Horner's syndrome after neck surgery.

Horner's syndrome (oculosympathetic paresis) is characterised by the classic triad of ipsilateral palpebral ptosis, pupillary miosis and facial anhidrosis. The syndrome arises from the interruption of sympathetic innervation to the eye and adnexa at varying levels. It is a rare complication of neck surgery.We describe 6 patients who presented with Horner's syndrome after a neck procedure in our department during the last 5 years and review the different neck procedures that can cause it.

Anterior exposure of the lumbar spine with and without an "access surgeon": morbidity analysis of 265 consecutive cases.

STUDY DESIGN: Retrospective review OBJECTIVE: To compare the incidence and type of exposure-related complications for anterior lumbar surgery performed with and without an "access" surgeon. SUMMARY OF BACKGROUND DATA: No data exist comparing the incidence and type of exposure-related complications for anterior lumbar surgery performed with and without a vascular surgeon's assistance. METHODS: A retrospective review was performed for 265 consecutive patients who underwent anterior lumbar spine surgery at our institution from 2003 to 2005. Each patient's records were reviewed for diagnosis, procedure, whether the surgical exposure was conducted by the spine surgeon (Spine) or with a vascular surgeon's assistance (Team), levels exposed, complications, and any lasting sequelae. RESULTS: The percentage of patients with at least 1 intraoperative complication was 8% and 12% for the Spine and Team cases, respectively. Two percent of the Spine patients experienced an intraoperative vascular complication compared with 7% of the Team cases. No intraoperative vascular complication occurred in the single-level Spine exposures. Four percent of the patients with single-level exposures with Team approaches sustained an intraoperative vascular complication. Eight percent of the multilevel Spine cases sustained an intraoperative vascular complication compared with 9% of the multilevel Team exposures. There were 14 vascular injuries appreciated intraoperatively in a total of 13 patients. These injuries were directly repaired in 10 patients without any residual sequelae. The rate of vascular complications was statistically higher for multiple-level exposures (9%) versus single-level exposure (3%; P = 0.0357). The rate of retrograde ejaculation was 6% in the Spine cases whereas it was 7% in the Team approach. CONCLUSIONS: Our results do not support the notion that the presence of an "access" surgeon will change the type and rate of complications. With adequate training and judgment, spine surgeons may safely perform such exposures, provided vascular surgical assistance is readily available.

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.

Reversible chest tube horner syndrome.

A 54-year-old woman who underwent chest tube placement after a lung biopsy was found on the first postoperative day to have ipsilateral ptosis and miosis, suggesting a Horner syndrome. A chest CT scan showed that the tip of the chest tube was apposed to the stellate ganglion. Repositioning of the chest tube later on the first postoperative day led to complete reversal of the Horner syndrome within 24 hours. We propose that the Horner syndrome arose as a result of pressure on the stellate ganglion, which interrupted neural conduction but did not sever the sympathetic pathway ("neurapraxia"). Whether prompt repositioning of the chest tube was critical in reversing the Horner syndrome is uncertain.

IL-1 alpha and TNF-alpha expression in rat periapical lesions and dental pulp after unilateral sympathectomy.

OBJECTIVES: Apical periodontitis is an inflammatory disease characterized by bone resorption, and sympathetic nerves are known to modulate bone resorption and bone remodeling. Higher numbers of osteoclasts and larger periapical lesions have been observed after sympathectomy in rats, but the mechanisms underlying the inhibitory effect of sympathetic nerves on osteoclasts are unknown. This study aimed to test the hypothesis that sympathetic nerves inhibit the production of the bone-resorbing pro-inflammatory cytokines IL-1 alpha and TNF-alpha in rat periapical lesions. METHODS: Rats were unilaterally sympathectomized and apical lesions were induced by exposing the dental pulp of molar teeth to the oral microflora. We quantified the cytokines IL-1 alpha and TNF-alpha by enzyme-linked immunosorbent assay, and immunohistochemical analysis was done for qualitative localization. Pulp from intact incisor teeth was tested as a control. RESULTS: We showed that IL-1 alpha was increased, but not TNF-alpha, in the periapical lesions on the sympathectomized side. Both IL-1 alpha and TNF-alpha were expressed in unexposed pulp. TNF-alpha was significantly decreased in the denervated incisor pulp, whereas the level of IL-1 alpha remained unchanged. CONCLUSIONS: This study suggests that sympathetic nerves have an inhibitory effect on IL-1 alpha in periapical lesions and a stimulatory effect on TNF-alpha in the intact rat pulp.

Hepatic blood flow responses to mechanical stimulation of the skin in anaesthetised rats.

The aim of the present study was to investigate how hepatic blood flow (HBF) changes in response to mechanical stimulation of different areas of the skin in anaesthetised rats, by focusing on involvement of the hepatic sympathetic nerves in and contribution of systemic circulatory changes to the HBF responses. HBF was measured at the surface of the left lateral lobe using the laser Doppler flowmetry. Both innocuous and noxious mechanical stimuli were applied to skin areas of the abdomen and hindlimb. Innocuous mechanical stimulation (brushing) of the abdomen and hindlimb did not significantly change HBF, while noxious mechanical stimulation (pinching) of the abdomen and hindlimb did. The responses to pinching were dependent on the sites stimulated. Pinching of the abdomen decreased, while pinching of the hindlimb increased the HBF. The decrease of HBF in response to abdominal pinching remained after the spinal cord was transected at T1-2 level, but the response was diminished after hepatic sympathetic nerves were severed. On the other hand, the increase of HBF in response to hindlimb pinching was dependent on the increase in blood pressure, and was not influenced by the severance of hepatic sympathetic nerves, and the responses to hindlimb pinching were almost absent after the spinal cord was transected. Based on these results, we suggest that noxious mechanical stimulation of the skin produces changes of HBF, either as a reflex response via activation of the hepatic sympathetic nerves or as a passive response to systemic circulatory changes, depending on the sites stimulated.

Modulation of parasympathetic neuron phenotype and function by sympathetic innervation.

Selective sympathetic nerve dysfunction occurs during aging and in certain disease states. Here, we review findings concerning the effects of chronic sympathetic denervation on parasympathetic innervation to orbital target tissues in the adult rat. Long-term sympathetic denervation was induced by excising the ipsilateral superior cervical ganglion for 5-6 weeks prior to analyses. Following sympathectomy, pterygopalatine ganglion parasympathetic neurons show reduced nitric oxide synthase protein in their somata and projections to vascular targets. Laser Doppler measurements of ocular blood flow indicate that sympathectomy is also accompanied by reduced nitrergic vasodilatation. In the superior tarsal muscle of the eyelid, parasympathetic varicosities, normally, are distant to smooth muscle cells but make axo-axonal contacts with sympathetic nerves, consistent with physiological evidence showing only prejunctional inhibitory effects on sympathetically mediated smooth muscle contraction. Following sympathectomy, parasympathetic varicosities proliferate and closely appose smooth muscle cells, and this is accompanied by establishment of parasympathetic-smooth muscle excitatory neurotransmission. Many pterygopalatine parasympathetic neurons normally contain nerve growth factor (NGF) protein and express NGF mRNA. However, following chronic sympathectomy or elimination of sympathetic impulse activity, NGF mRNA and protein are markedly reduced, indicating that sympathetic neurotransmission enhances NGF expression in parasympathetic neurons. Together, these findings portray a striking dependency of parasympathetic neurons on sympathetic nerves to maintain normal phenotype and function. Sympathetic influences on parasympathetic neurons may be mediated, in part, through axo-axonal synapses. NGF synthesis and release by parasympathetic neurons may represent a molecular basis underlying the formation of these synapses, and up-regulation of NGF synthesis by sympathetic nerve activity may act to reinforce these associations.

Nicotinic acetylcholine receptor subunit proteins alpha7 and beta4 decrease in the superior cervical ganglion after axotomy.

Synaptic transmission in the superior cervical ganglion (SCG) is mediated by nicotinic acetylcholine receptors (nAChR). After transection of the postganglionic nerves of the SCG in the adult rat, the transcript levels of four of the five nAChR subunits present in the ganglion, alpha3, alpha5, alpha7, and beta4, decrease dramatically. In the present study, the effect of axotomy on nAChR subunit expression was examined at the protein level, focusing on the alpha7 and beta4 subunits. Immunohistochemistry with monoclonal antibody mAb306 (for the alpha7 subunit) and polyclonal antibody 4886 (for the beta4 subunit) showed that immunoreactivities for both alpha7 and beta4 subunits were concentrated in neurons in the intact ganglion. Results from double staining with antibodies to these subunits and to tyrosine hydroxylase, the enzyme that catalyzes the rate-limiting step in the biosynthesis of the sympathetic neurotransmitter norepinephrine, demonstrated that most neurons in the SCG express both the alpha7 and beta4 subunits. Three days after axotomy, the number of immunolabeled neurons and the intensity of the immunostaining per labeled neuron were decreased for both subunits. Decreases in subunit levels were also observed by Western blot analysis. Observing changes in these subunits over time after surgery revealed that, while the protein level of the alpha7 subunit recovered substantially within 2 weeks after the lesion, that of the beta4 subunit stayed low. These data demonstrate that decreases in nicotinic receptor subunits are among the changes in proteins that occur in axotomized sympathetic neurons, and suggest that these decreases may contribute to the depression in ganglionic synaptic transmission observed in axotomized ganglia.

Peripheral nerve injury leads to the establishment of a novel pattern of sympathetic fibre innervation in the rat skin.

Peripheral nerve injury has been shown to result in sympathetic fibre sprouting around dorsal root ganglia (DRG) neurons. It has been suggested that this anomalous sympathetic fibre innervation of the DRG plays a role in neuropathic pain. Other studies have suggested an interaction between sympathetic and sensory fibres more peripherally. To date, no anatomical study of these possible interactions in the terminal fields of sensory and sympathetic fibres has been performed; therefore, the authors set out to study them in the rat lower lip after bilateral lesions of a sensory nerve, the mental nerve (MN). Immunocytochemistry for both substance P (SP) and dopamine-beta-hydroxylase (DbetaH) was performed. Within the first week post-MN lesions, the SP-immunoreactive (IR) fibres had degenerated almost completely, whereas DbetaH-IR fibres were found in the upper dermis, an area from which they normally are absent. These DbetaH-IR fibres were present in the upper dermis at all postsurgery times studied (1, 2, 3, 4, 6, and 8 weeks). It is noteworthy that, although, by week 6 post-MN lesions, SP-IR fibre reinnervation of the lower lip was occurring, the DbetaH-IR fibres still were present in the upper dermis. Quantification revealed that the migration and branching of the DbetaH-IR fibres into the upper dermis occurred gradually and was most significant at 4 weeks post-MN lesions, as demonstrated by the fact that the DbetaH-IR fibres were found 169.6 +/- 91.4 microm away from the surface of the skin compared with 407.1 +/- 78.4 microm away in sham-operated animals. These findings suggest that the ectopic innervation of the upper dermis by sympathetic fibres may be important in the genesis of neuropathic pain through the interactions of sympathetic and SP-containing sensory fibres.

Ontogeny of G-protein expression: control by beta-adrenoceptors.

Cardiac cell homeostasis is maintained in the face of excessive beta-adrenoceptor stimulation through the process of desensitization. Desensitization is not an inherent property of these cells but rather is acquired during development; neonates given beta-agonists actually show heterologous sensitization, involving changes in the expression and catalytic activity of adenylyl cyclase (AC) as well as an increased receptor/G-protein coupling. The current study examines the role of specific G-protein components, G(s)alpha and G(i)alpha, in the ontogeny of beta-adrenoceptor responses and in the transition from agonist-induced sensitization to desensitization. Between postnatal days (PN) 6 and 15 there was a significant decrease in the 52 kDa isoform of G(s)alpha with no accompanying change of the 45 kDa form; over the same period, G(i)alpha3 also declined substantially. In contrast, the 45 kDa isoform of G(s)alpha and G(i)alpha1,2 remained fairly constant over the same period and fluoride-stimulated AC activity increased. Treatment with isoproterenol on PN2-5 did not result in any significant changes in G(s)alpha expression but robustly decreased G(i)alpha1,2. These changes were accompanied by heterologous sensitization of AC activity at the level of AC itself, evidenced by equivalent increases in the enzymatic response to fluoride and forskolin-Mn2+. Isoproterenol given to older animals (PN11-14) also caused specific loss of G(i) protein, in this case targeting G(i)alpha3, whereas G(s)alpha again was unchanged; in contrast to the younger group, the older animals displayed heterologous desensitization of AC at the level of G-protein function (specific loss of the fluoride response). These results indicate that the normal ontogenetic increase of cardiac beta-adrenoceptor coupling to AC is not dependent on the absolute amount of G-proteins, nor on the relative balance of stimulatory (G(s)) and inhibitory (G(i)) subunits. However, the ability of receptor stimulation to downregulate G(i)alpha1,2, an event which is specific to immature cardiac cells, is likely to be an important component of the resistance of the fetal/neonatal heart to agonist-induced desensitization and hypertrophy. The maintenance of cardiac beta-adrenoceptor signaling in the face of intense stimulation is likely to play an important role in the physiologic adaptations necessary to the perinatal transition.

Monitoring of emission as direct intraoperative control for nerve sparing retroperitoneal lymphadenectomy.

An intraoperative test to identify emission relevant lumbar postganglionic nerves during nerve sparing retroperitoneal lymph node dissection is presented. The neurophysiological course of the ejaculation into the posterior urethra, the emission, is described. A retroperitoneal nerve sparing procedure was done for nonseminomatous testicular tumors bilaterally in 7 patients with pathological stage I disease and unilaterally in 4 with pathological stage IIa disease. While the isolated lumbar nerves were electrostimulated, the seminal vesicles and bladder neck were monitored by suprapubic transvesical sonography. Simultaneously, endoscopy of the posterior urethra was performed and time code was registered. Emission began with bladder neck closure, propulsive contraction of the seminal vesicles in the periphery and opening of the paracollicular region. Then, complete contraction of the seminal vesicles was associated with closure of the prostatic urethra and ended in the separate secretion from the ductuli prostatici and ejaculatorii. Descending from nerve L1 to L3, their importance for emission usually increased. For intraoperative monitoring of emission transvesical sonography alone is sufficient. In 2 patients this method allowed us to identify the relevant nerves within the retroperitoneal residual mass (fibrosis) after chemotherapy.