ABSTRACT
Deep brain stimulation (DBS) surgery typically involves placement of a single lead through a burr hole, either unilaterally or bilaterally. Rare indications, however, call for placement of 2 ipsilateral leads. To date, there have been no technical descriptions of how best to secure dual ipsilateral leads to the skull. We describe a method of placing and securing 2 ipsilateral DBS leads through a single burr hole using standard cranial plating equipment and a simple modification to a burr hole-mounted anchoring ring. This method has been used safely in 6 patients without detectable displacement of the first lead during implantation of the second lead.
Subject(s)
Craniotomy/methods , Deep Brain Stimulation/instrumentation , Deep Brain Stimulation/methods , Essential Tremor/surgery , Essential Tremor/therapy , Skull/surgery , Bone Plates , Electrodes, Implanted , Humans , Multiple Sclerosis/surgery , Multiple Sclerosis/therapy , Neurosurgical Procedures/instrumentation , Neurosurgical Procedures/methods , Postoperative Complications/prevention & control , Stereotaxic Techniques/instrumentation , Thalamus/physiology , Thalamus/surgeryABSTRACT
Traumatic brain injury (TBI) is the leading cause of morbidity and mortality among children and both clinical and experimental data reveal that the immature brain is unique in its response and vulnerability to TBI compared to the adult brain. Current therapies for pediatric TBI focus on physiologic derangements and are based primarily on adult data. However, it is now evident that secondary biochemical perturbations play an important role in the pathobiology of pediatric TBI and may provide specific therapeutic targets for the treatment of the head-injured child. In this review, we discuss three specific components of the secondary pathogenesis of pediatric TBI-- inflammation, oxidative injury, and iron-induced damage-- and potential therapeutic strategies associated with each. The inflammatory response in the immature brain is more robust than in the adult and characterized by greater disruption of the blood-brain barrier and elaboration of cytokines. The immature brain also has a muted response to oxidative stress compared to the adult due to inadequate expression of certain antioxidant molecules. In addition, the developing brain is less able to detoxify free iron after TBI-induced hemorrhage and cell death. These processes thus provide potential therapeutic targets that may be tailored to pediatric TBI, including anti-inflammatory agents such as minocycline, antioxidants such as glutathione peroxidase, and the iron chelator deferoxamine.
