Unmasking of the trigemino-accessory reflex in accessory facial anastomosis.
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OBJECTIVE: To evaluate the possible blink reflex responses in facial muscles reinnervated by the accessory nerve. METHOD: Eleven patients with a complete facial palsy were submitted to a surgical repair by an accessory facial nerve anastomosis (AFA). In this pathological group, blink reflex was studied by means of percutaneous electrical stimulation of the supraorbital nerve and recording from the orbicularis oculi muscle. A control group comprised seven normal people and seven patients with a complete Bell's facial palsy; in this group, responses on the sternocleidomastoideus (SCM) muscles were studied after supraorbital nerve stimulation. RESULTS: All the patients with AFA showed a consistent degree of facial reinnervation. Ten out of the 11 patients with AFA showed reflex responses; in six, responses were configured by a double component pattern, resembling the R1 and R2 components of the blink reflex; three patients had an R1-like response and one patient showed a unique R2 component. Mean values of latencies were 15.2 (SD 4.6) ms for the R1 and 85.3 (SD 9.6) ms for the R2. In the control group, eight out of 14 people had evidence of reflex responses in the SCM muscles; these were almost exclusively configured by a bilateral late component (mean latency 63.5 (SD15.9) ms) and only one of the subjects showed an early response at 11 ms. CONCLUSION: The trigemino-accessory reflex response in the pathological group was more complex and of a significantly higher incidence than in the control group. These differences could be tentatively explained by a mechanism of synaptic plasticity induced by the impairment of the efferent portion of the reflex. This could unmask the central linking between the trigeminal and the accessory limbs of the reflex. The findings described could be a demonstration of neurobionomic function in the repairing process of the nervous system. (+info)
The learning-related activity that develops in the pontine nuclei during classical eye-blink conditioning is dependent on the interpositus nucleus.
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A growing body of research now implicates the cerebellum in the formation and storage of the critical neural plasticity that subserves the classically conditioned eye-blink response. Previous anatomical, physiological, and behavioral research suggests that auditory-conditioned stimulus information is routed to the cerebellum by the pontine nuclei. However, it has also been observed from multiple unit recordings that some populations of pontine cells, in addition to showing auditory-evoked responses, also show changes in activity that is learning-related. It is unknown whether this learning-related activity is generated by the pontine cells or whether it is generated by some other structure and projected to the pontine nuclei. Because the cerebellum has been implicated in the formation of the essential plasticity that subserves this learned behavior, we examined how multiple unit recordings of learning-related activity within the pontine nuclei are affected by reversible inactivation of the interpositus nucleus of the cerebellum. The results indicated clearly that when the interpositus nucleus was inactivated, the learning-related activity in the pontine nuclei was abolished completely and the auditory stimulus-evoked activity was unaffected. In contract, when the facial nucleus was inactivated, both the auditory stimulus and the learning-related activity were still present. These results indicate that the learning-related activity exhibited by some populations of pontine nuclei cells is dependent on the interpositus nucleus and may represent feedback from the cerebellum. (+info)
Visualization of cranial motor neurons in live transgenic zebrafish expressing green fluorescent protein under the control of the islet-1 promoter/enhancer.
(11/372)
We generated germ line-transmitting transgenic zebrafish that express green fluorescent protein (GFP) in the cranial motor neurons. This was accomplished by fusing GFP sequences to Islet-1 promoter/enhancer sequences that were sufficient for neural-specific expression. The expression of GFP by the motor neurons in the transgenic fish enabled visualization of the cell bodies, main axons, and the peripheral branches within the muscles. GFP-labeled motor neurons could be followed at high resolution for at least up to day four, when most larval neural circuits become functional, and larvae begin to swim and capture prey. Using this line, we analyzed axonal outgrowth by the cranial motor neurons. Furthermore, by selective application of DiI to specific GFP-positive nerve branches, we showed that the two clusters of trigeminal motor neurons in rhombomeres 2 and 3 innervate different peripheral targets. This finding suggests that the trigeminal motor neurons in the two clusters adopt distinct fates. In future experiments, this transgenic line of zebrafish will allow for a genetic analysis of cranial motor neuron development. (+info)
Impaired axonal regeneration in alpha7 integrin-deficient mice.
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The interplay between growing axons and the extracellular substrate is pivotal for directing axonal outgrowth during development and regeneration. Here we show an important role for the neuronal cell adhesion molecule alpha7beta1 integrin during peripheral nerve regeneration. Axotomy led to a strong increase of this integrin on regenerating motor and sensory neurons, but not on the normally nonregenerating CNS neurons. alpha7 and beta1 subunits were present on the axons and their growth cones in the regenerating facial nerve. Transgenic deletion of the alpha7 subunit caused a significant reduction of axonal elongation. The associated delay in the reinnervation of the whiskerpad, a peripheral target of the facial motor neurons, points to an important role for this integrin in the successful execution of axonal regeneration. (+info)
Spatial relationship between vestibular schwannoma and facial nerve on three-dimensional T2-weighted fast spin-echo MR images.
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BACKGROUND AND PURPOSE: During surgical removal of a vestibular schwannoma, correct identification of the facial nerve is necessary for its preservation and continuing function. We prospectively analyzed the spatial relationship between vestibular schwannomas and the facial nerve using 3D T2-weighted and postcontrast T1-weighted spin-echo (SE) MR imaging. METHODS: Twenty-two patients with a unilateral vestibular schwannoma were examined with MR imaging. The position and spatial relationship of the facial nerve to adjacent tumor within the internal auditory canal (IAC) and cerebellopontine angle cistern (CPA) were assessed on multiplanar reformatted 3D T2-weighted fast spin-echo (FSE) images and on postcontrast transverse and coronal T1-weighted SE images. The entrance of the nerve into the bony canal at the meatal foramen and the nerve root exit zone along the brain stem were used as landmarks to follow the nerve course proximally and distally on all images. RESULTS: The spatial relationship between vestibular schwannoma and facial nerve could not be detected on postcontrast T1-weighted SE images. In 86% of the patients, the position of the nerve in relation to the tumor was discernible on multiplanar reformatted 3D T2-weighted FSE images. In tumors with a maximal diameter up to 10 mm, the entire nerve course was visible; in tumors with a diameter of 11 to 24 mm, only segments of the facial nerve were visible; and in tumors larger than 25 mm, the facial nerve could not be seen, owing to focal nerve thinning and obliteration of landmarks within the IAC and CPA. CONCLUSION: Identification of the facial nerve and its position relative to an adjacent vestibular schwannoma is possible on multiplanar reformatted 3D T2-weighted FSE images but not on postcontrast T1-weighted SE images. Detection of this spatial relationship depends on the tumor's size and location. (+info)
Acoustic neuroma surgery as an interdisciplinary approach: a neurosurgical series of 508 patients.
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OBJECTIVES: To evaluate an interdisciplinary concept (neurosurgery/ear, nose, and throat (ENT)) of treating acoustic neuromas with extrameatal extension via the retromastoidal approach. To analyse whether monitoring both facial nerve EMG and BAEP improved the functional outcome in acoustic neuroma surgery. METHODS: In a series of 508 patients consecutively operated on over a period of 7 years, functional outcome of the facial nerve was evaluated according to the House/Brackmann scale and hearing preservation was classified using the Gardner/Robertson system. RESULTS: Facial monitoring (396 of 508 operations) and continuous BAEP recording (229 of 399 cases with preserved hearing preoperatively) were performed routinely. With intraoperative monitoring, the rate of excellent/good facial nerve function (House/Brackmann I-II) was 88.7%. Good functional hearing (Gardner/Robertson 1-3) was preserved in 39.8%. CONCLUSION: Acoustic neuroma surgery via a retrosigmoidal approach is a safe and effective treatment for tumours with extrameatal extension. Functional results can be substantially improved by intraoperative monitoring. The interdisciplinary concept of surgery performed by ENT and neurosurgeons was particularly convincing as each pathoanatomical phase of the operation is performed by a surgeon best acquainted with the regional specialties. (+info)
Complete and long-term rescue of lesioned adult motoneurons by lentiviral-mediated expression of glial cell line-derived neurotrophic factor in the facial nucleus.
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To date, delivery of neurotrophic factors has only allowed to transiently protect axotomized facial motoneurons against cell death. In the present report, long-term protection of these neurons was evaluated by continuously expressing the neurotrophic factor glial cell line-derived neurotrophic factor (GDNF) within the facial nucleus using a lentiviral vector system. The viral vector was injected unilaterally into the facial nucleus of 4-month-old Balb/C mice. In contrast to axotomy in other adult rodents, facial nerve lesion in these animals leads to a progressive and sustained loss and/or atrophy of >50% of the motoneurons. This model thus represents an attractive model to evaluate potential protective effects of neurotrophic factors for adult-onset motoneuron diseases, such as amyotrophic lateral sclerosis. One month after unilateral lentiviral vector injection, the facial nerve was sectioned, and the animals were killed 3 months later. Viral delivery of the GDNF gene led to long-term expression and extensive diffusion of GDNF within the brainstem. In addition, axotomized motoneurons were completely protected against cell death, because 95% of the motoneurons were present as demonstrated by both Nissl staining and choline acetyltransferase immunoreactivity. Furthermore, GDNF prevented lesion-induced neuronal atrophy and maintained proximal motoneuron axons, despite the absence of target cell reinnervation. This is the first evidence that viral-mediated delivery of GDNF close to the motoneuron cell bodies of the facial nucleus of adult mice can lead to complete and long-term protection against lesion-induced cell death. (+info)
Neuronal propagation of HSV1 from the oral mucosa to the eye.
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PURPOSE: To identify possible neuronal pathways leading to herpetic ocular disease after primary oral infection in mice. METHODS: The SC16 strain of herpes simplex virus (HSV)-1 (10(6) plaque-forming units) was injected into the mucocutaneous border of the left upper lip. Animals were killed 2 to 10 days postinoculation (DPI). Spread of the virus in neural structures was studied by immunochemistry. RESULTS: HSV1 first replicated at the site of inoculation and then at the superior cervical ganglion (at 2 DPI). The trigeminal ganglion and the facial nerve fibers were infected by 4 DPI. Infection of the ciliary body and iris occurred at 6 DPI, together with several brain stem nuclei belonging to the autonomic or sensory pathways. Between 8 and 10 DPI, the neural infection gradually cleared up, except for the ipsilateral sympathetic ganglion, and ipsilateral keratitis appeared in some animals. CONCLUSIONS: The pattern of viral dissemination in this mouse model suggests that infection of iris and ciliary body results from transfer of virus in the superior cervical ganglion from sympathetic neurons innervating the lip to neighboring neurons innervating the anterior uvea. Later, zosteriform spread of virus from the trigeminal system may have contributed to the clinical and histologic findings. (+info)