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Trigeminal Nerve (trigeminal + nerve)
Selected AbstractsSurgical Management of an Unresectable Trigeminal Nerve (V2) Plexiform NeurofibromaTHE LARYNGOSCOPE, Issue S1 2009Urmen Desai MD MPH No abstract is available for this article. [source] Trigeminal Trophic Syndrome,Report of Four Cases and Review of the LiteratureDERMATOLOGIC SURGERY, Issue 5 2004Parrish Sadeghi MD Background. Trigeminal trophic syndrome is a unilateral, frequently crescent-shaped neurotrophic ulceration of the face occurring after injury to the trigeminal nerve. The appearance of the ulcers resembles other disease entities such as granulomatous disease, neoplasm, vasculitis, infection, and factitial dermatitis. Objectives. The objectives of this study are to increase awareness of this disorder and to emphasize the importance of eliciting a thorough neurologic history when evaluating facial ulcerations. Methods. Four cases are reported and, using MEDLINE, the English and non-English literature from 1982 to 2002 is reviewed. Results. Including this report, there have been 60 cases of trigeminal trophic syndrome reported from 1982 to 2002. The age at presentation ranged from 14 months to 93 years. Time of onset from injury to the trigeminal ganglion or its branches and the development of the ulcers ranged from 2 weeks to 30 years. One-third of the patients had undergone trigeminal nerve ablation for the treatment of trigeminal neuralgia and another third had a history of stroke. Other causes included craniotomy, head trauma, herpes infection. Conclusion. The majority of cases of trigeminal trophic syndrome are associated with a history of stroke or trigeminal nerve ablation. Successful surgical outcome can be achieved if the underlying neurologic pathology is addressed before the reconstructive procedure. [source] Caudal compression of the infraorbital nerve: A novel surgical technique for treatment of idiopathic headshaking and assessment of its efficacy in 24 horsesEQUINE VETERINARY JOURNAL, Issue 2 2009V. L. H. ROBERTS Summary Reasons for designing and reporting technique: Idiopathic headshaking has remarkable similarities to human neuropathic facial pain syndromes associated with post herpetic and trigeminal neuralgia. These derive from abnormal sensory function within the peripheral or central pathways of the trigeminal nerve (TgN). Limiting input from the TgN can be helpful in controlling the perception of pain. Rhizotomy of the infraorbital branch of the TgN as it emerges from the infraorbital canal has been reported but has a poor efficacy. A novel technique involves compression of the nerve at a more caudal location within the infraorbital canal and the technique requires validation. Hypothesis: Caudal compression of the infraorbital nerve with platinum coils, performed in horses diagnosed with idiopathic headshaking, results in a decrease in clinical signs. Methods: Caudal compression of the infraorbital nerve, using platinum embolisation coils, was performed under fluoroscopic guidance. Clinical records of 24 idiopathic headshakers that had undergone this procedure were reviewed. Follow-up information was obtained by telephone questionnaire with the owner or referring veterinary surgeon. Results: All 24 horses had at least one surgical procedure. Median follow-up time was 6 months. There were 2 horses which had surgery 2 weeks before follow-up and these were excluded from the analysis of outcome. Following one surgery, 13/22 horses (59.0%) had a successful outcome. Of the 9 horses that did not improve, surgery was repeated in 6 cases. Two of these horses had a successful outcome. Overall, a successful outcome was obtained in 16/19 horses (84.2%). Conclusions: This surgical technique is likely to prevent input from the TgN at a more caudal location then the previously described infraorbital neurectomy. The technique requires refinement. [source] Facial nerve injury-induced disinhibition in the primary motor cortices of both hemispheresEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2000Tamás Farkas Abstract Unilateral facial nerve transection induces plastic reorganization of the somatotopic order in the primary motor cortex area (MI). This process is biphasic and starts with a transient disinhibition of connections between cortical areas in both hemispheres. Little is known about the underlying mechanisms. Here, cortical excitability has been studied by paired pulse electrical stimulation, applied either within the MI or peripherally to the trigeminal nerve, while the responses were recorded bilaterally in the MI. The ratios between the amplitudes of the second and first evoked potentials (EPs or fEPSPs) were taken as measures of the inhibitory capacity in the MI ipsilateral or contralateral to the nerve injury. A skin wound or unilateral facial nerve exposure immediately caused a transient facilitation, which was followed by a reset to some level of inhibition in the MI on both sides. After facial nerve transection, the first relatively mild reduction of inhibition started shortly (within 10 min) after denervation. This was followed by a second step, involving a stronger decrease in inhibition, 40,45 min later. Previous publications have proved that sensory nerve injury (deafferentation) induces disinhibition in corresponding areas of the sensory cortex. It is now demonstrated that sham operation and, to an even greater extent, unilateral transection of the purely motoric facial nerve (deefferentation), each induce extended disinhibition in the MIs on both sides. [source] Generation of a transgenic mouse line expressing GFP-Cre protein from a Hoxb4 neural enhancerGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 2 2008Elena Rivkin Abstract Here, we describe a transgenic mouse line, in which expression of green fluorescent protein fused to Cre recombinase (GFP-Cre) is directed by the early neuronal enhancer (ENE) of Hoxb4. In E9.0,13.5 transgenic embryos, Cre activity coincided with endogenous Hoxb4 throughout the neural tube up to the r6/r7 boundary in the hindbrain, the dorsal root ganglia, and the Xth cranial ganglia. Unexpectedly, Cre activity was also consistently detected in the trigeminal (Vth) cranial nerve, which is devoid of endogenous Hoxb4 expression. Strong GFP dependent fluorescence appeared slightly later in E9.5,E11.5 embryos, and reflected the later expression pattern expected for Hoxb4-ENE directed expression in the neural tube up to the r7/r8 not r6/r7 boundary. Thus, with the exception of the trigeminal nerve, this reporter faithfully reproduces endogenous embryonic neural Hoxb4 expression, and provides an excellent reagent for in vivo gene manipulations in neuronal Hoxb4 positive cells as well as the developing trigeminal nerve. This transgenic mouse line should prove especially useful for determining the fate map of neuronal populations arising in rhombomeres 7 and 8 on its own and in combination with the small set of other existing rhombomere-specific Cre recombinase expressing lines. genesis 46:119,124, 2008. © 2008 Wiley-Liss, Inc. [source] Supraspinal Modulation of Trigeminal Nociception and PainHEADACHE, Issue 5 2009Amy E. Williams MA Objective., This study examined modulation of trigeminal pain/nociception by 2 supraspinal mechanisms: emotional controls of nociception and diffuse noxious inhibitory controls. Background., Prior research suggests emotional picture viewing (emotional controls) and tonic noxious stimuli (diffuse noxious inhibitory controls) engage supraspinal mechanisms to modulate pain and nociceptive processes. It is currently unknown, however, whether emotional controls modulate trigeminal pain and nociception. Additionally, the influences of emotional controls and diffuse noxious inhibitory controls have not been compared in the same group of participants. Methods., Noxious electrodermal stimuli were delivered to the trigeminal nerve using a concentric electrode designed to selectively activate nociceptive fibers. Trigeminal nociception and pain were assessed (34 participants) from the nociceptive blink reflex and pain ratings, respectively. Emotional controls were engaged by presentation of standardized picture stimuli (pleasant, neutral, and unpleasant) shown to reliably evoke pleasure-induced inhibition and displeasure-induced facilitation of pain and nociception. Diffuse noxious inhibitory controls were engaged with a forearm ischemia task. Results., Trigeminal pain (self-report ratings) and nociception (blinks) were facilitated by unpleasant pictures and inhibited by pleasant pictures. Emotion induction (as assessed from trend analysis) explained 51% of the variance in trigeminal pain and 25% of the variance in trigeminal nociception. Additionally, forearm ischemia inhibited trigeminal pain but not nociception. The baseline vs ischemia comparison explained 17% of the variance in pain report and 0.1% of the variance in blinks. Supraspinal modulation by emotional controls and diffuse noxious inhibitory controls were uncorrelated. Conclusions., Emotional controls and diffuse noxious inhibitory controls modulated trigeminal pain and emotional controls modulated trigeminal nociception. These procedures can be used to study supraspinal modulation of nociceptive processing in disorders of the trigeminal pain system, including headache. [source] Perineural Invasion of Sinonasal Lymphoma: A Rare Cause of Trigeminal NeuropathyHEADACHE, Issue 2 2007Chih-Wei Liang MD Trigeminal neuropathy is characterized by sensory disturbance of the division of trigeminal nerve, and sometimes is associated with pain. Trigeminal neuropathy secondary to perineural invasion of sinonasal lymphoma is extremely rare. Likewise, sinonasal lymphoma is infrequently demonstrated initially with cranial neuropathy. The present case served to broaden the differential diagnosis of secondary trigeminal neuropathy and to alert clinicians to cautiously assess perineural spread of occult neoplasm in sinonasal tract and larynx or pharynx for cases with evolving trigeminal neuropathy or even other cranial nerve neuropathy in which no definite cause is identified. [source] Repeat Trigeminal Nerve Radiosurgery for Refractory Cluster Headache Fails to Provide Long-Term Pain ReliefHEADACHE, Issue 2 2007Shearwood McClelland III MD Objective/Background.,Medically refractory cluster headache (MRCH) is a debilitating condition that has proven resistant to many modalities. Previous reports have indicated that radiosurgery for MRCH provides little long-term pain relief, with moderate/significant morbidity. However, there have been no reports of repeated radiosurgery in this patient population. We present our findings from the first reports of repeat radiosurgery for MRCH. Methods.,Two patients with MRCH underwent repeat gamma knife radiosurgery at our institution. Each fulfilled clinical criteria for treatment, including complete resistance to pharmacotherapy, pain primarily localized to the ophthalmic division of the trigeminal nerve, and psychological stability. Both patients previously received gamma knife radiosurgery (75 Gy) for MRCH with no morbidity, but no long-term improvement of pain relief (Patient 1 = 5 months, Patient 2 = 10 months) after treatment. For repeat radiosurgery, each patient received 75 Gy to the 100% isodose line delivered to the root entry zone of the trigeminal nerve, and was evaluated postretreatment. Pain relief was defined as: excellent (free of MRCH with minimal/no medications), good (50% reduction of MRCH severity/frequency with medications), fair (25% reduction), or poor (less than 25% reduction). Results.,Following repeat radiosurgery, long-term pain relief was poor in both patients. Neither patient sustained any immediate morbidity following radiosurgery. Patient 2 experienced right facial numbness 4 months postretreatment, while Patient 1 experienced no morbidity. Conclusion.,Repeat radiosurgery of the trigeminal nerve fails to provide long-term pain relief for MRCH. Given the reported failures of initial and repeat radiosurgery for MRCH, trigeminal nerve radiosurgery should not be offered for MRCH. [source] Neurotoxins in the Neurobiology of PainHEADACHE, Issue 2003Stephen D. Silberstein MD Migraine is a common, chronic, incapacitating, neurovascular disorder that affects an estimated 12% of the population. Understanding the basic mechanisms of pain is important when treating patients with chronic pain disorders. Pain, an unpleasant sensory and emotional experience, is usually triggered by stimulation of peripheral nerves and often associated with actual or potential tissue damage. Peripheral nerve fibers transmit pain signals from the periphery toward the spinal cord or brain stem. The different diameter pain fibers (A and C) vary in the speed of conduction and the type of pain transmitted (eg, sharp versus dull). When stimulated, peripheral pain fibers carrying sensory input from the body enter at different layers of the dorsal horn, which is then propagated toward the thalamus via the spinothalamic tract within the spinal cord. Conversely, sensory input from the face does not enter the spinal cord but enters the brain stem via the trigeminal nerve. This review describes in detail the neurobiological mechanisms and pathways for pain sensation, with a focus on migraine pain. [source] Surgical treatment of migraine headaches.HEADACHE, Issue 3 2003B Guyuron Plast Reconstr Surg. 2002 Jun;109(7):2183-2189 This prospective study was conducted to investigate the role of removal of corrugator supercilii muscles, transection of the zygomaticotemporal branch of the trigeminal nerve, and temple soft-tissue repositioning in the treatment of migraine headaches. Using the criteria set forth by the International Headache Society, the research team's neurologist evaluated patients with moderate to severe migraine headaches, to confirm the diagnosis. Subsequently, the patients completed a comprehensive migraine headaches questionnaire and the team's plastic surgeon injected 25 units of botulinum toxin type A (Botox) into each corrugator supercilii muscle. The patients were asked to maintain an accurate diary of their migraine headaches and to complete a monthly questionnaire documenting pertinent information related to their headaches. Patients in whom the injection of Botox resulted in complete elimination of the migraine headaches then underwent resection of the corrugator supercilii muscles. Those who experienced only significant improvement underwent transection of the zygomaticotemporal branch of the trigeminal nerve with repositioning of the temple soft tissues, in addition to removal of the corrugator supercilii muscles. Once again, patients kept a detailed postoperative record of their headaches. Of the 29 patients included in the study, 24 were women and five were men, with an average age of 44.9 years (range, 24 to 63 years). Twenty-four of 29 patients (82.8 percent, p < 0.001) reported a positive response to the injection of Botox, 16 (55.2 percent, p < 0.001) observed complete elimination, eight (27.6 percent, p < 0.04) experienced significant improvement (at least 50 percent reduction in intensity or severity), and five (17.2 percent, not significant) did not notice a change in their migraine headaches. Twenty-two of the 24 patients who had a favorable response to the injection of Botox underwent surgery, and 21 (95.5 percent, p < 0.001) observed a postoperative improvement. Ten patients (45.5 percent, p < 0.01) reported elimination of migraine headaches and 11 patients (50.0 percent, p < 0.004) noted a considerable improvement. For the entire surgical group, the average intensity of the migraine headaches reduced from 8.9 to 4.1 on an analogue scale of 1 to 10, and the frequency of migraine headaches changed from an average of 5.2 per month to an average of 0.8 per month. For the group who only experienced an improvement, the intensity fell from 9.0 to 7.5 and the frequency was reduced from 5.6 to 1.0 per month. Only one patient (4.5 percent, not significant) did not notice any change. The follow-up ranged from 222 to 494 days, the average being 347 days. In conclusion, this study confirms the value of surgical treatment of migraine headaches, inasmuch as 21 of 22 patients benefited significantly from the surgery. It is also evident that injection of Botox is an extremely reliable predictor of surgical outcome. Comment: Many small placebo-controlled studies and much anecdotal literature suggests that botulinum toxin may be effective in prevention of migraine, perhaps to the same extent as conventional prophylactic treatment. Larger, randomized clinical trials are underway to resolve this issue. In the meantime, those who believe in the effectiveness of botulinum toxin prophylaxis argue about how it works, that is whether its antinociceptive properties are due to peripheral effects, central or presynaptic effects, or both. Dr. Guyuron's group favors the idea that botulinum toxin interrupts a reflex arc between the central nervous system (CNS) and peripheral musculature, and that after establishing efficacy by low dose botulinum injection in the corrugator supercilii muscles, surgical resection of these muscles results in prolonged and effective prophylaxis. The idea is radical but intriguing and should not be dismissed out of hand. However, a trial is necessary in which both the botulinum toxin injections are blinded with vehicle, and the study of the surgery involves a sham surgery control group with extended long-term follow-up, before these forms of prophylaxis can be recommended to patients. SJT [source] Antiepileptic Drugs in the Management of Cluster Headache and Trigeminal NeuralgiaHEADACHE, Issue 2001Todd D. Rozen MD Cluster headache and trigeminal neuralgia are relatively rare but debilitating neurologic conditions. Although they are clinically and diagnostically distinct from migraine, many of the same pharmacologic agents are used in their management. For many patients, the attacks are so frequent and severe that abortive therapy is often ineffective; therefore, chronic preventive therapy is necessary for adequate pain control. Cluster headache and trigeminal neuralgia have several distinguishing clinical features. Cluster headache is predominantly a male disorder; trigeminal neuralgia is more prevalent in women. Individuals with cluster headaches often develop their first attack before age 25; most patients with trigeminal neuralgia are between age 50 and 70. Cluster headaches are strongly associated with tobacco smoking and triggered by alcohol consumption; trigeminal neuralgia can be triggered by such stimuli as shaving and toothbrushing. Although the pain in both disorders is excruciating, cluster headache pain is episodic and unilateral, typically surrounds the eye, and lasts 15 to 180 minutes; the pain of trigeminal neuralgia lasts just seconds and is usually limited to the tissues overlying the maxillary and mandibular divisions of the trigeminal nerve. Cluster headache is unique because of its associated autonomic symptoms. Although the pathophysiology of cluster headache and trigeminal neuralgia are not completely understood, both appear to have central primary processes, and these findings have prompted investigations of the effectiveness of the newer antiepileptic drugs for cluster headache prevention and for the treatment of trigeminal neuralgia. The traditional antiepileptic drugs phenytoin and carbamazepine have been used for the treatment of trigeminal neuralgia for a number of years, and while they are effective, they can sometimes cause central nervous system effects such as drowsiness, ataxia, somnolence, and diplopia. Reports of studies in small numbers of patients or individual case studies indicate that the newer antiepileptic drugs are effective in providing pain relief for trigeminal neuralgia and cluster headache sufferers, with fewer central nervous system side effects. Divalproex has been shown to provide effective pain control and to reduce cluster headache frequency by more than half in episodic and chronic cluster headache sufferers. Topiramate demonstrated efficacy in a study of 15 patients, with a mean time to induction of cluster headache remission of 1.4 weeks (range, 1 day to 3 weeks). In the treatment of trigeminal neuralgia, gabapentin has been shown to be effective in an open-label study. When added to an existing but ineffective regimen of carbamazepine or phenytoin, lamotrigine provided improved pain relief; it also may work as monotherapy. Topiramate provided a sustained analgesic effect when administered to patients with trigeminal neuralgia. The newer antiepileptic drugs show considerable promise in the management of cluster headache and trigeminal neuralgia. [source] Comparative innervation of cephalic photophores of the loosejaw dragonfishes (Teleostei: Stomiiformes: Stomiidae): Evidence for parallel evolution of long-wave bioluminescenceJOURNAL OF MORPHOLOGY, Issue 4 2010Christopher P. Kenaley Abstract Four genera of the teleost family Stomiidae, the loosejaw dragonfishes, possess accessory cephalic photophores (AOs). Species of three genera, Aristostomias, Malacosteus, and Pachystomias, are capable of producing far-red, long-wave emissions (>650nm) from their AOs, a character unique among vertebrates. Aristostomias and Malacosteus posses a single far-red AO, while Pachystomias possesses anterior and posterior far-red AOs, each with smaller separate photophores positioned in their ventral margins. The purpose of this study was to establish the primary homology of the loosejaw AOs based on topological similarity of cranial nerve innervation, and subject these homology conjectures to tests of congruence under a phylogenetic hypothesis for the loosejaw dragonfishes. On the basis of whole-mount, triple-stained specimens, innervation of the loosejaw AOs is described. The AO of Aristostomias and the anterior AO of Pachystomias are innervated by the profundal ramus of the trigeminal (Tpr), while the far-red AO of Malacosteus and a small ventral AO of Pachystomias are innervated by the maxillary ramus of the trigeminal (Tmx). The largest far-red AO of Pachystomias, positioned directly below the orbit, and the short-wave AO of Photostomias are innervated by a branch of the mandibular ramus of the trigeminal nerve. Conjectures of primary homology drawn from these neuroanatomical similarities were subjected to tests of congruence on a phylogeny of the loosejaws inferred from a reanalysis of a previously published morphological dataset. Optimized for accelerated transformation, the AO innervated by the Tpr appears as a single transformation on the new topology, thereby establishing secondary homology. The AOs innervated by the Tmd found in Pachystomias and Photostomias appear as two transformations in a reconstruction on the new topology, a result that rejects secondary homology of this structure. The secondary homology of AOs innervated by the Tmx found in Malacosteus and Pachystomias is rejected on the same grounds. Two short-wave cephalic photophores present in all four genera, the suborbital (SO) and the postorbital (PO), positioned in the posteroventral margin of the orbit and directly posterior to the orbit, respectively, are innervated by separate divisions of the Tmd. The primary homologies of the loosejaw PO and SO across loosejaw taxa are proposed on the basis of similar innervation patterns. Because of dissimilar innervation of the loosejaw SO and SO of basal stomiiforms, primary homology of these photophores cannot be established. Because of similar function and position, the PO of all other stomiid taxa is likely homologous with the loosejaw PO. Nonhomology of loosejaw long-wave photophores is corroborated by previously published histological evidence. The totality of evidence suggests that the only known far-red bioluminescent system in vertebrates has evolved as many as three times in a closely related group of deep-sea fishes. J. Morphol., 2010. © 2009 Wiley-Liss, Inc. [source] Direct Infiltration of Brainstem Glioma Along the Cranial NervesJOURNAL OF NEUROIMAGING, Issue 2 2005Alexander Ree ABSTRACT The authors describe a case of a low-grade brainstem glioma extending along the cranial nerves without any evidence of leptomeningeal spread. The tumor extended directly along the VII-VIIIth cranial nerve complex and also along the trigeminal nerve, which is quite an unusual characteristic of the glial tumors. [source] PERCUTANEOUS THERMORHIZOTOMY IN A CLINICAL SERIES OF 80 PATIENTS WITH TRIGEMINAL NEURALGIA.JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002F. Rychlicki At the time of this report, 80 patients have been operated upon for typical trigeminal neuralgia by the percutaneous rhizotomy approach. Through follow-up evaluation extending over a period of 1 to 20 years, it has been completed for 65 of these patients. The average age was 63 years and 60% of patients were female. In 60% of patients pain was located on the right, and the second and third division of the trigeminal nerve were commonly involved. Isolated pain in the first or third division was less frequent than the second division. The disease had been present for an average of 8 years and was characterized by increasingly severe episodes of paroxismal pain and shortening period of remission. Nearly all patients had been treated with either diphenylhydantoin or carbamazepine, as well as other forms of medical and physical remedies. Response to follow-up was obtained for all 65 patients. All were contacted by questionnaire on phone and a family member was contacted if the patient had died. At the time of evaluation, 94% of patients reported excellent to good results from the procedure. The remaining patients obtained only fair results because of undesirable side-effects or recurrence of pain. The authors emphasize the importance of surgical therapy in trigeminal neuralgia when medical therapy fails. [source] Alteration of central motor excitability in a patient with hemimasticatory spasm after treatment with botulinum toxin injectionsMOVEMENT DISORDERS, Issue 1 2006Pablo Mir MD Abstract Hemimasticatory spasm (HMS) is a condition characterized by paroxysmal involuntary contraction of masticatory muscles. We performed an electrophysiological investigation of a single patient with HMS to identify any pathophysiological changes associated with the condition. We identified a delayed M wave and jaw jerk on the affected side and an absent masseteric silent period during spasm. Botulinum toxin injections successfully treated the clinical symptoms and resulted in a significant reduction in the excitability of the blink reflex recovery cycle. These data suggest that HMS may be due to ectopic activity in the motor portion of the trigeminal nerve that is capable of inducing changes in the excitability of central reflex pathways. These changes can be altered by successful treatment with botulinum toxin. © 2005 Movement Disorder Society [source] Trigeminal nerve repetitive stimulation in myasthenia gravisMUSCLE AND NERVE, Issue 4 2004Devon I. Rubin MD Abstract The aim of this study was to evaluate the utility of repetitive nerve stimulation (RNS) of the trigeminal nerve in assessing patients with myasthenia gravis (MG). In 26 normal controls and 21 patients with myasthenia gravis (MG), 2-Hz repetitive stimulation of the trigeminal nerve was performed using a monopolar needle for percutaneous nerve stimulation and recording over the surface of the masseter. In the MG patients, repetitive stimulation of the ulnar, spinal accessory, and facial nerves was also performed. The mean percent decrement in the compound muscle action potential (CMAP) amplitude among the different nerves at rest were: ulnar, 4.3%; spinal accessory, 10.1%; facial, 14%; and trigeminal, 17.3%. The facial nerve demonstrated abnormal decrement in 57% of all patients, compared with the spinal accessory (48%), trigeminal (43%), and ulnar (20%) nerves. All patients tolerated trigeminal RNS better than or as well as facial RNS. The study demonstrates that trigeminal RNS is a safe, reliable, efficient, and well-tolerated technique that provides another cranial nerve,muscle combination that can be used to supplement repetitive stimulation of other limb or cranial nerves in the evaluation of patients with bulbar or generalized MG. Muscle Nerve 29: 591,596, 2004 [source] The dorsal raphe nucleus in schizophrenia: a post mortem study of 5-hydroxytryptamine neuronesNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 3 2005R. M. Craven The 5-hydroxytryptamine (5-HT, serotonin) system has been implicated in the pathophysiology and treatment of schizophrenia. In this study, we addressed the hypothesis that a deficit of 5-HT neurones, either inherited or acquired, is central to the developmental pathology of the disorder. We examined putative 5-HT neurones of the dorsal raphe nucleus (DRN) in post mortem, formalin-fixed tissue from 15 schizophrenic patients and 20 control subjects matched for age and gender. No significant difference was detected between these groups in the number or size (cross-sectional area or diameter) of tryptophan-hydroxylase-immunoreactive cell profiles viewed in transverse sections collected from the level of the trochlear decussation to the emergence of the trigeminal nerve. Profile number was not affected by age, gender, side of the brainstem (left or right) or post mortem interval; however, time in formalin correlated negatively with the number of neurones counted. Moreover, a significant negative correlation was detected between time in formalin and the levels of immunoreaction product (optical density), which in turn correlated positively with our profile counts. A positive correlation was found between the age of subjects and our estimates of cell size. Our results do not support the proposal that an abnormality in the number and/or size of DRN 5-HT neurones is central to the aetiopathology of schizophrenia. [source] Anatomically based guidelines for systematic investigation of the central somatosensory system and their application to a spinocerebellar ataxia type 2 (SCA2) patientNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 5 2003U. Rüb Dysfunctions of the somatosensory system are among the clinical signs that characterize a variety of polyglutamine or CAG-repeat diseases. Deficits within this system may hinder the perception of potential threats, be detrimental to somatomotor functions, and result in uncoordinated movements, ataxia, and falls. Despite the considerable clinical relevance of such deficits, however, no systematic pathoanatomical studies of the central somatosensory system in polyglutamine diseases are currently available. The present paper has two goals: (1) re-commendation of an economical tissue sampling method and optimized histological processing of this tissue to allow rapid and reliable evaluation of the structural integrity of all known relay stations and interconnecting fibre tracts within this complex system, and (2) the proposal of guidelines for a rapid and detailed pathoanatomical investigative procedure of the human central somatosensory system. In so doing, we draw on the current state of neuroanatomic research and apply the methods and guidelines proposed here to a 25-year-old female patient with spinocerebellar ataxia type 2 (SCA2). The use of 100 µm serial sections through the SCA2 patient's central somatosensory components showed that obvious neuronal loss occurred in nearly all of the relay stations of this system (Clarke's column; cuneate, external cuneate and gracile nuclei; spinal, principal and mesencephalic trigeminal nuclei; ventral posterior lateral and ventral posterior medial nuclei of the thalamus), whereas the majority of interconnecting fibre tracts (dorsal spinocerebellar tract; cuneate and gracile fascicles; medial lemniscus; spinal trigeminal tract, trigeminal nerve and mesencephalic trigeminal tract) displayed signs of atrophy accompanied by demyelinization. These pathological findings suffice to explain the patient's impaired senses of vibration, position and temperature. Moreover, together with the lesions seen in the motor cerebellothalamocortical feedback loop (pontine nuclei, deep cerebellar nuclei and cerebellar cortex, ventral lateral nucleus of the thalamus), they also account for the somatomotor deficits that were observed in the young woman (gait, stance, and limb ataxia, falls, and impaired writing). In proposing these new guidelines, we hope to enable others to study the hitherto unknown morphological counterparts of somatosensory dysfunctions in additional CAG-repeat disease patients. [source] Herpes zoster in HIV infection with osteonecrosis of the jaw and tooth exfoliationORAL DISEASES, Issue 5 2006P Siwamogstham Background:, Herpes zoster (HZ) infection of the trigeminal nerve is associated with complications such as postherpetic neuralgia, facial scarring, loss of hearing ability and conjunctivitis. Until 2005, postherpetic alveolar necrosis and spontaneous tooth exfoliation have been described in 20 cases unrelated to HIV infection. Objective:, The aim of this study was to describe HIV infection in patients (two women, two men, average age 30 years) who suffered from HZ attacks to their trigeminal nerves. Main outcome measures:, None of the patients had received antiherpetic medications or antiretroviral therapy. HIV infection was only diagnosed after the development of HZ. Facial scarring with depigmentation and hyperesthesia (postherpetic neuralgia) was diagnosed in all four patients. Oral findings consisted of spontaneous loss of both maxillary or mandibular teeth. Osteonecrosis of varying extent was also found. Treatment consisted of extractions of teeth and administration of antibiotics and analgesics. Healing of alveolar wounds was unremarkable. Conclusion:, Complications affecting the alveolar bone and teeth seem to be rare in HIV-infected patients. [source] OC7 Trigeminal neuropathy and autonomic neuropathy , a rare combinationORAL DISEASES, Issue 2006C Frezzini Introduction, Idiopathic trigeminal neuropathy is an uncommon orofacial symptom giving rise to paraesthesia and/or anaesthesia of one or more divisions of the trigeminal nerve in the absence of an obvious aetiology. Idiopathic autonomic neuropathy is a rare disorder giving rise to cholinergic and/or adrenergic dysfunction of the autonomic nervous system. The combination of trigeminal and autonomic neuropathy in the absence of diabetes mellitus is unusual. Signs and symptoms, A 45-year-old male was referred to the Oral Medicine Unit of UCL Eastman Dental Institute and UCLHT Eastman Dental Hospital for assessment of possible xerostomia secondary to autonomic neuropathy. Medical history & social history. The patient had long-standing trigeminal neuropathy, long-standing autonomic neuropathy giving rise to dysphagia, gastrointestinal and bladder function and orthostatic hypotension. There was a previous history of Hodgkin's disease. Oral disease history, Clinical examination revealed neurotrophic destruction of the nasal septum (trigeminal trophic syndrome), chronic periodontitis, but no features of long-standing xerostomia. Resting sialometry was >0.1 ml min,1. Diagnosis, Trigeminal trophic syndrome secondary to trigeminal neuropathy and partial autonomic neuropathy. Treatment, The patient was referred for appropriate periodontal therapy. Conclusion, This is a unique example of trigeminal sensory neuropathy and autonomic neuropathy in the absence of diabetes mellitus. Early diagnosis of both disorders is important to ensure avoidance of facial complications such as trigeminal trophic syndrome and the oral consequences of long-standing xerostomia. [source] MULTIDISCIPLINARY PAIN ABSTRACTS: 20PAIN PRACTICE, Issue 1 2004Article first published online: 15 MAR 200 Trigeminocervical reflex is a brainstem reflex that is evoked by stimulating the sensory branches of the trigeminal nerve and can be recorded from the neck muscles. Electric stimulation of the supraorbital nerve evokes a reflex response (C3) and early reflex response (C1). The mean latencies of C1 and C3 of patients with parallel fibers (PFS) were compared with normal values. In healthy volunteers, C3 latency ± standard deviation was 54.17 ± 6.00 ms ipsilaterally and 51.25 ± 9.26 ms contralaterally. The difference was not significant. The C1 latency was 17.46 ± 4.89 ms. In patients with PFS, C1 latency was 13.83 ± 4.48 ms and the C3 latency was 62.70 ± 18.22 ms. The difference was not significant between the patients and healthy volunteers. Conclude in patients with PFS having neck pain, trigeminocervical connections were not influenced and some other mechanisms may be responsible for pain in these patients. [source] Molecular determinants of the face map development in the trigeminal brainstemTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 2 2006Reha S. Erzurumlu Abstract The perception of external sensory information by the brain requires highly ordered synaptic connectivity between peripheral sensory neurons and their targets in the central nervous system. Since the discovery of the whisker-related barrel patterns in the mouse cortex, the trigeminal system has become a favorite model for study of how its connectivity and somatotopic maps are established during development. The trigeminal brainstem nuclei are the first CNS regions where whisker-specific neural patterns are set up by the trigeminal afferents that innervate the whiskers. In particular, barrelette patterns in the principal sensory nucleus of the trigeminal nerve provide the template for similar patterns in the face representation areas of the thalamus and subsequently in the primary somatosensory cortex. Here, we describe and review studies of neurotrophins, multiple axon guidance molecules, transcription factors, and glutamate receptors during early development of trigeminal connections between the whiskers and the brainstem that lead to emergence of patterned face maps. Studies from our laboratories and others' showed that developing trigeminal ganglion cells and their axons depend on a variety of molecular signals that cooperatively direct them to proper peripheral and central targets and sculpt their synaptic terminal fields into patterns that replicate the organization of the whiskers on the muzzle. Similar mechanisms may also be used by trigeminothalamic and thalamocortical projections in establishing patterned neural modules upstream from the trigeminal brainstem. © 2006 Wiley-Liss, Inc. [source] Pathogenesis of equine herpesvirus-1 infection in the mouse modelAPMIS, Issue 1 2009GEORG GOSZTONYI Equine herpesvirus-1 (EHV-1) is a major equine pathogen causing respiratory diseases, abortions and severe neurological disorders. The basis of neurological disturbances is, as in other organs, infection of endothelial cells, followed by vasculitis, thrombosis and ischaemic damage of the parenchyma. Here, a murine model was used to explore the mechanism of entry to, and spread within the brain, the cell affinity of the agent and the modulating role of the immune defence, which are all factors governing the pathogenesis of the neurological disease. Because controversial views exist about these mechanisms, we undertook a neuropathological study with intranasally infected adult mice. EHV-1 entered the brain through the olfactory neuroepithelium and along the olfactory nerves, and spread transsynaptically in rostro-caudal direction, using olfactory and limbic neuronal networks. Exclusively neurons were infected. The cellular immune reaction exerted a restraining effect on virus dissemination. Following nasal infection, the olfactory route was the major pathway for virus entry and dissemination, involvement of the trigeminal nerve in virus spread seems much less probable. In the adult mouse brain EHV-1 behaves as a typical neurotropic agent, using, similarly to other herpesviruses, the neuronal networks for dissemination. Vasculitis, the predominant type of lesion in natural infection, and endothelial cell positivity for EHV-1 were detectable only in the lung. Thus, this agent exhibits in the mouse a dual affinity: it is neurotropic in the brain, and endotheliotropic in visceral organs. Consideration of pathogenetic aspects of equine and experimental murine EHV-1 infections also helps a better understanding of human herpetic brain disease. [source] Repair of the trigeminal nerve: a reviewAUSTRALIAN DENTAL JOURNAL, Issue 2 2010RHB Jones Abstract Nerve surgery in the maxillofacial region is confined to the trigeminal and facial nerves and their branches. The trigeminal nerve can be damaged as a result of trauma, local anaesthesia, tumour removal and implant placement but the most common cause relates to the removal of teeth, particularly the inferior alveolar and lingual nerves following third molar surgery. The timing of nerve repair is controversial but it is generally accepted that primary repair at the time of injury is the best time to repair the nerve but it is often a closed injury and the operator does not know the nerve is injured until after the operation. Early secondary repair at about three months after injury is the most accepted time frame for repair. However, it is also thought that a reasonable result can be obtained at a later time. It is also generally accepted that the best results will be obtained with a direct anastamosis of the two ends of the nerve to be repaired. However, if there is a gap between the two ends, a nerve graft will be required to bridge the gap as the two ends of the nerve will not be approximated without tension and a passive repair is important for the regenerating axons to grow down the appropriate perineural tubes. Various materials have been used for grafting and include autologous grafts, such as the sural and greater auricular nerves, vein grafts, which act as a conduit for the axons to grow down, and allografts such as Neurotube, which is made of polyglycolic acid (PGA) and will resorb over a period of time. [source] The use of vein grafts in the repair of the inferior alveolar nerve following surgeryAUSTRALIAN DENTAL JOURNAL, Issue 2 2010RHB Jones Abstract Damage to the branches of the trigeminal nerve can occur as a result of a variety of causes. The most common damage to all divisions of this nerve occurs as a result of facial trauma. Unfortunately, iatrogenic damage to the inferior alveolar branch of the mandibular division of the trigeminal nerve is common because of its anatomical position within the mandible and its closeness to the teeth, particularly the third molar. It has been reported there is an incidence of approximately 0.5% of permanent damage to the inferior alveolar nerve following third molar removal. Extraction of other teeth within the mandible carries a lower incidence of permanent damage. However, damage can still occur in the premolar area, where the nerve exits the mandible via the mental foramen. Dental implants are a relatively new but increasing cause of damage to this nerve, particularly if the preoperative planning is inadequate. CT scanning is important for planning the placement of implants if this damage is to be reduced. Primary repair of the damaged nerve will offer the best chance of recovery. However, if there is a gap, and the nerve ends cannot be approximated without tension, a graft is required. Traditionally, nerve grafts have been used for this purpose but other conduits have also been used, including vein grafts. This article demonstrates the use of vein grafts in the reconstruction of the inferior dental branch of the mandibular division of the trigeminal nerve following injury, in this case due to difficulty in third molar removal, following sagittal split osteotomy and during the removal of a benign tumour from the mandible. In the five cases presented, this technique has demonstrated good success, with an acceptable return of function occurring in most patients. [source] Neuropathogenesis of Naturally Occurring Encephalitis Caused by Listeria monocytogenes in RuminantsBRAIN PATHOLOGY, Issue 2 2010Anna Oevermann DVM, Dipl. Abstract Listeriosis is a serious food-borne disease with increasing frequency in humans and ruminants. Despite the facts that in both hosts, listeriosis can occur as rhombencephalitis and ruminants are a reservoir of Listeria monocytogenes (LM) strains pathogenic for humans, little work has been done on the pathogenesis in ruminants. This study investigates the neuropathogenesis of listeric encephalitis in over 200 natural cases in cattle, sheep and goats by analyzing anatomical distribution, severity, bacterial load and temporal evolution of the lesions. Our results suggest that LM gains access to the brainstem of all three species via axonal migration not only along the trigeminal nerve, but also along other nerves. The ensuing encephalitis does not remain restricted to the brainstem. Rather, LM spreads further from the brainstem into rostral brain regions likely by intracerebral axonal migration. Significant differences in severity of the lesions and bacterial load were found between cattle and small ruminants, which may be caused by species-specific properties of antibacterial immune responses. As histopathological lesions of human rhombencephalitis caused by LM strongly resemble those of ruminants, the disease likely has a similar pathogenesis in both hosts. [source] CGRP blockers in migraine therapy: where do they act?BRITISH JOURNAL OF PHARMACOLOGY, Issue 7 2008L Edvinsson Calcitonin gene-related peptide (CGRP) is expressed throughout the CNS and peripheral nervous system, consistent with control of vasodilatation, nociception, motor function, secretion and olfaction. ,CGRP is prominently localized in primary afferent C and A, fibres of spinal and trigeminal ganglia. Activation of the trigeminal nerve results in antidromic release of CGRP, acting through a CGRP1 receptor. Antagonists of CGRP1 receptors reduce signalling in the trigeminovascular pathway at multiple sites, putatively inside the blood,brain barrier. Other ways of interacting with CGRP mechanisms have appeared limiting the availability of CGRP in the circulation with a specific CGRP antibody or with a CGRP-binding RNA-Spiegelmer. Either way reduces neurogenic inflammation and attenuates signalling within the trigeminovascular pathway. Specific CGRP receptor blockade has been shown to reduce the effect of released CGRP and to abort acute migraine attacks. The novel approach of reducing available CGRP is limited by the blood,brain barrier; its usefulness may be more as prophylaxis rather than as acute treatment of migraine. British Journal of Pharmacology (2008) 155, 967,969; doi:fn1; published online 8 September 2008 [source] Bony anomaly of Meckel's caveCLINICAL ANATOMY, Issue 1 2006R. Shane Tubbs Abstract This study describes the seemingly rare occurrence of bone formation within the proximal superior aspect of Meckel's cave thus forming a bony foramen for the proximal trigeminal nerve to traverse. The anatomy of Meckel's cave is reviewed and the clinical potential for nerve compression from this bony anomaly discussed. Clin. Anat. 19:75,77, 2006. © 2005 Wiley-Liss, Inc. [source] The Trigeminal Vasculature Pathology in Patients With NeuralgiaHEADACHE, Issue 9 2007Slobodan Marinkovi Objective.,To examine the possible pathological changes of the trigeminal vasculature in patients with neuralgia. Background.,Such a study has never been performed before. The alterations of the trigeminal vessels could have important pathophysiological implications in the trigeminal neuralgia pathogenesis. Methods.,The biopsy specimens for the electronmicroscopic (EM) and immunohistochemical examination were taken during a partial rhizotomy in 6 patients with trigeminal neuralgia and in 2 persons with trigeminal neuropathy. In addition, the 32 normal trigeminal nerves were used as the control specimens. Results.,The vascular pathological alterations were noticed in 3 out of 6 neuralgia patients. The EM study revealed signs of apoptosis or degeneration, respectively, of some endothelial and smooth muscle cells in the wall of the trigeminal arterioles. The immune reactions against CD31, CD34, and ,-smooth muscle actin in these cells were weaker than in the control specimens, but stronger against factor VIII. In addition, the arteriolar basement membranes, which were thickened, showed an intense laminin, fibronectin, and collagen IV immunoreactivity. Similarly, some endothelial cells and pericytes of the intratrigeminal capillaries also showed signs of apoptosis or degeneration, respectively. Their basement membrane was very thick and showed an intense immune reaction against laminin, fibronectin, and collagen IV. Conclusion.,The observed pathological changes of the trigeminal vasculature could be the primary factor, while demyelination of the trigeminal nerve fibers could be the secondary process in some patients with neuralgia. [source] Neuron,Glia Signaling in Trigeminal Ganglion: Implications for Migraine PathologyHEADACHE, Issue 7 2007Srikanth Thalakoti BS Objective.,The goal of this study was to investigate neuronal,glial cell signaling in trigeminal ganglia under basal and inflammatory conditions using an in vivo model of trigeminal nerve activation. Background.,Activation of trigeminal ganglion nerves and release of calcitonin gene-related peptide (CGRP) are implicated in the pathology of migraine. Cell bodies of trigeminal neurons reside in the ganglion in close association with glial cells. Neuron,glia interactions are involved in all stages of inflammation and pain associated with several central nervous system (CNS) diseases. However, the role of neuron,glia interactions within the trigeminal ganglion under normal and inflammatory conditions is not known. Methods.,Sprague,Dawley rats were utilized to study neuron,glia signaling in the trigeminal ganglion. Initially, True Blue was used as a retrograde tracer to localize neuronal cell bodies in the ganglion by fluorescent microscopy and multiple image alignment. Dye-coupling studies were conducted under basal conditions and in response to capsaicin injection into the TMJ capsule. S100B and p38 expression in neurons and glia were determined by immunohistochemistry following chemical stimulation. CGRP levels in the ganglion were measured by radioimmunoassay in response to capsaicin. In addition, the effect of CGRP on the release of 19 different cytokines from cultured glial cells was investigated by protein microarray analysis. Results.,In unstimulated control animals, True Blue was detected primarily in neuronal cell bodies localized in clusters within the ganglion corresponding to the V3 region (TMJ capsule), V2 region (whisker pad), or V1 region (eyebrow and eye). However, True Blue was detected in both neuronal cell bodies and adjacent glia in the V3 region of the ganglion obtained from animals injected with capsaicin. Dye movement into the surrounding glia correlated with the time after capsaicin injection. Chemical stimulation of V3 trigeminal nerves was found to increase the expression of the inflammatory proteins S100B and p38 in both neurons and glia within the V3 region. Unexpectedly, increased levels of these proteins were also observed in the V2 and V1 regions of the ganglion. CGRP and the vesicle docking protein SNAP-25 were colocalized in many neuronal cell bodies and processes. Decreased CGRP levels in the ganglion were observed 2 hours following capsaicin stimulation. Using protein microarray analysis, CGRP was shown to differentially regulate cytokine secretion from cultured trigeminal ganglion glia. Conclusions.,We demonstrated that activation of trigeminal neurons leads to changes in adjacent glia that involve communication through gap junctions and paracrine signaling. This is the first evidence, to our knowledge, of neuron,glia signaling via gap junctions within the trigeminal ganglion. Based on our findings, it is likely that neuronal,glial communication via gap junctions and paracrine signaling are involved in the development of peripheral sensitization within the trigeminal ganglion and, thus, are likely to play an important role in the initiation of migraine. Furthermore, we propose that propagation of inflammatory signals within the ganglion may help to explain commonly reported symptoms of comorbid conditions associated with migraine. [source] | |||||||||||||||||||||||||||||||