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- CANALICULAR SYNDROMES (Entrapment Neuropathies) OR SINGLE COMPRESSION OF PERIPHERAL NERVE: DEFINITION, PATHOPHYSIOLOGY AND LESIONAL DYNAMICS
- DOUBLE COMPRESSION SYNDROME OF THE PERIPHERAL NERVE (Double Crush Syndrome)
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 PAGES INSIDE THIS SITE FOR THE CANAL SYNDROMES
OF THE UPPER LIMB
AND OF THE LOWER LIMB
DOUBLE COMPRESSION SYNDROME OF THE PERIPHERAL NERVE (DOUBLE CRUSH SYNDROME)
FOR SCIENTIFIC AND INFORMATIONAL PURPOSES, CLICK HERE TO EXIT THIS WEBSITE AND CONNECT TO THE YOUTUBE CHANNEL OF PROFESSOR NABIL A. EBRAHEIM FROM THE UNIVERSITY OF TOLEDO, OHIO (USA) AND WATCH AN EDUCATIONAL VIDEO ON THE DOUBLE COMPRESSION SYNDROME OF THE PERIPHERAL NERVE, IN ENGLISH.
In the box below you can read the Italian translation of the English text.
THIS VIDEO IS MADE FOR EDUCATIONAL PURPOSES ONLY. PLEASE CONSULT YOUR PHYSICIAN BEFORE MAKING DECISIONS ABOUT YOUR CARE.
TRANSLATION FROM ENGLISH OF THE TEXT PRESENT IN THE ABOVE EDUCATIONAL VIDEO ON
DOUBLE CRUSH SYNDROME OF THE PERIPHERAL NERVE (DOUBLE CRUSH SYNDROME)
Dr. Ebraheim's animated educational video describes double crush syndrome of the peripheral nerve, its etiology, signs and symptoms, diagnosis, and management.
A patient with a peripheral nerve injury may also have a second injury elsewhere along the nerve pathway. Both injuries could contribute to the patient's symptoms.
The nerve cell body produces material necessary for the normal functioning of the axon. The material travels distally along the axon. Products are divided in a proximal direction from the axonal transport system. Disruption of synthesis or blockage of the transport of these materials (anterograde/retrograde) increases the vulnerability of the axon to compression. Other causes are edema and alteration of neural blood flow, neuropathy, diabetes, and reduced nerve elasticity as occurs in fibrosis.
Nerve compression at one point lowers the threshold for the onset of compression neuropathy at another point, distal or proximal, at the same point by interfering with the axonal transport mechanism. The outcome of surgical decompression may be disappointing unless both areas of compression are treated.
C5-C6 is the most common level at the cervical level. The patient's EMG will show fibrillation or sharp waves in the biceps, extensor carpi radialis longus, and extensor carpi radialis brevis muscles. This is different from the findings in carpal tunnel.
Common associations in double crush syndrome:
- Cervical root compression and carpal tunnel syndrome (median nerve). A minor compression in the median nerve in the carpal tunnel observed in EMG (distal sensory latency) will produce symptoms when a proximal cervical lesion is present. The coexistence of cervical root compression is one of the main reasons for persistent residual symptoms following carpal tunnel treatment. Physicians should not only think about carpal tunnel syndrome when examining patients; the possibility of other causes of symptoms should also be considered, and thus the possibility of a broader diagnostic approach that includes EMG and nerve studies from the neck down. The persistence of the symptom system after initial treatment of median nerve entrapment at the wrist is an indication to look for another site of compression;
- Thoracic outlet syndrome and carpal tunnel syndrome (median nerve);
- Cervical root compression and cubital tunnel syndrome (ulnar nerve);
- Cubital tunnel syndrome and Guyon's canal syndrome (ulnar nerve), the ulnar nerve enters the palm of the hand through Guyon's canal;
- Cervical root compression and radial tunnel syndrome (radial nerve).
THIS VIDEO IS MADE FOR EDUCATIONAL PURPOSES ONLY.
PLEASE CONSULT YOUR PHYSICIAN BEFORE MAKING CARE DECISIONS.
LAST MODIFIED 17 APRIL 2020
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