Subclinical femoral neuropathy after anterior cruciate ligament reconstruction

Background and aim of the study: Patients with anterior cruciate ligament (ACL) reconstruction and femoral catheter analgesia may develop quadriceps amyotrophy. We aimed to determine whether this amyotrophy might be related to a femoral neuropathy. Material and method: After Ethical Committee approval and patients' written informed consent, 17 patients ASA I and II scheduled to undergo ACL reconstruction were recruited. An electromyography (EMG) was performed before the operation in order to exclude a femoral neuropathy. A femoral nerve catheter was inserted before the surgery with the aid of a nerve stimulator, and 20 ml of 0.5% ropivacaine was injected. The operation was done under spinal or general anaesthesia. Postoperative analgesia was provided with 0.2% ropivacaine for 72 hours, in association with oxycodone, paracetamol and ibuprofen. A second EMG was performed 4 weeks after the ACL repair. A femoral neuropathy was defined as a reduction of the surface of the motor response of more than 20%, compared to the first EMG. A third EMG was performed at 6 months if a neuropathy was present. Results: Mean age of this group of patients was 27 years old (range 18-38 y.). Among the 17 patients, 4 developed a transient femoral neuropathy (incidence of 24%) without clinical complain. Conclusion: In this study, the incidence of subclinical femoral neuropathy after ACL reconstruction is high. This lesion may be caused by the femoral catheter (mechanical damage, toxicity of local anaesthesia) or by the Tourniquet. Further studies are needed to investigate the incidence of subclinical neuropathy, according to the type of analgesia (epidural analgesia, PCA) and surgery.

Anatomical landmarks for transnasal endoscopic skull base surgery.

Resection of midline skull base lesions involve approaches needing extensive neurovascular manipulation. Transnasal endoscopic approach (TEA) is minimally invasive and ideal for certain selected lesions of the anterior skull base. A thorough knowledge of endonasal endoscopic anatomy is essential to be well versed with its surgical applications and this is possible only by dedicated cadaveric dissections. The goal in this study was to understand endoscopic anatomy of the orbital apex, petrous apex and the pterygopalatine fossa. Six cadaveric heads (3 injected and 3 non injected) and 12 sides, were dissected using a TEA outlining systematically, the steps of surgical dissection and the landmarks encountered. Dissection done by the "2 nostril, 4 hands" technique, allows better transnasal instrumentation with two surgeons working in unison with each other. The main surgical landmarks for the orbital apex are the carotid artery protuberance in the lateral sphenoid wall, optic nerve canal, lateral optico-carotid recess, optic strut and the V2 nerve. Orbital apex includes structures passing through the superior and inferior orbital fissure and the optic nerve canal. Vidian nerve canal and the V2 are important landmarks for the petrous apex. Identification of the sphenopalatine artery, V2 and foramen rotundum are important during dissection of the pterygopalatine fossa. In conclusion, the major potential advantage of TEA to the skull base is that it provides a direct anatomical route to the lesion without traversing any major neurovascular structures, as against the open transcranial approaches which involve more neurovascular manipulation and brain retraction. Obviously, these approaches require close cooperation and collaboration between otorhinolaryngologists and neurosurgeons.

Glutathione deficit during development induces anomalies in the rat anterior cingulate GABAergic neurons: Relevance to schizophrenia.

A series of studies in schizophrenic patients report a decrease of glutathione (GSH) in prefrontal cortex (PFC) and cerebrospinal fluid, a decrease in mRNA levels for two GSH synthesizing enzymes and a deficit in parvalbumin (PV) expression in a subclass of GABA neurons in PFC. GSH is an important redox regulator, and its deficit could be responsible for cortical anomalies, particularly in regions rich in dopamine innervation. We tested in an animal model if redox imbalance (GSH deficit and excess extracellular dopamine) during postnatal development would affect PV-expressing neurons. Three populations of interneurons immunolabeled for calcium-binding proteins were analyzed quantitatively in 16-day-old rat brain sections. Treated rats showed specific reduction in parvalbumin immunoreactivity in the anterior cingulate cortex, but not for calbindin and calretinin. These results provide experimental evidence for the critical role of redox regulation in cortical development and validate this animal model used in schizophrenia research.

Pelvic floor dysfunction 6 years post-anal sphincter tear at the time of vaginal delivery.

INTRODUCTION AND HYPOTHESIS: This study aims to estimate fecal, urinary incontinence, and sexual function 6 years after an obstetrical anal sphincter tear. METHODS: Among 13,213 women who had a vaginal delivery of a cephalic singleton at term, 196 women sustained an anal sphincter tear. They were matched to 588 controls. Validated questionnaires grading fecal and urinary incontinence, and sexual dysfunction were completed by the participants. RESULTS: Severe fecal incontinence was more frequently reported by women who had sustained an anal sphincter tear compared to the controls. Women with an anal sphincter tear had no increased risk of urinary incontinence, but reported significantly more pain, difficulty with vaginal lubrication, and difficulty achieving orgasm compared to the controls. A fetal occiput posterior position during childbirth was an independent risk factor for both severe urinary incontinence and severe sexual dysfunction. CONCLUSIONS: Fecal incontinence is strongly associated with an anal sphincter tear. A fetal occiput posterior position represents a risk factor for urinary incontinence and sexual dysfunction.

Prise en charge des troubles oculomoteurs après effraction iatrogène de l'orbite au cours d'interventions sinusiennes endoscopiques [Management of motility disorders secondary to iatrogenic orbital fracture during endoscopic sinus surgery.]

PURPOSE: Orbital wall fracture may occur during endoscopic sinus surgery, resulting in oculomotor disorders. We report the management of four cases presenting with this surgical complication. METHODS: A non-comparative observational retrospective study was carried out on four patients presenting with diplopia after endoscopic ethmoidal sinus surgery. All patients underwent full ophthalmologic and orthoptic examination as well as orbital imaging. RESULTS: All four patients presented with diplopia secondary to a medial rectus lesion confirmed by orbital imaging. A large horizontal deviation as well as limitation of adduction was present in all cases. Surgical management consisted of conventional recession-resection procedures in three cases and muscle transposition in one patient. A useful field of binocular single vision was restored in two of the four patients. CONCLUSION: Orbital injury may occur during endoscopic sinus surgery and cause diplopia, usually secondary to medial rectus involvement due to the proximity of this muscle to the lamina papyracea of the ethmoid bone. Surgical management is based on orbital imaging, duration of the lesion, evaluation of anterior segment vasculature, results of forced duction testing and intraoperative findings. In most cases, treatment is aimed at the symptoms rather than the cause, and the functional prognosis remains guarded.

Retinal thickening in HLA-B27 associated acute anterior uveitis: evolution with time and association with severity of inflammatory activity.

Purpose: To describe the evolution of retinal thickness in eyes affected with acute anterior uveitis (AAU) in the course of follow-up and to assess its correlation with severity of inflammatory activity in the anterior chamber. Methods: Design: Prospective, cohort study Setting: Institutional study Patient population: 72 eyes (affected and fellow eyes) of 36 patients Observation procedure: Patients were followed daily until beginning of resolution of inflammatory activity and weekly thereafter. Optical coherence tomography and laser flare photometry were performed at each visit. Treatment consisted of topical corticosteroids Main outcome measures: Retinal thickness of affected eyes, difference in retinal thickness between affected and fellow eyes and their evolution in time, association between maximal retinal thickness and initial laser flare photometry. Results: Difference in retinal thickness between affected and fellow eyes became significant on average seven days from baseline and remained so through-out follow-up (p<0.001). There was a steep increase in retinal thickness of affected eyes followed by a progressive decrease after reaching a peak value. Maximal difference in retinal thickness between affected and fellow eyes was observed between 17 and 25 days from baseline and exhibited a strong, positive correlation with initial laser flare photometry values (p=0.015). Conclusions: Retinal thickness in eyes affected with AAU presents a steep increase over 3 to 4 weeks and then gradually decreases. Severity of inflammation at baseline predicts the amount of retinal thickening in affected eyes. A characteristic pattern of temporal response of retinal anatomy to inflammatory stimuli seems to arise.