Parasympathetic Fibers Research Articles

Pain relief during minor procedures: a challenge for gynaecologists.

Pain relief during minor procedures: a challenge for gynaecologists.

Anatomical basis of female pelvic cavity for nerve sparing radical hysterectomy.

The separation and sparing of the vesical branch of the inferior hypogastric plexus (IHP), to preserve the pelvic autonomic nerve, is critical and difficult in nerve sparing radical hysterectomy. Pelvic local anatomy was performed to provide the necessary anatomical information. Precise pelvic anatomy was performed in 15 adult corpses, and immunohistochemical analysis was carried out on the parametrial tissues of three fresh cadavers to analyze the nerve fiber type and content of the vesical branch of the IHP. The deep uterine vein is located in the upper region of the cardinal ligament (CL), with three to six multiple branches and anatomical variation, including one or two cervical branches, and two to four vesical branches. Three branches were found to be most common (63.3 %). The major distribution of the vesical branch of the IHP is dorsomedial to the middle and inferior vesical veins, with less ventral and lateral distribution. There are more sympathetic fibers than parasympathetic fibers in the vesical branch. There is a region rare of vasculature and nerve between the vaginal lateral margin and the vesical branch. The deep uterine vein is suggested as an anatomical landmark during surgery, to process the CL and preserve the pelvic splanchnic nerves. The middle and inferior vesical veins can be used as the landmark to preserve the vesical branch of the IHP.

Abstract 11392: Chronic Low-Level Transcutaneous Electrical Stimulation of the Auricular Branch of the Vagus Nerve: A New Approach to Attenuate Neural Remodeling and Reduce Ventricular Arrhythmias in a Post-Infarction Canine Model

Introduction: Left stellate ganglion (LSG) and cardiac neural remodeling, which are associated with ventricular arrhythmias (VAs) in post-infarction model, can be attenuated by low-level vagus nerve stimulation. However, whether chronic low-level transcutaneous electrical stimulation at the tragus, where the auricular branch of vagus nerve innervate, can attenuate neural remodeling both in heart and LSG and then reduce VAs is unknown. Hypothesis: We hypothesized that chronic low-level tragus stimulation (LL-TS) would attenuate cardiac and LSG nerve remodeling and then reduce inducibility of VAs in a post-infarction model. Methods: Twenty beagles after ligating coronary artery were randomly divided into normal control (NC, n=4), MI treated with LL-TS (MI-TS n=8)and MI treated with shame LL-TS (MI-NTS, n=8)groups. LL-TS was performed at 80% below the threshold, at which sinus rate or atrioventricular conduction slowing can be initially induced, for 2 hours a day for 2 months. Left stellate ganglionic nerve activity (SGNA) and left thoracic vagal nerve activity (VNA) was recorded. Slope of ventricular restitution curves (Smax) and programmed ventricular stimulation were performed to evaluate VAs. Nerve sprouting, nerve synaptic density and associated protein expression both in LSG and hearts were evaluated by immunostaining or Western blotting. Results: Two months later, the increased SGNA induced by MI was attenuated by LL-TS. However, the increased VNA was strengthened.In the MI-TS group, the number of sympathetic nerves both in peri-infarct zone and LSG were reduced, while the parasympathetic nerve fibers were increased compared to MI-NTS group. Moreover, the expression of synaptophysin, NGF in peri-infarct as well as in LSG in the MI-TS group was significantly lower than the MI-NTS group, while the level of SK2 was much higher.Chronic LL-TS also significantly decreased the Smax, LF/HF ratio and arrhythmia score of programmed ventricular stimulation induced VAs. Conclusions: These findings suggested that chronic LL-TS augmented cardiac vagal and reduced sympathetic tone, attenuated cardiac and LSG nerve remodeling, regulated nerve associated protein expression and potentially contributed to reducing vulnerability to VAs.

Patterns of innervation of the lacrimal gland with clinical application.

Parasympathetic stimulation of the lacrimal gland is responsible for tear production, and this innervation originates from fibers conveyed in the facial nerve. After synapse in the pterygopalatine ganglion, postsynaptic parasympathetic fibers travel within the zygomatic and zygomaticotemporal nerves (ZTN) into the orbit. As described in most anatomy texts, ZTN communicates with the lacrimal nerve (LN) posterior to the gland and then secretomotor fibers enter the gland. This study was performed to gain a better understanding of the innervation of the lacrimal gland. Seventeen cadaver heads were bisected for a total of 34 sides, which then underwent dissection of the superolateral orbital region to observe the course for the LN and ZTN. Three variations of the course of the LN and ZTN were found. In 20 (60.6%) dissections it was documented that the ZTN entered directly into the lacrimal gland with no communication with the LN. In 12 (36.4%) of the bisected heads, ZTN had both a direct connection into the gland and a communicating branch with the LN. In only one (3.0%) bisected head, ZTN communicated with the LN before entering the gland as it is commonly described in anatomy texts. Our study reveals that the ZTN usually takes a different course than is classically described in most anatomy textbooks. A greater understanding of the typical course these nerves take may help surgeons identify them more easily and avoid damaging them.

DLK1 regulates branching morphogenesis and parasympathetic innervation of salivary glands through inhibition of NOTCH signalling.

Delta-like proteins 1 and 2 (DLK1, 2) are NOTCH receptor ligands containing epidermal growth factor-like repeats, which regulate NOTCH signalling. We investigated the role of DLK and the NOTCH pathway in the morphogenesis of the submandibular salivary glands (SMGs), using in vitro organotypic cultures. DLK1 and 2 were present in all stages of SMG morphogenesis, where DLK1 inhibited both NOTCH activity and SMG branching. The addition of NOTCH inhibitory agents, either soluble DLK1 (sDLK1) or N-[N-(3, 5-difluorophenacetyl-L-alanyl]-S-phenylglycine t-buthyl ester (DAPT), to the SMG culture medium did not affect the rate of cell proliferation, but induced a strong reduction in SMG branching, increased epithelial apoptosis, and impaired innervation of the epithelial end buds by local parasympathetic ganglion neurons. SMG innervation could be restored by the acetylcholine analog carbachol (CCh), which also rescued cytokeratin 5 (CK5(+))-expressing epithelial progenitor cells. Despite this, CCh failed to restore normal branching morphogenesis in the presence of either sDLK1 or DAPT. However, it improved recovery of branching morphogenesis in SMGs, once DLK1 or DAPT were removed from the medium. Our data suggest that DLK1 regulates SMGs morphogenesis and parasympathetic nerve fibre outgrowth through inhibition of NOTCH signalling.

Maintenance of bladder innervation in diabetes: A stereological study of streptozotocin-treated female rats

Neuropathy and cystopathy are two common conditions in patients with chronic diabetes. Despite obvious bladder sensory and motor nerve dysfunction in diabetes, no studies have selectively explored whether sensory or motor innervation is affected in the bladder. In the present study, we tested the hypothesis that loss of bladder sensory and motor fibers is responsible for bladder sensory and motor dysfunction. Parasympathetic and sensory innervation of the bladder dome and neck were examined using immunohistochemistry (IHC) and stereology in adult female rats 12weeks after induction of diabetes by streptozotocin. Naïve and age matched rats were evaluated as controls. Diabetic rats had mean blood glucose level of >400mg/dl, and bladder weights and thicknesses that were more than doubled compared to naïve rats. In naïve rats, parasympathetic vesicular acetylcholine transporter (VAT) and sensory calcitonin gene-related peptide (CGRP) immunopositive nerve fibers were located in bladder smooth muscle and were more densely distributed in the neck compared to the dome. Within the urothelial region, CGRP nerve fibers were densely distributed while VAT nerve fibers were sparsely distributed in the bladder neck and both were virtually absent in the bladder dome. Streptozotocin induced diabetes did not change the total nerve fiber length of either VAT or CGRP stained fibers in either the neck or dome. These studies indicate that hyperglycemia, induced by streptozotocin treatment, does not result in a loss of parasympathetic VAT or CGRP sensory nerve fibers, per se, but the doubling of bladder weight and mass does indicate a decrease in innervation density.

Complexity of impaired parasympathetic heart rate regulation in diabetes.

The autonomic nervous system is crucial for blood pressure and heart rate regulation. Sympathetic efferent fibers elicit vasoconstriction, raise heart rate and cardiac contractility, and promote sodium reabsorption through direct renal tubular actions and renin-angiotensin system activation. Parasympathetic efferent fibers rapidly reduce heart rate. Both autonomic branches are tightly controlled by baroreflex, stabilizing blood pressure in a feedback fashion (1). Severe autonomic failure due to sympathetic and parasympathetic dysfunction typically occurs in patients with long-standing and poorly controlled diabetes. The condition is associated with profound orthostatic hypotension, postprandial hypotension, a fixed heart rate, and exercise intolerance. Positron emission tomography or single photon emission tomography imaging with tracers taken up by adrenergic sympathetic nerve endings suggest that autonomic efferent nerves are irreversibly damaged in these patients (2,3). There are no causative treatments for late-stage disease and symptomatic treatment is difficult. Clinicians caring for autonomic failure patients are faced with the therapeutic dilemma that blood pressure is often markedly elevated in the supine position (4). Yet, antihypertensive treatment exacerbates orthostatic hypotension. Conversely, treatment of orthostatic hypotension with pressor agents might hasten cardiovascular and renal disease progression. The condition carries a poor prognosis. More subtle changes in cardiovascular autonomic regulation are common early in the course of type 1 or type 2 diabetes. Typically, impaired parasympathetic heart rate control precedes sympathetic dysfunction. Simple bedside tests, such as respiratory sinus arrhythmia assessment during deep breathing, are often diagnostic (5). Heart rate variability and noninvasive baroreflex sensitivity measurements are also useful diagnostic tools, particularly in epidemiologic …

Autonomic nervous system changes associated with rheumatoid arthritis: Clinical and electrophysiological study

Aim of the workThe aim of this study was to evaluate clinically and electrophysiologically the autonomic nervous system changes associated with rheumatoid arthritis (RA). Patients and methodsThe present study included 25 patients with RA[22 women (88%)] and 30 apparently healthy control subjects[27 women (90%)]. A thorough clinical examination was carried out. Disease activity and functional disability were assessed. Tests for assessment of autonomic functions include active and passive orthostatic stress tests, and sympathetic skin response (SSR). The presence of abnormality in 2 tests or more was a clue for the presence of autonomic neuropathy (AN). Sural sensory nerve conduction study and posterior tibial motor nerve conduction study were done. ResultsThere was a statistically significant decrease in standing systolic and diastolic blood pressure (BP) components of the active orthostatic stress test and SSR amplitude as well as statistically significant prolongation of SSR latency of RA patients when compared to control. Three patients (12%) had clinical symptoms suggestive of AN; increased to 14 patients (56%) when orthostatic stress tests and SSR were utilized. There were no statistically significant differences between patients with different disease activity score 28 with 4 variables grades of RA activity and SSR latency and amplitude. There were no statistically significant differences between patients with different Stanford Health Assessment Questionnaire Disability Index grades of RA functional disability and SSR latency and amplitude. ConclusionsAutonomic neuropathy is a common extra-articular manifestation of RA affecting sympathetic and parasympathetic fibers.

English

Association of migraine and tonic pupil has been reported very rarely. We reported a young female with symptoms of migraine who developed a mydriatic pupil in one of her attacks. The pupil was unresponsive to light with little response to near reflex. In 0.125% pilocarpine test affected pupil responded significantly and tonic pupil was diagnosed. We discussed possible mechanisms and reviewed previous cases with the same diagnosis. Evidences show that this association may be caused by infarction of parasympathetic fibers secondary to prolonged vasospasm which sometimes occurs in migraine.

Nerves supplying the internal anal sphincter: an immunohistochemical study using donated elderly cadavers

Nerves serving the internal anal sphincter (NIAS) have been described as the lower rectal branches of the pelvic autonomic nerve plexus. However, their topographical anatomy and fiber components have remained unclear. Using histological sections from ten elderly donated cadavers, we investigated the topographical anatomy and composite fibers of the NIAS using immunohistochemistry for S100 protein, neuronal nitric oxide synthase (nNOS), vasoactive intestinal polypeptide (VIP) and tyrosine hydroxylase (TH). At the 2-3 o'clock position in the lower rectum, the NIAS originated from nerves at the posterolateral corner of the prostate in males or in the lower paracolpium in females. The nerves ran inferiorly along the internal aspect of the levator ani muscle, and joined branches of the myenteric plexus at a level slightly above the epithelial junction. The NIAS contained both nNOS-positive parasympathetic nerve fibers and TH-positive sympathetic fibers, but VIP-positive fibers were few in number. The origin of the NIAS at the posterolateral corner of the prostate as well as in the lower paracolpium might be sacrificed or damaged during radical prostatectomy or tension-free vaginal tape insertion. Low anterior resection of rectal cancer will most likely render damage to the NIAS because of its intersphincteric course. Although the nerve composition of the NIAS is characterized by a higher proportion of sympathetic nerve fibers than the myenteric plexus in the large intestine, their role is unclear. However, evaluation of sphincteric function after surgery would appear to be difficult because of the complex control mechanism independent of nerve supply.

Immunohistochemical evidence of a reduced vasodilatory capacity in vertebrobasilar arteries in pre‐hypertensive spontaneous hypertensive rats (1183.9)

Our earlier work has shown that vertebrobasilar artery remodelling causing high vascular resistance occurs in SHR prior to the development of hypertension. We hypothesise that a component of this remodelling results from reduced capacity of the vasodilatory parasympathetic innervation and that this contributes to the etiology of neurogenic hypertension via Cushing’s mechanism. Whole mounts of brainstem ventral brain vessels from hypertensive SHR (<12weeks), PH‐SHR (P28‐35) and age‐matched Wistars were immunostained for dopamine‐β hydroxylase (DBH), vesicular acetylcholine transporter (VAChT) and vasoactive intestinal peptide (VIP); the latter is co‐expressed in parasympathetic fibres. We found an age dependent reduction in the parasympathetic (~60‐85%) and sympathetic (10‐40%) innervation density of vertebrobasilar arteries in SHRs compared to Wistar rats (p<0.001). VAChT positive fibre densities were ~30‐50% lower than VIP‐ in all rat groups. In conclusion, SHRs have fewer parasympathetic fibres innervating the vertebrobasilar arteries than Wistars. Given the higher prevalence of both VAChT and VIP in Wistar rats, we speculate that the vasodilatory capacity of these cerebral vessels in SHR will be compromised.Grant Funding Source: Supported by BHF, NIH

An Investigation of the Relationship between Pelvic Pain and Density of Nerve Fibers in Peritoneal Lesions of Endometriosis

Purpose Endometriosis is a gynecological disease often characterized by severe pelvic pain, including perimenstrual and intermenstrual pain and dyspareunia. Sensory nerve fibers within peritoneal lesions have previously been shown to contribute to generation of pain in endometriosis; however, their association with different types of pelvic pain is currently uncertain. Methods Peritoneal endometriotic lesions (n = 30) were sectioned and stained immunohistochemically with protein gene product 9.5 (PGP 9.5; pan-neuronal marker), neuropeptide Y (NPY; sympathetic), vasoactive intestinal polypeptide (VIP; parasympathetic), substance P (SP; sensory) and nerve growth factor (NGF) to identify nerve fibers and neurotrophin levels. Densities were assessed within stroma of the lesions and in the adjacent peritoneum. Pelvic pain scores were obtained using a visual analogue scale (VAS), and correlation analysis was performed. Results Increased density of nerve fibers was observed within the stroma of lesions. NGF expression was significantly increased in glandular epithelium, compared with stromal regions (p = 0.026) and correlated inversely with menstrual pain scores (p = 0.05). Sympathetic nerve fiber density (NPY) in stroma showed a significant positive correlation with intensity of menstrual pain (p = 0.04). Parasympathetic nerve fiber density (VIP) also showed a strong trend toward a positive correlation with menstrual pain intensity (p = 0.056). Conclusions There is increased neurogenesis in the stromal region. Innervation of lesions correlates to intensity of menstrual pain. NGF in glandular epithelium may promote growth of nerve fibers into the core of lesions; however, the inverse correlation between NGF expression in glandular epithelium and menstrual pain indicates that mechanisms of pain generation in endometriosis are complex.

Decreased nerve fibers in the oviduct isthmus of women with endometriosis

Oviduct tubal motility is thought to be controlled by hormones and nerves and has been associated with endometriosis. However, it is still not known whether the fallopian tubes in women with endometriosis demonstrate an abnormal distribution of nerve fibers. The objective of this study was to determine the distribution of nerve fibers in the oviduct isthmus in women with and without endometriosis. Histological sections of the oviduct isthmus tissues were obtained from women undergoing hysterectomy for endometriosis (n=24) and other benign gynecologic diseases (n=24). The tissues were immunohistochemically stained for protein gene product (PGP) 9.5, substance P (SP), neuropeptide Y (NPY), and vasoactive intestinal peptide (VIP) to reveal all nerve fibers, sensory nerve fibers and sympathetic and parasympathetic nerve fibers. Nerve fibers stained with PGP9.5, VIP and NPY in the oviduct isthmus were all significantly decreased in women with endometriosis as compared with women without endometriosis (P<0.05). In women with endometriosis, reduced nerve fibers stained with PGP9.5 and SP in the serosal layer, NPY in the muscular and mucosal layers, and VIP in the mucosal layer of the oviduct isthmus were all associated with the severity of the disease (P<0.05). These results suggest that decreased nerve fibers in the oviduct isthmus in women with endometriosis in comparison to women without may imply a role in the pathogenesis of endometriosis.

(358) Neural cross-talk between the prostate and bladder is demonstrated by a retrograde labeling of DRGs

A high incidence of prostatic inflammation in patients with benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS) has been previously reported.1,2 One of the supportive mechanisms is that prostatic inflammation sensitizes afferent fibers from the bladder resulting in changes in bladder function. We show here that afferent innervation of the bladder and prostate originate from overlapping groups of dorsal root ganglia. To determine spinal segments having convergent DRGs, a retro-grade neuro-tracer Fast Blue (FB) was applied to each of the prostate lobes as the seminal vesicle and bladder in adult C57BL/6 mice. Tissues including pelvic organs and DRGs were harvested at post-application day 7. Our study clearly demonstrates that prostate and bladder share afferent innervation via convergent DRGs in spinal segment T13, L1, L2, L6 and S1. There are several features indicating the reliability and reproducibility of this technique in our laboratory. This includes (1) different intensity of staining in the same section of DRGs, (2) procedures confirming no-spillage from the origin of the neuro-tracer application via all pelvic organ sectioning, (3) positive parasympathetic (autonomic) nerve fibers in pelvic organs adjacent to the application orgin, (4) consistent staining pattern with two different application method; crystal powder and intramuscular injection, (5) co-staining with pan neural marker of PGP 9.5 and (6) size distribution of FB positive DRGs. We are the first group to successfully undertaken and accomplish these experiments and have now clearly shown that pelvic cross-talk occurs between the prostate and bladder. (1. Bushman, W. The Urologic clinics of North America, 2009; 2. i, V. Is chronic prostatic inflammation a new target in the medical therapy of lower urinary tract symptoms (LUTS) due to benign prostate hyperplasia (BPH), 2013.)

Oral lichen planus and neurogenic inflammation: new observations and therapeutic implications from four clinical cases

Oral lichen planus (OLP) is a usually chronic and relapsing mucocutaneous disease with unknown etiology. Immunosuppressive treatment is sometimes unsatisfactory. We describe four cases of reticular OLP localized on the internal side of cheek, in the territory innervated by sensory free endings of the buccinator nerve, poorly responding to immunosuppressive treatment (topical/systemic corticosteroids, topical cyclosporin). Addition of prazepam 10 mg/day to standard therapy achieved significant improvement and clinical healing in 30-40 days. Because of the complex interplay between the nervous and immune systems, neuroinflammation, acting through conventional axon reflex and/or indirect reflex mechanism involving localized efferent vasodilatory parasympathetic fibers, could have an important pathogenic role in OLP. Such hypothesis could explain, at least partly, the spreading of lesions in OLP primarily triggered (and possibly sustained) by infections, irritants, or autoimmunity. Moreover, neuroinflammation could have a relevant role in OLP related to psychosomatic diseases, where the nervous component is the primary trigger and the main pathogen responsible for the lesions observed. Benzodiazepines modulate neuroinflammation through central, and, possibly, peripheral action. In OLP patients with mild/subclinical psychological conditions, low doses may effectively modulate neuroinflammatory pathways that are not always completely inhibited by immunosuppressive treatment and can contribute to the persistence of inflammation.

Parasympathetic reflex vasodilation in the cerebral hemodynamics of rats

We investigated the role of parasympathetic reflex vasodilation in the regulation of the cerebral hemodynamics, and whether GABAA receptors modulate the response. We examined the effects of activation of the parasympathetic fibers through trigeminal afferent inputs on blood flow in the internal carotid artery (ICABF) and the cerebral blood vessels (rCBF) in parietal cortex in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited intensity- and frequency-dependent increases in ICABF that were independent of changes in external carotid artery blood flow. Increases in ICABF were elicited by LN stimulation regardless of the presence or absence of sympathetic innervation. The ICABF increases evoked by LN stimulation were almost abolished by the intravenous administration of hexamethonium (10 mg kg(-1)) and were reduced significantly by atropine administration (0.1 mg kg(-1)). Although the LN stimulation alone had no significant effect on rCBF, LN stimulation in combination with a blocker of the GABAA receptor pentylenetetrazole increased the rCBF markedly. This increase in rCBF was reduced significantly by the administration of hexamethonium and atropine. These observations indicate that the increases in both ICABF and rCBF are evoked by parasympathetic activation via the trigeminal-mediated reflex. The rCBF increase evoked by LN stimulation is thought to be limited by the GABAA receptors in the central nervous system. These results suggest that the parasympathetic reflex vasodilation and its modulation mediated by GABA receptors within synaptic transmission in the brainstem are involved in the regulation of the cerebral hemodynamics during trigeminal afferent inputs.

Exercising With Peripheral or Autonomic Neuropathy: What Health Care Providers and Diabetic Patients Need to Know

Both peripheral and autonomic neuropathies are characterized by a progressive loss of nerve fiber function. Most peripheral neuropathy affects the extremities, particularly the lower legs and the feet, but also the hands, whereas damage to the autonomic nervous system may lead to imbalances between the sympathetic and parasympathetic nerve fibers that innervate the heart and blood vessels, as well as abnormalities in heart rate control and vascular dynamics. To prescribe or engage in exercise that is both safe and effective, health care providers and patients with diabetes mellitus need to increase their understanding of the pathophysiological nature of neuropathies and the physical activity hurdles that may arise from the presence of a neuropathy. With proper care and preventative measures, patients with diabetes mellitus that experience either type of neuropathy can benefit from regular participation in mild to moderate aerobic, resistance, and balance activities, assuming they take any potential alterations into account to ensure that exercise is safe and effective.

Transplantation of iPSc Ameliorates Neural Remodeling and Reduces Ventricular Arrhythmias in a Post‐Infarcted Swine Model

Neural remodeling after myocardial infarction (MI) may cause malignant ventricular arrhythmia, which is the main cause of sudden cardiac death following MI. Herein, we aimed to examine whether induced pluripotent stem cells (iPSc) transplantation can ameliorate neural remodeling and reduce ventricular arrhythmias (VA) in a post-infarcted swine model. Left anterior descending coronary arteries were balloon-occluded to generate MI. Animals were then divided into Sham, PBS control, and iPS groups. Dynamic electrocardiography programmed electric stimulation were performed to evaluate VA. The spatial distribution of vascularization, Cx43 and autonomic nerve regeneration were evaluated by immunofluorescence staining. Associated protein expression was detected by Western blotting. Likewise, we measured the enzymatic activities of superoxide dismutase and content of malondialdehyde. Six weeks later, the number of blood vessels increased significantly in the iPSc group. The expression of vascular endothelial growth factor and connexin 43 in the iPS group was significantly higher than the PBS group; however, the levels of nerve growth factor and tyrosine hydroxylase were lower. The oxidative stress was ameliorated by iPSc transplantation. Moreover, the number of sympathetic nerves in the iPSc group was reduced, while the parasympathetic nerve fibers had no obvious change. The transplantation of iPSc also significantly decreased the low-/high-frequency ratio and arrhythmia score of programmed electric stimulation-induced VA. In conclusion, iPSc intramyocardial transplantation reduces vulnerability to VAs, and the mechanism was related to the remodeling amelioration of autonomic nerves and gap junctions. Moreover, possible mechanisms of iPSc transplantation in improving neural remodeling may be related to attenuated oxidative stress and inflammatory response.

Role of paravertebral block anaesthesia during percutaneous transhepatic thermoablation

This paper discusses the technique and preliminary results of right thoracic paravertebral block (TPVB) for percutaneous thermal ablation of liver tumours. Between October 2011 and August 2012 we treated 36 lesions (25 hepatocellular carcinoma and 11 metastases) in 30 patients aged 47-85 years (mean 67.5). Patients received ultrasound (US)-guided injection of 7 ml of naropin 0.75 % in T7, T9 and T11 levels, below the costo-vertebral ligament, until we observed an anterior displacement of the parietal pleura. For the subcapsular lesions, a cervical right phrenic nerve block was associated. The level of analgesia was evaluated during and after the percutaneous procedures with the Numerical Rating Scale. Finally, we investigated statistical correlations between pain and lesions (histological type, site, dimensions), and ablation time and technique (microwave or radiofrequency ablation). Technical success was achieved in all patients. Despite the correct anaesthetic diffusion during the ablation, 10 patients (33.3 %) reported medium/severe pain and intravenous sedation was required. Pain was not found to correlate with any variable. No complications were observed. In most cases, TPVB is a safe and effective technique for conscious anaesthesia during percutaneous thermal ablation of liver tumours. Failures probably derive from left sympathetic and parasympathetic fibre stimulation. We recommend performing a TPVB in the presence of the anaesthetist.

Posterior communicating aneurysm with oculomotor nerve palsy: clinical outcome after aneurysm clipping.

One of the clinical presentations of intracranial aneurysm is unilateral oculomotor nerve palsy (ONP). The most common location is the posterior communicating artery. Surgical clipping and/or endovascular coiling of the aneurysm are the treatments. The aim of this study was to identify the factors that influence the postoperative recovery of patients who have posterior communicating aneurysm with ONP. We included 13 patients diagnosed at our hospital from 1993 to 2008 with posterior communicating aneurysm with ONP. Ten patients underwent craniotomy to clip the aneurysm; 3 patients refused surgery. Five (50%) patients presented with periorbital pain. Seven (70%) patients had complete ONP recovery with a median recovery time of 58 days. We found that the first recovered component of ONP after clipping was the parasympathetic fibers with a mean recovery time of 4.4 days. Nine patients had a good recovery outcome; one patient died from postoperative vasospasm. There was no significant linear trend in complete recovery rate across palsy symptom periods. However, the palsy symptom period was significant correlated with recovery time. Early decompression of the posterior communicating aneurysm yielded satisfactory recovery and ONP can be reversible. In our patients, the first component of oculomotor function to recover was the parasympathetic fibers.