Trigeminal amyloidoma: case report and review of the literature.

The authors present a case of amyloid infiltration involving the trigeminal nerve that mimicked a malignant cavernous sinus tumor with perineural tumor infiltration. A 64-year-old man presented with trigeminal nerve numbness. Imaging revealed a plaque-like enhancing lesion along the right lateral cavernous sinus extending anteriorly into Meckel's cave and involving the proximal V2 and V3 branches of the trigeminal nerve. The patient underwent an extradural frontotemporal craniotomy with middle fossa exposure of the cavernous sinus to diagnose and treat the presumed malignant cavernous sinus tumor. A reddish mass involving the lateral dural wall of the cavernous sinus was resected. The gasserian ganglion, V2, and V3, the latter of which was biopsied, were enlarged. Permanent histopathological studies showed microscopic eosinophilic, amorphous material, which stained positive for Congo red, and an absence of neoplastic cells. The final diagnosis was amyloidoma. Thus, amyloidomas can involve the trigeminal nerve or ganglia and should be considered in the differential diagnosis of a cavernous sinus lesion mimicking a tumor. Patients may have symptomatic improvement of trigeminal neuropathy with resection of the amyloidoma outside the nerve capsule that is compressing the nerve, while resection of the lesion from within the capsule may result in permanent trigeminal nerve dysfunction.     

Timecourse of development of the wallaby trigeminal pathway. I. Periphery to brainstem

The development of the vibrissae and their innervation and the maturation of the brainstem trigeminal sensory nuclei have been studied in the wallaby, Macropus eugenii, from birth to adulthood. At birth, developing vibrissal follicles consist of solid epidermal pegs surrounded by dermal condensations. The developing follicles and adjacent skin are innervated by trigeminal afferents. Ten days after birth the follicle contains a dermal papilla and the deep vibrissal nerve can be recognised. A hair cone is present at postnatal day (P) 30 and hairs are apparent on the skin surface by P35. By P63 the deep vibrissal nerve can be seen innervating Merkel cells in the outer root sheath; in addition, the first signs of the blood sinus can be recognised. Innervation of the inner conical body and lanceolate and lamellated receptors supplying the mesenchymal sheath and waist region are not seen until P119, when the follicle resembles that seen in the adult. At birth, central processes of the trigeminal ganglion cells have entered the trigeminal tract and extend from the rostral pons to the upper cervical cord. Labelling with a carbocyanine dye at P0 shows afferents extending medially from the tract into the trigeminal subnuclei at all levels. At this stage the trigeminal nuclei appear as areas of increased cell density in the lateral brainstem. By P30–40 the four subnuclei can be distinguished on the basis of shape, cytoarchitecture, and succinic dehydrogenase reactivity. Adult morphology is not fully established until P210. In mature animals, nucleus principalis contains closely packed, polymorphic cells, frequently aligned parallel to thick fibre bundles that traverse the nucleus obliquely. Subnuclei oralis and interpolaris contain sparsely distributed, medium to large cells, randomly oriented, as well as prominent rostrocaudally directed fibre bundles. Subnucleus caudalis consists of the marginal layer, substantia gelatinosa, and magnocellular layers as described in other species. Patches of increased succinic dehydrogenase or cytochrome oxidase reactivity, presumably corresponding to the vibrissae, are present in subnuclei principalis, interpolaris, and caudalis in developing and adult animals, although the pattern is less clear than in rats. The brainstem patches are first seen at P40, approximately 6 weeks before the corresponding vibrissal-related pattern develops in the cortex. This suggests that the onset of patch formation may be regulated independently at different levels of the pathway. © 1994 Wiley-Liss, Inc.     

The influence of muscle-conditioned media on chick embryo brainstem neurons in culture

Brainstem pieces from the trigeminal region of the metencephalic basal plate of 10-day chick embryos were dissociated and cultured in control conditions or in the presence of muscle-conditioned medium (MCM). The MCM was derived from age-matched target tissue relevant to this neuronal region (jaw musculature), from relevant target tissue of an age at which innervation would initially be taking place (4 days), and from nonrelevant target tissue also of an early stage (4-day limb bud). Neuronal survival and differentiation was assessed daily, for 7 days. Survival and differentiation were significantly enhanced by the 4-day jaw MCM compared to both the controls and the cultures grown with 10-day jaw MCM and 4-day limb MCM. These measures in the presence of 10-day jaw MCM and 4-day limb MCM did not differ, but surpassed that seen in control cultures. The results are compared to the more specific responsiveness seen in earlier (2-day) neural tube cultures, and their relationship to in vivo regenerative nerve fiber outgrowth is considered.     

实验性单纯疱疹病毒Ⅰ型感染兔眼部扫描电镜观察研究

应用ＤＭＳＯ（Ｄｉｍｅｔｈｙｌｓｕｌｆｏｘｉｄｅ二甲基亚砜）冷冻割断制样扫描电镜技术首次动态观察了不同感染阶段（ｐｏｓｔＩｎｆｅｃｔｉｏｎ，ＰＩ）实验性单纯疱疹病毒性角膜炎（ＨＳＫ）兔的角膜、三叉神经节（ＴＧ）泪腺等组织的病变情况。初步报告并分析了各组织病变的扫描图像结果，并对冷冻割断法观察扫描电镜的原理及优缺点予以讨论，认为该技术应用于眼部单疱病毒感染的研究图像清晰、直观、简便可行，是一种有实用价值的方法。     

颈交感神经对血管源性头痛痛觉传导的影响

目的采用电刺激大鼠上矢状窦(SSS)区硬脑膜,观察颈上交感神经节(SCG)摘除术前后在延髓和上颈段三叉神经脊束核一氧化氮合酶(NOS)阳性神经元数目的变化,以探讨交感神经系统在血管源性头痛(如偏头痛)涉及的伤害觉信息传递中的作用。方法以雄性SD大鼠(体重为220～250g)为实验对象,行颈上交感神经节摘除术后再手术暴露其SSS,然后电刺激SSS区硬脑膜,应用免疫组织化学染色技术,观察延髓和上颈段三叉神经脊束核NOS表达的变化。结果NOS免疫反应阳性神经元主要分布在三叉神经脊束核和上颈段脊髓的第Ⅰ、Ⅱ板层,双侧对称。假手术对照组、SCG摘除组每张切片的NOS阳性神经元数分别为150.2±10.3、223.0±11.6,SCG摘除组NOS阳性神经元数目较假手术对照组明显增加(P<0.05)。结论颈交感神经系统参与了头部血管源性疼痛(如偏头痛)中伤害性感觉信息导致的疼痛的产生、传导及调节过程。     

Pathological forms of brain electrical activity and localization of its sources in patients with trigeminal neuralgia

No significant differences from the typical electroencephalogram were observed in patients with trigeminal neuropathy. In patients with typical trigeminal neuralgia, the electroencephalogram variations were detected both in the changes of dominant activity and in the appearance of individual pathological phenomena. The three-dimensional localization of pathological activity generators points to the involvement of the median nonspecific brainstem structures into pathological process evoked by trigeminal neuralgia. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 9, pp. 275–279, September, 1997     

The organization of trigeminotectal and trigeminothalamic neurons in rodents: a double-labeling study with fluorescent dyes

Retrogradely transported fluorescent dyes (fast blue and diamidino-dihydrochloride yellow) were used to compare the distributions of trigeminofugal neurons that project to the superior colliculus and/or the thalamus in three rodent species. The objective was to determine what the projection and collateralization patterns of these trigeminofugal pathways are and whether they are similar among different species. In each anesthetized animal, one dye was injected into the superior colliculus and the other into the topographically congruent area of the thalamus. Counts of the numbers of yellow, blue, and double-labeled neurons were made throughout the trigeminal complex: principalis, pars oralis, pars interpolaris, and pars caudalis. Trigeminothalamic projections were similar in each of the rodent species studied. The densest concentration of retrogradely labeled neurons was in principalis, with substantially fewer neurons in pars interpolaris, and fewer still in pars oralis and pars caudalis. These neurons were generally small and tended to have round or fusiform somata. A common pattern was also noted among the three species for trigeminotectal neurons. Most trigeminotectal projections originated from neurons in pars interpolaris, somewhat fewer from pars oralis, and the fewest from principalis and pars caudalis. These neurons tended to be the largest in each subdivision and were often multipolar. Following paired injections of the tracers, double-labeled neurons were scattered throughout the sensory trigeminal complex and had morphologies characteristic of single-labeled trigeminotectal neurons. Although comparatively few double-labeled neurons were observed in any species, most of those seen were restricted to the ventrolateral portion of pars interpolaris, a position that corresponds to the representation of the vibrissae. These data indicate that, regardless of the rodent species, the vast majority of labeled trigeminal neurons project either to the superior colliculus or the thalamus, but not to both targets. This might be expected on the basis of the very different behavioral roles these structures play. On the other hand, a subpopulation of trigeminal neurons exists (mainly in pars interpolaris) that does project to both the superior colliculus and the thalamus, perhaps because both structures require some of the same somatosensory information to perform their behavioral functions.     

NGF Augmentation rescues trigeminal ganglion and principalis neurons,but not brainstem or cortical whisker patterns,after infraorbital nerve injury at birth

Prior studies indicate that neonatal nerve injury kills many trigeminal (V) first- and second-order cells, and interrupts pattern formation in the brainstem and cerebral cortex. Yet it is not known whether effects upon cell survival and pattern formation are causally related. To determine whether axotomized V ganglion cells can be rescued by an exogenous trophic agent, rats received 5 mg/kg of nerve growth factor (NGF) prior to, and every day after, infraorbital nerve section on the day of birth until sacrifice on postnatal day (PND) 1, 3, 5, 7, or 14. Other animals received identical lesions without NGF. Ganglion cell numbers were significantly reduced by PNDl in pups not given NGF, while NGF-treated rats displayed no significant cell loss through PND7. However, NGF did not permanently rescue V neurons because ganglion cell numbers were reliably reduced by PND14. Cell numbers in V nucleus principalis were reduced by PNDl in pups not given NGF, while NGF-treated animals displayed no cell loss through PND14. NGF's rescue of second-order cells is probably an indirect effect of NGF actions upon V ganglion cells because, in other newborns, NGF failed to maintain principalis cells after direct lesion of the left V ganglion. To determine whether preventing cell death permits whisker-related pattern formation, other rats also received NGF prior to and after infraorbital nerve section at birth. After 3–14 days, patterns were assessed in the brainstem and cortex with cytochrome oxidase histochemistry and serotonin immunocytochemistry. Whisker-related patterns failed to develop as in cases not given NGF. These data indicate that communication with the periphery is necessary for the maintenance of central whisker-related patterns. They also suggest that V ganglion cells can be rescued, albeit temporarily, from rapid injury-induced death by NGF, thereby delaying injury-induced cell death in nucleus principalis. However, the mechanism(s) responsible for injury-induced pattern alterations in the developing V system remains to be elucidated. © 1993 Wiley-Liss, Inc.     

Transient GABA immunoreactivity in cranial nerves of the chick embryo

The distribution and time course of gamma-aminobutyric acid (GABA) immunoreactivity was investigated in the cranium of the chick embryo from 2 to 16 days of incubation (E2-16). A fraction of nerve fibers transiently stains GABA-positive in all cranial motor nerves and in the vestibular nerve. Cranial motor nerves stain GABA-positive from E4 to E11, including neuromuscular junctions at E8-11; labeled fibers are most frequent in the motor trigeminal root (E6-9.5). Substantial GABA staining is present from E4 to E10 in a subpopulation (1-2%) of vestibular ganglion cells. Their peripheral processes are labeled in the vestibular endorgan, predominantly in the posterior crista. Some GABA-positive fibers are present in the olfactory nerve (after E5) and in the optic nerve (after E9.5); their immunoreactivity persists throughout the period investigated. Transient GABA immunoreactivity follows "pioneer" fiber outgrowth and coincides with the formation of early synaptic contacts. GABA-containing neurons may change their neuronal phenotype (loss of GABA expression) or they may be eliminated by embryological cell death. Periods of cell death were determined in cranial ganglia and motor nuclei by aggregations of pycnotic cells in the same embryonic material. The periods of embryonic cell death partly coincide with transient GABA immunoreactivity. The function(s) of transient GABA expression is unknown. Some lines of evidence suggest that GABA has neurotrophic functions in developing cranial nerves or their target tissue. In the developing neuromuscular junction, GABA may be involved in the regulation of acetylcholine receptors.