First Bite Syndrome: Presentation of a Patient Status-Post Right Carotid Endarterectomy.

First bite syndrome (FBS) is a sharp unilateral pain in the vicinity of the angle of the mandible after taking the first bite of a meal that presents typically after surgery in the area of the ipsilateral parapharyngeal space. It is not confirmed what the pathophysiology is that causes this pain, but the proposed mechanism is the iatrogenic damage of sympathetic fibers that extend from the superior cervical ganglion (SCG) to innervate the parotid gland. The presentation of this syndrome has been acknowledged in patients who have undergone head and neck tumor resections, but it has not been documented in the same thorough manner among vascular surgery cases in the parapharyngeal space, possibly because of a higher risk of development in other head and neck surgeries, or to under-reporting of cases. To date, only 5 cases of FBS status post carotid endarterectomy have been documented in the literature. Definitive treatment of FBS has not been established. Some studies have shown improvement with amitriptyline, and carbamazepine as well as botulinum toxin injections. We will present the case of a 75 year old male who developed first bite syndrome after a right carotid endarterectomy with efforts of raising awareness of a potential acute complication of carotid endarterectomy.

Oxidative stress damage circumscribed to the central temporal retinal pigment epithelium in early experimental non-exudative age-related macular degeneration.

Non-exudative age-related macular degeneration (NE-AMD) represents the leading cause of blindness in the elderly. The macular retinal pigment epithelium (RPE) lies in a high oxidative environment because its high metabolic demand, mitochondria concentration, reactive oxygen species levels, and macular blood flow. It has been suggested that oxidative stress-induced damage to the RPE plays a key role in NE-AMD pathogenesis. The fact that the disease limits to the macular region raises the question as to why this area is particularly susceptible. We have developed a NE-AMD model induced by superior cervical ganglionectomy (SCGx) in C57BL/6J mice, which reproduces the disease hallmarks exclusively circumscribed to the temporal region of the RPE/outer retina. The aim of this work was analyzing RPE regional differences that could explain AMD localized susceptibility. Lower melanin content, thicker basal infoldings, higher mitochondrial mass, and higher levels of antioxidant enzymes, were found in the temporal RPE compared with the nasal region. Moreover, SCGx induced a decrease in the antioxidant system, and in mitochondria mass, as well as an increase in mitochondria superoxide, lipid peroxidation products, nuclear Nrf2 and heme oxygenase-1 levels, and in the occurrence of damaged mitochondria exclusively at the temporal RPE. These findings suggest that despite the well-known differences between the human and mouse retina, it might not be NE-AMD pathophysiology which conditions the localization of the disease, but the macular RPE histologic and metabolic specific attributes that make it more susceptible to choroid alterations leading initially to a localized RPE dysfunction/damage, and secondarily to macular degeneration.

Retrograde influences of SCG axotomy on uninjured preganglionic neurons.

There is evidence that neuronal injury can affect uninjured neurons in the same neural circuit. The overall goal of this study was to understand the effects of peripheral nerve injury on uninjured neurons located in the central nervous system (CNS). As a model, we examined whether axotomy (transection of postganglionic axons) of the superior cervical ganglion (SCG) affected the uninjured, preganglionic neurons that innervate the SCG. At 7 days post-injury a reduction in choline acetyltransferase (ChAT) and synaptophysin immunoreactivity in the SCG, both markers for preganglionic axons, was observed, and this reduction persisted at 8 and 12 weeks post-injury. No changes were observed in the number or size of the parent cell bodies in the intermediolateral cell column (IML) of the spinal cord, yet synaptic input to the IML neurons was decreased at both 8 and 12 weeks post-injury. In order to understand the mechanisms underlying these changes, protein levels of brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) were examined and reductions were observed at 7 days post-injury in both the SCG and spinal cord. Taken together these results suggest that axotomy of the SCG led to reduced BDNF in the SCG and spinal cord, which in turn influenced ChAT and synaptophysin expression in the SCG and also contributed to the altered synaptic input to the IML neurons. More generally these findings provide evidence that the effects of peripheral injury can cascade into the CNS and affect uninjured neurons.

Sympathetic reinnervation of peripheral targets following bilateral axotomy of the adult superior cervical ganglion.

The ability of adult injured postganglionic axons to reinnervate cerebrovascular targets is unknown, yet these axons can influence cerebral blood flow, particularly during REM sleep. The objective of the present study was to assess quantitatively the sympathetic reinnervation of vascular as well as non-vascular targets following bilateral axotomy of the superior cervical ganglion (SCG) at short term (1 day, 7 day) and long term (8 weeks, 12 weeks) survival time points. The sympathetic innervation of representative extracerebral blood vessels [internal carotid artery (ICA), basilar artery (BA), middle cerebral artery (MCA)], the submandibular gland (SMG), and pineal gland was quantified following injury using an antibody to tyrosine hydroxylase (TH). Changes in TH innervation were related to TH protein content in the SCG. At 7 day following bilateral SCG axotomy, all targets were significantly depleted of TH innervation, and the exact site on the BA where SCG input was lost could be discerned. Complete sympathetic reinnervation of the ICA was observed at long term survival times, yet TH innervation of other vascular targets showed significant decreases even at 12 weeks following axotomy. The SMG was fully reinnervated by 12 weeks, yet TH innervation of the pineal gland remained significantly decreased. TH protein in the SCG was significantly decreased at both short term and long term time points and showed little evidence of recovery. Our data demonstrate a slow reinnervation of most vascular targets following axotomy of the SCG with only minimal recovery of TH protein in the SCG at 12 weeks following injury.

Chronic pain related to first bite syndrome: report of two cases.

First bite syndrome is the classic symptomatology of pain in the parotid region that occurs in response to the first bite of a meal. We report two cases of this syndrome in patients after operations to the parapharyngeal space.

Neuroanatomy of cervical sympathetic trunk: a cadaveric study.

To reduce the risk of iatrogenic injury to sympathetic chain during anterior and anterolateral approaches to the cervical spine, its location has to be well defined and known by surgeons. We analyzed the course of sympathetic chain and its ganglia from C7 up to its entry into the cranial base and its relationship mainly with the longus colli (LC). Formalin fixed 20 human cadavers were dissected under operating microscope. Measurement of the dimensions of the ganglia, distance of the trunk to the LC, and the angles identifying the course of the chain were performed. Superior and inferior cervical/cervicothoracic ganglion were observed in all specimens, the middle cervical ganglion was observed in 48% of the specimens. The middle ganglion consisted of two ganglia in 10% of the dissected sides. Forty percent of the inferior cervical/cervicothoracic ganglion was at the C7 level, 25% was at C7-Th1 disc level, and 35% was at Th1 level. Vertebral ganglion was detected in only 8% of the specimens. The course of the sympathetic trunk converges medially descending from upper cervical levels to the lower levels. Anterior surgical approach to the cervical spine is a commonly used procedure. Although Horner syndrome due to sympathetic injury is not a common sequence of cervical operations, our findings support the current few reports on the subject and should be useful to any surgeon who operates in the cervical region to avoid this uncommon complication.

[Dynamics of neural connection remodeling in rat superior cervical ganglion after dosated preganglionic trunk compression].

The objective of this study was to obtain a quantitative characteristic of posttraumatic regeneration of neural connections in the superior cervical ganglion (SCG) using the ratio of ganglionic neurons (N) to preganglionic myelinated axons (A) in the cervical sympathetic trunk (N/A) as an index of this process. Light and electron microscopy methods were used to study albino male rats which were divided into three groups: intact animals (7 months-old), age control group (19 months-old animals) and experimental group (1 year after compression of sympathetic trunk at SCG base made at the age of 7 months). The results have demonstrated that in intact animals N/A index was equal to 1:210. In the age control group it became equal to 1:173 and ione year after the compression--to 1:745. These data may indicate that the normalization of the neural connections in the SCG did not occur. The process of posttraumatic regeneration was not completed and became chronic.

Head-turned rear impact causing dynamic cervical intervertebral foramen narrowing: implications for ganglion and nerve root injury.

OBJECT: A rotated head posture at the time of vehicular rear impact has been correlated with a higher incidence and greater severity of chronic radicular symptoms than accidents occurring with the occupant facing forward. No studies have been conducted to quantify the dynamic changes in foramen dimensions during head-turned rear-impact collisions. The objectives of this study were to quantify the changes in foraminal width, height, and area during head-turned rear-impact collisions and to determine if dynamic narrowing causes potential cervical nerve root or ganglion impingement. METHODS: The authors subjected a whole cervical spine model with muscle force replication and a surrogate head to simulated head-turned rear impacts of 3.5, 5, 6.5, and 8 G following a noninjurious 2-G baseline acceleration. Continuous dynamic foraminal width, height, and area narrowing were recorded, and peaks were determined during each impact; these data were then statistically compared with those obtained at baseline. The authors observed significant increases (p < 0.05) in mean peak foraminal width narrowing values greater than baseline values, of up to 1.8 mm in the left C5-6 foramen at 8 G. At the right C2-3 foramen, the mean peak dynamic foraminal height was significantly narrower than baseline when subjected to rear-impacts of 5 and 6.5 G, but no significant increases in foraminal area were observed. Analysis of the results indicated that the greatest potential for cervical ganglion compression injury existed at C5-6 and C6-7. Greater potential for ganglion compression injury existed at C3-4 and C4-5 during head-turned rear impact than during head-forward rear impact. CONCLUSIONS: Extrapolation of present results indicated potential ganglion compression in patients with a non-stenotic foramen at C5-6 and C6-7; in patients with a stenotic foramen the injury risk greatly increases and spreads to include the C3-4 through C6-7 as well as C4-5 through C6-7 nerve roots.

Calcium entry through L-type calcium channels is essential for neurite regeneration in cultured sympathetic neurons.

Previous work showed that a post-neuritotomy rise in [Ca2+]i is required for regeneration. We tested the following hypotheses in cultured sympathetic neurons: (1) blocking L-type channels at the time of injury inhibits regeneration; (2) enhancing Ca2+ entry through L-type Ca2+ channels enhances regeneration; (3) L-type Ca2+ channel distribution is predominantly on the soma and proximal neurites of uninjured and injured neurons. To visualize L-type Ca2+ channels and block Ca2+ influx, the fluorescent dihydropyridine antagonist, DM-BODIPY, was used. Our results show that regeneration is markedly inhibited by the antagonist when administered 20 min. prior to injury, in the presence or absence of nerve growth factor (NGF) (p < 0.0001). Severe degeneration of proximal and distal neurites was seen 48 h after injury. Regeneration was minimally inhibited by the antagonist when administered 5 min after injury (p < 0.05), but not inhibited when administered 2 or 24 h after injury (p > 0.05). We found that L-type channels are distributed ubiquitously on the soma and neurites of uninjured and injured cells, and on regenerating neurites. The addition of the L-type channel agonist, BayK8644, (1 microM) 20 min prior to injury enhanced neurite length at 24 h post-injury (p = 0.002). Blocking L-type channels did not affect the viability of uninjured or injured cells. For the first time, it has been shown that Ca2+ entry through L-type Ca2+ channels is essential for post-neuritotomy sympathetic neurite regeneration, and that this effect shows a strict temporal dependency. We also demonstrated that regeneration can be enhanced by increasing Ca2+ influx through L-type channels.

Nicotinic acetylcholine receptor subtypes in the rat sympathetic ganglion: pharmacological characterization, subcellular distribution and effect of pre- and postganglionic nerve crush.

Nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission in autonomic ganglia, which innervate and control the activity of most visceral organs. By combining ultrastructural, immunocytochemical, and pharmacological analyses, we characterized the nAChR subtypes in the rat superior cervical ganglion (SCG) and the effect of pre- and postganglionic nerve crush on their number in the ganglion and their distribution at the intraganglionic synapses. Binding with radioactive nicotinic ligands, immunoprecipitation, and immunolocalization experiments revealed the presence of different nAChR subtypes: those containing the alpha3 subunit associated with beta4 and/or beta2 subunits that bind 3H-Epibatidine with high affinity, and those containing the alpha7 subunit that bind 125I-alphaBungarotoxin. After postganglionic nerve crush, the number of nicotinic receptors and immunopositive intraganglionic synapses for each nAChR subunit strongly decreased. Both the number of nAChRs and immunoreactivity recovered 26 days after injury, when regenerating postganglionic fibers had reinnervated the peripheral target organs, as shown by the restoration of tyrosine hydroxylase immunoreactivity in the iris. This observation and the lack of any effect of preganglionic nerve crush on the number of nicotinic receptors suggest that the peripheral targets affect the organization of intraganglionic synapses in adult SCG.

Evidence of neuroanatomical connection between the superior cervical ganglion and hypoglossal nerve in the hamster as revealed by tract-tracing and degeneration methods.

Previous studies have shown the existence of a sympathetic component in some cranial nerves including the hypoglossal nerve. In this study, the horseradish peroxidase (HRP) tract-tracing retrograde technique and experimental degeneration method were used to elucidate the possible neuroanatomical relationship between the superior cervical ganglion (SCG) and the hypoglossal nerve of hamsters. About 10% of the SCG principal neurons were HRP positive following the tracer application to the trunk of hypoglossal nerve. Most of the HRP-labelled neurons were multipolar and were randomly distributed in the ganglion. When HRP was injected into the medial branch of the hypoglossal nerve, some of the SCG neurons were labelled, but they were not detected when HRP was injected into the lateral branch. The present findings suggest that postganglionic sympathetic fibres from the SCG may travel along the hypoglossal nerve trunk via its medial branch to terminate in visceral targets such as the intralingual glands. By electron microscopy, the HRP reaction product was localised in the neuronal somata and numerous unmyelinated fibres in the SCG. In addition, HRP-labelled axon profiles considered to be the collateral branches of the principal neurons contained numerous clear round and a few dense core vesicles. Besides the above, some HRP-labelled small myelinated fibres, considered to be visceral afferents, were also present. Results of experimental degeneration following the severance of the hypoglossal nerve showed the presence of degenerating neuronal elements both in the hypoglossal nucleus and the SCG. This confirms that the hypoglossal nerve contains sympathetic component from the SCG which may be involved in regulation of the autonomic function of the tongue.

Monocyte chemoattractant protein (MCP)-1 is rapidly expressed by sympathetic ganglion neurons following axonal injury.

EDI-immunoreactive macrophages, absent from the superior cervical ganglia (SCG) of normal rats, appear in these ganglia within 48h after postganglionic axotomy. Further, resident macrophages show changes after axotomy. Since chemokines function as chemoattractants and activators of leukocytes, the effects of axotomy on chemokine expression in the SCG were examined. Within 6 h after nerve transection, increases were seen in mRNA levels for monocyte chemoattractant protein (MCP)-1. MCP-1 mRNA was concentrated in a population of neurons, while MCP-1 protein was localized to endothelial cells. This axotomy-induced neuronal MCP-1 expression may trigger the infiltration and/or activation of macrophages in SCG after injury.

Superior cervical ganglionectomy leads to dampening of amplitude of temperature rhythm in rats.

The circadian rhythm of body temperature (CRT) is a robust marker of the endogenous pacemaker function and is one of the most frequently studied rhythms. Melatonin, the main secretion of the pineal gland seems to have more of a thermomodulatory role in controlling the body temperature than having a direct role in thermoregulation. The sympathetic innervation to the pineal via the superior cervical ganglion determines the melatonin secretion, and superior cervical ganglionectomy (SCGx) decreases the secretion of melatonin. The present study was conducted on the Wistar rats (n = 12) to determine the role of melatonin in modulation of CRT. Adult male rats were either ganglionectomised (n = 6) or sham ganglionectomised (n = 6). Rectal temperature was recorded for CRT analysis. Cosinar analysis of the temperature record was done to get the acrophase, amplitude and mesor. Our results show that SCGx decreases the amplitude to the rhythm but has no effect on the mesor of the rhythm. Our study confirms that melatonin has little role to play in the thermoregulation and its role is mainly in thermomodulation.

[Claude Bernard-Horner syndrome and its opposite, Pourfour du Petit syndrome, in anesthesia and intensive care]. / Le syndrome de Claude Bernard-Horner et son contraire, le syndrome de pourfour du petit, en anesthésie-réanimation.

OBJECTIVE: To analyse cases of Horner's syndrome (HS) and its opposite, Pourfour du Petit's syndrome (PPS), occurring in anaesthesia and intensive therapy with consideration of the data of current literature. DATA SOURCES: For this paper we have reviewed the French, English and German literature published in anaesthesia and intensive care journals using Medline search and the current textbooks. STUDY SELECTION: All observational studies on these syndromes, whether clinical cases or letters to the editor, form the basis for this article. DATA EXTRACTION: The articles were analysed mainly with regard to diagnosis, therapy and prognosis of syndromes due to iatrogenic causes. DATA SYNTHESIS: HS is caused by a paralysis of the ipsilateral sympathetic cervical chain and includes a ptosis of the upper eyelid, a slight elevation of the lower lid, a sinking of the eyeball, a constriction of the pupil, a narowing of the palpebral fissure, a nasal stuffiness associated with anhidrosis, and flushing of the affected side of the face. Regional anaesthesia (intra-oral anaesthesia, brachial plexus block, epidural anaesthesia whether by thoracic, lumbar or caudal approach, as well as interpleural analgesia) is the main anaesthetic cause for HS. HS due to the effect of a local anaesthetic is transient, it can precede a high spinal block and a cardiovascular collapse. HS from puncture of the internal jugular vein is most often permanent. When transient, HS regresses within 3 months after puncture. Other causes of HS include intraoperative posture, pleural drain, neck surgery, neck trauma. A mydriatic collyrium, such as phenylephrine, resolves ptosis for less than 1 hour and results in blurred vision from pupillary dilation. Major ptosis requires surgery. PPS is the reciprocal HS and is caused by a stimulation of the ipsilateral sympathetic cervical chain. PPS can precede HS. It carries a risk for conjunctivitis, keratitis and epiphora in case of major exophthalmia. PPS is often reported as an unilateral mydriasis. PPS has the same causes as HS. Myotic collyriums are relatively inefficient. Major lid retraction requires a tarsorraphy, pomades and nocturnal lid occlusion. A part of HS and most PPS occurring in anaesthesia and intensive care remain unrecognized or are recognized with delay, especially if they remain minor and transient or when they occur in unconscious patients, in horizontal posture.

Isolated superior gluteal nerve injury: two case reports.

Isolated superior gluteal nerve injury has been infrequently described in the literature, mainly from injections or hip surgery. Its course through the greater sciatic foramen renders it at risk in pelvic or hip trauma. We report 2 cases of electromyographically documented isolated superior gluteal nerve injury following pelvic trauma. These cases illustrate that weakness in hip abduction following pelvic trauma may indicate the presence of a superior gluteal nerve injury, warranting further clinical and electrodiagnostic evaluation.

Pourfour du Petit syndrome: a case following a traffic accident with severe cranioencephalic trauma.

Poufour du Petit syndrome is an extraordinarily unusual clinical condition produced by hyperactivity of the sympathetic cervical chain as a consequence of irritation of these nerves. It causes an ipsilateral mydriasis, which, in patients suffering a head injury as in the case reported here, can confuse the diagnosis and disconcert physicians.

Histochemical detection of age- and injury-related changes in signal transduction in the superior cervical ganglion.

The superior cervical ganglion (SCG) is thought to be a good model for correlation studies of morphology, function and metabolism of neurons. The SCG has a relatively simple organization, it can be easily manipulated in situ, and it maintains synaptic transmission and a high metabolic rate during in vitro incubations. The histology and structure of SCG neurons have been characterized in detail, and physiologic stimuli, injury and aging have all been found to induce changes in the SCG morphology. During the last decade, research in the field of signal transduction has greatly expanded. Several signal transduction pathways have been identified that participate in the regulation of neurotransmitter synthesis, gene expression, neuronal excitability and growth factor responses of sympathetic neurons. We have been interested in using the SCG to study some of the second and third messengers involved in converting external stimuli received by sympathetic neurons into cellular short- and long-term events. Using immunohistochemistry, we have investigated protein kinase C-subtypes and the immediate early gene product Fos in the SCG, and characterized some of the changes induced by injury and aging in these messenger molecules. We will review the results and discuss the advantages and disadvantages of using histological methods in the study of signal transduction in sympathetic neurons.

Neuropeptide Y-immunoreactive primary afferents in the dental pulp and periodontal ligament following nerve injury to the inferior alveolar nerve in the rat.

The distribution of neuropeptide Y (NPY)-immunoreactive (IR) primary afferents in the dental pulp and periodontal ligament of the rat mandible were examined following combined chronic constriction injury (CCI) of the inferior alveolar nerve (IAN) and sympathectomy of the superior cervical ganglion (SCG). NPY-IR nerve fibers were observed around the blood vessels in the trigeminal ganglion, dental pulp and periodontal ligament in normal animals. Following combined CCI of the IAN and sympathectomy of SCG (SCGx), perivascular NPY-IR nerve fibers originating from SCG disappeared completely, but many NPY-IR nerve fibers coming from the trigeminal ganglion appeared in the dental pulp and periodontal ligament. In the molar dental pulp, thick NPY-IR nerve fibers were observed within the nerve bundle, and some thin NPY-IR nerve fibers ran towards the odontoblast layer; very few NPY-IR nerve fibers were observed in the incisor pulp. In the periodontal ligament of molar, thick NPY-IR nerve fibers appeared at the alveolar part following combined CCI of IAN and SCGx. In the lingual portion of the periodontal ligament of the incisor, many thick NPY-IR nerve fibers were observed. These occasionally showed a tree-like appearance, resembling immature Ruffini endings; slowly adapting mechanoreceptors. The present results indicate that periodontal mechanoreceptors are among the main targets of injury-evoked NPY following IAN injury.