The ENTRTAPMENT SYNDROMES are the compression syndromes of the peripheral nervous system since they refer to the suffering of a nerve trunk when passing from one anatomical compartment to another (eg the passage from the trunk to the limbs or from one segment of the limbs themselves).
Compression can occur due to the narrowness of the anatomical osteofibrosis channels or structures formed by soft tissues.
The clinical symptoms can be irritative with pain, hypoaesthesia (decreased sensitivity of the skin) or paresthesia (tingling, sensation of skin electric shock) in initial or less severe cases, or injury with strength deficiency.
The anatomopathological findings inherent in this category of neuropathies are practically limited to the occasional findings of autopsy findings. There are, however, numerous clinical studies on experimental animal models that have made it possible to know the events that result from a chronic compression of a peripheral nerve.
Electrophysiology allows you to have an in vivo projection of what are the most common subversions 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 allows to highlight the primary involvement of the myelin, with the slowing of the conduction speed, and eventually to detect axonal damage in the form of amplitude alterations and form of action potentials.
The compressive action, although widely applied on all the components of the peripheral nerve, finds its most frequent expression in the damage to the myelin fibers of large diameter.
The forces involved in the development of nerve pathology are those of stretching and compression. With regard to stretching, Sunderland has established with electrophysiological method that conduction progressively slows down when traction is exerted to cease when it reaches 6% of the original length. At this degree of elongation, the true stretching of the nerve fiber begins, until then compensated by the serpiginous course of the fascicles immersed in the inter-vascular connective elastic.
The connective structure is the only one that offers mechanical resistance to the lengthening of the system. When there is a failure of the connective fibers, the distracting energy is transferred to the nerve fiber that enters tension. At this point, the immediate block of conduction occurs on the basis of the deformation of the Ranvier nodes. Continuing the traction, damage to the nerve fiber occurs up to the anatomical discontinuity of the same (axonotmesis) or of the entire nerve (neurotmesis).
As regards compression, Ochoa, with electron microscopy has shown, in experimental cases, what it happens to the fiber wrapped in the myelin sheath. In the case of both acute and chronic compression, the pathology initially affects only Schwann cells.
In acute compressions, the picture is characterized by an intussusception of the myelin sheath upstream and downstream of the point of application of the force. The applied force produces, in the two directions of the fiber, a sliding of the myelin sheaths like the cylinders of a telescope.
In chronic compressions (which better reflect the pathomechanics of the canalicular syndromes) there is instead a "bulb" formation of the myelin: the the outermost layers slip, moving away from the point of application of the force, and lose their disposition.
For both types of myelin destructuring there is a consequent deformation and closure of the "knots" of Ranvier. The physiological result is the interruption of the ability to conduct impulses. There is, at this moment, an anatomical interruption of the fiber, which can 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 affects preferably the fibers of small diameter unmyelinated.
Under normal conditions, in order for oxygenation of the nerve to be guaranteed, there must be a pressure gradient (arterial> arteriolar> capillary> endonevrial> venular> venous); if this is canceled or reversed, the blood cannot reach the axon with its consequent suffering.
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