Trigeminal Injury Research Articles

Editorial: Microvascular decompression for trigeminal neuralgia

The contribution of Sekula et al.1 highlights several aspects of the surgical treatment of trigeminal neuralgia (TN) that are worthy of consideration and discussion. Their paper continues a previous theme of microvascular decompression (MVD) in the elderly.2 Their thesis is strengthened by a prospective design and a more discrete, standardized classification of the facial pain syndromes and postoperative outcomes. Several limitations of the study are apparent. Their prospective series is small and the follow-up is short, although the authors concede both of these points. Further, the literature review is not independent of their current prospective series given that the authors included their recent results in the meta-analysis. Nevertheless, the evidence from their unique prospective series could be classified as Class II, which further strengthens the literature on this subject. The authors do make a good point in their suggestion that the risks of trigeminal destructive procedures in the elderly have tended to be underemphasized. The risks of facial neuropathic pain from radiofrequency lesioning, glycerol injection, balloon compression, and radiosurgery are substantial and probably increase with advancing age. With repeated destructive procedures, the burden of trigeminal neuropathy is also probably cumulative. The risks of MVD are certainly serious but uncommon, while the potential adverse consequences of a destructive procedure cannot be underestimated. Specifically, although the incidence of cerebellar hemorrhage or stroke from MVD appears to be quite small, the risks of trigeminal deafferentation pain from destructive procedures are in the neighborhood of 15%. An elderly patient who suffers a complication of intentional trigeminal injury, such as facial dysesthesias or, worse, full-blown anesthesia dolorosa, is not at all happy with the outcome or the surgeon. The authors’ conclusions will stir some controversy, but they derive from an increasing evidence base. Thoughtful patient selection is clearly a hallmark of any surgical practice. However, the results of this series and the systematic review suggest that in contrast to previous assumptions, elderly patients with TN can undergo MVD as safely and effectively as a younger cohort.

Use of Decellularized Nerve Allograft for Inferior Alveolar Nerve Reconstruction: A Case Report

Injury to the inferior alveolar nerve (IAN) has been reported to occur in 0.4% to 22% of patients undergoing routine removal of third molars. 1 Zuniga J.R. LeBanc J.P. Advances in microsurgical nerve repair. J Oral Maxillofac Surg. 1993; 51: 62 Abstract Full Text PDF PubMed Scopus (31) Google Scholar Within this group, 25% of patients might not have recovered within 1 year of the nerve injury, and up to 0.9% of patients might have permanent injury. 2 Ziccardi V.B. Assael L.A. Mechanisms of trigeminal nerve injuries. Atlas Oral Maxillofac Surg Clin North Am. 2001; 9: 1 PubMed Google Scholar Other than the removal of impacted teeth, osteotomies and dental implants are the most common procedures associated with IAN injury. Sacrifice of the IAN can also complicate tumor resections, resulting in anatomic continuity defects of the IAN. Injury to the IAN can cause significant patient morbidity such as bite wounds and burn injuries of the lower lip. Therefore, any treatment that provides functional recovery after IAN injury is of potential value to the patient. In rare and specific situations, procedures such as IAN lateralization or transposition can be performed to avoid nerve injuries.

Differential activation of mitogen-activated protein kinases and glial cells in the trigeminal sensory nuclear complex following lingual nerve injury

Mitogen-activated protein kinases (MAPKs) play a pivotal role in the mediation of cellular responses to a variety of signaling molecules. The current study demonstrates phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in each subdivision of the trigeminal sensory nuclear complex (TSNC) following lingual nerve injury. Immunohistochemical labeling for phosphorylated ERK (p-ERK) or phosphorylated p38 (p-p38) MAPK was performed in histological sections of the brainstem. A transient increase in the immunoreactivity for p-ERK was found in each subdivision of the TSNC followed by a prolonged increase in the immunoreactivity for p-p38 MAPK after nerve injury. Double immunofluorescence labeling with cell-specific markers revealed that ERK and p38 MAPK were phosphorylated predominantly by OX-42-positive microglia or GFAP-positive astrocytes. Increased immunofluorescence labeling for OX-42 and GFAP indicated that microglia and astrocytes were activated by nerve injury in the TSNC. Activation of MAPKs and glial cells in the rostral subdivisions of the TSNC was comparable with that in the subnucleus caudalis of the trigeminal spinal tract nucleus (Vc). We conclude that differential activation of MAPKs and glial cells in the rostral subdivisions of the TSNC as well as the Vc may have a substantial role in the pathogenesis of neuropathic pain following trigeminal nerve injury.

Summary of: Trigeminal nerve injuries in relation to the local anaesthesia in mandibular injections

This study reports the signs and symptoms that are the features of trigeminal nerve injuries caused by local anaesthesia (LA). Thirty-three patients with nerve injury following LA were assessed. All data were analysed using the SPSS statistical programme and Microsoft Excel. Lingual nerve injury (LNI; n = 16) and inferior alveolar nerve injury (IANI; n = 17) patients were studied. LNI were more likely to be permanent. Neuropathy was demonstrable in all patients with varying degrees of paraesthesia, dysaesthesia (in the form of burning pain) allodynia and hyperalgesia. All injuries were unilateral. A significantly greater proportion of LNI patients (75%) had received multiple injections, in comparison to IANI patients (41%) (p <0.05). Fifty percent of patients with LNI reported pain on injection. The presenting signs and symptoms of both LNI and IANI included pain. These symptoms of neuropathy were constant in 88% of the IANI group and in 44% of LNI patients. Functional difficulties were different between the LNI and IANI groups, a key difference being the presence of severely altered taste perception in nine patients with LA-induced LNI. Chronic pain is often a symptom after local anaesthetic-induced nerve injury. Patients in the study population with lingual nerve injury were significantly more likely to have received multiple injections compared to those with IANI.

Trigeminal nerve injuries in relation to the local anaesthesia in mandibular injections

This study reports the signs and symptoms that are the features of trigeminal nerve injuries caused by local anaesthesia (LA). Thirty-three patients with nerve injury following LA were assessed. All data were analysed using the SPSS statistical programme and Microsoft Excel. Lingual nerve injury (LNI; n = 16) and inferior alveolar nerve injury (IANI; n = 17) patients were studied. LNI were more likely to be permanent. Neuropathy was demonstrable in all patients with varying degrees of paraesthesia, dysaesthesia (in the form of burning pain) allodynia and hyperalgesia. All injuries were unilateral. A significantly greater proportion of LNI patients (75%) had received multiple injections, in comparison to IANI patients (41%) (p <0.05). Fifty percent of patients with LNI reported pain on injection. The presenting signs and symptoms of both LNI and IANI included pain. These symptoms of neuropathy were constant in 88% of the IANI group and in 44% of LNI patients. Functional difficulties were different between the LNI and IANI groups, a key difference being the presence of severely altered taste perception in nine patients with LA-induced LNI. Chronic pain is often a symptom after local anaesthetic-induced nerve injury. Patients in the study population with lingual nerve injury were significantly more likely to have received multiple injections compared to those with IANI.

Characteristics of patients referred to a UK trigeminal nerve injury service

AbstractAim: Patients suffering from a persistent sensory disturbance or pain following a trigeminal nerve injury are frequently referred to a specialist centre for evaluation. This study reports the characteristics of the patients seen on a designated nerve injury clinic during 2008.Methods: Information from 100 consecutive patients was collated, including demographic details, source of referral, nerve damaged, cause of the injury, presence or absence of dysaesthesia and nature of the treatment, if offered.Results: There were 70 females and 30 males, with a mean age at presentation of 42 years (range 21–78 years). Sixty‐five per cent of referrals were from a consultant, and patients travelled from a wide geographical distribution across England, Wales and Ireland. The delay between nerve injury and referral ranged from 1 month to 5 years. Fifty‐six per cent of the patients had sustained an inferior alveolar nerve (IAN) injury and 44% had a lingual nerve injury. Most injuries (59%) were caused by lower third molar removal, but there were numerous other causes, including 10% associated with local anaesthetic administration. A similar proportion of patients reported symptoms of dysaesthesia after lingual nerve (41%) and IAN (45%) injuries. Only 41% of patients were treated (52% of lingual nerve injuries and 32% of IAN injuries), and this usually involved microsurgical repair (lingual nerve injuries) or decompression and neurolysis (IAN injuries).Conclusions: The highly selected population of patients that received tertiary referral to a specialist nerve injury clinic were most commonly female and 30–50 years old. A substantial proportion had dysaesthesia, and these patients were most likely to be offered treatment.

Microsurgical Repair of the Peripheral Trigeminal Nerve After Mandibular Sagittal Split Ramus Osteotomy

Injuries to the inferior alveolar nerve (IAN) and lingual nerves (LNs) have long been known complications of the mandibular sagittal split ramus osteotomy (SSRO). Most postoperative paresthesias resolve without treatment. However, microsurgical exploration of the nerve may be indicated in cases of significant persistent sensory dysfunction associated with observed or suspected localized IAN or LN injury. We report the demographics and outcome of microsurgical exploration and repair of peripheral branches of the trigeminal nerve injured because of the SSRO. A retrospective chart review was completed on all patients who had microsurgical repair of peripheral trigeminal nerve injuries caused by mandibular SSRO and were operated on by the senior author (R.A.M.) between March 1986 and December 2005. A physical examination, including standardized neurosensory testing (NST) as described by Zuniga et al, was completed on each patient preoperatively. All patients were followed periodically after surgery for at least 1 year with NST repeated at each visit. NST results obtained at the last patient visit were used to determine the final level of recovery of sensory function. Sensory recovery was evaluated using guidelines established by the Medical Research Council scale. The following data were collected and analyzed: age of patient, gender, nerve injured, chief sensory complaint (numbness, pain, or both), duration (months) from injury to surgical intervention, intraoperative findings, surgical procedure, and neurosensory status at final evaluation. Given the retrospective nature of this study, the research was exempt from our institutional review board ethics committee. There were 54 (n = 54) patients (8 males and 46 females) with an average age of 36.9 years (range, 16 to 55 years) and a follow-up of at least 12 months. The most commonly injured/repaired nerve was the IAN (n = 39), followed by the LN (n = 14), and the long buccal nerve (n = 1). In 31 patients (57.4%), the chief sensory complaint was numbness, while 20 patients (37%) complained of pain and numbness, and 3 patients (5.5%) complained of pain without mention of numbness. The average time from nerve injury to repair was 9.4 months (range, 3 to 50 months). The most common intraoperative finding was a discontinuity defect (n = 18, 33.3%), followed by partial nerve severance (n = 15, 27.8%), neuroma-in-continuity (n = 11, 20.3%), and compression injury (n = 10, 18.5%). The most frequent surgical procedure was autogenous nerve graft reconstruction of the IAN using the sural or great auricular nerve (n = 22, 40.7%), followed by excision of a neuroma with or without neurorrhaphy (n = 13, 24.1%). All the LN injuries (n = 14) were partial or complete severances, of which 2 were reconstructed with autogenous nerve grafts and the other 12 underwent neurorrhaphy. The long buccal nerve injury required excision of a proximal stump neuroma without neurorrhaphy. After a minimum of 1-year follow-up, NST showed that 8 nerves (14.8%) showed no sign of recovery; 19 nerves (35.2%) had regained "useful sensory function," and 27 nerves (50%) showed full recovery as described by the Medical Research Council scale. Microsurgical repair of the IAN or LN injured during the SSRO can be considered in patients with persistent, unacceptable sensory dysfunction in the distribution of the involved nerve. Modifications of surgical technique may be helpful in reducing the incidence of such injuries. Based on our experience, an algorithm for evaluation and treatment is presented.

Radiosurgery for large-volume (&gt; 10 cm3) benign meningiomas

Stereotactic radiosurgery (SRS) has proven to be a safe and effective treatment for many patients with intracranial meningiomas. Nevertheless, the morbidity associated with radiosurgery of larger meningiomas is poorly understood. The authors performed a retrospective review of 116 patients who underwent SRS for meningiomas (WHO Grade I) > 10 cm3 between 1990 and 2007, with a minimum follow-up of 12 months. Patients with atypical or malignant meningiomas and those who received prior radiotherapy were excluded. The average tumor volume was 17.5 cm3 (range 10.1-48.6 cm3); the average tumor margin dose was 15.1 Gy (range 12-18 Gy); and the mean follow-up duration was 70.1 months (range 12-199 months). Tumor control was 99% at 3 years and 92% at 7 years after radiosurgery. Thirty complications after radiosurgery were noted in 27 patients (23%), including 7 cases of seizures, 6 cases of hemiparesis, 5 cases of trigeminal injury, 4 cases of headaches, 3 cases of diplopia, 2 cases each of cerebral infarction and ataxia, and 1 case of hearing loss. Patients with supratentorial tumors experienced a higher complication rate compared with patients with skull base tumors (44% compared with 18%) (hazard ratio 2.9, 95% CI 1.3-6.7, p = 0.01). The morbidity associated with SRS for patients with benign meningiomas > 10 cm(3) is greater for supratentorial tumors compared with skull base tumors. Whereas radiosurgery is relatively safe for patients with large-volume skull base meningiomas, resection should remain the primary disease management for the majority of patients with large-volume supratentorial meningiomas.

Use of Botulinum Toxin Type A Injection for Neuropathic Pain after Trigeminal Nerve Injury

To present a case that neuropathic pain following traumatic injury of the inferior alveolar nerve, which was relieved by the injection of BTX-A. Case report. Tertiary care University hospital. A 62-year-old female was referred by her general dentist to our clinic due to numbness and pain over the left side of her lower lip and chin region. Botulinum toxin type A injected into the middle of chin area subcutaneously. At 1 month after BTX-A injection, the affected area had decreased in size. And at 2 months, the patient reported a slight decreased in pain, and CPT differences being sustained at a reduced level. This case report suggests an effective new modality for treating neuropathic pain after trigeminal nerve injury. A further randomized controlled study involving a large number of patients is needed.

Pain Remapping in Migraine: A Novel Characteristic Following Trigeminal Nerve Injury

The location of pain during the headache phase of migraine varies between individuals as well as between attacks in some individuals. We have observed a "remapping" or a change in the location of migraine pain following injury to the trigeminal system that is a novel characteristic to migraine and has not been described in other trigeminal pain syndromes of the head, neck, and face. Recognition of this clinical feature implies that the pathophysiology of migraine is impressionable and may be why diagnosis and treatment are often delayed.

Trigeminal injury causes kappa opioid-dependent allodynic, glial and immune cell responses in mice

Trigeminal injury causes kappa opioid-dependent allodynic, glial and immune cell responses in mice

Painful Neuron-Microglia Interactions in the Trigeminal Sensory System

The trigeminal sensory system is unique in its innervation of structures specific to the orofacial area. Nocicep- tive trigeminal afferents are known to synapse with second-order neurons in the trigeminal subnucleus caudalis (Sp5C) in the brain stem. The activity of neurons within the Sp5C is responsible for the relay of nociceptive signals to higher brain centers. Recent evidence suggests that central sensitization may be fundamental to many trigeminal-specific painful neu- ropathies, including trigeminal neuralgia and migraine. Glia within the Sp5C are emerging as prime suspects in trigeminal central sensitization. In particular, microglial activation has been implicated in the development of neuropathic pain. It is possible that activated microglia release factors that alter the activity of second-order neurons or the synaptic activity of peripheral terminals within the Sp5C. Microglial activation has been characterized by changes in morphology, expression of membrane receptors and ion chan- nels, as well as alterations to cytokine and chemokine release. In addition, microglia have been studied in brain slice and dissociated culture where activation is characterized by changes to P2X receptor and potassium channel membrane cur- rents. However, little is known about resting and activated microglial membrane properties in the Sp5C and, furthermore, how these properties are affected following trigeminal nerve injury. This review summarizes the anatomical and patho- physiological importance of the Sp5C and focuses on recent studies on neurons and microglia in the trigeminal sensory system. The final part of the review aims to link important aspects of microglial membrane physiology with their potential role in chronic trigeminal pain conditions.

Trigeminal injury causes kappa opioid-dependent allodynic, glial and immune cell responses in mice.

BackgroundThe dynorphin-kappa opioid receptor (KOR) system regulates glial proliferation after sciatic nerve injury. Here, we investigated its role in cell proliferation following partial ligation of infraorbital nerve (pIONL), a model for trigeminal neuropathic pain. Mechanical allodynia was enhanced in KOR gene deleted mice (KOR-/-) compared to wild type mice. Using bromodeoxyuridine (BrdU) as a mitotic marker, we assessed cell proliferation in three different areas of the trigeminal afferent pathway: trigeminal nucleus principalis (Vp), trigeminal root entry zone (TREZ), and trigeminal ganglion (TG).ResultsIn KOR-/- mice or norBNI-treated mice, the number of proliferating cells in the Vp was significantly less than in WT mice, whereas cell proliferation was enhanced in TREZ and TG. The majority of the proliferating cells were nestin positive stem cells or CD11b positive microglia in the Vp and macrophages in the TG. GFAP-positive astrocytes made a clear borderline between the CNS and the PNS in TREZ, and phosphorylated KOR staining (KOR-p) was detectable only in the astrocytes in CNS in WT mice but not in KOR-/- or norBNI-treated mice.ConclusionsThese results show that kappa opioid receptor system has different effects after pIONL in CNS and PNS: KOR activation promotes CNS astrocytosis and microglial or stem cell proliferation but inhibits macrophage proliferation in PNS. The trigeminal central root has a key role in the etiology and treatment of trigeminal neuralgia, and these newly identified responses may provide new targets for developing pain therapies.

Distinctive response of CNS glial cells in oro-facial pain associated with injury, infection and inflammation.

Oro-facial pain following injury and infection is frequently observed in dental clinics. While neuropathic pain evoked by injury associated with nerve lesion has an involvement of glia/immune cells, inflammatory hyperalgesia has an exaggerated sensitization mediated by local and circulating immune mediators. To better understand the contribution of central nervous system (CNS) glial cells in these different pathological conditions, in this study we sought to characterize functional phenotypes of glial cells in response to trigeminal nerve injury (loose ligation of the mental branch), infection (subcutaneous injection of lipopolysaccharide-LPS) and to sterile inflammation (subcutaneous injection of complete Freund's adjuvant-CFA) on the lower lip. Each of the three insults triggered a specific pattern of mechanical allodynia. In parallel with changes in sensory response, CNS glial cells reacted distinctively to the challenges. Following ligation of the mental nerve, both microglia and astrocytes in the trigeminal nuclear complex were highly activated, more prominent in the principal sensory nucleus (Pr5) and subnucleus caudalis (Sp5C) area. Microglial response was initiated early (days 3-14), followed by delayed astrocytes activation (days 7-28). Although the temporal profile of microglial and astrocyte reaction corresponded respectively to the initiation and chronic stage of neuropathic pain, these activated glial cells exhibited a low profile of cytokine expression. Local injection of LPS in the lower lip skin also triggered a microglial reaction in the brain, which started in the circumventricular organs (CVOs) at 5 hours post-injection and diffused progressively into the brain parenchyma at 48 hours. This LPS-induced microglial reaction was accompanied by a robust induction of IκB-α mRNA and pro-inflammatory cytokines within the CVOs. However, LPS induced microglial activation did not specifically occur along the pain signaling pathway. In contrast, CFA injection led to minor microglial morphological changes and an induction of IκB-α mRNA in the CVO regions; a significant increase in IL-1β and IL-6 mRNA started only at 48 hours post-injection, when the induced pain-related behavior started to resolve. Our detailed analysis of CNS glial response clearly revealed that both nerve injury and oro-facial infection/inflammation induced CNS glial activation, but in a completely different pattern, which suggests a remarkable plasticity of glial cells in response to dynamic changes in their microenvironment and different potential involvement of this non-neuronal cell population in pathological pain development.

VARIANT INTRANEURAL VEIN-TRIGEMINAL NERVE RELATIONSHIPS

Trigeminal neuralgia is often caused by compression, demyelination, and injury of the trigeminal nerve root entry zone by an adjacent artery and/or vein. Previously described variations of the nerve-vessel relationship note external nerve compression. We offer a detailed classification of intraneural vessels that travel through the trigeminal nerve and safe, effective surgical management. We report 3 microvascular decompression operations for medically refractory trigeminal neuralgia during which the surgeon encountered a vein crossing through the trigeminal nerve. Two types of intraneural veins are described: type 1, in which the vein travels between the motor and sensory branches of the trigeminal nerve (1 patient), and type 2, in which the vein bisects the sensory branch (portio major) (2 patients). We recommend sacrificing the intraneural vein between the motor and sensory branches if the vein is small (most likely type 1). If the intraneural vein is large and bisects the sensory branch (most likely type 2), vein mobilization can be achieved, but often requires extensive dissection through the nerve. Because this maneuver may lead to trigeminal nerve injury and result in uncomfortable neuropathy and numbness (including corneal hypoesthesia), we recommend against mobilization of the vein through the nerve, suggesting instead, consideration of a selective trigeminal nerve rhizotomy. Because aggressive dissection of intraneural vessels can lead to higher than normal complication rates, preoperative knowledge of vein-trigeminal nerve variants is crucial for intraoperative success.

Astroglia in Medullary Dorsal Horn (Trigeminal Spinal Subnucleus Caudalis) Are Involved in Trigeminal Neuropathic Pain Mechanisms

The aim of this study was to investigate whether astroglia in the medullary dorsal horn (trigeminal spinal subnucleus caudalis; Vc) may be involved in orofacial neuropathic pain following trigeminal nerve injury. The effects of intrathecal administration of the astroglial aconitase inhibitor sodium fluoroacetate (FA) were tested on Vc astroglial hyperactivity [as revealed by glial fibrillary acid protein (GFAP) labeling], nocifensive behavior, Vc extracellular signal-regulated kinase phosphorylation (pERK), and Vc neuronal activity in inferior alveolar nerve-transected (IANX) rats. Compared with sham-control rats, a significant increase occurred in GFAP-positive cells in ipsilateral Vc at postoperative day 7 in IANX rats, which was prevented following FA administration. FA significantly increased the reduced head withdrawal latency to high-intensity heat stimulation of the maxillary whisker pad skin in IANX rats, although it did not significantly affect the reduced escape threshold to low-intensity mechanical stimulation of the whisker skin in IANX rats. FA also significantly reduced the increased number of pERK-like immunoreactive cells in Vc and the enhanced Vc nociceptive neuronal responses following high-intensity skin stimulation that were documented in IANX rats, and glutamine administration restored the enhanced responses. These various findings provide the first documentation that astroglia is involved in the enhanced nociceptive responses of functionally identified Vc nociceptive neurons and in the associated orofacial hyperalgesia following trigeminal nerve injury.

Microsurgical Repair of Peripheral Trigeminal Nerve Injuries From Maxillofacial Trauma

Microsurgical Repair of Peripheral Trigeminal Nerve Injuries From Maxillofacial Trauma

S121: Microsurgical Repair of Trigeminal Nerve Injuries

Sensory disturbances to the peripheral branches of the trigeminal nerve can be a debilitating disruption to patients leading to problems with speech, mastication, food and liquid incompetence and difficulty with activities of daily living. These injuries may arise from a number of causes in oral and maxillofacial surgery. The most common cause of trigeminal nerve injury results from the removal of impacted third molars. There are a variety of other causes including orthognathic surgery, endodontic surgery, implant placement, fractures, preprosthetic surgery and treatment of maxillofacial pathology.

Microsurgical Repair of Peripheral Trigeminal Nerve Injuries From Maxillofacial Trauma

Injuries to the peripheral branches of the trigeminal nerve from maxillofacial trauma can have distressing sensory or functional sequelae. The present study reports the results of trigeminal microneurosurgical repair in a series of patients with maxillofacial trauma. A retrospective chart review was completed of all patients who had undergone microneurosurgical repair of peripheral trigeminal nerve injuries caused by maxillofacial trauma and who had been treated by one of us (R.A.M.) from March 1986 through December 2005. A physical examination, including standardized neurosensory testing, was completed on each patient preoperatively. All patients were followed up periodically after surgery for at least 1 year with neurosensory testing repeated at each visit. Sensory recovery was evaluated using the guidelines established by the Medical Research Council. The following data were collected and analyzed: patient age, gender, nerve injured, etiology (location of fracture), chief sensory complaint (ie, numbness or pain, or both), interval from injury to surgical intervention, intraoperative findings, surgical procedure, and neurosensory status at the final evaluation. A total of 42 patients (25 males and 17 females) with average age of 37.1 years (range 11 to 61) and a follow-up of at least 12 months were included in the study. The most commonly injured/repaired nerve was the inferior alveolar nerve caused by mandibular angle fracture (n = 21), followed by the mental nerve due to mandibular parasymphysis fracture (n = 12), the infraorbital nerve from zygomaticomaxillary complex fracture (n = 7), and lingual nerve and long buccal nerve from mandibular body fracture (n = 1 each). In 17 patients, the chief sensory complaint was numbness, and 25 patients complained of pain with or without mention of numbness. The average interval from nerve injury to repair was 12.5 months (range 2 to 24). The most common intraoperative finding was a compression injury (n = 19), followed by partial nerve severance (n = 9). The most frequent surgical procedure was external decompression/internal neurolysis (n = 20). Ten injured nerves required reconstruction of a discontinuity defect with an autogenous nerve graft (donor sural or great auricular nerve), all of which were associated with mandibular angle or parasymphysis fractures. After a minimum of 1 year of follow-up, neurosensory testing demonstrated that 6 nerves (14%) showed no sign of recovery, 23 nerves (55%) had regained "useful sensory function," and 13 nerves (31%) showed full recovery as described by the Medical Research Council scale. Microsurgical repair of peripheral branches of the trigeminal nerve injured by maxillofacial trauma produced significant improvement or complete recovery in 36 (86%) of 42 patients. These results compare favorably with the microsurgical repair of peripheral trigeminal nerve injuries resulting from other causes.

Insular cortex representation of dynamic mechanical allodynia in trigeminal neuropathic rats

Dynamic mechanical allodynia is a widespread symptom of neuropathic pain for which mechanisms are still poorly understood. The present study investigated the organization of dynamic mechanical allodynia processing in the rat insular cortex after chronic constriction injury to the infraorbital nerve (IoN-CCI). Two weeks after unilateral IoN-CCI, rats showed a dramatic bilateral trigeminal dynamic mechanical allodynia. Light, moving stroking of the infraorbital skin resulted in strong, bilateral upregulation of extracellular-signal regulated kinase phosphorylation (pERK-1/2) in the insular cortex of IoN-CCI animals but not sham rats, in whose levels were similar to those of unstimulated IoN-CCI rats. pERK-1/2 was located in neuronal cells only. Stimulus-evoked pERK-1/2 immunopositive cell bodies displayed rostrocaudal gradient and layer selective distribution in the insula, being predominant in the rostral insula and in layers II–III of the dysgranular and to a lesser extent, of the agranular insular cortex. In layers II–III of the rostral dysgranular insular cortex, intense pERK also extended into distal dendrites, up to layer I. These results demonstrate that trigeminal nerve injury induces a significant alteration in the insular cortex processing of tactile stimuli and suggest that ERK phosphorylation contributes to the mechanisms underlying abnormal pain perception under this condition.