Microvascular decompression for hemifacial spasm: Outcome on spasm and complications. A review

Over the last decades microvascular decompression (MVD) has been established as the curative treatment of the primary Hemifacial Spasm (HFS), proven to be linked in almost all cases to a neurovascular compression of the facial nerve. Because the disease is not life-threatening and MVD not totally innocuous, efficacy and safety have to be weighted before decision taken of indicating surgery. The authors have been charged by the French Speaking Society of Neurosurgery to conduct a detailed evaluation of the probability of relief of the spasm that MVD is able to obtain, together with its potential complications. For the review, the authors have gone through the reports available from the Pubmed system. Eighty-two publications have been read and analysed, totalizing more than 10,000 operated cases. In most series, the percentage of patients with total relief ranged between 85% and 90%. Relief was obtained after a certain delay in as many as in 33%±8% of the patients in many series. For those, delay lasted around one year in 12% of them. When effect of MVD was considered achieved, relief remained permanent in all but 1%-2% of the long-term followed patients. As regards to complications, risk of permanent cranial nerve deficit was evaluated at 1%-2% for facial palsy, 2%-3% for non-functional hearing loss, 0.5%-1% for lower cranial nerve dysfunction. Risk of stroke was at 0.1% and mortality at 0.1%. CSF leakage and related complications could be reduced at less than 2% in most series provided careful closing techniques be applied. Complications were at a higher rate in repeated MVD. MVD is an effective curative method for almost all the patients affected with primary HFS. Because MVD for HFS is functional surgery, scrupulous consideration of its potential risks, together with the ways to avoid complications are of paramount importance. When MVD is estimated to have failed, it is wise to wait one year before considering to repeat surgery, as number of patients may benefit from delayed effect. This is the more so as important as repeated surgery entails a higher rate of complications

Morphological and functional anatomy of the trigeminal triangular plexus as an anatomical entity: a systematic review

PURPOSE: The sensory trigeminal nerve in the trigeminal cave of Meckel-which is an individualized lodge-is classically segmented into two parts: the trigeminal ganglion (TG) and the triangular plexus (TP). The TP has been defined as the portion of the trigeminal nerve from the posterior margin of the TG to the path over the upper ridge of the petrous bone. Due to its relatively unrecognized status, its morphological and functional anatomy has been reviewed by the authors through a PRISMA systematic review of the literature. METHODS: The authors have carried out a systematic review of the TP according to the PRISMA model with various bibliographical bases. Before 1947: Medic @ Library (BIU Santé Paris, 2017); Index-Catalog of the Library of the Surgeon-General\u27s Office (US National Library of Medicine, 2017); Gallica (French National Library, 2017). After 1947: PUBMED, PubMed Central and MEDLINE. RESULTS: 56 articles were retained for full-text examination, of which 23 were chosen and included. The TP was described as having a triangular shape (30.2%), a plexual organization (97.4%) with sensory-, motor- and sympathetic-anastomoses (96.7%) that, however, respect the somatotopic trigeminal distribution (93.3%). The direct electrical stimulation of the root at the level of the TP (during radiofrequency-thermorhizotomy procedures) confirmed a clear-cut somatotopy. CONCLUSION: An understanding of both the morphological and the functional anatomy of the triangular plexus can contribute to accuracy and safety on the surgeries performed for trigeminal neuralgia and tumor removal inside the trigeminal cave

The tethered effect of the arachnoid in vago-glossopharyngeal neuralgia: a real associated alternative mechanism?

Vago-glossopharyngeal neuralgia (VGPN) is a rarely seen disease when compared to trigeminal neuralgia. When the pain is resistant to medical therapy, microvascular decompression can be performed if a vascular conflict is suspected on magnetic resonance imaging (MRI). In addition, arachnoid pathology may play a role in VGPN. We report two cases of VGPN caused by tethered arachnoid, associated with a vascular contact in which pain was reduced by freeing rootlets from arachnoid compression. We report two cases relating to 50-year-old and 30-year-old men with a history of electric shooting pain triggered by swallowing in the right pharyngeal and auricular regions. Preoperative MRI documented a neurovascular conflict in the first case and an arachnoid cyst in the second. Surgery was performed via a retrosigmoid craniotomy. In both cases, the intraoperative findings documented a tethered arachnoid membrane compressive to cranial nerves IX and X. Untethering was performed by liberation of the rootlets from the arachnoid with microvascular decompression. No additional rhizotomy was performed. The postoperative course was uneventful and pain was relieved in the first case and decreased in the second. In VGPN, a tethered arachnoid may play a role in causing the neuralgia, either alone or associated with a neuro-vascular conflict

The Political Economy of Aid for Power Sector Reform

Recent literature on the effectiveness of donor programmes points to the importance of understanding the political context within which reforms are taking place. The characteristics of the power sector make reform intensely political in almost all countries and donor projects have sometimes failed because of an inability to navigate the local politics of reform. This article reviews what is known about how donors have taken politics into account in designing and implementing power sector reform programmes in sub-Saharan Africa. It illustrates the challenges which donors have faced with reference to a case study of donor attempts to support power sector reform in Tanzania. The article draws on documentary evidence from major donors as well as a set of qualitative interviews with experienced project supervisors to provide a set of lessons for donors about how to incorporate political context into the design and implementation of power sector projects

Correction to: Arachnoiditis as an outcome factor for microvascular decompression in classical trigeminal neuralgia

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Trigeminal neuralgia: new classification and diagnostic grading for practice and research

Trigeminal neuralgia (TN) is an exemplary condition of neuropathic facial pain. However, formally classifying TN as neuropathic pain based on the grading system of the International Association for the Study of Pain is complicated by the requirement of objective signs confirming an underlying lesion or disease of the somatosensory system. The latest version of the International Classification of Headache Disorders created similar difficulties by abandoning the term symptomatic TN for manifestations caused by major neurologic disease, such as tumors or multiple sclerosis. These diagnostic challenges hinder the triage of TN patients for therapy and clinical trials, and hamper the design of treatment guidelines. In response to these shortcomings, we have developed a classification of TN that aligns with the nosology of other neurologic disorders and neuropathic pain. We propose 3 diagnostic categories. Classical TN requires demonstration of morphologic changes in the trigeminal nerve root from vascular compression. Secondary TN is due to an identifiable underlying neurologic disease. TN of unknown etiology is labeled idiopathic. Diagnostic certainty is graded possible when pain paroxysms occur in the distribution of the trigeminal nerve branches. Triggered paroxysms permit the designation of clinically established TN and probable neuropathic pain. Imaging and neurophysiologic tests that establish the etiology of classical or secondary TN determine definite neuropathic pain

Introduction to primary hemifacial spasm: A neurosurgical disease

Primary hemifacial spasm is a hyperactive cranial nerve syndrome. The cause is always a neurovascular compression, generally at the root exit zone from the brainstem. Its curative treatment is microvascular decompression, that may be performed as a first option, or secondarily when botulinum toxin injections fail

Trigeminal neuralgia: New classification and diagnostic grading for practice and research

Trigeminal neuralgia (TN) is an exemplary condition of neuropathic facial pain. However, formally classifying TN as neuropathic pain based on the grading system of the International Association for the Study of Pain is complicated by the requirement of objective signs confirming an underlying lesion or disease of the somatosensory system. The latest version of the International Classification of Headache Disorders created similar difficulties by abandoning the term symptomatic TN for manifestations caused by major neurologic disease, such as tumors or multiple sclerosis. These diagnostic challenges hinder the triage of TN patients for therapy and clinical trials, and hamper the design of treatment guidelines. In response to these shortcomings, we have developed a classification of TN that aligns with the nosology of other neurologic disorders and neuropathic pain. We propose 3 diagnostic categories. Classical TN requires demonstration of morphologic changes in the trigeminal nerve root from vascular compression. Secondary TN is due to an identifiable underlying neurologic disease. TN of unknown etiology is labeled idiopathic. Diagnostic certainty is graded possible when pain paroxysms occur in the distribution of the trigeminal nerve branches. Triggered paroxysms permit the designation of clinically established TN and probable neuropathic pain. Imaging and neurophysiologic tests that establish the etiology of classical or secondary TN determine definite neuropathic pain

Neurotrophins are expressed in giant cell arteritis lesions and may contribute to vascular remodeling

International audienceIntroduction: Giant cell arteritis (GCA) is characterized by intimal hyperplasia leading to ischaemic manifestations that involve large vessels. Neurotrophins (NTs) and their receptors (NTRs) are protein factors for growth, differentiation and survival of neurons. They are also involved in the migration of vascular smooth muscle cells (VSMCs). Our aim was to investigate whether NTs and NTRs are involved in vascular remodelling of GCA.Methods: We included consecutive patients who underwent a temporal artery biopsy for suspected GCA. We developed an enzymatic digestion method to obtain VSMCs from smooth muscle cells in GCA patients and controls. Neurotrophin protein and gene expression and functional assays were studied from these VSMCs. Neurotrophin expression was also analysed by immunohistochemistry in GCA patients and controls.Results: Whereas temporal arteries of both GCA patients (n = 22) and controls (n = 21) expressed nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB) and sortilin, immunostaining was more intense in GCA patients, especially in the media and intima, while neurotrophin-3 (NT-3) and P75 receptor (P75NTR) were only detected in TA from GCA patients. Expression of TrkB, a BDNF receptor, was higher in GCA patients with ischaemic complications. Serum NGF was significantly higher in GCA patients (n = 28) vs. controls (n = 48), whereas no significant difference was found for BDNF and NT-3. NGF and BDNF enhanced GCA-derived temporal artery VSMC proliferation and BDNF facilitated migration of temporal artery VSMCs in patients with GCA compared to controls.Conclusions: Our results suggest that NTs and NTRs are involved in vascular remodelling of GCA. In GCA-derived temporal artery VSMC, NGF promoted proliferation and BDNF enhanced migration by binding to TrkB and p75NTR receptors. Further experiments are needed on a larger number of VSMC samples to confirm these results