Intraoperative electrophysiological monitoring for C1-2 spinal cord stimulation.

OBJECTIVE This study is a retrospective case series involving C1-2 spinal cord stimulation in patients with complex regional pain syndrome (CRPS) under general endotracheal anesthesia. Currently, C1-2 paddle lead placement is an accepted practice, which provides effective cervical stimulation to ameliorate upper-extremity and sometimes lower-extremity symptoms experienced by patients with CRPS. However, this technique must be performed under general endotracheal anesthesia rather than in an awake or semiconscious state due to intraoperative safety concerns and patient comfort. The authors aim to provide additional data to support the following novel technique: the use of somatosensory evoked potential (SSEP) diminution data to assist with proper midline placement of C1-2 leads under general anesthesia. METHODS SSEP median nerve (MN) and posterior tibial nerve (PTN) data were collected from 6 patients undergoing placement of C1-2 leads under general anesthesia. Fluoroscopy was used as an initial guide for proper anatomical midline placement. This was followed by the activation of the spinal cord stimulator and simultaneous collection of primarily MN SSEPs as well as PTN SSEPs for physiological midline placement. Unilateral and bilateral reductions in SSEPs assisted with the correct lateralization of the lead to ensure effective postoperative coverage according to the patient's individual preoperative symptoms. RESULTS Six patients were monitored using SSEPs and repeatable, reliable MN and PTN baseline responses were obtained from all. A reduction in amplitude ranging from 5% to 87% was observed, confirming inhibition of dorsal column conduction, and an average pain relief of 63% at short-term and 64% at long-term follow-up was recorded with 6 of 6 and 5 of 6 patients responding, respectively. CONCLUSIONS Intraoperative SSEP collision study testing appears to be a safe technique to monitor placement of C1-2 paddle leads intraoperatively under general anesthesia.

Postlesion estradiol treatment increases cortical cholinergic innervations via estrogen receptor-α dependent nonclassical estrogen signaling in vivo.

17ß-Estradiol (E2) treatment exerts rapid, nonclassical actions via intracellular signal transduction system in basal forebrain cholinergic (BFC) neurons in vivo. Here we examined the effect of E2 treatment on lesioned BFC neurons in ovariectomized mice and the role of E2-induced nonclassical action in this treatment. Mice given an N-methyl-d-aspartic acid (NMDA) injection into the substantia innominata-nucleus basalis magnocellularis complex (SI-NBM) exhibited cholinergic cell loss in the SI-NBM and ipsilateral cholinergic fiber loss in the cortex. A single injection of E2 after NMDA lesion did not have an effect on cholinergic cell loss in the SI-NBM, but it restored the ipsilateral cholinergic fiber density in the cortex in a time- and dose-dependent manner. The most effective cholinergic fiber restoration was observed with 33 ng/g E2 treatment at 1 h after NMDA lesion. The E2-induced cholinergic fiber restoration was absent in neuron-specific estrogen receptor-α knockout mice in vivo. Selective activation of nonclassical estrogen signaling in vivo by estren induced E2-like restorative actions. Selective blockade of the MAPK or protein kinase A pathway in vivo prevented E2's ability to restore cholinergic fiber loss. Finally, studies in intact female mice revealed an E2-induced restorative effect that was similar to that of E2-treated ovariectomized mice. These observations demonstrate that a single E2 treatment restores the BFC fiber loss in the cortex, regardless of endogenous E2 levels. They also reveal the critical role of nonclassical estrogen signaling via estrogen receptor-α and protein kinase A-MAPK pathways in E2-induced restorative action in the cholinergic system in vivo.

Action of estrogen on survival of basal forebrain cholinergic neurons: promoting amelioration.

Extensive studies during the past two decades provide compelling evidence that the gonadal steroid, estrogen, has the potential to affect the viability of basal forebrain cholinergic neurons. These observations reflect a unique ameliorative feature of estrogen as it restores and protects the cholinergic neurons against noxious stimuli or neurodegenerative processes. Hence, we first address the ameliorative function of estrogen on basal forebrain cholinergic neurons such as the actions of estrogen on neuronal plasticity of cholinergic neurons, estrogen-induced memory enhancement and the ameliorative role of estrogen on cholinergic neuron related neurodegenerative processes such as Alzheimer's disease. Second, we survey recent data as to possible mechanisms underlying the ameliorative actions of estrogen; influencing the amyloid precursor protein processing, enhancement in neurotrophin receptor signaling and estrogen-induced non-classical actions on second messenger systems. In addition, clinical relevance, pitfalls and future aspects of estrogen therapy on basal forebrain cholinergic neurons will be discussed.