Effects of anode position on pedicle screw testing during lumbosacral spinal fusion surgery.

OF BACKGROUND DATA: Pedicle screws are commonly placed with lumbar/lumbosacral fusions. Triggered electromyography (tEMG), which employs the application of electrical current between the screw and a complementary anode to determine thresholds of conduction, may be utilized to confirm the safe placement of such implants. While previous research has established clinical thresholds associated with safe screw placement, there is variability in clinical practice of anode placement which could lead to unreliable measurements. PURPOSE: To determine the variance in pedicle screw stimulation thresholds when using four unique anode locations (ipsilateral/contralateral and paraspinal/gluteal relative to tested pedicle screws). STUDY DESIGN: Prospective cohort study. Tertiary medical center. PATIENT SAMPLE: Twenty patients undergoing lumbar/lumbosacral fusion with pedicle screws using tEMG OUTCOME MEASURES: tEMG stimulation return values are used to assess varied anode locations and reproducibility based on anode placement. METHODS: Measurements were assessed across node placement in ipsilateral/contralateral and paraspinal/gluteal locations relative to the screw being assessed. R2 coefficients of correlation were determined, and variances were compared with F-tests. RESULTS: A total of 94 lumbosacral pedicle screws from 20 patients were assessed. Repeatability was verified using two stimulations at each location for a subset of the screws with an R2 of 0.96. Comparisons between the four anode locations demonstrated R2 values ranging from 0.76 to 0.87. F-tests comparing thresholds between each anode site demonstrated all groups not to be statistically different. CONCLUSION: The current study, a first-of-its-kind formal evaluation of anode location for pedicle screw tEMG testing, demonstrated very strong repeatability and strong correlation with different locations of anode placement. These results suggest that there is no need to change the side of the anode for testing of left versus right screws, further supporting that placing an anode electrode into gluteal muscle is sufficient and will avoid a sharp ground needle in the surgical field.

MK-801 disrupts and nicotine augments 40 Hz auditory steady state responses in the auditory cortex of the urethane-anesthetized rat.

Patients with schizophrenia show marked deficits in processing sensory inputs including a reduction in the generation and synchronization of 40 Hz gamma oscillations in response to steady-state auditory stimulation. Such deficits are not readily demonstrable at other input frequencies. Acute administration of NMDA antagonists to healthy human subjects or laboratory animals is known to reproduce many sensory and cognitive deficits seen in schizophrenia patients. In the following study, we tested the hypothesis that the NMDA antagonist MK-801 would selectively disrupt steady-state gamma entrainment in the auditory cortex of urethane-anesthetized rat. Moreover, we further hypothesized that nicotinic receptor activation would alleviate this disruption. Auditory steady state responses were recorded in response to auditory stimuli delivered over a range of frequencies (10-80 Hz) and averaged over 50 trials. Evoked power was computed under baseline condition and after vehicle or MK-801 (0.03 mg/kg, iv). MK-801 produced a significant attenuation in response to 40 Hz auditory stimuli while entrainment to other frequencies was not affected. Time-frequency analysis revealed deficits in both power and phase-locking to 40 Hz. Nicotine (0.1 mg/kg, iv) administered after MK-801 reversed the attenuation of the 40 Hz response. Administered alone, nicotine augmented 40 Hz steady state power and phase-locking. Nicotine's effects were blocked by simultaneous administration of the α4ß2 antagonist DHßE. Thus we report for the first time, a rodent model that mimics a core neurophysiological deficit seen in patients with schizophrenia and a pharmacological approach to alleviate it.

Recovery from monocular deprivation using binocular deprivation.

Ocular dominance (OD) plasticity is a robust paradigm for examining the functional consequences of synaptic plasticity. Previous experimental and theoretical results have shown that OD plasticity can be accounted for by known synaptic plasticity mechanisms, using the assumption that deprivation by lid suture eliminates spatial structure in the deprived channel. Here we show that in the mouse, recovery from monocular lid suture can be obtained by subsequent binocular lid suture but not by dark rearing. This poses a significant challenge to previous theoretical results. We therefore performed simulations with a natural input environment appropriate for mouse visual cortex. In contrast to previous work, we assume that lid suture causes degradation but not elimination of spatial structure, whereas dark rearing produces elimination of spatial structure. We present experimental evidence that supports this assumption, measuring responses through sutured lids in the mouse. The change in assumptions about the input environment is sufficient to account for new experimental observations, while still accounting for previous experimental results.

Instructive effect of visual experience in mouse visual cortex.

We describe a form of experience-dependent response enhancement in the visual cortex of awake mice. Repeated presentations of grating stimuli of a single orientation result in a persistent enhancement of responses evoked by the test stimulus. Response potentiation is specific to the orientation of the test stimulus, develops gradually over the course of several training sessions, and occurs in both juvenile and adult mice. The stimulus-selective response potentiation (SRP) can mask deprivation-induced response depression in adult mice. SRP requires NMDA receptor activation and is prevented by viral delivery of a peptide that interferes with AMPA receptor trafficking. SRP may reveal the mechanisms involved in certain forms of perceptual learning.

How monocular deprivation shifts ocular dominance in visual cortex of young mice.

We used a chronic recording method to document the kinetics of ocular dominance (OD) plasticity induced by temporary lid closure in young mice. We find that monocular deprivation (MD) induces two separate modifications: (1) rapid, deprivation-induced response depression and (2) delayed, deprivation-enabled, experience-dependent response potentiation. To gain insight into how altering retinal activity triggers these cortical responses, we compared the effects of MD by lid closure with monocular inactivation (MI) by intravitreal injection of tetrodotoxin. We find that MI fails to induce deprived-eye response depression but promotes potentiation of responses driven by the normal eye. These effects of MI in juvenile mice closely resemble the effects of MD in adult mice. Understanding how MI and MD differentially affect activity in the visual system of young mice may provide key insight into how the critical period ends.

NMDA receptor-dependent ocular dominance plasticity in adult visual cortex.

The binocular region of mouse visual cortex is strongly dominated by inputs from the contralateral eye. Here we show in adult mice that depriving the dominant contralateral eye of vision leads to a persistent, NMDA receptor-dependent enhancement of the weak ipsilateral-eye inputs. These data provide in vivo evidence for metaplasticity as a mechanism for binocular competition and demonstrate that an ocular dominance shift can occur solely by the mechanisms of response enhancement. They also show that adult mouse visual cortex has a far greater potential for experience-dependent plasticity than previously appreciated. These insights may force a revision in how data on ocular dominance plasticity in mutant mice have been interpreted.