin) in the initial or less severe cases, or lesional with strength deficits.
PATHOPHYSIOLOGY
The anatomopathological findings related to this category of neuropathies are practically limited to occasional findings from autopsy examinations. However, there are numerous clinical studies on experimental animal models that have made it possible to understand the events that follow chronic compression of a peripheral nerve.
Electrophysiology allows for an in vivo projection of the most common disruptions of the structures that make up the nerve. The course of the lesion and its localization in the nerve trunk are well reflected by electroneurography, which makes it possible to highlight the primary involvement of the myelin, with the slowing of conduction velocity, and possibly to detect axonal damage in the form of changes in amplitude and shape of the action potentials.
The compressive action, even if exerted diffusely on all the components of the peripheral nerve, most frequently manifests itself as damage to the large-diameter myelinated fibers.
LESIONAL DYNAMICS
The forces involved in the development of nerve pathology are those of stretching and compression. Regarding stretching, Sunderland established with electrophysiological methods that conduction progressively slows down when traction is applied, ceasing when it reaches 6% of the original length. At this degree of elongation, true stretching of the nerve fiber begins, up to that point compensated by the serpentine course of the fascicles immersed in the interfascicular elastic connective tissue.
The connective structure is the only one that offers mechanical resistance to the elongation of the system. When there is a failure of the connective fibers, the distractive energy is transferred to the nerve fiber, which becomes tense. At this point, immediate conduction block occurs due to deformation of the nodes of Ranvier. If traction continues, damage to the nerve fiber occurs up to anatomical discontinuity of the fiber itself (axonotmesis) or of the entire nerve (neurotmesis).
As for compression, Ochoa, using electron microscopy, showed in experimental cases what happens to the fiber wrapped in the myelin sheath. In both acute and chronic compression, the pathology initially affects only the Schwann cells.
In acute compressions, the picture is characterized by an intussusception of the myelin sheath upstream and downstream of the point of force application. The applied force produces, in both directions along the fiber, a sliding of the myelin sheaths like the cylinders of a telescope.
In chronic compressions (which more closely reflect the pathomechanics of canalicular syndromes), there is instead a "bulb-like" formation of the myelin: the outermost layers slip, moving away from the point of force application, and lose their arrangement.
For both types of myelin destructuring, there is a consequent deformation and closure of the "nodes" of Ranvier. The physiological result is the interruption of the ability to conduct impulses. At this moment, there is no anatomical interruption of the fiber, which may instead occur later due to progressive ischemia, after a phase of metabolic reduction (axonocachexia).
Another type of noxa concerns the vascular suffering of the nerve, which preferentially affects the small-diameter unmyelinated fibers.
Under normal conditions, in order to guarantee oxygenation of the nerve, there must be a pressure gradient (arterial > arteriolar > capillary > endoneurial > venular > venous); if this is nullified or reversed, blood cannot reach the axon, resulting in its suffering.
MOST COMMON CANALICULAR SYNDROMES
UPPER LIMB:
- Carpal tunnel
- Cubital tunnel
- Thoracic outlet
LOWER LIMB:
- Meralgia paresthetica
- Tarsal tunnel
- Compression and paralysis of the Peroneal nerve
SEE DEDICATED PAGES WITHIN THIS SITE FOR THE ABOVE-MENTIONED CANALICULAR SYNDROMES