Detectable Deficits Research Articles

The Significance of Upper Extremity Neuromonitoring Changes During Thoracolumbar Spine Surgery.

This is a retrospective matched-pair cohort study. To investigate the significance of upper extremity (UE) neuromonitoring changes in patients undergoing thoracolumbar surgery in prone position. Peripheral nerve injuries in the UEs due to the prone positioning during prolonged thoracolumbar spinal procedures can cause diminished postsurgical outcomes. Intraoperative neuromonitoring has been utilized to alert the surgeon of the development of such injuries. Patients who developed intraoperative ulnar somatosensory-evoked potential (SSEP) signal changes during posterior thoracolumbar surgery were identified and compared with a group of patients who did not develop such signal changes. The patients in 2 groups were pair-matched on the number of vertebral levels undergoing surgery. Data regarding intraoperative attempts to resolve signal changes and outcomes were collected. In total, 843 patients underwent thoracic, lumbar, or thoracolumbar spine surgeries in the prone position with intraoperative ulnar SSEPs neuromonitoring data available. Of these, 37 patients (4.4%) had intraoperative signal changes in the UEs. An equal number of patients without signal changes were also selected. In each group, 6 patients underwent thoracic, 20 patients underwent lumbar, and 11 patients underwent thoracolumbar procedures. In 8 patients (21.6%), there was no resolution of SSEP signal changes despite intraoperative attempts. The 2 groups were similar with respect to age and comorbidities. There was no significant difference in the mean body mass index (P=0.22). The mean duration of the procedures was 324 minutes in the SSEP signal change patients and 260 minutes in the patients without SSEP signal changes (P=0.03). No patient with UE SSEP changes had a clinically detectable neurological deficit postoperatively. UE SSEP signal changes during multilevel posterior thoracolumbar procedures are more likely to occur as the duration of the operation increases. The presence of UE signal changes does not coincide with clinically significant peripheral neuropathies. Level III.

Tone-in-noise detection deficits in elderly patients with clinically normal hearing

PurposeOne of the most common complaints among the elderly is the inability to understand speech in noisy environments. In many cases, these deficits are due to age-related hearing loss; however, some of the elderly that have difficulty hearing in noise have clinically normal pure-tone thresholds. While speech in noise testing is informative, it fails to identify specific frequencies responsible for the speech processing deficit. Auditory neuropathy patients and animal models of hidden hearing loss suggest that tone-in-noise thresholds may provide frequency specific information for those patients who express difficulty, but have normal thresholds in quiet. Therefore, we aimed to determine if tone-in-noise thresholds could be a useful measure in detecting age-related hearing deficits, despite having normal audiometric thresholds. Materials & methodsWe tested this hypothesis by measuring tone-in-noise thresholds in 11 Old (62.4 ± 5 years) and 21 Young (23.1 ± 2.2 years) patients with clinically normal thresholds. Tone thresholds were measured in a quite sound field, then in 20, 30 and 40 dB HL broadband noise. ResultsDespite having normal hearing (thresholds ≤25 dB HL), the Old patients had significantly worse tone-in-noise thresholds than the Young patients at 0.125, 4, and 8 kHz. Linear regression analysis showed that the growth of masking in Old and Young patients was nearly identical at all frequencies. However, the amount of masking at low and high frequencies was typically 10–18 dB greater in the Old patients compared to the Young, except near 1 kHz. The frequency-dependent changes in masking are discussed in the context of a “line busy” model and temporal bone studies of auditory nerve fiber loss.

“It’s Not a Tumor”: A Framework for Capitalizing on Individual Diversity to Boost Target Detection

Even experts routinely miss infrequent targets, such as weapons in baggage scans or tumors in mammograms, because the visual system is not equipped to notice the unusual. To date, limited progress has been made toward improving human factors that mediate such critical diagnostic tasks. Here, we present a novel framework for pairing individuals’ estimates to increase target detection. Using a wisdom-of-crowds approach that capitalizes on the visual system’s ability to efficiently combine information, we demonstrated how averaging two noninteracting individuals’ continuous estimates of whether a briefly presented image contained a prespecified target can significantly boost detection across a range of tasks. Furthermore, we showed how pairing individuals’ estimates to maximize decorrelated patterns of performance in one task can optimize performance on a separate task. These results make significant advances toward combating severe deficits in target detection using straightforward applications for maximizing performance within limited pools of observers.

The Influence of Hearing Aid Gain on Gap-Detection Thresholds for Children and Adults With Hearing Loss.

The objective of this experiment was to examine the contributions of audibility to the ability to perceive a gap in noise for children and adults. Sensorineural hearing loss (SNHL) in adulthood is associated with a deficit in gap detection. It is well known that reduced audibility in adult listeners with SNHL contributes to this deficit; however, it is unclear the extent to which hearing aid amplification can restore gap-detection thresholds, and the effect of childhood SNHL on gap-detection thresholds have not been described. For adults, it was hypothesized that restoring the dynamic range of hearing for listeners with SNHL would lead to approximately normal gap-detection thresholds. Children with normal hearing (NH) exhibit poorer gap-detection thresholds than adults. Because of their hearing loss, children with SNHL have less auditory experience than their peers with NH. Yet, it is unknown the extent to which auditory experience impacts their ability to perceive gaps in noise. Even with the provision of amplification, it was hypothesized that children with SNHL would show a deficit in gap detection, relative to their peers with normal hearing, because of reduced auditory experience. The ability to detect a silent interval in noise was tested by adapting the stimulus level required for detection of gap durations between 3 and 20 ms for adults and children with and without SNHL. Stimulus-level thresholds were measured for participants with SNHL without amplification and with two prescriptive procedures-the adult and child versions of the desired sensation level i/o program-using a hearing aid simulator. The child version better restored the normal dynamic range than the adult version. Adults and children with NH were tested without amplification. When fitted using the procedure that best restored the dynamic range, adults with SNHL had stimulus-level thresholds similar to those of adults with normal hearing. Compared to the children with NH, the children with SNHL required a higher stimulus level to detect a 5-ms gap, despite having used the procedure that better restored the normal dynamic range of hearing. Otherwise, the two groups of children had similar stimulus-level thresholds. These findings suggest that apparent deficits in temporal resolution, as measured using stimulus-level thresholds for the detection of gaps, are dependent on age and audibility. These novel results indicate that childhood SNHL may impair temporal resolution as measured by stimulus-level thresholds for the detection of a gap in noise. This work has implications for understanding the effects of amplification on the ability to perceive temporal cues in speech.

Modeling subjective relevance in schizophrenia and its relation to aberrant salience.

In schizophrenia, increased aberrant salience to irrelevant events and reduced learning of relevant information may relate to an underlying deficit in relevance detection. So far, subjective estimates of relevance have not been probed in schizophrenia patients. The mechanisms underlying belief formation about relevance and their translation into decisions are unclear. Using novel computational methods, we investigated relevance detection during implicit learning in 42 schizophrenia patients and 42 healthy individuals. Participants underwent functional magnetic resonance imaging while detecting the outcomes in a learning task. These were preceded by cues differing in color and shape, which were either relevant or irrelevant for outcome prediction. We provided a novel definition of relevance based on Bayesian precision and modeled reaction times as a function of relevance weighted unsigned prediction errors (UPE). For aberrant salience, we assessed responses to subjectively irrelevant cue manifestations. Participants learned the contingencies and slowed down their responses following unexpected events. Model selection revealed that individuals inferred the relevance of cue features and used it for behavioral adaption to the relevant cue feature. Relevance weighted UPEs correlated with dorsal anterior cingulate cortex activation and hippocampus deactivation. In patients, the aberrant salience bias to subjectively task-irrelevant information was increased and correlated with decreased striatal UPE activation and increased negative symptoms. This study shows that relevance estimates based on Bayesian precision can be inferred from observed behavior. This underscores the importance of relevance detection as an underlying mechanism for behavioral adaptation in complex environments and enhances the understanding of aberrant salience in schizophrenia.

Wednesday, September 26, 2018 9:00 AM – 10:00 AM Best Papers: 5. The significance of upper extremity neuromonitoring changes in patients undergoing thoracolumbar surgery

BACKGROUND CONTEXT Peripheral nerve injuries of the upper extremities in patients undergoing posterior thoracolumbar surgery is a well described, yet preventable complication. Upper extremity (UE) neuromonitoring has been utilized to alert the surgeon of the development of such an injury. PURPOSE The purpose of this study is to investigate the occurrence of upper extremity neuromonitoring changes in patients undergoing thoracolumbar surgery in prone position and to assess the significance of these changes in terms of procedure and patient characteristics, and in preventing postoperative UE neuropathy. STUDY DESIGN/SETTING Pair-matched case-control study (Level III) design, university hospital setting. PATIENT SAMPLE A total of 843 consecutive patients from single institution. OUTCOME MEASURES Presence or absence of postoperative upper extremity neuropathy. METHODS All patients who underwent posterior thoracic, lumbar, or thoracolumbar surgery at a single institution from 2014 to 2016 with neuromonitoring were included in the study. UE neuromonitoring consisted of ulnar somatosensory evoked potentials (SSEPs). Patients with intraoperative ulnar SSEP signal changes were identified and compared with a group of pair-matched patients who did not develop intraoperative ulnar SSEP signal changes. The groups were matched based on the number of vertebral levels undergoing surgery. Data regarding intraoperative attempts to resolve signal changes and outcomes were collected. The two groups were compared to identify the risk factors for the development of UE neuromonitoring changes. RESULTS Between January 2014 and December 2016, 843 patients in our institution underwent thoracic, lumbar or thoracolumbar spine surgeries in prone position with intraoperative bilateral ulnar SSEPs neuromonitoring data available. Of these, 37 patients (4.4%) had intraoperative signal changes in the UE; an equal number of patients without signal changes were also selected. In each group, six patients underwent thoracic, 20 patients underwent lumbar, and 11 patients underwent thoracolumbar procedures. In eight patients (21.6%), there was no resolution of SSEP signal changes despite intraoperative attempts. The two groups were similar with respect to age and co-morbidities including diabetes, ischemic heart disease, and peripheral arterial disease. There was also no significant difference in the mean BMI (p=0.22). The mean duration of the procedures was 324 minutes in the SSEP signal change patients and 260 minutes in the patients who did not experience SSEP signal changes (p=0.03). No patient with UE SSEP changes had a clinically detectable neurologic deficit postoperatively. CONCLUSIONS Upper extremity SSEP signal changes during multilevel posterior thoracolumbar procedures are more likely to occur as the duration of the operation increases. The presence of UE signal changes does not coincide with clinically significant peripheral neuropathies. FDA DEVICE/DRUG STATUS This abstract does not discuss or include any applicable devices or drugs.

Single olfactory receptors set odor detection thresholds

In many species, survival depends on olfaction, yet the mechanisms that underlie olfactory sensitivity are not well understood. Here we examine how a conserved subset of olfactory receptors, the trace amine-associated receptors (TAARs), determine odor detection thresholds of mice to amines. We find that deleting all TAARs, or even single TAARs, results in significant odor detection deficits. This finding is not limited to TAARs, as the deletion of a canonical odorant receptor reduced behavioral sensitivity to its preferred ligand. Remarkably, behavioral threshold is set solely by the most sensitive receptor, with no contribution from other highly sensitive receptors. In addition, increasing the number of sensory neurons (and glomeruli) expressing a threshold-determining TAAR does not improve detection, indicating that sensitivity is not limited by the typical complement of sensory neurons. Our findings demonstrate that olfactory thresholds are set by the single highest affinity receptor and suggest that TAARs are evolutionarily conserved because they determine the sensitivity to a class of biologically relevant chemicals.

Hypoglossal-facial nerve "side-to-side" neurorrhaphy for facial paralysis resulting from closed temporal bone fractures.

Closed temporal bone fractures due to cranial trauma often result in facial nerve injury, frequently inducing incomplete facial paralysis. Conventional hypoglossal-facial nerve end-to-end neurorrhaphy may not be suitable for these injuries because sacrifice of the lesioned facial nerve for neurorrhaphy destroys the remnant axons and/or potential spontaneous innervation. we modified the classical method by hypoglossal-facial nerve "side-to-side" neurorrhaphy using an interpositional predegenerated nerve graft to treat these injuries. Five patients who experienced facial paralysis resulting from closed temporal bone fractures due to cranial trauma were treated with the "side-to-side" neurorrhaphy. An additional 4 patients did not receive the neurorrhaphy and served as controls. Before treatment, all patients had suffered House-Brackmann (H-B) grade V or VI facial paralysis for a mean of 5 months. During the 12-30 months of follow-up period, no further detectable deficits were observed, but an improvement in facial nerve function was evidenced over time in the 5 neurorrhaphy-treated patients. At the end of follow-up, the improved facial function reached H-B grade II in 3, grade III in 1 and grade IV in 1 of the 5 patients, consistent with the electrophysiological examinations. In the control group, two patients showed slightly spontaneous innervation with facial function improved from H-B grade VI to V, and the other patients remained unchanged at H-B grade V or VI. We concluded that the hypoglossal-facial nerve "side-to-side" neurorrhaphy can preserve the injured facial nerve and is suitable for treating significant incomplete facial paralysis resulting from closed temporal bone fractures, providing an evident beneficial effect. Moreover, this treatment may be performed earlier after the onset of facial paralysis in order to reduce the unfavorable changes to the injured facial nerve and atrophy of its target muscles due to long-term denervation and allow axonal regrowth in a rich supportive environment.

Late maturation of backward masking in auditory cortex.

Speech perception relies on the accurate resolution of brief, successive sounds that change rapidly over time. Deficits in the perception of such sounds, indicated by a reduced ability to detect signals during auditory backward masking, strongly relate to language processing difficulties in children. Backward masking during normal development has a longer maturational trajectory than many other auditory percepts, implicating the involvement of central auditory neural mechanisms with protracted developmental time courses. Despite the importance of this percept, its neural correlates are not well described at any developmental stage. We therefore measured auditory cortical responses to masked signals in juvenile and adult Mongolian gerbils and quantified the detection ability of individual neurons and neural populations in a manner comparable with psychoacoustic measurements. Perceptually, auditory backward masking manifests as higher thresholds for detection of a short signal followed by a masker than for the same signal in silence. Cortical masking was driven by a combination of suppressed responses to the signal and a reduced dynamic range available for signal detection in the presence of the masker. Both coding elements contributed to greater masked threshold shifts in juveniles compared with adults, but signal-evoked firing suppression was more pronounced in juveniles. Neural threshold shifts were a better match to human psychophysical threshold shifts when quantified with a longer temporal window that included the response to the delayed masker, suggesting that temporally selective listening may contribute to age-related differences in backward masking. NEW & NOTEWORTHY In children, auditory detection of backward masked signals is immature well into adolescence, and detection deficits correlate with problems in speech processing. Our auditory cortical recordings reveal immature backward masking in adolescent animals that mirrors the prolonged development seen in children. This is driven by both signal-evoked suppression and dynamic range reduction. An extended window of analysis suggests that differences in temporally focused listening may contribute to late maturing thresholds for backward masked signals.

A blunted phasic autonomic response to errors indexes age-related deficits in error awareness.

Conscious error detection is impaired in older age, yet it is unclear which age-related changes in the nervous system contribute to this deficit. In younger adults, error commission is accompanied by phasic autonomic arousal, which purportedly contributes to conscious error detection. Because aging is associated with declining autonomic reactivity, reduced phasic arousal to errors may therefore contribute to age-related error detection deficits. To test this, we measured pupil dilation in younger (<30years) and older (60-80years) healthy adults during an eye movement task. The task required a subjective assessment of response accuracy, as well as a "meta-judgment" of the certainty underlying that accuracy-assessment. This allowed for a precise quantification of subjective error awareness. Behaviorally, we found reduced error awareness in older adults. Furthermore, while younger adults showed "residual" awareness of error commission on unreported errors (indicated by decreased rating certainty compared with correct responses), this effect was absent in older adults. Notably, pupil dilation correlated with both measures: between subjects, greater pupil dilation to reported errors was correlated with greater subjective certainty of error detection, and greater pupil dilation to unreported errors was correlated with greater "residual" awareness of unreported errors. In line with this association, older adults showed a reduced pupil response to both reported and unreported errors. Notably, older adults showed no pupil dilation to unreported errors, in line with their lack of "residual" error awareness on such trials. Taken together, our results suggest that reduced autonomic reactivity may contribute to age-related error awareness deficits.

Automatic Processing of Changes in Facial Emotions in Dysphoria: A Magnetoencephalography Study.

It is not known to what extent the automatic encoding and change detection of peripherally presented facial emotion is altered in dysphoria. The negative bias in automatic face processing in particular has rarely been studied. We used magnetoencephalography (MEG) to record automatic brain responses to happy and sad faces in dysphoric (Beck’s Depression Inventory ≥ 13) and control participants. Stimuli were presented in a passive oddball condition, which allowed potential negative bias in dysphoria at different stages of face processing (M100, M170, and M300) and alterations of change detection (visual mismatch negativity, vMMN) to be investigated. The magnetic counterpart of the vMMN was elicited at all stages of face processing, indexing automatic deviance detection in facial emotions. The M170 amplitude was modulated by emotion, response amplitudes being larger for sad faces than happy faces. Group differences were found for the M300, and they were indexed by two different interaction effects. At the left occipital region of interest, the dysphoric group had larger amplitudes for sad than happy deviant faces, reflecting negative bias in deviance detection, which was not found in the control group. On the other hand, the dysphoric group showed no vMMN to changes in facial emotions, while the vMMN was observed in the control group at the right occipital region of interest. Our results indicate that there is a negative bias in automatic visual deviance detection, but also a general change detection deficit in dysphoria.

Emotion Detection Deficits and Decreased Empathy in Patients with Alzheimer's Disease and Parkinson's Disease Affect Caregiver Mood and Burden.

Background: Changes in social cognition occur in patients with Alzheimer’s disease (AD) and Parkinson’s disease (PD) and can be caused by several factors, including emotion recognition deficits and neuropsychiatric symptoms (NPS). The aims of this study were to investigate: (1) group differences on emotion detection between patients diagnosed with AD or PD and their respective caregivers; (2) the association of emotion detection with empathetic ability and NPS in individuals with AD or PD; (3) caregivers’ depression and perceived burden in relation to patients’ ability to detect emotions, empathize with others, presence of NPS; and (4) caregiver’s awareness of emotion detection deficits in patients with AD or Parkinson.Methods: In this study, patients with probable AD (N = 25) or PD (N = 17), and their caregivers (N = 42), performed an emotion detection task (The Awareness of Social Inference Test—Emotion Evaluation Test, TASIT-EET). Patients underwent cognitive assessment, using the Behavioral Neurology Assessment (BNA). In addition, caregivers completed questionnaires to measure empathy (Interpersonal Reactivity Index, IRI) and NPS (Neuropsychiatric Inventory, NPI) in patients and self-reported on depression (Geriatric Depression Scale, GDS) and burden (Zarit Burden Interview, ZBI). Caregivers were also interviewed to measure dementia severity (Clinical Dementia Rating (CDR) Scale) in patients.Results: The results suggest that individuals with AD and PD are significantly worse at recognizing emotions than their caregivers. Moreover, caregivers failed to recognize patients’ emotion recognition deficits and this was associated with increased caregiver burden and depression. Patients’ emotion recognition deficits, decreased empathy and NPS were also related to caregiver burden and depression.Conclusions: Changes in emotion detection and empathy in individuals with AD and PD has implications for caregiver burden and depression and may be amenable to interventions with both patients and caregivers.

Post-stroke unilateral spatial neglect: virtual reality-based navigation and detection tasks reveal lateralized and non-lateralized deficits in tasks of varying perceptual and cognitive demands

BackgroundUnilateral spatial neglect (USN), a highly prevalent and disabling post-stroke impairment, has been shown to affect the recovery of locomotor and navigation skills needed for community mobility. We recently found that USN alters goal-directed locomotion in conditions of different cognitive/perceptual demands. However, sensorimotor post-stroke dysfunction (e.g. decreased walking speed) could have influenced the results.Analogous to a previously used goal-directed locomotor paradigm, a seated, joystick-driven navigation experiment, minimizing locomotor demands, was employed in individuals with and without post-stroke USN (USN+ and USN-, respectively) and healthy controls (HC).MethodsParticipants (n = 15 per group) performed a seated, joystick-driven navigation and detection time task to targets 7 m away at 0°, ±15°/30° in actual (visually-guided), remembered (memory-guided) and shifting (visually-guided with representational updating component) conditions while immersed in a 3D virtual reality environment.ResultsGreater end-point mediolateral errors to left-sided targets (remembered and shifting conditions) and overall lengthier onsets in reorientation strategy (shifting condition) were found for USN+ vs. USN- and vs. HC (p < 0.05). USN+ individuals mostly overshot left targets (− 15°/− 30°). Greater delays in detection time for target locations across the visual spectrum (left, middle and right) were found in USN+ vs. USN- and HC groups (p < 0.05).ConclusionUSN-related attentional-perceptual deficits alter navigation abilities in memory-guided and shifting conditions, independently of post-stroke locomotor deficits. Lateralized and non-lateralized deficits in object detection are found. The employed paradigm could be considered in the design and development of sensitive and functional assessment methods for neglect; thereby addressing the drawbacks of currently used traditional paper-and-pencil tools.

Scene and human face recognition in the central vision of patients with glaucoma.

Primary open-angle glaucoma (POAG) firstly mainly affects peripheral vision. Current behavioral studies support the idea that visual defects of patients with POAG extend into parts of the central visual field classified as normal by static automated perimetry analysis. This is particularly true for visual tasks involving processes of a higher level than mere detection. The purpose of this study was to assess visual abilities of POAG patients in central vision. Patients were assigned to two groups following a visual field examination (Humphrey 24–2 SITA-Standard test). Patients with both peripheral and central defects and patients with peripheral but no central defect, as well as age-matched controls, participated in the experiment. All participants had to perform two visual tasks where low-contrast stimuli were presented in the central 6° of the visual field. A categorization task of scene images and human face images assessed high-level visual recognition abilities. In contrast, a detection task using the same stimuli assessed low-level visual function. The difference in performance between detection and categorization revealed the cost of high-level visual processing. Compared to controls, patients with a central visual defect showed a deficit in both detection and categorization of all low-contrast images. This is consistent with the abnormal retinal sensitivity as assessed by perimetry. However, the deficit was greater for categorization than detection. Patients without a central defect showed similar performances to the controls concerning the detection and categorization of faces. However, while the detection of scene images was well-maintained, these patients showed a deficit in their categorization. This suggests that the simple loss of peripheral vision could be detrimental to scene recognition, even when the information is displayed in central vision. This study revealed subtle defects in the central visual field of POAG patients that cannot be predicted by static automated perimetry assessment using Humphrey 24–2 SITA-Standard test.

Abstract WP250: Evaluating &amp; Optimizing the Model of Thrombotic MCAO in Mice

Background: The embolic model of middle cerebral artery occlusion (MCAO) by thrombus mimics the ischemic stroke in human and is amenable to thrombolytic therapies with recombinant tissue plasminogen activator. However, this model has not been thoroughly investigated and standardized. The present study was performed to optimize this model in mice. Methods: Male C57BL/6 mice (8-10 week old) were subjected to MCAO induced by autologous or allogeneic thrombus measuring 5, 10, or 15 mm in length. Blood was placed in a tube (20μm diameter) with thrombin before injecting with sterile saline into internal carotid artery (ICA). Cerebral blood flow (CBF) was monitored by laser-Doppler or laser speckle before MCAO. Infarct was assessed by TTC staining 24 hours after MCAO. Neurological deficits were evaluated by modified neurological severity score (mNSS), rotarod test and corner test 1-7 days after ischemia. Results: Thrombus injection resulted in an abrupt drop of CBF to less than 30% of baseline in the MCA territory. The areas with more than 50% CBF decrease at 3 h after thrombus injection was significantly correlated to infarct volume at 24 h after MCAO (r=0.792, P=0.019, Pearson′s correlation analysis), suggesting that continuous decrease in CBF within 3 h can predict brain damage after stroke. No significant differences in infarct volume between autologous and allogeneic thrombus were observed (25.31±6.45 mm 3 vs 23.00±6.31 mm 3 , p&gt;0.05). Allogeneic thrombi of 10 mm and 15 mm lengths caused reproducible infarct with detectable neurological deficits in mice. The 10 mm thrombus was chosen as the optimal thrombus length as it caused similar morphological and functional alterations compared with 60 min suture model of MCAO. In contrast, 15 mm thrombus resulted in significantly larger infract volume, worse sensorimotor functions and higher mortality in mice. Conclusion: Embolic MCAO did not yield stable CBF reduction compared to the classical suture MCAO. However, continuous decrease in CBF in the embolic model for at least 3 h resulted in successful infarct induction. The 10 mm autologous thrombus is suitable to induce reproducible infarct with neurological deficits in adult mice.

Incidence of peripheral nerve injury during shoulder arthroplasty when motor evoked potentials are monitored.

To report the incidence of clinically detectable nerve injuries when utilizing transcranial electrical motor evoked potentials (MEPs) during shoulder arthroplasty. A retrospective review of patients undergoing shoulder arthroplasty with continuous IONM was performed. The criteria for nerve alerts was an 80% amplitude reduction in MEPs. The primary outcome measure was post-operative clinically detectable nerve deficit. An additional retrospective analysis on a subset of cases using an all-or-none (100% amplitude reduction) criterion applied to the deltoid was performed. Two hundred eighty four arthroplasty cases were included. There were no permanent post-operative nerve injuries and two transient nerve injuries (0.7%). MEP alerts occurred in 102 cases (36.2%). Nineteen (6.7%) cases did not have signals return above alert threshold at closure. These cases were significantly associated with post-operative nerve injury (p = 0.03). There were no false negatives, making sensitivity 100% and specificity was 93.9%. In the subset of cases in which an all-or-none criterion was retrospectively applied to just the deltoid, MEP alerts occurred in just 17.9% of cases; specificity improved to 98.0%. We conclude that utilization of the real-time diagnostic MEP data during shoulder arthroplasty aids surgeons in decision making regarding impending peripheral nerve injuries.

Anserine (beta-alanyl-3-methyl-L-histidine) improves neurovascular-unit dysfunction and spatial memory in aged A\u03b2PPswe/PSEN1dE9 Alzheimer\u2019s-model mice

Anserine/carnosine supplementation improves cerebral blood flow and verbal episodic memory in elderly people, as we previously reported. Anserine’s buffering activity is superior to that of carnosine at neutral pH. In human sera, carnosine but not anserine is rapidly cleaved by carnosinase, limiting its effectiveness. This study examined the effects of anserine on AβPPswe/PSEN1dE9 Alzheimer’s disease (AD) model mice over 18-months old, an age at which these mice exhibit detectable memory deficits. We found that 8 weeks of anserine treatment completely recovered the memory deficits, improved pericyte coverage on endothelial cells in the brain, and diminished chronic glial neuroinflammatory reactions in these mice. These results suggest that anserine (beta-alanyl-3-methyl-L-histidine) supplementation improved memory functions in AD-model mice by exerting a protective effect on the neurovascular units, which are composed of endothelial cells, pericytes, and supporting glial cells.

Testing the Sarcocystis neurona vaccine using an equine protozoal myeloencephalitis challenge model

Equine protozoal myeloencephalitis (EPM) is an important equine neurologic disorder, and treatments for the disease are often unrewarding. Prevention of the disease is the most important aspect for EPM, and a killed vaccine was previously developed for just that purpose. Evaluation of the vaccine had been hampered by lack of post vaccination challenge. The purpose of this study was to determine if the vaccine could prevent development of clinical signs after challenge with Sarcocystis neurona sporocysts in an equine challenge model. Seventy horses that were negative for antibodies to S. neurona and were neurologically normal were randomly assigned to vaccine or placebo groups and divided into short-term duration of immunity (study #1) and long-term duration of immunity (study #2) studies. S. neurona sporocysts used for the challenge were generated in the opossum/raccoon cycle isolate SN 37-R. Study #1 horses received an initial vaccination and a booster, and were challenged 34days post second vaccination. Study #2 horses received a vaccination and two boosters and were challenged 139days post third vaccination. All horses in study #1 developed neurologic signs (n=30) and there was no difference between the vaccinates and controls (P=0.7683). All but four horses in study #2 developed detectable neurologic deficits. The neurologic signs, although not statistically significant, were worse in the vaccinated horses (P=0.1559). In these two studies, vaccination with the S. neurona vaccine failed to prevent development of clinical neurologic deficits.

A modified deltoid splitting approach with axillary nerve bundle mobilization for proximal humeral fracture fixation

IntroductionThe deltopectoral and the deltoid splitting approach are commonly used for the treatment of proximal humeral fractures. While the deltopectoral approach requires massive soft tissue devascularization, the deltoid splitting approach needs an additional skipped incision to avoid axillary nerve injury. The purpose of this study was to describe a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization in the treatment of proximal humeral fractures and to assess its radiologic and clinical outcomes. Patients and methodsTwenty-two consecutive patients with proximal humeral fractures were treated with minimally invasive plate osteosynthesis by using a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization. The patients were divided into two groups: 10 patients of Neer type 2 or 3 fractures vs. 12 patients of Neer type 4 fractures. The mean age of the study population was 63.5 years (range: 30–80 years). Six patients had valgus impacted fractures, and nine had fractures with medial comminution. ResultsFracture union was achieved in all cases. The mean time to union was 8.6 weeks (range: 6–12 weeks). Major complications, such as avascular necrosis of the humeral head and varus collapse at the fracture site, were not observed. No patients had clinically detectable sensory deficits in the axillary nerve distribution or paralysis of the anterior deltoid muscle. The mean neck-shaft angle at the final follow-up was 136.9° (range, 115°–159°). The mean visual analog score for patient satisfaction was 9.1 (range, 6–10), and the mean Neer scores were 93.5 (range, 84–100). There were no significant differences between the two groups with respect to radiologic and clinical outcomes except Neer scores: 95.8 (range: 86–100) in Neer type 2 or 3 fractures and 91.7 (range: 84–99) in Neer type 4 fractures. ConclusionThe use of a modified anterolateral deltoid splitting approach with axillary nerve bundle mobilization in the treatment of proximal humeral fractures yielded excellent outcomes. This approach is a useful alternative to the deltopectoral or the deltoid splitting approaches in the treatment of proximal humeral fractures.

312 An Evaluation of the Clinical and Histological Effects of High Dose Radiosurgery on the Rat Dorsal Root Ganglion

Abstract INTRODUCTION Stereotactic radiosurgery (SRS) is a safe and effective technique to create lesions of the brain and trigeminal nerve (TGN) in order to achieve neuromodulation. The lumbar dorsal root ganglion (DRG) contains the body of the sensory neurons responsible for pain sensitivity and can be targeted to treat chronic and debilitating pain in the extremities. Neuromodulation of the DRG might therefore improve chronic peripheral pain. This study was performed to determine the feasibility as well as clinical and histological effects of delivering high dose SRS targeted to the lumbar DRG in a rat model. METHODS Four Sprague Dawley male rats underwent 80 Gy maximum dose single-fraction SRS to the left L5 and L6 DRG using the Leksell Gamma Knife Icon (Elekta, Atlanta, GA) with onboard cone-beam CT imaging using 4 mm diameter collimators. The right L5 and L6 DRGs served as the controls. The animals were evaluated for motor and sensory deficits every two weeks. Two animals were sacrificed at 3 and two at 6 months after SRS. The lumbar spines were harvested and decalcified. Common histological techniques (Masson trichrome, Prussian blue) were used to assess for fibrosis and demyelination. RESULTS &gt;No detectable motor or sensory deficits were seen in any animal. Histological changes including fibrosis and loss of myelin were noted to the left L5 and L6 DRGs, but not the right side control DRGs. Fibrotic changes within the vertebral body were also evident on the treated sides of the vertebral bodies. CONCLUSION We were able to detect a demyelinating histopathological response from SRS delivered to the DRG in rats. Since such changes mimic those seen after trigeminal SRS in experimental animals, we hypothesize that radiosurgery may be a potential option in chronic spinal radicular pain amenable to neuromodulation.