Radiological evaluation of the localization of sympathetic ganglia in the cervical region.

PURPOSE: To determine local variations of cervical sympathetic ganglia (CSG) according to vertebral levels on preoperative neck magnetic resonance imaging (MRI) by designating carotid artery (CA) as the standard landmark at the center, in attempts to prevent injury to CSG in the anterior-anterolateral approaches performed in the cervical spinal region. MATERIALS AND METHODS: The retrospective study reviewed neck MRI images of 281 patients, of which the images of 231 patients were excluded from the study based on the exclusion criteria. As a result, the MRI images of the remaining 50 patients were included in the study. The circumference of carotid artery (CA) was divided into eight equal zones with CA defined as the standard landmark at the center. High-risk zones were determined based on the anterior-anterolateral approaches. RESULTS: At C1 level, a superior ganglion was located on the right side in 32 (64%) and on the left side in 30 (60%) patients. At this level, it was most commonly located in Zone 6. Middle ganglion was observed most frequently at C3 level, which was detected on the right side in 17 (34%) and on the left side in 17 (34%) patients. At this level, it was most commonly located in Zone 2. CONCLUSION: Variations in the localizations of superior and middle cervical ganglia should be taken into consideration prior to surgical procedures planned for this region. This study sheds light on high-risk zones in the surgical site and could guide surgeons to better understand the location of cervical sympathetic ganglia before surgical planning.

Axotomy-induced changes in the chemical coding pattern of colon projecting calbindin-positive neurons in the inferior mesenteric ganglia of the pig.

The present study examines the response of colon-projecting neurons localized in the inferior mesenteric ganglia (IMG) to axotomy in the pig animal model. In all animals (n = 8), a median laparotomy was performed under anesthesia and the retrograde tracer Fast Blue was injected into the descending colon wall. In experimental animals (n = 4), the descending colon was exposed and the bilateral caudal colonic nerves were identified and severed. All animals were euthanized and the inferior mesenteric ganglia were harvested and processed for double-labeling immunofluorescence for calbindin-D28k (CB) in combination with either tyrosine hydroxylase (TH), neuropeptide Y (NPY), somatostatin (SOM), vasoactive intestinal polypeptide (VIP), nitric oxide synthase (NOS), Leu-enkephalin (LENK), substance P, vesicular acetylcholine transporter, or galanin. Immunohistochemistry revealed significant changes in the chemical coding pattern of injured inferior mesenteric ganglion neurons. In control animals, Fast Blue-positive neurons were immunoreactive to TH, NPY, SOM, VIP, NOS, LENK, and CB. In the experimental group, the numbers of TH-, NPY-, and SOM-expressing neurons were reduced, whereas the number of neurons immunoreactive to LENK was increased. Our data indicate that the colon-projecting neurons of the porcine IMG react to the axotomy in a similar, but not an identical manner in a comparison to other species, especially rodents. Further studies are needed to elucidate the detailed factors/mechanisms involved in the response to nerve injury.

Horner syndrome after carotid sheath surgery in a pig: anatomic study of cervical sympathetic chain.

In an experimental model, iatrogenic Horner syndrome developed after a right carotid sheath surgery in an infant pig (Sus scrofa). Horner syndrome is a classic clinical triad consisting of ipsilateral eyelid ptosis, pupil miosis, and facial anhydrosis. This syndrome results from cervical sympathetic chain (CSC) paresis and usually is acquired in humans. To determine whether the development of Horner syndrome in this situation could be attributed to pig anatomy, we compared the anatomy of the CSC in pigs and humans, by using 10 infant (age, 1 to 3 wk) pig cadavers. The CSC and cranial cervical sympathetic ganglion (CCG) were dissected bilaterally under a surgical microscope. These structures were consistently within the carotid sheaths of the pigs. In contrast, the CSC and CCG are outside the carotid sheath in humans. Awareness of the anatomic variation of the CSC and CCG within the carotid sheath in the pig and the possibility of the same variation in humans may help surgeons to identify and preserve important structures while performing cervical surgery in pigs and humans. Furthermore, this knowledge can aid in the diagnosis and prognosis of schwannoma.

CT-guided blocks and neuroablation of the ganglion impar (Walther) in perineal pain: anatomy, technique, safety, and efficacy.

OBJECTIVE: An alternate approach to the ganglion impar was chosen to minimize the risk of adverse events. Efficacy of the procedure was evaluated. METHODS: Charts and computed tomography (CT)-scans of patients who underwent block and neuroablation of the ganglion impar (Walther) between 2003 and 2007 were systematically reviewed with respect to adverse events and efficacy by rating pain intensity. A total of 76 blocks were performed, 48 of them being diagnostic blocks and 28 neuroablations. Chemical destruction was performed with ethanol, if pain recurred despite injection of local anesthetic. RESULTS: Interventional pain therapy was performed in 43 patients (age: 64.6+/-12.4 y, median 49.5 y, range: 36 to 86 y, male/female: 27/16) presenting with perineal pain of unknown origin (n=15), carcinoma of the prostate (n=8), colorectal carcinoma (n=7), postsurgery of thrombosis of perineal veins (n=3), postherpetic neuralgia (n=4), malformation of the spinal cord (n=2), vaginal protrusion (n=2), failed back surgery syndrome (n=1), and ablation of testis (n=1). CT-guided puncture was not associated with any adverse events and resulted in a reduction of numeric rating scale values from 8.2+/-1.6 to 2.2+/-1.6 (P<0.0001, 95% confidence interval 0.5) immediately at discharge and to 2.2+/-1.4 (P<0.0001, 95% confidence interval 0.4) at 4 months on follow up. DISCUSSION: CT-guided block and neuroablation of the ganglion impar (Walther) results in a significant reduction of pain scores and carries virtually no hazards.

Horner's syndrome: a complication of experimental carotid artery surgery in rats.

PURPOSE: To report on the occurrence of iatrogenic Horner's syndrome (HS) in epileptic rats after implantation of an electrode for vagus nerve stimulation and to describe the possible consequences of this new complication of carotid artery surgery in rats. METHODS: A bipolar circular electrode was placed around the left carotid artery and vagus nerve of 31 rats. The incidence of HS was evaluated by visual inspection within 24 h after surgery. RESULTS: 68% of rats suffered from HS immediately after surgery. This complication did not affect epileptogenesis. CONCLUSION: The occurrence of HS in the rat is a frequent complication of vagus nerve electrode implantation, which does not affect epileptogenesis in this study. However, rats affected by HS may suffer from damage to the sympathetic innervation of the gut, due to rat-specific neuroanatomy. Therefore, caution towards other research questions is warranted.

Neurturin suppresses injury-induced neuronal activating transcription factor 3 expression in cultured guinea pig cardiac ganglia.

Cultured guinea pig atrial whole mounts containing the intrinsic cardiac ganglia were used as an in vitro model to investigate the induction of the stress/injury marker activating transcription factor 3 (ATF-3). ATF-3 expression was quantified by using immunocytochemical labeling and real-time PCR. In freshly isolated ganglia, no neuronal or Schwann cell nuclei exhibited ATF-3 immunoreactivity. In 2-hour cultures, the induction of ATF-3 expression was evident in many Schwann cell nuclei, whereas no neuronal nuclei were ATF-3 immunoreactive. Beginning at 4 hours, the percentage of neurons with ATF-3-immunoreactive nuclei increased progressively, and, by 48 hours in culture, approximately 95% of the cardiac neurons had ATF-3-immunoreactive nuclei. Neurturin significantly suppressed ATF-3 expression in 48-hour-cultured neurons without effect on ATF-3 expression in Schwann cell nuclei. Neuturin also could reverse neuronal ATF-3 expression after its induction. The suppression of ATF-3 induction by neurturin was mediated by activation of the phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. Glial-derived neurotrophic factor (GDNF) also suppressed neuronal ATF-3 induction during culture. However, culture in serum-free media, presence of nerve growth factor, or addition of pituitary adenylate cyclase-activating polypeptide had no effect on ATF-3 induction in the 48-hour-cultured cardiac neurons. By 4 hours in culture, there was a significant increase in ATF-3 transcript levels, and neurturin partially suppressed ATF-3 transcript levels in 48-hour cultures. It is proposed that the loss of target-derived neurturin is a potential mechanism stimulating injury-induced expression of ATF-3 in cardiac neurons.

Horner Syndrome due to a solitary osteochondroma of C7: a case report and review of the literature.

STUDY DESIGN: Case report and review of the literature. OBJECTIVE: To report a 23-year-old woman with osteochondroma of the lower cervical spine who presented with Horner syndrome and to review the relevant literature. SUMMARY OF BACKGROUND DATA: Osteochondroma is the most common benign lesion of bone but rarely affects the spine. METHODS: Clinical history, routine radiographs, and computed tomography study of the patient were described. A review of the relevant literature was also done. RESULTS: The patient demonstrated a complete disappearance of clinical symptoms on the follow-up examination 60 days after surgery. No patients with Horner syndrome due to a solitary cervical osteochondroma have been previously reported in English-language medical literature. CONCLUSION: Vertebral involvement of osteochondroma is rare, especially with neurologic compromise. A young patient is presented with a symptomatic solitary osteochondroma of the seventh cervical vertebra who had Horner syndrome. This case report supports surgical intervention of symptomatic osteochondroma of the cervical spine.

Cervical angina caused by atlantoaxial instability.

Cervical angina is defined as a paroxysmal precordialgia that resembles true cardiac angina caused by cervical spondylosis. Cervical angina most commonly results from compression of the C7 ventral root. We present here a case of cervical angina caused by atlantoaxial instability. This case had marked atlantoaxial instability but no flexibility of the middle to lower levels of the cervical spine. Although there was mild C7 root compression on the radiologic findings, the chest pain was induced by neck motion, and the precordialgia disappeared after posterior atlantoaxial fusion without C7 root decompression. Therefore, we diagnosed this case as cervical angina caused by spinal cord compression at the C1-C2 level. It was speculated that a perturbation of the sympathetic nervous system or a hypofunction of the pain suppression pathway in the posterior horn of the spinal cord caused the pectoralgia. Although cervical angina is a rare disease, physicians should be aware of it; if there are no abnormal findings on cardiac examinations for angina pectoris, they should examine the cervical spine. Cervical angina due to atlantoaxial instability is one of the differential diagnoses of precordialgia.

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.

Modeling axonal injury in vitro: injury and regeneration following acute neuritic trauma.

Traumatic injury to axons was modeled in vitro using sympathetic principal neurons from the rat superior cervical ganglion. Neurons were grown as a pure culture on collagen in parallel tracks, with cell somata confined to the center, and neurites occupying the periphery of the culture dish. Growing as fascicles on tracks, the neurites demonstrated periodic varicosities. Neuritic transection was reliably and reproducibly achieved with a motor driven rubber impactor injury device. During a period lasting at least 1 h, dieback involving the proximal neurites averaged 105 +/- 10 microm. This was followed by neurite regeneration, with the injured segment being traversed within 36 h at an average rate of regeneration of 595 +/- 15 microm/day. The distal neurite segments showed degenerative changes within 1 h following transection, with initial receding of neurites progressing to vacuolation, beading, blebbing, and eventual detachment from the underlying matrix. This in vitro model of axonal injury allows neuritic injury to be studied at the cellular and molecular levels, and also provides a unique opportunity to test potential neuromodulatory and neuroprotective strategies.

Anatomical variants of the cervical sympathetic chain to be considered during neck dissection.

Horner's syndrome, as a complication of radical neck dissection, is given little attention in textbooks of head and neck surgery. To investigate which topographical anatomic factors, if any, might influence damage to the sympathetic chain during neck dissection, we undertook a series of 12 cadaveric neck dissections. The axial position of the cervical sympathetic chain varied. The chain could be clearly delineated from the carotid sheath except in two cadavers, in which it was found within the sheath. The presence of cervical ganglia also varied. We suggest that if the chain is within the sheath, it may be more likely to be injured during operation.

LIF-and IL-1 beta-mediated increases in substance P receptor mRNA in axotomized, explanted or dissociated sympathetic ganglia.

Regulation of substance P receptor (SPR) mRNA was examined in the rat sympathetic superior cervical ganglion (SCG) in vitro and in vivo after axotomy. Interleukin-1 beta (IL-1 beta) treatment of explanted ganglia elevated levels of SPR mRNA. By contrast, dissociated cultures of purified sympathetic neurons, purified fibroblasts, and purified Schwann cells each expressed only low levels of SPR mRNA, and treatment with the cytokine did not alter levels of the receptor mRNA. Treatment of Schwann cell or fibroblast cultures with leukemia inhibitory factor (LIF) also did not alter SPR mRNA. However, treatment of pure neuronal cultures with LIF significantly elevated levels of the receptor mRNA. Further, SPR mRNA increased in pure sympathetic neurons cultured in the presence of conditioned medium from IL-1 beta treated fibroblasts or Schwann cells; this effect was blocked in the presence of LIF antibody. This suggests that the stimulatory effects of IL-1 beta on SPR mRNA in explants is mediated by LIF release. Axotomy of the SCG in vivo resulted in a significant increase in LIF mRNA. Further, axotomy resulted in a significant increase in SPR mRNA, suggesting that LIF may mediate the increase in SPR mRNA. In view of the known effects of substance P (SP) on inflammatory responses, these observations suggest that coordinated expression of SP and SPR mRNA in neurons after nerve injury may participate in inflammatory and repair processes in the ganglion.

Postoperative mydriasis after repair of orbital floor fracture.

Mydriasis after operative repair of orbital floor fracture has been attributed to manipulation of the inferior oblique muscle. We treated two patients with mydriasis, one with an isolated mydriatic pupil and the other with a tonic pupil, which followed posterior orbital floor injuries and repair. The posterior location of the fractures suggests that surgical manipulation of or near the ciliary ganglion may account for these phenomena. Patients should be warned before posterior orbital floor repair about possible mydriatic or tonic pupils as a complication.

Secretomotor rhinopathy after Le Fort I maxillary osteotomy. Case report.

Severe secretomotor (vasomotor) rhinopathy is a very uncommon nasal condition which is believed to result from marked autonomic neural imbalance to the nasal and lacrimal glands. It has not, to our knowledge, been reported after trauma or elective surgery. A patient is described who developed this condition after a Le Fort maxillary osteotomy. The clinical difficulties of establishing this diagnosis are highlighted, and contemporary management options are discussed.

Injury-induced long-term expression of immediate early genes in the rat superior cervical ganglion.

Using in situ hybridization histochemistry and immunocytochemistry the induction of immediate early genes (IEGs) was studied in the rat superior cervical ganglion (SCG) after deafferentation, axotomy and sialectomy (removal of the submandibular gland). Control SCGs showed very low levels of IEGs, whereby Fos proteins were found in 1% and Jun protein in 6% of neurons, but not in non-neuronal cells. Denervation and axotomy induced c-fos, NGFI-A, c-jun, jun B and jun D mRNA expression for up to 6 days in non-neuronal cells, whereas in sympathetic neurons the expression of only c-jun mRNA was induced after axotomy and sialectomy. The induction of Fos and Jun proteins by neuronal injury was demonstrated by immunocytochemistry. The results indicate that neuronal injury induces IEGs mainly in non-neuronal cells and that in neurons only c-jun is induced after axotomy. It is hypothesized that the induction of IEG other than c-jun in neurons after brain injury is an indirect event unrelated to the neuronal response to injury.

Colocalization of NGF binding sites, trk mRNA, and low-affinity NGF receptor mRNA in primary sensory neurons: responses to injury and infusion of NGF.

The distributions of mRNAs for the protooncogene trk and the low-affinity NGF receptor (LNGFR) were studied by hybridization with oligonucleotide probes on sections of adult rat primary sensory and sympathetic ganglia. For comparison with high-affinity binding sites, adjacent sections were processed for NGF receptor radioautography. Among neurons in lumbar dorsal root ganglia and trigeminal ganglia, trk mRNA and NGF-binding sites were closely colocalized; this finding together with previous direct evidence in other cell types is taken to indicate that trk protein is an essential component of the high-affinity NGF receptor in adult sensory neurons. In lumbar dorsal root ganglia and trigeminal ganglia, abundant LNGFR mRNA was found in all neurons with strong 125I-NGF labeling and on additional neurons lacking high-affinity NGF-binding sites. The presence of abundant LNGFR in neurons with high-affinity receptors could be the cause and/or consequence of their ability to respond to NGF. Neurons with abundant LNGFR mRNA but few high-affinity NGF-binding sites may have receptors for other members of the neurotrophin family. In nodose ganglia, neurons with high concentrations of LNGFR mRNA greatly outnumbered the small percentage with abundant trk mRNA. Following intrathecal infusion of NGF to otherwise normal dorsal root ganglia, the concentrations of LNGFR mRNA but not those of trk mRNA and NGF-binding sites were increased in NGF-responsive neurons. The usual single normal pattern of frequency histograms of LNGFR labeling indices became bimodal in response to NGF. Concentrations of NGF-binding sites, LNGFR mRNA, and trk mRNA were all decreased by peripheral nerve transection and restored by exogenous NGF, the restoration being complete for LNGFR mRNA and partial for trk mRNA and NGF-binding sites. The data indicate that NGF can regulate both LNGFR and trk mRNAs but do not clarify the possible contribution of the LNGFR protein to high-affinity binding sites.