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OBJECTIVE: Our objective was to facilitate the in vivo identification of the celiac ganglia on MRI by using MRI to identify the celiac ganglia in cadavers. CONCLUSION: MRI can show the celiac ganglia accurately in cadavers when the ganglia are large and labeled with gadolinium. The findings in cadavers can be a reference for identifying the celiac ganglia in vivo.
OBJECTIVE: Creutzfeldt-Jakob disease is a rare dementing illness that usually affects older adults. Currently, neuroradiologic examinations play a minor role in the diagnosis of Creutzfeldt-Jakob disease. Several single case reports have noted a distinctive finding of hyperintense signal abnormalities in the basal ganglia on T2-weighted MR images of patients with Creutzfeldt-Jakob disease. In order to assess the diagnostic utility of this finding, we studied the imaging features of four patients with Creutzfeldt-Jakob disease in whom this MR finding was present. MATERIALS AND METHODS: Two neuroradiologists retrospectively reviewed the MR images of four patients who had pathologically proved Creutzfeldt-Jakob disease and signal abnormalities in the basal ganglia on T2-weighted MR images. The patients' clinical findings were also analyzed. RESULTS: The four patients had MR examinations between 6 months and 1 year after the onset of symptoms. In all four cases, the hyperintense signal abnormalities in the basal ganglia on T2-weighted images were diffuse and bilaterally symmetric. The T1-weighted images were normal. A CT scan was obtained on a single patient and was normal. CONCLUSION: Although a lack of signal abnormality in the basal ganglia on MR imaging cannot be used to rule out a diagnosis of Creutzfeldt-Jakob disease, our experience and review of published reports suggest that in the proper clinical setting, bilaterally symmetric, diffuse hyperintense abnormalities in the basal ganglia on T2-weighted images may be a specific sign of Creutzfeldt-Jakob disease.
OBJECT: The peroneal nerve is the most common site of intraneural ganglia. The neurological deficit associated with these cysts is often severe and the operation to eradicate them is difficult The aims of this multicenter study were to collate the authors' experience with a relatively rare lesion and to improve clinical outcomes by better understanding its controversial pathogenesis. METHODS: Part I of this paper offers a description of 24 patients with peroneal intraneural ganglia who were treated by surgeons aware of the importance of the peroneal nerve's articular branch. Part II offers a description of three more patients who were seen after earlier operations in which the ganglion was excised, but the articular branch was not identified (all reportedly gross-total resections). Twenty-six of the 27 patients presented with clinical electrophysiological, and imaging evidence of a common peroneal nerve (CPN) lesion, predominantly affecting the deep peroneal nerve (DPN) division, and one patient presented with a painful mass of the CPN that was not accompanied by a neurological deficit. In all 24 patients in Part I there was magnetic resonance (MR) imaging evidence of a connection between the cyst and the superior tibiofibular joint, including one patient in whom high-resolution (3-tesla) MR neurography demonstrated the pathological articular branch itself. At the operation, the communication proved to extend through the articular branch of the CPN in all cases. The operation consisted of drainage of the cyst and ligation of the articular branch. At a minimum follow-up period of 1 year, these patients experienced significant improvements in their neuropathic pain, but only mild improvements in their functional deficits. In none of the 24 patients was there evidence of an intraneural recurrence. In three patients, however, extraneural ganglia developed: two patients with symptoms subsequently underwent resection of the superior tibiofibular joint without further recurrence and one patient with no symptoms was followed clinically after the recurrence was detected incidentally on 1-year postoperative imaging. As predicted, in Part II all three patients in whom the articular branch had not been ligated experienced early intraneural recurrence; both postoperative MR images and original studies, which were retrospectively examined, demonstrated a connection with the superior tibiofibular joint. CONCLUSIONS: The clinical presentation, electrical studies, imaging characteristics, and operative observations regarding peroneal intraneural ganglia are predictable. Treatment must address the underlying pathoanatomy and should include decompression of the cyst and ligation of the articular branch of the nerve. To avoid extraneural recurrence, resection of the superior tibiofibular joint may also be necessary, but indications for this additional procedure need to be defined. These recommendations are based on the authors' belief that intraneural peroneal ganglia arise from the superior tibiofibular joint and are connected to it by the articular branch.
Metabotropic glutamate receptors (mGluRs) coupled to G-proteins have important roles in the regulation of basal ganglia function. We have examined the localization of the mGluR7 mRNA and mGluR7a protein in the basal ganglia of the rat. Strong mGluR7 hybridization signals are found in cerebral cortex and striatum, but much less intense signals are present in other components of the basal ganglia. Abundant mGluR7a immunoreactivity was found in striatum, globus pallidus (GP), and substantia nigra pars reticulata (SNr). Examination using confocal microscopy together with dendritic and presynaptic markers as well as studies in lesion models provided evidence for the presence of mGluR7a on presynaptic terminals in all three structures. Electron microscopic studies confirmed the presence of mGluR7a in axon terminals in both the striatum and the GP and also revealed the presence of mGluR7a at postsynaptic sites in both of these regions. Our data demonstrate that mGluR7a is located not only on presynaptic glutamatergic terminals of the corticostriatal pathway, where it may serve as an autoreceptor, but also on terminals of striatopallidal and striatonigral projections, where it may modulate the release of gamma-aminobutyric acid (GABA). The presence of mGluR7 at these multiple sites in the basal ganglia suggests that this receptor has a particularly crucial role in modulating neurotransmitter release in major basal ganglia pathways.
INTRODUCTION: The cerebral cortex of mammals is massively interconnected with the basal ganglia. The manner in which the basal ganglia process information has been accepted since it was described in the 1980s. It is not a definitive model and many aspects of it still need clarification. DEVELOPMENT: The corpus striatum (ST) forms the entrance to the basal ganglia circuit (BG) and receives numerous afferent fibres from the cerebral cortex. Similarly, the internal segment of the globus pallidus (GPi) and the substantia nigra pars reticulata (SNpr) form the main nuclei for exit from the circuit and have an inhibitory effect on the pre-motor neurones of the ventral lamina of the thalamus. Between the entrance nucleus and the exit structures are two parallel systems of projection known as the direct and indirect pathways. The direct pathway projects monosynaptically only on the Gpi/SNpr complex. The indirect pathway projects polysynaptically on to the GR/SNpr complex after passing through the external segment of the globus pallidus (Gpe) and subthalamic nucleus. Imbalance in the activity of these two circuits will lead to alterations in discharge from the Gpi/SNpr complex which will cause bradykinesia or hyperkinesia. The bradykinesia or akinesia would be caused by increased gabaergic inhibition of the thalamic premotor neurones as a result of excessive discharge of the Gpi/SNpr complex. CONCLUSION: Current exploration of the electrophysiology of the basal ganglia and careful analysis of the clinical findings in lesions circumscribed to certain parts of the thalamus, subthalamus and internal globus pallidus in patients with Parkinson's disease, have led to the appearance of paradoxical effects, according to the current basal ganglia model.
We injected the anterograde fluorescent tracer 1,1;-dioleyl-3,3,3;, 3;-tetramethylindocarbocyanine methanesulfonate (DiI) into the nucleus ambiguus (NA) and used confocal microscopy to inventory NA fibers and axon terminals in whole-mounts of rat atrial tissues. Both the axons projecting to cardiac ganglia and the innervated principal neurons (PNs) were counted. Rats were injected unilaterally in the NA with DiI, either at four sites (between 600 microm rostral and 600 microm caudal to the obex) or at nine sites (1,600 microm rostral to 1,600 microm caudal). Fluoro-Gold was administered intraperitoneally to retrogradely label neurons of the dorsal motor nucleus of the vagus (DmnX), NA, and cardiac ganglia. To verify that the DiI-labeled fibers examined in the atria originated exclusively from the NA, neurons of the DmnX and the nodose ganglia were surveyed for DiI labeling. Our observations established that (1) NA fibers in the cardiac branches of the vagus numbered in the range of 82-151, left; or 60-122, right. (2) Both left and right NA supplied substantial numbers of fibers to each of the three major cardiac ganglionic plexuses. (3) NA axons terminated in dense basket, or calyx, endings around individual PNs. (4) By issuing divergent collaterals, individual NA fibers supplied numerous PNs with these calyx endings. (5) Labeled axons innervated 2,248 (left vagus) and 1,784 (right), or at least 56% and 45%, of the cardiac PNs. (6) Divergence (i.e., NA axons:PNs innervated) averaged between 1:27 (left vagus) and 1:30 (right vagus). Several features of these NA projections to cardiac ganglia contrasted sharply with those of DmnX projections that we have recently characterized with the same tracing protocol: (1) NA fibers did not innervate small intensely fluorescent cell clusters in cardiac ganglia, whereas DmnX axons did. (2) NA efferent fascicles contained more large fibers (presumably B-type), whereas the DmnX issued more fine caliber fibers (presumably C-type). (3) NA fibers diverged about three times as extensively as did DmnX axons. Taken together, our data strongly suggest that vagal control of the heart involves the convergence and integration of distinct NA and DmnX projections within the cardiac plexuses.
OBJECTIVE: To evaluate the role of CT and MR imaging in diagnosing germinomas arising in the basal ganglia and thalamus. METHODS: MR imaging of 11 boys (ranging in age from 3-15 years with a median of 10.7 years) with germinomas arising from the basal ganglia and thalamus was reviewed retrospectively and the imaging findings were compared with the features of 86 germinomas in other regions. The tumors located at basal ganglia in 9 and at thalamus in 2. All diagnosis was proved operatively and pathologyically. Five cases were studied using both CT and MR, 4 were examined with MR and 2 with CT only. RESULTS: In this series of 11 tumors, 9 were located in the basal ganglia and 2 in the thalamus. The shape of six tumors was global and 5 was lobulated. The cystic components or necrosis were intratumoral in 5 patients and hemorrhage in 4. Patchy enhancement was found in 9 patients and ring-enhancing lesions in 2. Tumor spread oppositely in 4 patients. Five patients demonstrated cortical atrophy ipsilaterally. CONCLUSION: The germinomas arising from the basal ganglia and thalamus have sex, location and imaging characteristics. Therefore, it is possible to make preoperative diagnosis using CT or MR.
Over the past few years, the role of the basal ganglia in epilepsy has been widely debated, the debate being mainly based on experimental data obtained from several animal models. In the present review, the possibility that basal ganglia circuits can generate some forms of seizure or participate to their initiation will first be addressed. In the second part of this chapter, recent data suggesting the involvement of the basal ganglia in the control of seizures will be discussed. Although it is clear that basal ganglia circuits cannot generate seizures and are unlikely to be involved in their initiation, numerous experimental data have revealed that seizures modify the activity of this system. More recently, the collection of pharmacological and electrophysiological data in animal models of epilepsy has led to the emergence of the basal ganglia as a possible control circuit for the seizures. These experimental data have already led to initial clinical trials in epileptic patients. The preliminary clinical data encourage the further development of experimental research in chronic models of epilepsy to better determine the exact output circuits involved in seizure interruption, the mechanisms participating in seizure control and whether the same circuits are involved in the control of different types of seizures. These studies may allow the identification of crucial structures and the types of epilepsy likely to benefit from this new therapeutic approach.
The effects of two barbiturates on calcium uptake by sympathetic ganglia have been examined. Sodium pentobarbital (0.4-0.75 mM) and sodium thiopental (0.3 mM) block the preganglionic stimulation-induced uptake of 45Ca by rat superior cervical ganglia but not action potential conduction in the presynaptic axons. The ganglionic-blocking agent, tetraethylammonium, does not inhibit stimulation-induced Ca uptake and does not prevent the blocking effect of thiopental. This effect is therefore probably presynaptic. Postassium-rich media also stimulate Ca uptake by the ganglia, and this effect is markedly inhibited by pentobarbital. Since the K stimulation effect is also observed in deafferented ganglia but not in guanethidine-denervated ganglia, this effect is probably associated primarily with postsynaptic elements. In sum, the data suggest that the barbiturates inhibit Ca permeability changes in both pre- and postsynaptic neurons.
The aim of this study was to obtain the normative data on the age-dependent transformation of morphometric and histochemical characteristics of neurocytes in different ganglia in albino rats. Cell cross-sectional area, activities of cholinesterase (demonstrated with thioacetic acid method) monoamine oxidase (demonstrated with Glenner method) were measured in neurocytes of stellate, spinal, trigeminal and gastric ganglia in rats aged 2 to 360 days. Measurements were made with the help of "Bioscan" videoanalyzer. Informational analysis was used for the evaluation of the degree of maturation of neurocyte systems. General features, age- and organ-related peculiarities of morphometric and enzyme-histochemical characteristics were established for neurocytes of different ganglia, as well as a heterochronism of their definitive state attainment. The time of stabilization for neurocytes of stellate and I thoracic spinal ganglia was the age of 60 days, for those of trigeminal ganglion and intramural gastric ganglia -90 and 120 days, respectively. By this time, neurocyte systems turned from a determined state into a probabilistic-determined one, this transformation being considered as a population stabilization.
Autonomic dysfunction is an increasingly recognized problem in aging animals and man. The pathologic changes that produce autonomic dysfunction in human aging are largely unknown; however, in experimental animal models specific pathologic changes have been found in selected sympathetic ganglia. To address whether similar neuropathologic changes occur in aging humans, the authors have examined paravertebral and prevertebral sympathetic ganglia from a series of 56 adult autopsied nondiabetic patients. They found significant, specific, age-related neuropathologic lesions in the prevertebral sympathetic superior mesenteric ganglia of autopsied patients. Markedly swollen dystrophic preterminal axons compressed or displaced the perikarya of principal sympathetic neurons. Ultrastructurally, these swollen presynaptic axons contained abundant disoriented neurofilaments surrounded by peripherally marginated dense core vesicles. Immunohistochemical studies demonstrated that dystrophic axons contained tyrosine hydroxylase and neuropeptide tyrosine (NPY)-like immunoreactivity but not other neuropeptides (VIP, substance P, gastrin-releasing peptide [GRP]/bombesin, met-enkephalin). Similar to the animal models of aging, lesions were much more frequent in the prevertebral superior mesenteric ganglia than in the paravertebral superior cervical ganglia. These studies demonstrate anatomic, peptidergic, and pathologic specificity in the aging human nervous system similar in many respects to that which the authors have described in experimental animal models. Neuroaxonal dystrophy in the sympathetic nervous system may underlie poorly understood alterations in clinical autonomic nervous system function that develop with age.
Antibodies to small cardioactive peptide (SCP) label a segmentally iterated subset of cells in the leech nerve cord, including the previously identified alternating SCP (AS) neurons. Unlike the majority of leech neurons, these cells are asymmetrically distributed in the adult nerve cord. Moreover, each AS neuron shows a strong tendency to lie on alternate right and left sides in successive ganglia. Previous work has shown that these unpaired neurons arise from bilaterally paired embryonic homologues, only 1 of which takes on the mature immunoreactive phenotype. The 2 AS homologues within a ganglion compete for this fate, in that either the right or the left homologue will become a mature AS neuron with a high degree of reliability if its contralateral homologue is ablated during embryogenesis. In this paper, we demonstrate the existence of interactions between neurons in adjacent ganglia that could account for the alternation of sides observed during normal development. The unilateral ablation of a single AS homologue neuron forced its contralateral homologue to take on the mature AS fate, and this consistently biased the side of AS development in adjacent, unlesioned ganglia both anterior and posterior to the lesion. One of the AS neurons, the caudal alternating SCP (CAS) cell, was injected with Lucifer yellow in adult nerve cords and was shown to have a large primary axon that extends into more anterior ganglia, as well as other, finer axons that are variable in number and arrangement. If the interganglionic interaction of AS neuron homologues is mediated by their primary axons, signals of developmental import must be transmitted both anterogradely and retrogradely along the axon's length. The present results indicate that the development of individual AS neurons is influenced by homologous cells located in the same and neighboring ganglia and suggest that the final, multisegmental patterning of the AS neuron distribution is not predetermined, but rather, arises as an emergent property of the cell interactions that occur during nervous system differentiation.
The metabolism of catecholamines in rat superior cervical ganglia in organ culture was examined by biochemical and histofluorescence methods. Pronounced increases in both norepinephrine and dopamine content were observed in the cultured ganglia. Norepinephrine levels were more than doubled after 12 hours in culture and reached a maximum after 24 hours. The greatest increase in norepinephrine concentration occurred in the region of the postganglionic nerve trunks and was correlated with an accumulation of intense catecholamine fluorescence in the stumps of the severed postganglionic nerves. Since the rate of norepinephrine synthesis was unaltered, the increase in norepinephrine levels in cultured ganglia appears to be a result of blocked axoplasmic transport of this amine out of the ganglia. The dopamine content of the cultured preparations was not altered after 24 hours but increased rapidly thereafter and attained a maximum at 48 hours. The changes in dopamine did not parallel the changes in norepinephrine either in time course or distribution. The elevated levels of dopamine were accompanied by an increased rate of dopamine synthesis. It is suggested that the increased dopamine content in cultured ganglia is the result of an enhanced synthesis of this amine by specific dopaminergic cells.
Electron microscopy was used to study synapse development in the cardiac ganglia of human fetuses ranging from 8 to 27 weeks of ovulation time. Staining with ethanolic phosphotungstic acid was used for analysis of synaptic active zones. Specialization of interneuronal links begins with the appearance of electron dense material on plasmalemmas of nerve cells in the places of simple contacts. First synapses with single synaptic vesicles and short osmiophilic zones were found in cardiac ganglia in 8-week-old fetuses. Large granular vesicles and mitochondria vesicles are formed from cisternae of agranular endoplasmic reticulum in the preterminal parts of axons and moved by axoplasmic transport to the osmiophilic zones of future synapses. Axodendritic synapses appeared earlier in the cardiac ganglia than axosomatic ones, the latter were observed from the middle of gestation. Transient neuroglial synapse-like contacts were found in the cardiac ganglia. Staining with phosphotungstic acid made it possible to distinguish the degree of synapse maturation according to active synaptic zones. The peculiarities of synaptic development in cardiac ganglia in comparison with that in the central nervous system may be accounted for by different origins of the neural tube and of neural crest and by the level of their phylogenic development.
A two-site enzyme immunoassay was used to determine the nerve growth factor (NGF) contents of sympathetic ganglia and their corresponding target tissues in adult rats. The destruction of sympathetic nerve terminals by 6-hydroxydopamine (6-OHDA) and the blockade of axonal transport by colchicine resulted in a rapid increase in the NGF levels of sympathetically innervated organs and a rapid decrease in the sympathetic ganglia. NGF levels in heart atrium, heart ventricle, submandibular gland, and iris increased 2- to 4-fold 12 hr after injection of 6-OHDA, whereas the NGF contents of stellate and superior cervical ganglia dropped to a minimal level of 3 to 4% of control 24 hr after injection. Twelve hours after treatment with colchicine the NGF levels in sympathetically innervated organs increased 2- to 3-fold, whereas the NGF contents of sympathetic ganglia fell to one-third of control values. The half-lives of NGF in the superior cervical and stellate sympathetic ganglia were 4.5 and 4.8 hr, respectively, as determined by the decrease of NGF content after treatment with 6-OHDA. These results indicate that the synthesis of NGF is normally confined to the innervated target organs with no significant contribution of ganglionic cells. This is consistent with the concept that NGF acts as a retrograde messenger between target organs and innervating sympathetic neurons.
By using selective dopamine (DA) receptor agonists and antagonists, we have demonstrated previously the presence of DA-2- and DA-1-like DA receptors in the stellate ganglia of the dog. Activation of either DA-2- or DA-1-like receptors by quinpirole or fenoldopam, respectively, leads to inhibition of ganglionic transmission. In the present study we have examined the involvement of DA receptor subtypes in the action of DA on ganglionic transmission. Inasmuch as stimulation of DA receptors is linked to the activation (DA-1) or inhibition (DA-2) of the enzyme adenylate cyclase, we have also measured the accumulation of cyclic AMP (cAMP) for biochemical characterization of ganglionic DA receptors. In isolated stellate ganglia treated with phentolamine and propranolol, DA caused concentration-dependent inhibition of ganglionic transmission as evidenced by reductions in the amplitude of the evoked postganglionic compound action potentials. The inhibitory effect of DA on ganglionic transmission was antagonized by both the DA-1 receptor antagonist, R-sulpiride, and the DA-2 receptor antagonist, S-sulpiride. However, the more potent and selective DA-1 receptor antagonist, SCH-23390, failed to antagonize the DA-induced inhibition of ganglionic transmission. Isolated stellate ganglia were also utilized for the measurement of cAMP. Neither DA nor the selective DA-1 receptor agonist, fenoldopam, caused any significant changes in cAMP, suggesting the lack of an adenylate cyclase-linked DA-1 receptor in the ganglia. On the other hand, beta adrenoceptor activation by isoproterenol produced a 3-fold increase in cAMP content of the stellate ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)
The timetable of cell generation, neuronal death and neuron numbers in the fused proximal glossopharyngeal (IX) and vagal (X) ganglion and distal IX and X ganglia were studied in normal and nerve growth factor (NGF) treated chick embryos. 3H-thymidine was injected between the 3rd and 7th days of incubation and embryos sacrificed on the 11th day. Neurons in the distal IX and X ganglia were generated between the 2nd and 5th days of incubation, the peak mitotic activity occurring on the 4th and 3rd days, respectively. Neurons of the proximal IX and X ganglion were generated between the 4th and 7th days, with maximum neuron generation on the 5th day of incubation. Counts of neurons in the 3 ganglia between the 5th and 18th days of incubation showed a maximum of 22,000 on the 8th day in the proximal IX and X ganglion and this decreased to 12,000 by the 13th day. In the distal IX ganglion, the neuron number decreased by 44% from 4,500 on the 6th day to 2,500 by the 11th day. A similar decrease of 43% was found in the distal X ganglion, the neuron number falling from 11,500 on the 7th day to 6,500 by the 11th day of incubation. Neuronal cell death in these ganglia extended from the 5th to the 12th day of incubation, maximum cell death occurring at or after the cessation of mitotic activity. NGF administration from the 5th to the 11th day of incubation did not have a measurable effect on the neurons of proximal IX and X and distal IX ganglia, but increased neuronal survival by 30% in the distal X ganglion.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of the present research is to study the development of spinal ganglia implanted onto chorio-allantoic membrane (CAM), where they are supplied by 'foreign', extraembryonic vessels. Small blocks including a segment of the neural tube and 4 pairs of somites were isolated from the brachial or thoracic or lumbar region (neuromeres C13 - T1 or T3 - T6 or L1 - L4) of thirty 3-day donor chick embryos and grafted on the CAM of as many 10-day host chick embryos. At regular time intervals after grafting, the implants were fixed, embedded in paraffin, serially cross-sectioned and stained. The preliminary results are similar for the ganglia from the 3 regions: they seem to indicate that in the spinal ganglia grafted on the CAM the developing blood vessels do not exert any morphogenetic influence on the substratum; this corroborates results from previous researches (2) on the normally 'in situ' developing ganglia. It is now the author purpose to submit to a careful analysis a datum from the present research: namely, the earlier appearance of the endoganglionic vessels in the brachial and lumbar grafted ganglia than in the thoracic ones.