Horner Syndrome After Lumbar Epidural Analgesia in a Patient with Ehlers-danlos Syndrome

Horner syndrome is a facial triad of miosis, ptosis, and anhidrosis. It is produced by a lesion of the sympathetic pathway supplying the head, eye, and neck. Causes range from benign to serious. Epidural anesthesia is widely used during obstetrics and general surgery. Although generally a safe procedure, it can cause neurologic and ophthalmologic complications. We report a case of unilateral Horner syndrome in a 43-year-old woman with Ehlers-Danlos syndrome (EDS). The patient underwent bowel and urogenital surgery under general anesthesia supplemented with L4-L5 epidural anesthesia. Horner syndrome may have been promoted by increased local anesthetic spread permitted by the connective tissue dysfunction of EDS. Furthermore, the patient suffered chronic constipation as a complication of EDS, and straining may have promoted upward spread of the local anesthetic. In addition, weakness of the dura and/or ligamentum flavum might predispose to subdural migration of epidural catheters in patients with EDS. Accordingly, EDS may increase the likelihood of a Horner syndrome following epidural anesthesia.

Defective adaptive thermogenesis contributes to metabolic syndrome and liver steatosis in obese mice

Defective adaptive high-fat diet (HFD)- and cold-induced thermogenesis, due to impaired sympathetic pathway in brown adipose tissue (BAT), contribute to metabolic syndrome and fatty liver. Improving thermogenic capacities by repeated cold exposure alleviates metabolic and hepatic complications of obesity.

Abstract P304: A Sympathetic-cholinergic Pathway Performs a Connection Between Brain and Spleen, to Prime Immune System and Induce Arterial Hypertension

It is now widely recognized that immune system has a crucial role in hypertension. Various studies have demonstrated that the activation of adaptive immunity, and in particular of T cells, is a crucial moment in the onset and maintaining of hypertension induced by various stimuli in mice. Our previous studies have shown that hypertensive stimuli couple the sympathetic nervous system to determine the activation of splenic immune system. However, how the brain-to-spleen connection is realized in hypertension remains unknown. In this study we demonstrate that mice subjected to various hypertensive stimuli (AngII, DOCA-salt) show an increase of sympathetic nervous activity recorded in vivo in the splenic nerve (Firing Frequency: AngII 131±17 vs Veh 30±10 spikes/10 min, p<0.001). We also show how the sympathetic pathway induced by pro-hypertensive stimuli has its origin in the brain, converging into the spleen through a cholinergic-sympathetic connection that is realized through the vagus-splenic nerve drive and mediated at the molecular level by cholinergic nicotinic receptors at the level of celiac ganglion. In fact, we show that in celiac vagotomized mice, i.e. mice subjected to a procedure inhibiting vagal efferents but not central afferents, the splenic nervous drive induced by AngII was absent (AngII+VagX 21±4 vs AngII+sham 148±29 spikes/10 min, p<0.001). The same result was shown in α7 cholinergic nicotinic receptor KO mice, a receptor typically expressed by neurons in the peripheral ganglia (α7nAChR KO AngII 43±8 vs WT AngII 141±27 spikes/10 min, p<0.01). Moreover, we found that this cholinergic-sympathetic pathway was necessary to allow the activation of T cell costimulation and egression upon hypertensive challenges. Our results highlight a cholinergic-sympathetic pathway played by vagus-splenic nerves and responsible for immune system activation in response to hypertensive stimuli. We believe our results are significant because they reveal a previously unknown sympathetic pathway in hypertension for the first time. The brain-to-spleen connection realized through a cholinergic-sympathetic nervous drive that resembles the cholinergic anti-inflammatory pathway identified by immunologists in endotoxemia.

The role of apraclonidine in Horner’s syndrome: A case report

Introduction. Horner?s syndrome is an interruption of the sympathetic nervous system at any point along its course between the hypothalamus and the orbit. Horner?s syndrome is classically presented as an ipsilateral miosis, subtle ptosis, and facial anhidrosis. Pharmacologic testing is very useful in the diagnosis of Horner?s syndrome as it could help to localize the lesioned neuron in the sympathetic pathway, suggesting an etiology. Case Outline. We present a case report of a 41-year-old woman who reported right eyelid drooping immediately after operation of sympathetic chain schwannoma. We performed apraclonidine test for the diagnosis of Horner?s syndrome, which produced mydriasis on the affected eye, while there was no significant change of the normal eye. Based on the clinical presentation of anisocoria and one-sided ptosis, and previous medical history of surgical removal of the mediastinal tumor, the patient was diagnosed with a right-sided, partial Horner?s syndrome. Conclusion. Timely recognition, exact localization of the lesioned neuron, and referral for urgent imaging studies are important for ophthalmologists in order to prevent and treat life-threatening conditions. Besides its diagnostic value in Horner?s syndrome, topical apraclonidine could correct ptosis for the sake of esthetics or when ptosis reduces the superior visual field.