| Neurosensory disturbance after bilateral sagittal split osteotomy | ||
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The nerve trunk is composed of four connective tissue sheaths. From the outside inward these are the mesoneurium, epineurium, perineurium, and endoneurium (Daniel & Terzis 1977, May 1986, Millesi & Terzis 1987, Lundborg 1988). The mesoneurium is a connective tissue sheath analogous to the mesentery of the intestine. It suspends the nerve trunk within the soft tissue, contains the segmental blood supply of the nerve, and is continuous with the epineurium. The epineurium is the loose connective tissue sheath that defines the nerve trunk and protects it against mechanical stress. Fascicles are delineated by the perineurium, which surrounds the axons and endoneurial sheaths. The fascicles form a complex branching pattern that varies from millimetre to millimetre along the path of the nerve trunk. The fascicular pattern can be monofascicular (one large fascicle), oligofascicular (2-10 rather large fascicles) or polyfascicular (more than 10 fascicles of different sizes). Individual nerve fibers and their Schwann cells are surrounded by the endoneurium. Together, the perineurium and endoneurium provide elasticity. Polyfascicular nerves such as the IAN with many small fascicles are better able to withstand stretch than are monofascicular or oligofascicular nerves (Sunderland 1951).
The nerve fiber is the functional component of the peripheral nerve responsible for transmitting stimuli. The nerve fiber is composed of an axon, a Schwann cell, and a myelin sheath in myelinated nerve fibers. The axon is an extension of a neuron and can be characterized by morphology, conduction velocity and function. A-alpha fibers are the largest myelinated fibers, functionally they are encoded for the transmission of muscle spindle and tendon organ afferents and skeletal muscle efferents. The A-beta fibers are the next largest myelinated axons. The sensation of touch is attributed to these axons. The smallest of the myelinated fibers are the A-delta fibers, which transmit stimuli encoded for temperature and pain. The smallest axons are the unmyelinated C-fibers. They transmit stimuli encoded for slow or second pain, temperature, and efferent sympathetic fibers (LaBanc1992).
In 1943, Seddon described a triple classification of mechanical nerve injuries to characterize the morphophysiologic types of mechanical nerve injuries. Seddon’s classification (neuropraxia, axonotmesis and neurotmesis) is based on the time course and completeness of sensory recovery.
The majority of IAN injuries following BSSO are neuropraxias. A neuropraxia is characterized by a conduction block, the rapid and virtually complete return of sensation or function, and no degeneration of the axon. It may be the result of nerve trunk manipulation, traction, or compression of a nerve such as might occur during sagittal ramus osteotomy. Trauma of sufficient magnitude to injure the endoneurial capillaries causes intrafascicular edema, resulting in a conduction block. Normal sensation or function returns within 1 to 2 days following the resolution of intrafascicular edema, generally within 1 week following nerve injury. Pressure on the nerve may also result in segmental demyelinisation or mechanical disruption of the myelin sheaths. In this case sensory and functional recovery are complete within 1 to 2 months. The response to this type of injury is paresthesia (LaBanc 1992).
An axonotmesis is characterized by axonal injury with subsequent degeneration or regeneration. Traction and compression are the usual mechanisms of this type of injury and may cause severe ischemia, intrafascicular edema, or demyelination. Even though the axons are damaged, there is no disruption of the endoneurial sheath, perineurium, or epineurium. Complete recovery occurs in 2 to 4 months, but improvement leading to complete recovery may take as long as 12 months. It is important to know that within 2 to 4 months following injury there are signs of sensation or function which continue to improve over the next 8 to 10 months. The psychophysical response to an axonotmesis is an initial anesthesia followed by a paresthesia as recovery begins (LaBanc 1992).
A neurotmesis is characterized by severe disruption of the connective tissue components of the nerve trunk with compromised sensory and functional recovery. The etiology of nerve injury is traction, compression, injection injury, chemical injury or in a complete distruption of the nerve trunk laceration and avulsion. With this type of nerve injury there is a poor prognosis for recovery, and sensory and functional recovery is never complete. The psychophysical response to these injuries is an immediate anestesia. This may be followed by paresthesia or possibly neuropathic responses such as allodynia, hyperpathia, hyperalgesia, or chronic pain. This type of nerve injury has a high probability of development of a central neuroma (LaBanc 1992).