ABSTRACT
OBJECTIVE: To demonstrate the role of intraoperative multichannel electromyographic (EMG) monitoring to reduce postoperative deterioration and achieve full untethering of complex occult dysraphisms. METHODS: A retrospective analysis was performed on 66 patients who underwent operation for lumbosacral lipomas. Twenty recent cases were submitted to EMG monitoring and stimulation. RESULTS: All patients presented symptoms at the time of surgery, and 74% exhibited progressive deterioration during the lengthy preoperative period. Postoperative surgery-related deterioration was observed in 6% of patients. This number was reduced to zero with the introduction of intraoperative EMG monitoring. CONCLUSION: Intraoperative multichannel EMG monitoring can be carried out and requires only minimal changes to anesthetic procedures. With this method, it is possible to better identify the neural structures of complex malformations, reducing the risks of surgical damage and incomplete detethering.
Subject(s)
Electromyography , Lipoma/surgery , Lumbar Vertebrae , Monitoring, Intraoperative , Neurosurgical Procedures , Sacrum , Spinal Cord Neoplasms/surgery , Adolescent , Adult , Child , Child, Preschool , Female , Follow-Up Studies , Humans , Infant , Lipoma/complications , Lipoma/diagnosis , Lipoma/physiopathology , Male , Middle Aged , Monitoring, Intraoperative/methods , Neural Tube Defects/etiology , Neurosurgical Procedures/adverse effects , Retrospective Studies , Spinal Cord Neoplasms/diagnosis , Spinal Cord Neoplasms/physiopathology , Treatment OutcomeABSTRACT
Experimental autoimmune myasthenia gravis (EAMG), a model for human myasthenia (MG), is routinely induced in susceptible rat strains by a single immunization with Torpedo acetylcholine receptor (TAChR). TAChR immunization induces anti-AChR Abs that cross-react with self AChR, activate the complement cascade, and promote degradation of the postsynaptic membrane of the neuromuscular junction. In parallel, TAChR-specific T cells are induced, and their specific immunodominant epitope has been mapped to the sequence 97-116 of the AChR alpha subunit. A proliferative T cell response against the corresponding rat sequence (R97-116) was also found in TAChR-immunized rats. To test whether the rat (self) sequence can be pathogenic, we immunized Lewis rats with R97-116 or T97-116 peptides and evaluated clinical, neurophysiological, and immunological parameters. Clinical signs of the disease were noted only in R97-116-immunized animals and were confirmed by electrophysiological signs of impaired neuromuscular transmission. All animals produced Abs against the immunizing peptide, but anti-rat AChR Abs were observed only in animals immunized with the rat peptide. These findings suggested that EAMG in rats can be induced by a single peptide of the self AChR, that this sequence is recognized by T cells and Abs, and that breakdown of tolerance to a self epitope might be an initiating event in the pathogenesis of rat EAMG and MG.
