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dissection of the IAN from the mandibular canal during changes result from molecular and cellular changes at the
surgery has been shown to significantly increase the level of the primary afferent nociceptor that are triggered
risk of neurosensory disturbance, while patients with a by the nerve lesion. They are expressed as increased
laceration of the IAN have higher chance of developing spontaneous firing, lowered activation threshold, and
neuropathic pain. [29] expanded receptive fields. [33]
Genioplasty and age at the time of surgery are significant Central sensitization
predictors of hypoesthesia after BSSO, a 1‑year increase in Hyperactivity of the peripheral nociceptor results in
age may increase the odds of hypoesthesia of the lower secondary changes in the dorsal horn of the spinal cord
lip by 5%, and the odds of hypoesthesia for patients with with an associated increase in general excitability of
concurrent genioplasty are 4.5‑fold greater than the odds multi‑receptive spinal cord neurons. This hyper‑excitability
for patients without concurrent genioplasty. Other factors is manifested by increased neuronal activity in response
include smoking and gender (women are at higher risk for to noxious stimuli, expansion of neuronal receptive fields,
hypoesthesia). [27,29] and spread of spinal hyper‑excitability to other segments.
Patients most likely to develop neuropathic pain after Central sensitization is initiated and maintained by
BSSO are older than fourty‑five years and have undergone activity in pathologically sensitized C‑fibers. Importantly,
a procedure involving compression or partial severance the activation of both descending facilitatory and
of the IAN or complete discontinuity of the LN with a inhibitory supraspinal pain control systems requires
proximal stump neuroma. Others at risk include those intense noxious stimulation, resulting in activation of
with nerve injury repair delayed past twelve months, these brainstem centers to finally activate the descending
[26]
patients with chronic illnesses that compromise healing arm of thespino‑bulbo‑spinal circuit. An imbalance
or enhance the risk for developing peripheral neuropathy between facilitatory and inhibitory systems, with higher
(e.g. diabetes mellitus) and patients with preexisting activity in the former and lower in the latter, contributes
chronic pain from any cause (e.g. lower back pain, to central neuronal sensitization and to the development
postthoracotomy syndrome). Furthermore, potentially at and maintenance of pain. [26]
risk are patients with certain psychological features such Deafferentation: hyperactivity of central pain
as depression, anger issues, posttraumatic stress disorder, transmission neurons
and victims of abuse who have lost the ability to trust. Some patients experience a profound cutaneous
[19,26,30,31] Patients undergoing orthognathic surgery are deafferentation of the painful area without significant
usually young and healthy, which may explain the low allodynia. In BSSO and orofacial neuropathic pain,
incidence of neuropathic pain after BSSO surgery. the simultaneous occurrence of an exposed nerve or
partial axonal IAN injury together with disruption of
THE PATHOPHYSIOLOGY OF the bony environment of the IAN is a risk factor. The
[34]
NEUROPATHIC PAIN formation of a neuroma from a severed nerve ending
has been associated with neuropathic pain, which is
Chronic neuropathic pain represents a heterogeneous attributed to altered sensory processing in either the
group of diseases in which pain is caused by nerve damage trigeminal ganglion or the central trigeminal nerve
[35]
owing to various etiologies. Before pain is perceived in the center. Politis et al. found no visible nerve damage
[20]
central nervous system, different descending mechanisms on panoramic radiographs or magnetic resonance
must modulate the initial nociceptive stimulus. The imaging (MRI) or computerized tomography (CT) scans in
imbalance between the amount of stimuli and the efficacy their case series of neuropathic pain after BSSO surgery,
of modulation mechanisms is processed as the sensation except in one patient in whom neuropathic pain started
of pain. High‑magnitude or repetitive nociceptive after loss of fixation and pathological movement of the
impulses cause peripheral and central neuronal changes, bone segments due to pseudarthrosis. In this patient,
leading to the maintenance and exacerbation of the pain the neuropathic pain disappeared after bone grafting and
sensation. These alterations are often irreversible and stabilization of the segments with adequate fixation.
[26]
responsible for patient reports of long‑term pain, even Compression or crush lesions cannot be routinely
after many unsuccessful treatments. Most of the current visualized after orthognathic surgery by either CT or
ideas regarding the pathophysiology of neuropathic pain MRI secondary to artifacts from orthodontic appliances.
originated from experimental work in animal models. The Pathologic elongation of the nerve in BSSO surgery is
underlying mechanisms are described below. [26]
certainly possible when the mandible has been surgically
Peripheral sensitization widened after a BSSO advancement with a midline split.
Pain sensations are normally elicited by activity in Here too, cone beam CT, CT, and MRI cannot be used to
unmyelinated (C‑) and thinly myelinated (Aδ‑) primary directly visualize the nerve damage.
afferent neurons. These nociceptors are usually silent
in the absence of stimulation and respond best to DIAGNOSIS
potentially noxious stimuli. Neurons become abnormally
sensitive after damage to peripheral nerves and develop The diagnosis of neuropathic pain should be made only
pathological spontaneous activity. These pathological when the history and signs are indicative of neuropathy
[32]
Plast Aesthet Res || Vol 2 || Issue 4 || Jul 15, 2015 173