Novel Hexb-based tools for studying microglia in the CNS.

Microglia and central nervous system (CNS)-associated macrophages (CAMs), such as perivascular and meningeal macrophages, are implicated in virtually all diseases of the CNS. However, little is known about their cell-type-specific roles in the absence of suitable tools that would allow for functional discrimination between the ontogenetically closely related microglia and CAMs. To develop a new microglia gene targeting model, we first applied massively parallel single-cell analyses to compare microglia and CAM signatures during homeostasis and disease and identified hexosaminidase subunit beta (Hexb) as a stably expressed microglia core gene, whereas other microglia core genes were substantially downregulated during pathologies. Next, we generated HexbtdTomato mice to stably monitor microglia behavior in vivo. Finally, the Hexb locus was employed for tamoxifen-inducible Cre-mediated gene manipulation in microglia and for fate mapping of microglia but not CAMs. In sum, we provide valuable new genetic tools to specifically study microglia functions in the CNS.

GFP-labeled Schwann cell-like cells derived from hair follicle epidermal neural crest stem cells promote the acellular nerve allografts to repair facial nerve defects in rats.

BACKGROUND: Acellular nerve allografts (ANAs) have been successfully applied to bridge facial nerve defects, and transplantation of stem cells may enhance the regenerative results. Up to now, application of hair follicle epidermal neural crest stem cell-derived Schwann cell-like cells (EPI-NCSC-SCLCs) combined with ANAs for bridging facial nerve defects has not been reported. METHODS: The effect of ANAs laden with green fluorescent protein (GFP)-labeled EPI-NCSC-SCLCs (ANA + cells) on bridging rat facial nerve trunk defects (5-mm-long) was detected by functional and morphological examination, as compared with autografts and ANAs, respectively. RESULTS: (1) EPI-NCSC-SCLCs had good compatibility with ANAs in vitro. (2) In the ANA + cells group, the GFP signals were observed by in vivo imaging system for small animals within 8 weeks, and GFP-labeled EPI-NCSC-SCLCs were detected in the tissue slices at 16 weeks postoperatively. (3) The facial symmetry at rest after surgery in the ANA + cells group was better than that in the ANA group (p < 0.05), and similar to that in the autograft group (p > 0.05). The initial recovery time of vibrissal and eyelid movement in the ANA group was 2 weeks later than that in the other two groups. (4) The myelinated fibers, myelin sheath thickness and diameter of the axons of the buccal branches in the ANA group were significantly worse than those in the other two groups (P < 0.05), and the results in the ANA + cells group were similar to those in the autograft group (p > 0.05). CONCLUSIONS: EPI-NCSC-SCLCs could promote functional and morphological recovery of rat facial nerve defects, and GFP labeling could track the transplanted EPI-NCSC-SCLCs in vivo for a certain period of time. These may provide a novel choice for clinical treatment of peripheral nerve defects.

Motoneuron-Specific PTEN Deletion in Mice Induces Neuronal Hypertrophy and Also Regeneration after Facial Nerve Injury.

In postmitotic neurons, several tumor suppressor genes (TSGs), including p53, Rb, and PTEN, modulate the axon regeneration success after injury. Particularly, PTEN inhibition is a key driver of successful CNS axon regeneration after optic nerve or spinal cord injury. In contrast, in peripheral neurons, TSG influence in neuronal morphology, physiology, and pathology has not been investigated to the same depth. In this study, we conditionally deleted PTEN from mouse facial motoneurons (Chat-Cre/PtenloxP/loxP ) and analyzed neuronal responses in vivo with or without peripheral facial nerve injury in male and female mice. In uninjured motoneurons, PTEN loss induced somatic, axonal, and nerve hypertrophy, synaptic terminal enlargement and reduction in physiological whisker movement. Despite these morphologic and physiological changes, PTEN deletion positively regulated facial nerve regeneration and recovery of whisker movement after nerve injury. Regenerating PTEN-deficient motoneurons upregulated P-CREB and a signaling pathway involving P-Akt, P-PRAS40, P-mTOR, and P-4EBP1. In aged mice (12 months), PTEN deletion induced hair loss and facial hyperplasia of the epidermis. This suggests a time window in younger mice with PTEN loss stimulating axon growth after injury, however, at the risk of hyperplasia formation at later time points in the old animal. Overall, our data highlight a dual TSG function with PTEN loss impairing physiological neuron function but furthermore underscoring the positive effects of PTEN ablation in axon regeneration also for the PNS.SIGNIFICANCE STATEMENT Tumor suppressor genes (TSGs) restrict cell proliferation and growth. TSG inhibition, including p53 and PTEN, stimulates axon regeneration after CNS injury. In contrast, in PNS axon regeneration, TSGs have not been analyzed in great depth. Herein we show enhanced peripheral axon regeneration after PTEN deletion from facial motoneurons. This invokes a signaling cascade with novel PTEN partners, including CREB and PRAS40. In adult mice, PTEN loss induces hyperplasia of the skin epidermis, suggesting detrimental consequences when reaching adulthood in contrast to a beneficial TSG role for regeneration in young adult mice. Thus, our data highlight the double-edged sword nature of interfering with TSG function.

The SELENOT mimetic PSELT promotes nerve regeneration by increasing axonal myelination in a facial nerve injury model in female rats.

Peripheral nerve injury (PNI) is frequent and many patients suffer lifelong disabilities in severe cases. Although the peripheral nervous system is able to regenerate, its potential is limited. In this study, we tested in a nerve regeneration model in rat the potential beneficial effect of a short mimetic peptide, named PSELT, which derives from SELENOT, an essential thioredoxin-like selenoprotein endowed with neuroprotective and antioxidant activities. For this purpose, the right facial nerve of female Long-Evans rats was axotomized then bridged with a free femoral vein interposition graft. PSELT (1 µM) was injected into the vein immediately and 48 h after the injury, and the effects observed were compared to those found after an end-to-end suture used as a gold standard treatment. Whisking behavior, electrophysiological potential, and histological analyses were performed 3 months after injury to determine the effects of these treatments. These analyses revealed that PSELT-treated animals exhibit a better motor recovery in terms of protraction amplitude and velocity of vibrissae compared to control and end-sutured nerve animal groups. Moreover, administration of PSELT following injury enhanced muscle innervation, axonal elongation, and myelination of newly formed nerve fibers. Altogether, these results indicate that a PSELT-based treatment is sufficient to enhance facial nerve myelination and regeneration and could represent a new therapeutic tool to treat PNI.

Overexpression of Foxc1 regenerates crushed rat facial nerves by promoting Schwann cells migration via the Wnt/ß-catenin signaling pathway.

Facial paralysis can result in severe implications for patients. A good prognosis depends on the degree of nerve regeneration. Schwann cells (SCs) play an important role in facial nerve development and regeneration through migration. Forkhead box C1 (Foxc1), a member of the forkhead transcription factor family, is implicated in cell migration. However, the role of Foxc1 in the progression after facial nerve crush remains unknown. Our aim was to evaluate the effect of Foxc1 overexpression on SC migration and recovery of facial nerves after crush injury. The rat facial nerve crush injury model was established through the use of unilateral surgery. The results showed that the expression of Foxc1 was increased in the surgery group compared to that of the control group. SCs were isolated from the sciatic nerves and cultured. Foxc1, delivered by an adeno-associated virus in vivo, or adenovirus in vitro, both induced overexpression of Foxc1, and increased the expression of CXCL12 and ß-catenin. After the transfection of Foxc1, the migration of SC was increased both in vitro and in vivo, was reduced by the inhibition of CXCL12 or ß-catenin. The facial nerve function and the nerve axon remyelination of the rats transfected with Foxc1 were significantly improved after nerve crush injury. Overall, the results demonstrated that overexpression of Foxc1 promoted SC migration by regulating CXCL12 via the Wnt/ß-catenin pathway, thus contributing to improved facial nerve function after crush injury.

Facial nerve management in patients with malignant skull base tumors.

INTRODUCTION: The course of the facial nerve through the cerebellopontine angle, temporal bone, and parotid gland puts the nerve at risk in cases of malignancy. In contrast to Bell's palsy, which presents with acute facial paralysis, malignancies cause gradual or fluctuating weakness. METHODS: We review malignancies affecting the facial nerve, including those involving the temporal bone, parotid gland, and cerebellopontine angle, in addition to metastatic disease. Intraoperative management of the facial nerve and long term management of facial palsy are reviewed. RESULTS: Intraoperative management of the facial nerve in cases of skull base malignancy may involve extensive exposure, mobilization, or rerouting of the nerve. In cases of nerve sacrifice, primary neurorrhaphy or interposition grafting may be used. Cranial nerve substitution, gracilis free functional muscle transfer, and orthodromic temporalis tendon transfer are management options for long term facial paralysis. CONCLUSION: Temporal bone, parotid gland, and cerebellopontine angle malignancies pose a tremendous risk to the facial nerve. When possible, the facial nerve is preserved. If the facial nerve is sacrificed, static and dynamic reanimation strategies are used to enhance facial function.

Altered axonal excitability properties in facial palsy.

INTRODUCTION: Axonal excitability measures give insight into the biophysical properties of peripheral nerve axons. In this study we applied these techniques to the study of facial palsy. METHODS: Thirty patients with established facial palsy due to unresolved Bell's palsy or herpes zoster (>6 months duration), tumor invasion of the facial nerve, or traumatic facial nerve injury were assessed using facial nerve excitability techniques. RESULTS: Full recordings were obtained in 23 patients (15 unrecovered Bell's palsy or herpes zoster, 5 trauma, 3 tumor-related). Compared with normal controls, the facial palsy group demonstrated changes in stimulus response properties, threshold electrotonus, refractoriness, superexcitability, and I/V slope. Depolarizing threshold electrotonus distinguished between viral and non-viral etiologies on subgroup analysis. DISCUSSION: In this cross-sectional study, established facial palsy demonstrated findings similar to those seen in studies of regenerated axons. The improved understanding of underlying axonal characteristics offered by the technique may guide future treatment. Muscle Nerve 57: 268-272, 2018.

Bilateral Post-Traumatic Facial Paralysis That Contains Longitudinal and Transverse Temporal Fracture.

Acute bilateral post-traumatic facial paralysis is rare in the literature. Post-traumatic facial paralysis is frequently accompanied transverse fractures of temporal more. The incidence of acute bilateral post-traumatic facial paralysis has been reported as 1 to 5 per million in the literature. Trauma and concurrent facial paralysis are usually in the same subsite (right temporal bone fracture and right facial paralysis). There is one pathophysiological pattern for a single temporal bone fracture in a subsite. The authors present a bilateral isolated different pathophysiological pattern sudden onset facial paralysis in a patient herein.

Neurochemical effects of photobiostimulation in the trigeminal ganglion after inferior alveolar nerve injury.

Orofacial pain is associated with peripheral and central sensitization of trigeminal nociceptive neurons. Nerve injury results in release of chemical mediators that contribute to persistent pain conditions. The activation of the transient receptor potential vanilloid 1 (TRPV1), promotes release of calcitonin gene-related peptide (CGRP) and substance P (SP) from trigeminal nerve terminals. CGRP and SP contribute to the development of peripheral hyperalgesia. The expression of SP and CGRP by primary afferent neurons is rapidly increased in response to peripheral inflammation. CGRP receptor activation promotes activation of AMPA receptors, leading to increased firing of neurons which is reflected as central sensitization. In this study we investigated whether inferior alveolar nerve (IAN) injury influences AMPA receptors, CGRP, SP and TRPV1 expression in the trigeminal ganglion (TG). The relative expression of the protein of interest from naive rats was compared to those from injured rats and animals that received low level laser therapy (LLLT). IAN-injury did not change expression of GluA1, GluA2 and CGRP, but increased the expression of TRPV1 and SP. LLLT increases GluA1 and GluA2 expression and decreases TVPV1, SP and CGRP. These results, together with previous behavioral data, suggest that IAN-injury induced changes in the proteins analyzed, which could impact on nociceptive threshold. These data may help to understand the molecular mechanisms of pain sensitization in the TG.

Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury.

An increased risk of ALS has been reported for veterans, varsity athletes, and professional football players. The mechanism underlying the increased risk in these populations has not been identified; however, it has been proposed that motor nerve injury may trigger immune responses which, in turn, can accelerate the progression of ALS. Accumulating evidence indicates that abnormal immune reactions and inflammation are involved in the pathogenesis of ALS, but the specific immune cells involved have not been clearly defined. To understand how nerve injury and immune responses may contribute to ALS development, we investigated responses of CD4(+) T cell after facial motor nerve axotomy (FNA) at a presymptomatic stage in a transgenic mouse model of ALS (B6SJL SOD1(G93A)). SOD1(G93A) mice, compared with WT mice, displayed an increase in the basal activation state of CD4(+) T cells and higher frequency of Th17 cells, which were further enhanced by FNA. In conclusion, SOD1(G93A) mice exhibit abnormal CD4(+) T cell activation with increased levels of Th17 cells prior to the onset of neurological symptoms. Motor nerve injury exacerbates Th17 cell responses and may contribute to the development of ALS, especially in those who carry genetic susceptibility to this disease.

Nicotine effects on muscarinic receptor-mediated free Ca[Formula: see text] level changes in the facial nucleus following facial nerve injury.

It was suggested that muscarinic, and nicotinic receptors increase free Ca[Formula: see text] levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca[Formula: see text] overload can trigger either necrotic or apoptotic cell death. It is assumed that, following facial nerve injury, the interactions of nicotinic and muscarinic acetylcholine receptors in facial nerve nucleus may negatively regulate free Ca[Formula: see text] concentrations in the facial nerve nucleus, which provide important information for the repair and regeneration of the facial nerve. The present study investigated the regulatory effects of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus in a rat model of facial nerve injury at 7, 30, and 90 days following facial nerve injury using laser confocal microscopy. The dose-dependent regulation of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus may decrease the range of free Ca[Formula: see text] increases following facial nerve injury, which is important for nerve cell regeneration. It is concluded that the negative effects of nicotine on muscarinic receptors are related to the [Formula: see text] subtype of nicotinic receptors.

The effect of tacrolimus on facial nerve injury: Histopathological findings in a rabbit model.

HYPOTHESIS: Tacrolimus helps healing of facial nerve injury. BACKGROUND: Positive effects of tacrolimus on axon regeneration and healing of injured peripheral nerves (eg. sciatic nerve) have been reported in the literature. Tacrolimus may be an additional treatment method that could improve the nerve healing after surgical treatment of cut injury of facial nerve. METHODS: 20 New Zealand rabbits were randomly separated into control and study groups of 10. In control group, no medical treatment was given after facial nerve anastomosis, and the animals were followed up for 2months. In the study group rabbits were given 1mg/kg/day tacrolimus subcutaneously for 2months after the facial nerve anastomosis. The histopathologic findings of axon regeneration like axon myelination were analyzed in both groups under electron and light microscopy. The data obtained in the groups were compared. RESULTS: Greater axon diameters, thicker myelin sheaths, and higher total number of myelinated axons were found in the tacrolimus group, suggesting better regeneration in this group when compared to the control group. There was less vacuolar degeneration in the study group. All these findings suggest that tacrolimus positively affects healing after facial nerve anastomosis. CONCLUSION: The results of this study indicate that tacrolimus has favorable effects on the healing process of the facial nerve after end-to-end anastomosis. Tacrolimus may be a promising agent in the future for nerve regeneration following traumatic facial paralysis surgery.

The histopathological and electrophysiological effects of thymoquinone and methylprednisolone in a rabbit traumatic facial nerve paralysis model.

OBJECTIVE: We aimed to determine the effects of methylprednisolone and thymoquinone on nerve healing in a traumatic facial nerve paralysis animal model. SUBJECTS AND METHODS: Twenty-four rabbits were randomly divided into 4 groups: group I: control group received no medication and no trauma; group II: sham group received no medication after facial nerve trauma group III: 5mg/kg/day thymoquinone administered; group IV: 1mg/kg/day methylprednisolone administered. An initial electrophysiological assessment was performed in all the animals. The buccal branch of the facial nerve was then clipped to form a traumatic facial paralysis model. The drugs were administered for two weeks once a day. At the end of the second month, the electrophysiological assessments were performed and the distal part of the traumatic facial nerve were dissected and examined under light microscopy. RESULTS: Best nerve regeneration was observed in the control and the thymoquinone groups, respectively, whereas the weakest regeneration was determined in the sham group. Thymoquinone and methylprednisolone significantly increased nerve recovery, as measured by histopathological scores and electrophysiological assessment. In the thymoquinone group, due to postoperative amplitude, axon diameter and thickness of myelin sheath values were significantly further increased nerve regeneration compared to that of the methylprednisolone group and these values were close to those of the values of the control group. CONCLUSION: Thymoquinone was slightly better than methylprednisolone for functional nerve recovery. The neuroprotective effect of thymoquinone was attributed to its antioxidant and anti-inflammatory effects. Thymoquinone can have a new treatment option to ameliorate the nerve injury.

Extra and Intramuscular Distribution of the Thoracodorsal Nerve with Regard to Nerve Reconstruction Surgeries.

Background The lateral branch of the thoracodorsal nerve (LBTN) is used for nerve transfer in facial, musculocutaneous, axillary nerve injuries and for irreparable C5, C6 spinal nerve lesions and accessory nerve defects. For a successful surgical outcome, the nerve to be used in nerve transfer should be of adequate length and thickness for nerve coaptation. Aim Our objective was to evaluate the length of the LBTN that could be obtained as a donor nerve, externally and within the muscle. Method Eight (8) cadavers with intact upper limbs and thorax which could be positioned in the anatomical position were selected for the study. Cadavers with dissected axillae, brachial plexus or upper limbs were excluded. The thoracodorsal neurovascular bundle was dissected and the number of branches of the thoracodorsal nerve was identified along with its lateral branch. The lateral branch was dissected up to the latissimus dorsi muscle and further intramuscularly. All lengths were measured using a vernier caliper. Results The mean length of the LBTN, up to its first intramuscular branch, is 8.14 cm (range 5.99-12.29 cm). Beyond this, the intramuscular nerve branched further and was of very minute diameter. The mean unbranched intramuscular length of the nerve is 3.36 cm (range 1.3-7.71 cm) which is 41.28% of the total length of the LBTN. Conclusion A significant proportion of the LBTN is found within the latissimus dorsi muscle. This length could potentially be used for direct nerve coaptation by intrafascicular dissection.

ZPK/DLK and MKK4 form the critical gateway to axotomy-induced motoneuron death in neonates.

Motoneuron death after transection of the axons (axotomy) in neonates is believed to share the same mechanistic bases as naturally occurring programmed cell death during development. The c-Jun N-terminal kinase pathway is activated in both forms of motoneuron death, but it remains unknown to what extent these two forms of motoneuron death depend on this pathway and which upstream kinases are involved. We found that numbers of facial motoneurons are doubled in neonatal mice deficient in either ZPK/DLK (zipper protein kinase, also known as dual leucine zipper kinase), a mitogen-activated protein kinase kinase kinase, or in MKK4/MAP2K4, a mitogen-activated protein kinase kinase directly downstream of ZPK/DLK, and that the facial motoneurons in those mutant mice are completely resistant to axotomy-induced death. Conditional deletion of MKK4/MAP2K4 in neurons further suggested that ZPK/DLK and MKK4/MAP2K4-dependent mechanisms underlying axotomy-induced death are motoneuron autonomous. Nevertheless, quantitative analysis of facial motoneurons during embryogenesis revealed that both ZPK/DLK and MKK4/MAP2K4-dependent and -independent mechanisms contribute to developmental elimination of excess motoneurons. In contrast to MKK4/MAP2K4, mice lacking MKK7/MAP2K7, another mitogen-activated protein kinase kinase directly downstream of ZPK/DLK, conditionally in neurons did not have excess facial motoneurons. However, some MKK7/MAP2K7-deficient facial motoneurons were resistant to axotomy-induced death, indicating a synergistic effect of MKK7/MAP2K7 on axotomy-induced death of these facial motoneurons. Together, our study provides compelling evidence for the pivotal roles of the ZPK/DLK and MKK4/MAP2K4-dependent mechanism in axotomy-induced motoneuron death in neonates and also demonstrates that axotomy-induced motoneuron death is not identical to developmental motoneuron death with respect to the involvement of ZPK/DLK, MKK4/MAP2K4 and MKK7/MAP2K7.

Astrocyte-targeted production of IL-10 induces changes in microglial reactivity and reduces motor neuron death after facial nerve axotomy.

Interleukin-10 (IL-10) is a cytokine that plays a crucial role in regulating the inflammatory response and immune reactions. In the central nervous system (CNS), IL-10 is mainly produced by astrocytes and microglia and it is upregulated after various insults, such as experimental autoimmune encephalomyelitis, middle cerebral artery occlusion, excitotoxicity and traumatic brain injury. To better understand the effects of IL-10 in the normal and injured CNS, we generated transgenic mice (termed GFAP-IL-10Tg) that expressed the murine IL-10 gene under the transcriptional control of the glial fibrillary acidic protein (GFAP) promoter. Previous studies demonstrated marked changes in the microglial phenotype in these mice under basal conditions. The objective of the present study was to investigate the effects of local astrocyte-targeted IL-10 production on glial activation, neuronal degeneration and leukocyte recruitment after axotomy. GFAP-IL-10Tg mice had marked changes in the phenotype of activated microglial cells, as well as in the number of microglial clusters and in microglial cell density. These microglial changes are accompanied by a twofold increase in lymphocyte infiltration in GFAP-IL-10Tg mice and around twofold decrease in neuronal cell death at 21 dpi. Altogether, our findings suggested that astrocyte-targeted production of IL-10 impacted the microglial response and lymphocyte recruitment and culminated in a beneficial effect on neuronal survival.

Electrical stimulation characteristics of denervated orbicularis oculi muscle.

This research is to study the electrical stimulation characteristics of orbicularis oculi muscle and the characteristics of the mechanical contraction. We observed the stimulus current diffusion regularity and its relationship with mechanical contraction in the orbicularis oculi muscle using an electrode gathering line. Under different stimulus intensities of 2 or 4 mA, the closer the recording electrodes were to the stimulating electrode, the larger was the amplitude. When the recording electrode and stimulating electrode distance increased, the amplitude declined linearly with decreasing function. In addition, current conduction across the muscle fiber was studied. Under different stimulus intensities of 2 or 4 mA, it was found that the closer the recording electrodes were to the stimulating electrode, the larger was the amplitude. When the recording electrode and stimulating electrode distance increased, the amplitude declined linearly with decreasing function. The transverse current reached a maximum 4 mA range, and increasing the current intensity did not increase the propagation range. Under different stimulation intensities, the larger the stimulus intensity, the greater is the potential change and the faster is the attenuation. Longitudinal current, even in the range of 6 mm, can still record electrical activity. While a transverse current diffuser has a maximum range of 4 mm, increasing the current intensity does not increase the propagation range.

Facial and Cochlear Nerve Complications following Microsurgical Resection of Vestibular Schwannomas in a Series of 221 Cases.

BACKGROUND: Despite improvements in microsurgical technique and the use of intraoperative electrophysiological monitoring, the potential for facial and cochlear nerve injury remains a possibility in the resection of vestibular schwannomas (VS). We reviewed a series of 221 cases of VS resected via a retrosigmoid approach at our institution from October 2008 to April 2014 and determined the incidence of postoperative facial and cochlear deficits. MATERIAL AND METHODS: A total of 221 patients - 105 (47.5%) male and 116 (52.5%) female - with a mean age of 46.1 years (range 29-73 years), with VS ≥3 cm (n=183, 82.8%) and <3 cm (n=38, 17.2%) underwent surgical resection via a retrosigmoid approach and were evaluated for postoperative facial and cochlear nerve deficits. RESULTS: Near-total resection (>95% removal) was achieved in 199 cases (90%) and subtotal resection (>90% removal) in 22 cases (10%). At 6 month follow-up, House-Brackmann grades I-III were observed in 183 cases (82.8%), grade IV in 16 cases (7.2%), and grade V in 22 cases (10%). Of the 10 patients that had preoperative functional hearing, 3 (33%) retained hearing postoperatively. Cerebrospinal fluid leakage occurred in 6 patients (2.7%), lower cranial nerve palsies in 9 patients (4.1%), and intracranial hematomas 3 cases (1.4%). CONCLUSIONS: The observed incidence of persistent postoperative nerve deficits is very low. Meticulous microsurgical dissection of and around the facial and cochlear nerves with the aid of intraoperative electrophysiological nerve monitoring in the retrosigmoid approach allows for near-total resection of medium and large VS with the possibility of preservation of facial and cochlear nerve function.

The effect of coenzyme Q10 on the regeneration of crushed facial nerve.

OBJECTIVE: The aim of this study is to show the possible positive effect of coenzyme Q10 (Co Q10) on regenerating in facial palsy. MATERIALS AND METHODS: Sixteen female Sprague-Dawley albino rats were randomly divided into 2 groups as Co Q10 and control groups. Group Q10 (n = 8) received Co Q10 of 10 mg/kg/d intraperitoneally for 30 days, and group C (n = 8) received saline solution of 1 mL/d intraperitoneally once daily for 30 days. The right facial nerve stimulation thresholds were determined before crush, immediately after crush, and after 1 month.After determination of the thresholds, the crushed part of the facial nerve was then excised. All specimens were examined by a pathologist using a light microscope. RESULTS: No statistically significant difference in stimulation threshold was found between the Co Q10 and saline groups after crushing (P = 0.645). After 1 month of treatment, stimulation thresholds were significantly lower in both the Co Q10 and saline groups (Ps = 0.028 and 0.016). However, the Co Q10 group showed greater improvement than the saline group (P = 0.050).After 1 month of treatment, neither the Co Q10 group nor the saline group had reached the precrushing amplitude levels (Ps = 0.027 and 0.011).Significant differences were found in vascular congestion, macrovacuolization, and myelin thickness between the Co Q10 and control groups by light microscopy (P < 0.05). CONCLUSIONS: Although many treatment methods have been tried to accelerate facial nerve regeneration after trauma, a definitive method has not been found yet. Co Q for the treatment of acute facial paralysis is promising on both physiologic assessments and pathologic evaluation.

Relationships between facial canal dehiscence and other intraoperative findings in chronic otitis media with cholesteatoma.

OBJECTIVE: We investigated the relationship between facial canal dehiscence and intraoperative middle ear and mastoid findings in patients operated on for cholesteatoma. METHODS: We examined retrospectively 334 patients who had been operated on for cholesteatoma in Izmir Katip Celebi University, Ataturk Research and Training Hospital, ENT Clinic, between April 1997 and April 2010. The patients were examined for facial canal dehiscence according to age, gender, side of the ear, surgery type, first or revision surgery, localization of the facial canal dehiscence, spread of the cholesteatoma, with the presence of lateral semi-circular canal (LSCC) fistula and any defect in the ossicle chain, and destruction in the posterior wall of the external auditory canal(EAC). RESULTS: Of the patients, 23.6% had facial canal dehiscence and detected most commonly in the right ear 28.9% and tympanic segment, 83.5%. Facial canal dehiscence was found to be 24.2-fold more common in patients with LSCC fistula and 4.1-fold more common in patients with destruction in the posterior wall of the (EAC). In patients located cholesteatoma in tympanic cavity+antrum and the tympanic cavity+all mastoid cells and with incus and stapes defect, increased incidence of dehiscence. Age, first or revision operation and canal wall down tympanoplasty (CWDT) or canal wall up tympanoplasty (CWUT) did not affect the incidence of dehiscence. CONCLUSIONS: That the likelihood of facial canal dehiscence occurrence is increased in patients with LSSC fistulas, destruction in the posterior wall of the EAC, or a stapes defect is important information for surgeons.