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Results for “Trigeminal Nerve Injuries”

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At least 19 recordsLinked to original sources
PubMed2001

Mechanisms of trigeminal nerve injuries.

Injuries to the trigeminal nerve branches are a known and accepted risk in oral and maxillofacial surgery. It is prudent for the practitioner to explain the risks to patients as part of the informed consent process and to recognize and document the presence of nerve injury postoperatively. Patients should be referred to a surgeon experienced in microsurgical techniques in a timely fashion for evaluation and possible surgical intervention if an injury is not resolving.

Dental Implantation, Endosseous↗
PubMed2002

Strain-dependent modification of neuropathic pain behaviour in the rat hindpaw by a priming painful trigeminal nerve injury.

The aim of the present study was to test the behavioural effect of infraorbital (IO) chronic constriction injury (CCI) on the development of neuropathic pain in the rat hindpaw following sciatic nerve CCI performed 7 days later. Control groups consisted of rats that underwent sham infraorbital surgery followed by sciatic CCI at identical time points. Sensory testing of the rat's face and hindpaw was performed at baseline and at 4, 11, 14, 17 and 21 days postoperative (dpo) relative to the IOCCI, at which time all rats were euthanized. To test for strain differences the experiment was performed on Sprague-Dawley, Sabra and Lewis rats. In Lewis rats the trigeminal nerve injury significantly accelerated the development of hindpaw mechanoallodynia (11th, 14th and 17th dpo, unpaired t-test, P<0.05) and mechanohyperalgesia (14th and 17th dpo, unpaired t-test, P<0.05), following a second sciatic nerve CCI relative to the control group. This effect was not observed in Sprague-Dawley or Sabra rats.

Animals↗
PubMed1996

[Simple assessment of trigeminal nerve injury].

This paper describes a simple method to assess trigeminal nerve injury. An easy and feasible technique, in particular for the dental surgeon, is scanning the area with altered sensation as indicated by the patient. It is important to refer the eligible patient in time for microsurgical repair of the damaged nerve.

Anesthesia, Dental↗
PubMed2002

Management of patients with trigeminal nerve injuries after mandibular implant placement.

BACKGROUND: Placement of mandibular endosseous implants can result in damage to the lingual nerve, the inferior alveolar nerve or both nerves. All dentists who place mandibular implants should be aware of the appropriate early management of these injuries, as well as the appropriate time to refer patients with these injuries to a microneurosurgeon. OVERVIEW: The lingual nerve is less likely to undergo spontaneous regeneration than is the inferior alveolar nerve, which is protected within the inferior alveolar canal. Since the inferior alveolar canal can be seen on most panoramic radiographs and on all high-quality computed tomographic scans, it is easier to avoid damage to the inferior nerve than to the lingual nerve, which is not visualized on radiographs and whose relationship to the posterior portion of the mandible varies from person to person. RESULTS: The authors reviewed one study that showed that lingual nerve repair helped 90 percent of patients. A second study found that patients who underwent lingual nerve repair reported a mean score of 7 on a scale from 0 to 10 in regard to the postoperative return of nerve function. Several other studies reported favorable patient responses to inferior alveolar nerve repair. CONCLUSIONS AND CLINICAL IMPLICATIONS: These results reinforce the need for early referral and intervention when inferior alveolar nerve injuries occur. Failure to refer patients with trigeminal nerve injury before distal nerve degeneration develops prevents minimization of the injury through microneurosurgical repair.

Dental Implantation, Endosseous↗
PubMed2004

Peripheral mechanisms for the initiation of pain following trigeminal nerve injury.

Injury to a branch of the trigeminal nerve may lead to the development of chronic pain in the affected area. The etiology of this condition is not clear, but there is strong evidence to suggest that spontaneous and mechanically induced neural discharge from the injury site plays a crucial role. In laboratory studies, we have characterized this discharge following injury to the inferior alveolar or lingual nerves and have shown a temporal association with the accumulation of neuropeptides in the damaged axons. Substance P, calcitonin gene-related peptide, and vasoactive intestinal polypeptide were all found to be capable of increasing the discharge when applied systemically, and enkephalin caused a decrease. There were also changes in the expression of specific sodium channels and nitric oxide synthase, both at the injury site and in the trigeminal ganglion. Studies on lingual nerve neuromas taken from patients undergoing nerve repair also revealed accumulation of peptides, as well as inflammatory and structural changes, but the presence of these features did not correlate directly with the reported symptoms. The application of corticosteroids to an experimental injury site decreased the mechanically induced discharge, and the anticonvulsant carbamazepine reduced the spontaneous discharge in some axons. Some of the responses that result from damage to a branch of the trigeminal nerve appear to differ from those that follow damage to other peripheral nerves. These differences will need to be taken into account when developing new therapeutic approaches for the management of injury-induced trigeminal pain.

Action Potentials↗
PubMed2000

Trigeminal nerve injuries.

Injuries to peripheral branches of the trigeminal nerve are relatively uncommon; however, they are fairly debilitating to the patient when they do occur. Treating clinicians should evaluate and document baseline neurosensory testing results on patients and perform serial examinations approximately every two weeks. If there are no changes after one month, consideration should be given for referral to an oral and maxillofacial surgeon trained in trigeminal nerve microsurgery. Many patients will go on to spontaneous recovery; however, a number will require microsurgery. It is prudent for the treating clinician to recognize, document and discuss the injury with the patient prior to referring to the oral and maxillofacial surgeon trained in microsurgery.

Dental Records↗
PubMed1994

Diagnosis and treatment of trigeminal nerve injuries.

Microneurosurgery has become a valuable technique in the field of oral and maxillofacial surgery. It is now possible to microsurgically repair injuries to the inferior alveolar and lingual nerves resulting from routine oral surgery or dental or oncologic treatment. Sensation may be improved or restored, and painful pares thesias relieved, by timely, well-performed microsurgery.

Humans↗
PubMed1996

Trigeminal nerve injury and repair.

Injuries to the inferior alveolar nerve (IAN) and the lingual nerve are relatively uncommon. However, there are certain routine surgical and non-surgical procedures that have the potential, albeit small, for injuring these neural structures. A review of the diagnosis, classification and management of these injuries is presented.

Humans↗
PubMed2006

Changes in sodium channel expression following trigeminal nerve injury.

We have investigated the expression of TTX-sensitive (TTXs) and TTX-resistant (TTXr) sodium channel subtypes following injury to the inferior alveolar nerve (IAN), in order to determine their potential role in the development of trigeminal neuropathic pain. In seven anaesthetised ferrets, fluorogold (2%) was injected into the left IAN to identify cell bodies with axons in this nerve. In four animals, the nerve was sectioned distal to the injection site and the remaining three served as controls. After 3 days, the animals were perfused with 4% paraformaldehyde. The left and right IANs and trigeminal ganglia were processed using indirect immunofluorescence with specific primary antibodies to TTXs subtypes Na(v)1.3 and Na(v)1.7 and TTXr subtypes Na(v)1.8 and Na(v)1.9. Image analysis was used to quantify the percentage area of staining (PAS) in the nerves. In the ganglia, counts were made of positively labelled cells in the fluorogold population. PAS for Na(v)1.8 and Na(v)1.9 was significantly greater in injured nerves than in either contralateral or control nerves. After injury, significantly fewer cells in the ganglia expressed Na(v)1.3 (controls 36.9%; injured 13.1%), Na(v)1.7 (controls 17.0%; injured 8.1%) and Na(v)1.9 (controls 60.3%; injured 29.0%) (p<0.05, unpaired t test). These changes are different from those previously reported in the dorsal root ganglion following damage to peripheral nerves of spinal origin. As they occur at a time of known high abnormal neural discharge, it seems likely that changes in sodium channel expression may play a role in nerve injury-induced trigeminal pain.

Animals↗
PubMedDate not supplied

Trigeminal nerve injuries after mandibular implant placement--practical knowledge for clinicians.

Endosseous mandibular implant placement can result in injuries to the peripheral branches of the trigeminal nerve even with the most careful preoperative planning and intraoperative technique. In the past, many patients have been discouraged from seeking repair for such injuries because of the unreliability of the techniques for correcting the injury. It is now possible to perform microneurosurgical repair of such injuries. If the repair is done in a timely fashion, sensation can be improved or restored and painful nerve dysesthesia can be relieved. This article reviews the different types of nerve injuries, their symptoms and diagnosis, and provides information for clinicians to manage their implant patients with neurosensory disturbance.

Dental Implantation, Endosseous↗
PubMedDate not supplied

Peripheral trigeminal nerve injuries.

Certain dental procedures being performed routinely can result in nerve damage. The following is a review of some of these surgical procedures coupled with a discussion of ways to avoid, diagnose and manage the nerve injuries associated with them.

Humans↗
PubMed1996

Experimental trigeminal nerve injury.

The successful reinnervation of peripheral targets after injury varies with the axonal population of the nerve that is injured and the extent of the dislocation of its central component from the peripheral endoneurial tube. Larger-diameter axons such as those supplying mechanoreceptors recover more readily than narrower axons such as those supplying taste. A complex, bi-directional interaction between lingual epithelium and sprouting nerve results in the redifferentiation of taste buds after denervation. Dentin and the dental pulp provide a strong attraction to sprouting nerves and will become reinnervated from collateral sources if recovery of the original innervation is blocked. The most effective repair technique for transected lingual nerves is one which brings the cut ends together rather than one that provides a temporary bridge. Injuries can result in cell death in the trigeminal ganglion but only if the injury is severe and recovery is prevented. Lesser damage results in chromatolysis and the increased expression of neuropeptides. All nerve injuries bring about changes in the trigeminal nucleus. These occur as changes in receptive field and the incidence of spontaneously active neurons, effects which are consistent with the unmasking of existing afferents. These functional changes are short-lived and reversible. Morphologically, nerve injury results in terminal degeneration in the nuclei and an increased expression of the c-Fos gene and some neuropeptides. Only a chronic constriction injury induces behavioral changes. The adult trigeminal system retains considerable plasticity that permits it to respond successfully to nerve injury. Much remains to be learned about this response, particularly of the trophic factors that control peripheral recovery and the central response to more severe injuries.

Adult↗
PubMed2001

Interleukin-6 and nerve growth factor levels in peripheral nerve and brainstem after trigeminal nerve injury in the rat.

Earlier studies have demonstrated that inflammation plays a role in the development of evoked pain following partial nerve injury. In this report, we demonstrate bilateral changes in interleukin-6 (IL-6) and nerve growth factor (nerve growth factor) levels following unilateral infraorbital nerve (infraorbital nerve) constriction. infraorbital nerve constriction resulted in an initial period of decreased mechanical sensitivity (1 and 3 days), followed by recovery (7 days) and then a marked bilateral mechanical hypersensitivity (10 and 28 days). nerve growth factor levels in the injured infraorbital nerve were elevated on all days, but peak concentrations of nerve growth factor were observed on day 3. A smaller increase was also observed on days 1, 3, and 7 in the uninjured nerve. A bilateral elevation of IL-6 was also seen on days 3 and 10 in the infraorbital nerve, and in the brainstem on days 3, 7 and 10 after constriction. No changes in mechanical sensitivity were found after a sham-injury, but there was a small increase in brainstem IL-6 ipsilaterally at 7 days. We conclude from these data that increases in IL-6 and nerve growth factor may contribute to the development of mechanical allodynia after trigeminal nerve injury, but they are not specifically correlated with the onset or duration of pain behaviors.

Analysis of Variance↗
PubMed2002

[Repair and revision 9. Peripheral trigeminal nerve injury].

A review is given about long-term incidence of sensory disturbance in the areas of innervation of the n. trigeminus for different types of trauma and/or treatment. Diagnosis, clinical course and possible types of treatment are in addition reviewed. Regarding diagnosis, the outcome of a test on sensory function is not always related to the degree of nerve damage because methods differ in the type of afferent nerve fibers of which function is tested, and some specificity might occur in nerve damage, i.e. either thick or thin afferent fibers might be predominantly affected at a particular time. An initial quick testing of sensory function is recommended. This testing includes examining two sensory modalities, which are related to functioning of thick and thin afferent fibers respectively and which have a dichotomous yes/no outcome on the incidence of a pronounced sensory disturbance.

Humans↗