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A commercial fast pyrolysis probe coupled with a high-resolution tandem mass spectrometer was employed to identify the initial reactions and products of fast pyrolysis of xylobiose and xylotriose, model compounds of xylans. Fragmentation of the reducing end by loss of an ethenediol molecule via ring-opening and retro-aldol condensation was found to be the dominant pyrolysis pathway for xylobiose, and the structure of the product-ß-d-xylopyranosylglyceraldehyde-was identified by comparing collision-activated dissociation of the ionized product and an ionized authentic compound. This intermediate can undergo further decomposition via the loss of formaldehyde to form ß-d-xylopyranosylglycolaldehyde. In addition, the mechanisms of reactions leading to the loss of a water molecule or dissociation of the glycosidic linkages were explored computationally. These reactions are proposed to occur via pinacol ring contraction and/or Maccoll elimination mechanisms.

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Glucuronidation, a common phase II biotransformation reaction, is one of the major in vitro and in vivo metabolism pathways of xenobiotics. In this process, glucuronic acid is conjugated to a drug or a drug metabolite via a carboxylic acid, a hydroxy, or an amino group to form acyl-, O-, and/or N-glucuronide metabolites, respectively. This process is traditionally thought to be a detoxification pathway. However, some acyl-glucuronides react with biomolecules in vivo, which may result in immune-mediated idiosyncratic drug toxicity (IDT). In order to avoid this, one may attempt in early drug discovery to modify the lead compounds in such a manner that they then have a lower probability of forming reactive acyl-glucuronide metabolites. Because most drugs or drug candidates bear multiple functionalities, e.g., hydroxy, amino, and carboxylic acid groups, glucuronidation can occur at any of those. However, differentiation of isomeric acyl-, N-, and O-glucuronide derivatives of drugs is challenging. In this study, gas-phase ion-molecule reactions between deprotonated glucuronide metabolites and BF3 followed by collision-activated dissociation (CAD) in a linear quadrupole ion trap mass spectrometer were demonstrated to enable the differentiation of acyl-, N-, and O-glucuronides. Only deprotonated N-glucuronides and deprotonated, migrated acyl-glucuronides form the two diagnostic product ions: a BF3 adduct that has lost two HF molecules, [M - H + BF3 - 2HF]-, and an adduct formed with two BF3 molecules that has lost three HF molecules, [M - H + 2BF3 - 3HF]-. These product ions were not observed for deprotonated O-glucuronides and unmigrated, deprotonated acyl-glucuronides. Upon CAD of the [M - H + 2BF3 - 3HF]- product ion, a diagnostic fragment ion is formed via the loss of 2-fluoro-1,3,2-dioxaborale (MW of 88 Da) only in the case of deprotonated, migrated acyl-glucuronides. Therefore, this method can be used to unambiguously differentiate acyl-, N-, and O-glucuronides. Further, coupling this methodology with HPLC enables the differentiation of unmigrated 1-ß-acyl-glucuronides from the isomeric acyl-glucuronides formed upon acyl migration. Quantum chemical calculations at the M06-2X/6-311++G(d,p) level of theory were employed to probe the mechanisms of the reactions of interest.

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Evaluation of the feasibility of various mechanisms possibly involved in cellulose fast pyrolysis is challenging. Therefore, selectively 13C-labeled cellotriose, 18O-labeled cellobiose, and 13C- and 18O-doubly-labeled cellobiose were synthesized and subjected to fast pyrolysis in an atmospheric pressure chemical ionization source of a linear quadrupole ion trap/orbitrap mass spectrometer. The initial products were immediately quenched, ionized using ammonium cations, and subsequently analyzed using the mass spectrometer. The loss or retention of isotope labels upon pyrolysis unambiguously revealed three major competing mechanisms-sequential losses of glycolaldehyde/ethenediol molecules from the reducing end (the reducing-end unraveling mechanism), hydroxymethylene-assisted glycosidic bond cleavage (HAGBC mechanism), and Maccoll elimination. Important discoveries include the following: (1) Reducing-end unraveling is the predominant mechanism occurring at the reducing end; (2) Maccoll elimination facilitates the cleaving of aglyconic bonds, and it is the mechanism leading to formation of reducing carbohydrates; 3) HAGBC occurs for glycosides but not at the reducing end of cellodextrins; 4) HAGBC and water loss are the predominant reactions for fast pyrolysis of 1,6-anhydrocellodextrins; and 5) HAGBC can proceed after reducing-end unraveling but unraveling does not occur once the HAGBC reaction pathway is initiated. Moreover, hydrolysis was conclusively ruled out for fast pyrolysis of cellobiose, cellotriose, and 1,6-anhydrocellodextrins up to cellotetraosan. No radical reactions were observed.

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A full understanding of all possible elementary reactions applicable to cellulose fast pyrolysis is key to developing a comprehensive kinetic model for fast pyrolysis of cellulose. Since water is an observed product of fast pyrolysis of cellulose, the energetics of the dehydration reactions of cellulose were explored computationally by using density functional theory. Glucose and cellobiose were selected as the cellulose model compounds. The four water loss mechanisms studied are Maccoll elimination, Pinacol ring contraction, cyclic Grob fragmentation, and alcohol condensation, some of which have not been considered previously in the literature. Levoglucosan formation via alcohol condensation has the lowest calculated free-energy barrier (50.4 kcal mol-1) for glucose dehydration. All other water loss reactions have calculated free-energy barriers greater than 60 kcal mol-1. Cellobiose dehydration shows similar trends to those of glucose, suggesting that these reactions are applicable to glucooligosaccharides with higher degrees of polymerization. Secondary reactions of dehydrated glucose and dehydrated cellobiose via retro-Diels-Alder and aldol rearrangement mechanisms are also explored computationally.

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Isomeric O- and N-glucuronides are common drug metabolites produced in phase II of drug metabolism. Distinguishing these isomers by using common analytical techniques has proven challenging. A tandem mass spectrometric method based on gas-phase ion/molecule reactions of deprotonated glucuronide drug metabolites with trichlorosilane (HSiCl3) in a linear quadrupole ion trap mass spectrometer is reported here to readily enable differentiation of the O- and N-isomers. The major product ion observed upon reactions of HSiCl3 with deprotonated N-glucuronides is a diagnostic HSiCl3 adduct that has lost two HCl molecules ([M - H + HSiCl3 - 2HCl]-). This product ion was not observed for deprotonated O-glucuronides. Reaction mechanisms were explored with quantum chemical calculations at the M06-2X/6-311++G(d,p) level of theory.

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BACKGROUND: Biofilm has been suggested as a cause of disinfection failures in flexible endoscopes where no lapses in the decontamination procedure can be identified. To test this theory, the activity of peracetic acid, one of the widely used disinfectants in the reprocessing of flexible endoscopes, was evaluated against both planktonic and sessile communities of Pseudomonas aeruginosa. AIM: To investigate the ability of P. aeruginosa biofilm to survive high-level peracetic acid disinfection. METHOD: The susceptibility of planktonic cells of P. aeruginosa and biofilms aged 24, 48, 96, and 192 h to peracetic acid was evaluated by estimating their viability using resazurin viability and plate count methods. The biomass of the P. aeruginosa biofilms was also quantified using Crystal Violet assay. Planktonic cells of P. aeruginosa were treated with 5-30 ppm concentration of peracetic acid in the presence of 3.0 g/L of bovine serum albumin (BSA) for 5 min. Biofilms of P. aeruginosa were also treated with various peracetic acid concentrations (100-3000 ppm) for 5 min. FINDINGS: Planktonic cells of P. aeruginosa were eradicated by 20 ppm of peracetic acid, whereas biofilms showed an age-dependent tolerance to peracetic acid, and 96 h biofilm was only eradicated at peracetic acid concentration of 2500 ppm. CONCLUSION: Ninety-six-hour P. aeruginosa biofilm survives 5 min treatment with 2000 ppm of peracetic acid, which is the working concentration used in some endoscope washer-disinfectors. This implies that disinfection failure of flexible endoscopes might occur when biofilms build up in the lumens of endoscopes.

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Epidural spinal cord stimulation has a long history of application for improving motor control in spinal cord injury. This review focuses on its resurgence following the progress made in understanding the underlying neurophysiological mechanisms and on recent reports of its augmentative effects upon otherwise subfunctional volitional motor control. Early work revealed that the spinal circuitry involved in lower-limb motor control can be accessed by stimulating through electrodes placed epidurally over the posterior aspect of the lumbar spinal cord below a paralyzing injury. Current understanding is that such stimulation activates large-to-medium-diameter sensory fibers within the posterior roots. Those fibers then trans-synaptically activate various spinal reflex circuits and plurisegmentally organized interneuronal networks that control more complex contraction and relaxation patterns involving multiple muscles. The induced change in responsiveness of this spinal motor circuitry to any residual supraspinal input via clinically silent translesional neural connections that have survived the injury may be a likely explanation for rudimentary volitional control enabled by epidural stimulation in otherwise paralyzed muscles. Technological developments that allow dynamic control of stimulation parameters and the potential for activity-dependent beneficial plasticity may further unveil the remarkable capacity of spinal motor processing that remains even after severe spinal cord injuries.

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BACKGROUND: The human lumbosacral spinal circuitry can generate rhythmic motor output in response to different types of inputs after motor-complete spinal cord injury. OBJECTIVE: To explore spinal rhythm generating mechanisms recruited by phasic step-related sensory feedback and tonic posterior root stimulation when provided alone or in combination. METHODS: We studied stepping in 4 individuals with chronic, clinically complete spinal cord injury using a robotic-driven gait orthosis with body weight support over a treadmill. Electromyographic data were collected from thigh and lower leg muscles during stepping with 2 hip-movement conditions and 2 step frequencies, first without and then with tonic 30-Hz transcutaneous spinal cord stimulation (tSCS) over the lumbar posterior roots. RESULTS: Robotic-driven stepping alone generated rhythmic activity in a small number of muscles, mostly in hamstrings, coinciding with the stretch applied to the muscle, and in tibialis anterior as stance-phase synchronized clonus. Adding tonic 30-Hz tSCS increased the number of rhythmically responding muscles, augmented thigh muscle activity, and suppressed clonus. tSCS could also produce rhythmic activity without or independent of step-specific peripheral feedback. Changing stepping parameters could change the amount of activity generated but not the multimuscle activation patterns. CONCLUSIONS: The data suggest that the rhythmic motor patterns generated by the imposed stepping were responses of spinal reflex circuits to the cyclic sensory feedback. Tonic 30-Hz tSCS provided for additional excitation and engaged spinal rhythm-generating networks. The synergistic effects of these rhythm-generating mechanisms suggest that tSCS in combination with treadmill training might augment rehabilitation outcomes after severe spinal cord injury.

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STUDY DESIGN: Prospective cohort study. OBJECTIVE: This study was designed to neurophysiologically characterize motor control recovery after spinal cord injury (SCI). SETTING: University of Louisville, Louisville, Kentucky, USA. MATERIAL: Eleven acute SCI admissions and five non-injured subjects were recruited for this study. METHODS: The American Spinal Injury Association Impairment Scale (AIS) was used to categorize injury level and severity at onset. Multimuscle surface electromyography (sEMG) recording protocol of reflex and volitional motor tasks was initially performed between the day of injury and 11 days post onset (6.4±3.6, mean±s.d. days). Follow-up data were recorded for up to 17 months after injury. Initial AIS distribution was as follows: 4 AIS-A; 2 AIS-C; 5 AIS-D. Multimuscle activation patterns were quantified from the sEMG amplitudes of selected muscles using a vector-based calculation that produces separate values for the magnitude and similarity of SCI test-subject patterns to those of non-injured subjects for each task. RESULTS: In SCI subjects, overall sEMG amplitudes were lower after SCI. Prime mover muscle voluntary recruitment was slower and multimuscle patterns were disrupted by SCI. Recovery occurred in 9 of the 11 subjects, showing an increase in sEMG amplitudes, more rapid prime mover muscle recruitment rates and the progressive normalization of the multimuscle activation patterns. The rate of increase was highly individualized, differing over time by limb and proximal or distal joint within each subject and across the SCI group. CONCLUSIONS: Recovery of voluntary motor function can be quantitatively tracked using neurophysiological methods in the domains of time and multimuscle motor unit activation.

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STUDY DESIGN: The study design used is prospective cohort study. OBJECTIVES: This study was designed to neurophysiologically characterize spinal motor activity during recovery from spinal cord injury (SCI). SETTING: University of Louisville, Louisville, Kentucky, USA. METHODS: Twenty-five consecutive acute SCI admissions were recruited for this study. The American Spinal Injury Association Impairment Scale (AIS) was used to categorize injury level and severity at onset. Surface EMG recording was carried out initially between the day of admission and 17 days post-onset (6.0 ± 4.3, mean ± s.d. days). Follow-up recordings were performed for up to 9 months after injury. Initial AIS distribution was 7 AIS-A; 3 AIS-B; 2 AIS-C; 13 AIS-D. RESULTS: Twelve subjects (48%) showed long-duration involuntary motor-unit activation during relaxation. This activity was seen on initial examination in nine and on follow-up by 3 months post-injury in three others. It was seen in muscles innervated from the injury zone in 11 and caudal to the lesion in 9 subjects. This activity was independent of the presence or absence of tendon reflexes and the ability to volitionally suppress plantar stimulation elicited reflex withdrawal. CONCLUSION: The form of involuntary activity described here is the likely result of the altered balance of excitation and inhibition reaching spinal motor neurons because of the loss of inhibitory interneurons or their reduced activation by damaged supraspinal drive and the synaptic reorganization that follows SCI. As such, this activity may be useful for monitoring the effects of neuroprotective and restorative intervention strategies in persons with SCI.

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BACKGROUND: Increased BMI may increase the body's capacity to store potent inhaled anaesthetics, more so with more soluble agents. Accordingly, we asked whether increased BMI and longer anaesthesia prolonged airway reflex recovery. METHODS: We measured time from anaesthetic discontinuation until first response to command (T1); from response to command until ability to swallow (T2); and from anaesthetic discontinuation to recovery of ability to swallow (T3) in 120 patients within three BMI ranges (18-24, 25-29, and >or=30 kg m(-2)). All received sevoflurane or desflurane, delivered via an LMA. RESULTS: T1 and T3 after sevoflurane exceeded T1 and T3 after desflurane: 6.6 (sd 4.2) vs 4.0 (1.9) min (P<0.001), and 14.1 (sd 8.3) vs 6.1 (2.0) min (P<0.0001). T3 correlated more strongly with BMI after sevoflurane (28 s per kg m(-2), P=0.02) than desflurane (7 s per kg m(-2), P=0.03). Regarding T2, patients receiving sevoflurane with BMI >or=30 kg m(-2) were less often able to swallow 2 min after response to command than were those with BMI 18-24 or 25-29 kg m(-2) (3/20 vs 10/20 or 9/20, P<0.05). Each sevoflurane MAC-hour delayed T3 by 4.5 min (268 s) (R=0.46, P<0.001) whereas each desflurane MAC-hour delayed T3 by 0.2 min (16 s) (R=0.10, P=0.44). CONCLUSIONS: Prolonged sevoflurane administration and greater BMI delay airway reflex recovery. The contribution of BMI to this delay is more pronounced after sevoflurane than desflurane.

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BACKGROUND: Morphine decreases gut peristalsis, and ketamine decreases morphine use after surgery, and does not slow peristalsis. Thus, the combination should result in faster return of bowel function after surgery than morphine alone. METHOD: A double-blind randomized controlled trial of saline vs. ketamine with intravenous patient-controlled-analgesia morphine for post-operative pain control was conducted on 42 patients having bowel resection. Bowel function was assessed by auscultation, time to passage of flatus and stool, and time to first retained oral intake; pain by visual analog scale. Time to return of all four measures of bowel function was the primary outcome. RESULTS: Despite a ketamine dose that in other studies had decreased morphine use without side-effects, there was no difference in bowel function, pain control, or morphine use between the two groups. Ketamine resulted in hallucinations in six out of 19 patients, with none in the placebo group (P =0.018). CONCLUSION: Low-dose ketamine was not efficacious for hastening return of bowel function, or for decreasing post-operative pain after surgery for bowel resection. It resulted in hallucinations in some patients. Those reporting hallucinations all wished to remain in the study.

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In this review we describe clinical and neurophysiological features of motor control in human spinal cord injury based on two models. First, motor control is considered in subjects with injury-induced complete division of the spinal cord from brain and brainstem structures, and second, in those in which the division is partial. We describe motor control in terms of segmental and plurisegmental reflex activity that dominates motor unit output to the muscles following complete separation from the brain motor structures by accidental injury. With incomplete separation of the spinal cord from brain structures, motor control is defined as the voluntary manipulation of reflex and automatic activity integrated with internal and external feedback signals. We review here motor control found after complete spinal cord injury with paradigm of single and regular-repeating stimuli applied to elicit cutaneous and muscle stretch reflex responses. We argue, that isolated spinal cord neural circuitry is capable of organizing characteristic reflex events that depend on the characteristics of the stimulus. Also, the profile of residual brain and brainstem, modified by the reduction in descending long spinal tract fibers arriving at their targets in the spinal gray matter, produces characteristic changes in motor output to the muscles that leads to the development of new neural strategies for control of segmental and plurisegmental neural circuitry. In the second part of this review, we discuss available treatment modalities for impaired cord function and briefly outline neurobiological interventions under development for repair of spinal cord injury.

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STUDY DESIGN: Cross-sectional retrospective study of a neurophysiological method of voluntary motor control characterization. OBJECTIVES: This study was undertaken to validate the surface electromyography (sEMG)-based voluntary response index (VRI) as an objective, quantitative, laboratory measure of spinal cord injury severity in terms of voluntary motor control disruption. SETTING: VA Medical Centers in Houston and Dallas Texas, USA. METHODS: A total of 67 subjects with incomplete spinal cord injury (iSCI), American Spinal Injury Association Impairment Scale (AIS)-C (n = 32) and -D (n = 35) were studied. sEMG recorded during a standardized protocol including eight lower-limb voluntary motor tasks was analyzed using the VRI method that relates multi-muscle activation patterns of SCI persons to those of healthy-subject prototypes (n = 15). The VRI is composed of a measure of the amount of the sEMG activity (magnitude) and the distribution of activity across muscle groups compared to that of healthy subjects for each motor task (similarity index, SI). These resulting VRI components, normalized magnitude and SI, were compared to AIS clinical findings in this study. Receiver operating characteristic analysis was performed to determine the SI values best separating AIS-C and AIS-D subjects. RESULTS: Magnitude and SI for AIS-C subjects had mean values of 0.27 +/- 0.32 and 0.65 +/- 0.21, respectively. Both parameters were significantly larger in the AIS-D subjects (0.78 +/- 0.43 and 0.93 +/- 0.06), respectively (P < 0.01). An SI value of 0.85 was found to separate AIS-C and AIS-D groups with a sensitivity of 0.89 and a specificity of 0.81. Further, the VRI of each leg strongly correlated with the respective AIS motor score (0.80, r < 0.01). CONCLUSIONS: In the domains of voluntary motor control, the sEMG-based VRI demonstrated adequate face validity and sensitivity to injury severity as currently measured by the AIS. SPONSORSHIP: Veterans Affairs Medical Center.

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This study employed neurophysiological methods to relate the condition of the corticospinal system with the voluntary control of lower-limb muscles in persons with motor-incomplete spinal cord injury. It consisted of two phases. In a group of ten healthy subjects, single and paired transcranial magnetic stimulation (TMS) of the motor cortex was used to study the behavior of the resulting motor evoked potentials (MEP) in lower-limb muscles. Interstimulus intervals (ISIs) of 15-100 ms were examined for augmentation of test MEPs by threshold or subthreshold conditioning stimuli. The second phase of this study examined eight incomplete spinal cord injured (iSCI) subjects, American Spinal Injury Association Impairment Scale C (n = 5) and D (n = 3) in whom voluntary motor control was quantified using the surface EMG (sEMG) based Voluntary Response Index (VRI). The VRI is calculated to characterize relative output patterns across ten lower-limb muscles recorded during a standard protocol of elementary voluntary motor tasks. VRI components were calculated by comparing the distribution of sEMG in iSCI subjects with prototype patterns collected from 15 healthy subjects using the same rigidly administered protocol, The resulting similarity index (SI) and magnitude values provided the measure of voluntary motor control. Corticospinal system connections were characterized by the thresholds for MEPs in key muscles. Key muscles were those that function as the prime-movers, or agonists for the voluntary movements from which the VRI data were calculated. Results include healthy-subject data that showed significant increases in conditioned MEP responses with paired stimuli of 15-50 ms ISI. Stimulus pairs of 75 and 100 ms showed no increase in MEP peak amplitude over that of the single-pulse conditioning stimulus alone, usually no response. For the iSCI subjects, 42% of the agonists responded to single-pulse TMS and 25% required paired-pulse TMS to produce an MEP. American Spinal Injury Association Impairment Scale component motor scores for agonist muscles, Quadriceps, Tibialis Anterior, and Triceps Surae, were significantly lower where MEPs could not be obtained (p < 0.05). VRI values were also significantly lower for motor tasks with agonists that had no resting MEP (p < 0.01). Therefore, the presence of a demonstrable connection between the motor cortex and spinal motor neurons in persons with SCI was related to the quality of post-injury voluntary motor control as assessed by the VRI.

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In this paper, a method for analyzing surface electromyographic (sEMG) data recorded from the lower-limb muscles of incomplete spinal-cord injured (iSCI) subjects is evaluated. sEMG was recorded bilaterally from quadriceps, adductor, hamstring, tibialis anterior, and triceps surae muscles during voluntary ankle dorsiflexion performed in the supine position as part of a comprehensive motor control assessment protocol. Analysis of the sEMG centered on two features, the magnitude of activation and the degree of similarity [similarity index (SI)] of the sEMG distribution to that of healthy subjects performing the same maneuver (n = 10). The analysis calculations resulted in response vectors (RV) that were compared to healthy-subject-derived prototype response vectors resulting in a voluntary response index (VRI). Incomplete SCI subjects (n = 9) were used to test the sensitivity of this analysis method. They were given supported-weight treadmill ambulation training, which is expected to improve or at least not cause a deterioration of voluntary motor control. The VRI provided evidence that the quantitative sEMG analysis method used was able to differentiate between healthy subjects and those with iSCI, characterize individual differences among iSCI subjects, and track motor control changes occurring over time.

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OBJECTIVE: This study was designed to characterize the rudimentary residual lower-limb motor control that can exist in clinically paralyzed spinal-cord-injured individuals. METHODS: Sixty-seven paralyzed spinal-cord-injured subjects were studied using surface electromyography recorded from muscles of the lower limbs and analyzed for responses to a rigidly administered protocol of reinforcement maneuvers, voluntary movement attempts, vibration, or the ability to volitionally suppress withdrawal evoked by plantar surface stimulation. RESULTS: Markers for the subclinical discomplete motor syndrome were found in 64% of the subjects. The tonic vibration response was recorded in 37%, volitional plantar surface stimulation response suppression in 27%, and reinforcement maneuver responses in 6% of the subjects. Three subjects, 4%, produced reliable but very low amplitude surface electromyography during the voluntary movement segment of the protocol. Surface electromyography recorded during passive leg movement was related to Ashworth scores as was the tonic vibration response marker (P < 0.05). CONCLUSIONS: Multimuscle surface electromyography patterns recorded during a rigidly administered protocol of motor tasks can be used to differentiate between clinically paralyzed spinal-cord-injured individuals using subclinical motor output to identify the translesional neural connections that remain available for intervention testing and treatment planning after spinal cord injury.

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Individuals with incomplete spinal cord injuries (SCI) retain varying degrees of voluntary motor control. The complexity of the motor control system and the nature of the recording biophysics have inhibited efforts to develop objective measures of voluntary motor control. This paper proposes the definition and use of a voluntary response index (VRI) calculated from quantitative analysis of surface electromyographic (sEMG) data recorded during defined voluntary movement as a sensitive measure of voluntary motor control in such individuals. The VRI is comprised of two numeric values, one derived from the total muscle activity recorded for the voluntary motor task (magnitude), and the other from the sEMG distribution across the recorded muscles (similarity index (SI)). Calculated as a vector, the distribution of sEMG from the test subject is compared to the average vector calculated from sEMG recordings of the same motor task from 10 neurologically intact subjects in a protocol called brain motor control assessment (BMCA). To evaluate the stability of the VRI, a group of five healthy subjects were individually compared to the prototype, average healthy-subject vectors for all of the maneuvers. To evaluate the sensitivity of this method, the VRI was obtained from two SCI subjects participating in other research studies. One was undergoing supported treadmill ambulation training, and the other a controlled withdrawal of anti-spasticity medications. The supported treadmill training patient's VRI, calculated from pre- and post-training BMCA recordings, reflected the qualitative changes in sEMG patterns and functional improvement of motor control. The VRI of the patient followed by serial BMCA during medication withdrawal also reflected changes in the motor control as a result of changes in anti-spasticity medication. To validate this index for clinical use, serial studies using larger numbers of subjects with compromised motor control should be performed.

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