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Background: Traumatic brachial plexus injuries are rare but serious consequences of major traumas. Pre-ganglionic lesions are considered irreparable, while post-ganglionic injuries can be potentially treated if an early diagnosis is available. Pre-surgical diagnosis is important to distinguish low-grade from high-grade lesions and to identify their location. The aim of the review is to evaluate the diagnostic accuracy of magnetic resonance imaging (MRI) in the identification of adult post-ganglionic lesions due to traumatic brachial plexus injuries, compared to intraoperative findings. Methods: Research on the main scientific electronic databases was conducted. Studies of adults with traumatic post-ganglionic brachial plexus injuries were included. The index test was preoperative MRI and the reference standard was surgical exploration. Pooled sensitivity and specificity were calculated. Results: Four studies were included for the systematic review, of which three articles met the inclusion criteria for the meta-analysis. Pooled sensitivity and pooled specificity values resulted high. The sensitivity value is associated with a high heterogeneity index of the selected literature. Conclusion: MRI can be considered, despite the limits, the gold standard exam in morphological evaluation of brachial plexus injuries, particularly in the diagnosis of post-ganglionic traumatic injuries.

We have previously shown that sudomotor dysfunction in autoimmune autonomic ganglionopathy is severe, widespread, and predominantly post-ganglionic. However, the long-term changes in sudomotor function have not been studied in detail. Our objective was to characterize the long-term changes in sudomotor dysfunction in patients with autoimmune autonomic ganglionopathy.Changes in sudomotor function were compared in a cohort of nine α3 nAChR antibody positive autoimmune autonomic ganglionopathy patients over an approximate 5-year period. Standard measurements of sudomotor function were used including the thermoregulatory sweat test and quantitative sudomotor axon reflex test.Total body anhidrosis on thermoregulatory sweat testing showed improvement in four of nine patients. Quantitative sudomotor axon reflex testing for both forearm and foot sites was variable with four of nine patients showing improvement in total sweat output. Distribution of sudomotor dysfunction at follow-up was post-ganglionic in seven of nine patients at the foot site and three of nine patients at the forearm site. Overall, sudomotor dysfunction was post-ganglionic in seven of nine patients throughout the follow-up period (62.4 ± 19.4 months).Sudomotor dysfunction in autoimmune autonomic ganglionopathy was severe and widespread throughout the follow-up period for the majority of patients studied. Sudomotor dysfunction was predominantly post-ganglionic throughout the follow-up period.

Quantitative Sudomotor Axon Reflex Testing is a useful measure of post ganglionic sudomotor function. The test is based on the iontophoresis of an acetylcholine solution which induces a local sweat response. We have previously described a gel-based vehicle that may provide another option for the iontophoresis of acetylcholine. It was our objective to compare the influence of the vehicle (gel versus solution) on sudomotor recordings and perceived discomfort. Results show gel-based vehicles are very similar to solution-based vehicles during Quantitative Sudomotor Axon Reflex Testing.

1. The present report documents evidence suggesting that endothelin (ET) is a mediator and modulator of post-ganglionic sympathetic neuronal development. 2. Endothelin is produced by post-ganglionic neurons and by cells adjacent to these neurons. 3. Post-ganglionic sympathetic neurons express functional receptors for ET. 4. Endothelin promotes the survival of cultured post-ganglionic sympathetic neurons and modulates the morphological and biochemical differentiation of these neurons. 5. Endothelin enhances the activity of nerve growth factor and modulates the release of neurotransmitter from post-ganglionic sympathetic nerve terminals.

Summary Applying double-fluorescence immunohistochemistry, adrenergic and non-adrenergic postganglionic sympathetic neurons, in the porcine inferior mesenteric ganglion (IMG) are subdivided according to size and cotransmitter content. Calcitonin gene related peptide (CGRP)-immunoreactive (IR) neurons are demonstrated to belong to the non-adrenergic, i.e. tyrosine hydroxylase- and DOPAmine-s-hydroxylase-(DsH)-negative subpopulation of postganglionic perikarya. Virtually all of the CGRP-IR postganglionic neurons exhibit colocalization with somatostatin (SOM), and, some of them with neuropeptide tyrosine (NPY). Additionally, NPY-, SOM-, and NPY/SOM-IR subpopulations of adrenergic and non-adrenergic neurons are observed. CGRP-immunoreactivity is seen in dense networks of intraganglionic varicose nerve fibres, adjacent to the TH-and SOM-IR neurons. NPY-IR perikarya are sparsely supplied by CGRP-IR fibres. SOM- and NPY-IR nerve fibres also exist in the inferior mesenteric ganglion. The functional relevance of CGRP-IR postganglionic neurons, as well as target organs of these neurons remain to be elucidated.

Axotomy of a major cranial post ganglionic branch of the superior cervical ganglion of an adult rat resulted in increased radiolabeling of tubulin and microtubule-associated proteins after an in vitro 5-h incubation with [14C]-methionine. The increased incorporation of the radiolabel began at day 1 postoperatively and exhibited a biphasic response, peaking at days 3 and 8.

Noradrenaline uptake is a property not only of sympathetic axons but also of their ganglion cells. This has been shown by electronautoradiography which indicates higher than background levels of 3H-noradrenaline in ganglion cells (incubated in isotope solution) following post-ganglionic nerve ligation. Under these circumstances noradrenaline concentrations have been found specifically related to the Golgi complex and granular endoplasmic reticulum in hypogastric ganglion cells.

1. The spontaneous activity recorded from the central ends of the uterine nerves of the rabbit is described. The discharges resembled those reported from other post-ganglionic sympathetic nerves; the individual units appeared to discharge remarkably regularly at frequencies between 4/sec and 1 per 3 sec. 2. The resting discharge in late pregnant rabbits was usually more intense than in non-pregnant rabbits; otherwise no clear relation existed between variations in the discharges and in the sexual state. 3. The discharge was reduced by stimulation of the central end of the depressor nerve and increased by asphyxia. 4. Stimulation of either the preganglionic or the post-ganglionic nerve by a single shock evoked a long after-discharge in the post-ganglionic nerve. It is shown that this after-discharge is a property of some of the post-ganglionic neurones supplying the rabbit's uterus which does not depend on the integrity of the preganglionic nerves or of the spinal cord, or on transmission through the ganglia, and that it is not a general property of the sympathetic post-ganglionic neurones of the rabbit. 5. Repetitive stimulation of the preganglionic nerve at low frequencies augmented the after-discharge in some cases and depressed it in others; stimulation at high frequencies invariably depressed the after-discharge. Repetitive stimulation of the post-ganglionic nerve at low or high frequencies depressed the after-discharge. 6. If the normal preganglionic activity was interrupted abruptly by an anode block, the post-ganglionic discharge also stopped abruptly. 7. A ganglion-stimulating action of hexamethonium is described. 8. Adrenaline inhibited the post-ganglionic neurones with no sign of excitation. This effect was antagonized by Rogitine without affecting the resting discharge, the action of the depressor nerve or the after-discharge in any way.

1. Electrophysiological studies showed that injury of post-ganglionic nerve fibres leads to severe and prolonged depression of synaptic transmission through the rat superior cervical ganglion, beginning within 24 h. This is in line with the results of previous studies in other species and upon other neurones. 2. electron microscopy after post-ganglionic axotomy revealed nerve endings of presynaptic type with all the specialized membrane-related features of a synaptic zone, but which were not apposed to any post-synaptic nervous element. These umusual profiles were interpreted as detached presynaptic nerve endings. In normal and control ganglia, such profiles formed at most 0-5% of all vesicle-containing profiles of presynaptic type; in ganglia with all major post-ganglionic branches cut the proportion rose to approximately 7%, between 3 and 7 d post-operatively. Over this period, the mean incidence of chromatolytic neurones was 74-6%. 3. Concomitantly, the incidence of synapses within the ganglion fell by about 75%, reaching its lowest levels between 3 and 7 d post-operatively. There was strikingly little evidence of persistence of post-synaptic membrane specializations ('membrane thickenings') following detachment of synapses. 4. At longer survival intervals the incidence of synapses gradually increased, and that of detached nerve endings gradually decreased; recovery was well advanced by 42 d. 5. The fall in the incidence of synapses was closely paralleled by a fall in the incidence of desmosome-like attachments in the ganglion; the incidence of such attachments was found to be correlated to a significant degree with that of synapses. 6. It is concluded that most or all of the synapses upon sympathetic neurones become physically dissociated during the chromatolytic reaction of these neurones to axotomy. The failure to persist of ultrastructurally specialized post-synaptic sites, and the loss of desmosomes (particularly marked for those involving purely post-ganglionic nervous elements) suggest that the post-ganglionic neurone is losing all its specializations for attachment. 7. Some evidence suggests that the satellite cells may effect the final separation between pre- and post-synaptic structures.

Parotid glands of rat have been examined 12, 24 and 48 hours after avulsion of the cervical sympathetic ganglion and compared with the normally innervated left glands. Formaldehyde-induced fluorescence showed a relatively normal complement of adrenergic nerves at 12 hours but most of the nerves had lost their noradrenaline content by 24 hours and no fluorescent nerves were detected at 48 hours. Ultrastructural degenerative changes in axons were rare at 12 hours, common at 24 hours, and the degenerating axons appeared to have disappeared by 48 hours. The glands looked whitish and pale and similar to the controls at 12 and 48 hours but were pinkish and oedematous on the sympathectomised side at 24 hours. Correspondingly the acini were loaded with secretory granules at 12 and 48 hours but were extensively depleted of granules at 24 hours. This loss of granules is considered to be due to sympathetic “degeneration secretion” caused by the release of noradrenaline from the degenerating adrenergic nerves between 12 and 24 hours after ganglionectomy. This is thought to be the first example of morphological change resulting from “degeneration activation” to be recorded microscopically.

The action of neuromuscular blocking agents on the spontaneous sympathetic activity has been quantitated. “On line” spectrum analysis has been applied to the action potential of pre- and post ganglionic nerves of the coeliac plexus. The activity, the frequency spectrum and their changes after the injection of clinical and high doses of decamethonium, D-tubocurarine, succinylcholine, gallamine and pancuronium are determined.

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1. Using field stimulation with short trains of pulses (< 10 per train), the post-ganglionic motor transmission in the mammalian vas deferens has been further analysed pharmacologically. 2. In preparations taken from guinea-pigs, rats and rabbits the effects of the indirectly sympathomimetic drugs, tyramine and cocaine, could be explained entirely on the basis of the actions of released, endogenous noradrenaline. 3. Tyramine produced a contraction in vasa taken from normal rats but not from normal guinea-pigs. The tyramine contraction was due to release of endogenous noradrenaline because it was not seen in preparations taken from reserpinized rats and because it was abolished in normal vasa by phenoxybenzamine or phentolamine, thus denying the supposed inaccessibility, to α-blockers, of the motor α-adrenoceptors activated by endogenous noradrenaline. 4. Phenoxybenzamine or phentolamine failed to block post-ganglionic motor transmission in rat and in guinea-pig vasa. 5. Tyramine strongly inhibited motor transmission in vasa taken from normal but not from reserpinized guinea-pigs. 6. Tyramine produced inhibition of motor transmission in phenoxybenzamine-treated preparations taken from normal but not from reserpinized rats. 7. Cocaine inhibited motor transmission in guinea-pig and in rat vasa. This effect was not due to a local anaesthetic or to a smooth-muscle depressant action because it did not occur in preparations taken from reserpinized animals. 8. The inhibitory effect of tyramine or cocaine was not abolished by β-adrenoceptor blockade with propranolol. 9. Whereas reserpinization abolished the tyramine- and cocaine-inhibitions, it did not affect the inhibitory actions of noradrenaline or of PGE2. 10. Indomethacin and sodium meclofenamate, which suppress prostaglandin synthesis, did not affect the twitch-inhibiting actions of noradrenaline, tyramine or cocaine. 11. These results provide further support for the conclusion that post-ganglionic motor transmission to the vas deferens is non-adrenergic in these species and assign to endogenously released noradrenaline an inhibitory role upon motor transmission.

Publisher Summary This chapter describes sympathetic ganglia in culture. Freshly excised ganglia contain terminals of preganglionic cholinergic neurons, cell bodies of sympathetic neurons whose axonal processes extend into the post ganglionic nerve trunk or possibly on other ganglion cells and small numbers of other catecholamine-containing cells some of which are intensely fluorescent. In addition, there are a variety of non-neuronal supporting elements. In a recent careful study of neurons in cultured sympathetic ganglia from neonatal rodents and chick embryos, two types of neurons were distinguished. Most of the neurons, which were called Type II, were relatively large, egg-shaped cells with eccentric round clear nuclei, abundant clear cytoplasm, and one or more processes. The catecholamine fluorescence of these cells was usually low and always evenly distributed. About 5–10% of the cells were small, with scant cytoplasm and variable intensity of catecholamine fluorescence. These small Type I cells were most outstanding because of their ability to migrate out of the cultured ganglion.

Thirty-one patients with pain in one or both hands associated with sympathetic dystrophy or Raynaud's disease were studied before and after the administration of a placebo and guanethidine 10mg i.v. Before and after the injections each patient reported his pain and had sympathetic activity assessed by: (1) palmar sweating; (2) skin temperature; (3) hand blood flow and (4) the ice response of hand blood flow. There was no significant change in any index after the placebo injection, nor was there any change in palmar sweating after guanethidine. Following guanethidine there were significant changes in reported pain (P less than 0.001), skin temperature (P less than 0.05), hand blood flow (P less than 0.001) and the ice response of hand blood flow (P less than 0.001). The results confirm the importance of the post-ganglionic sympathetic nervous system in the transmission of pain in these patients.