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Vibration, a potent mechanical stimulus for activating muscle spindle primary afferents, may improve gait performance in persons with multiple sclerosis (MS), but has yet to be developed and deployed for multiple leg muscles with application during walking training. This study explored the development of a cyclic focal muscle vibration (FMV) system, and the deployment feasibility to correct MS walking swing phase deficits in order to determine whether this intervention warrants comprehensive study. The system was deployed during twelve, two-hour sessions of walking with cyclic FMV over six weeks. Participants served as their own control. Blood pressure, heart rate, walking speed, kinematics (peak hip, knee and ankle angles during swing), toe clearance, and step length were measured before and after deployment with blood pressure and heart rate monitored during deployment. During system deployment, there were no untoward sensations and physiological changes in blood pressure and heart rate, and volitional improvements were found in walking speed, improved swing phase kinematics, toe clearance and step length. This FMV training system was developed and deployed to improve joint flexion during walking in those with MS, and it demonstrated feasibility and benefits. Further study will determine the most effective vibration frequency and dose, carryover effects, and those most likely to benefit from this intervention.

Gait deficits are often persistent after stroke, and current rehabilitation methods do not restore normal gait for everyone. Targeted methods of focused gait therapy that meet the individual needs of each stroke survivor are needed. Our objective was to develop and test a combination protocol of simultaneous brain stimulation and focused stance phase training for people with chronic stroke (>6 months). We combined Transcranial Direct Current Stimulation (tDCS) with targeted stance phase therapy using Virtual Reality (VR)-assisted treadmill training and overground practice. The training was guided by motor learning principles. Five users (>6 months post-stroke with stance phase gait deficits) completed 10 treatment sessions. Each session began with 30 min of VR-assisted treadmill training designed to apply motor learning (ML)-based stance phase targeted practice. During the first 15 min of the treadmill training, bihemispheric tDCS was simultaneously delivered. Immediately after, users completed 30 min of overground (ML)-based gait training. The outcomes included the feasibility of protocol administration, gait speed, Timed Up and Go (TUG), Functional Gait Assessment (FGA), paretic limb stance phase control capability, and the Fugl–Meyer for lower extremity coordination (FMLE). The changes in the outcome measures (except the assessments of stance phase control capability) were calculated as the difference from baseline. Statistically and clinically significant improvements were observed after 10 treatment sessions in gait speed (0.25 ± 0.11 m/s) and FGA (4.55 ± 3.08 points). Statistically significant improvements were observed in TUG (2.36 ± 3.81 s) and FMLE (4.08 ± 1.82 points). A 10-session intervention combining tDCS and ML-based task-specific gait rehabilitation was feasible and produced clinically meaningful improvements in lower limb function in people with chronic gait deficits after stroke. Because only five users tested the new protocol, the results cannot be generalized to the whole population. As a contribution to the field, we developed and tested a protocol combining brain stimulation and ML-based stance phase training for individuals with chronic stance phase deficits after stroke. The protocol was feasible to administer; statistically and/or clinically significant improvements in gait function across an array of gait performance measures were observed with this relatively short treatment protocol.

Background: In ≈25% of patients with heart failure and reduced left-ventricular ejection fraction, right-ventricular (RV), and left-ventricular (LV) filling pressures are discordant (ie, one is elevated while the other is not). Whether clinical assessment allows detection of this discordance is unknown. We sought to determine the agreement of clinically versus invasively determined patterns of ventricular congestion. Methods: In 156 heart failure and reduced LV ejection fraction subjects undergoing invasive hemodynamic assessment, we categorized patterns of ventricular congestion (no congestion, RV only, LV only, or both) based on clinical findings of RV (jugular venous distention) or LV (hepatojugular reflux, orthopnea, or bendopnea) congestion. Agreement between clinically and invasively determined (RV congestion if right atrial pressure [RAP] ≥10 mm Hg and LV congestion if pulmonary capillary wedge pressure [PCWP] ≥22 mm Hg) categorizations was the primary end point. Results: The frequency of clinical patterns of congestion was: 51% no congestion, 24% both RV and LV, 21% LV only, and 4% RV only. Jugular venous distention had excellent discrimination for elevated RAP (C=0.88). However, agreement between clinical and invasive congestion patterns was poor, к=0.44 (95% CI, 0.34–0.55). While those with no clinical congestion usually had low RAP and PCWP (67/79, 85%), over one-half (24/38, 64%) with isolated LV clinical congestion had PCWP Conclusions: While clinical examination allows accurate detection of elevated RAP, it does not allow accurate detection of discordant RV and LV filling pressures.

Morbidity and mortality (M&M) conferences were originally developed in surgical and procedural-related fields as an attempt to identify errors leading to patient harm [(1)][1]. Following a mandate from the Accreditation Council for Graduate Medical Education (ACGME) in 1983 [(2)][2], M&M conferences

We present the design, control, and experimental evaluation of an energy regenerative powered transfemoral prosthesis. Our prosthesis prototype is comprised of a passive ankle and a powered knee joint. The knee joint is actuated by an ultracapacitor based regenerative drive mechanism. A novel varying impedance control approach controls the prosthesis in both the stance and swing phase of the gait cycle, while explicitly considering energy regeneration. This control method varies the impedance of the knee joint based on the amount of force exerted on the shank of the prosthesis. Furthermore, the controller promotes energy regeneration by precisely injecting a designated amount of negative damping into the system. Our control approach leads to a few tuning parameters that cover all of the gait phases for walking and all of the tested walking speeds and eliminates the need for tedious target impedance scheduling. Experimental evaluation is done with an amputee test subject walking at different speeds on a treadmill. The results validate the effectiveness of the control method. In addition, net energy regeneration is achieved while walking with near-natural gait across all speeds.

Pulmonary arterial hypertension is characterized by abnormalities in the small pulmonary arteries including increased vasoconstriction, vascular remodeling, proliferation of smooth muscle cells, and in situ thrombosis. Selexipag, a novel, oral prostacyclin receptor agonist, has been shown to improve hemodynamics in a phase II clinical trial and reduce clinical worsening in a large phase III clinical trial involving patients with pulmonary arterial hypertension. In this paper, we describe the prostacyclin signaling pathway, currently available oral prostanoid medications, and the development and clinical use of selexipag.

Walking is possible for many patients with a spinal cord injury. Avenues enabling walking include braces, robotics and FES. Among the benefits are improved musculoskeletal and mental health, however unrealistic expectations may lead to negative changes in quality of life. Use rigorous assessment standards to gauge the improvement of walking during the rehabilitation process, but also yearly. Continued walking after discharge may be limited by challenges, such as lack of accessibility in and outside the home, and complications, such as shoulder pain or injuries from falls. It is critical to determine the risks and benefits of walking for each patient.

Background: Previous research suggests that a subset of individuals with intolerance to low levels of environmental chemicals have increased levels of premorbid and/or comorbid psychiatric disorders such as depression, anxiety, and somatization. The purpose of this study was to evaluate the psychological profiles and quantitative electroencephalographic (qEEG) profiles at baseline of women with and without chemical intolerance (CI). Methods: Participants were middle-aged women who reported illness from the odor of common chemicals (CI, n = 14), depressives without such intolerances (D, n = 10), and normal controls (N, n = 11). They completed a set of psychological scales and underwent two separate qEEG recording laboratory sessions spaced 1 week apart, at the same time of day for each subject. Results: CI were similar to D with increased lifetime histories of physician-diagnosed depression (71% vs. 100%), Symptom Checklist 90 (revised) (SCL-90-R) so-matization scores, Barsky Somatic Symptom Amplification, and perceived life stressfulness, although D had more distress than either CI or N on several other SCL-90-R subscales. CI scored significantly higher on the McLean Limbic Symptom Checklist somatic symptom subscale than did either D or N. On qEEG, CI exhibited significantly greater overall resting absolute alpha activity with eyes closed, especially at the parietal midline site (Pz), and increased (sensitized) frontal alpha from session 1 to 2, in contrast with the D and N groups. D showed right frontal asymmetry in both sessions, in comparison with CI. Conclusions: The data indicate that CI with affective distress diverge from both D without chemical intolerance and N in qEEG alpha patterns at resting baseline. Although CI descriptively resemble D with increased psychological distress, the CI's greater alpha suggests the possibility of a) central nervous system hypo-, not hyper-, activation; and/or b) an overlap with EEG alpha patterns of persons with positive family histories of alcoholism.

This paper summarizes the key features of the olfactory-limbic, neural sensitization model for multiple chemical sensitivity (MCS) and presents relevant data on chemically intolerant human subjects from laboratory studies using quantitative electroencephalography, polysomnography, neuropsychological tests, cardiovascular measurements, and blood markers. MCS is a poorly understood chronic, polysymptomatic condition in which some prior controlled research studies have failed to find evidence to differentiate active from placebo tests. Closer examination of past MCS research, however, reveals that studies have failed to incorporate the design and methodological approaches necessary to test for nonimmunological sensitization. Time-dependent sensitization (TDS) is a well-documented phenomenon in the pharmacology literature involving the progressive increase in a given response by the passage of time between the initial and subsequent exposures to a substance or a stressor. As in MCS, multiple, chemically unrelated agents can trigger TDS. Females time-sensitize more readily than do males. Pharmacological and nonpharmacological (stress) stimuli can cross-sensitize. Dopaminergic pathways in the brain and the hypothalamic–pituitary–adrenal axis are likely involved in TDS. Data on the symptomatology of MCS point to central nervous system involvement, including limbic regions that receive input from both olfactory (odor) and trigeminal (irritant) pathways. Limbic and mesolimbic brain regions are among the most sensitizable to repeated, intermittent environmental stimuli. Sensitizable individuals can show no difference or lesser responses to a test substance on initial exposure, but later exhibit much greater increases in responsivity on the next exposure after a period of days. For future research, it is essential to distinguish chemical intolerance symptoms such as derealization, sudden mood changes, musculoskeletal pain, menstrual dysfunction, and uncontrollable sleepiness from chemical phobia and avoidance behaviors. This model permits hypothesis-driven research on MCS and has major implications for interpretation of apparently positive and negative tests for “true” as opposed to “perceived” sensitivity to low levels of environmental chemicals.

We previously hypothesized that individual differences in (a) limbic system reactivity and (b) central nervous system sensitizability underlie vulnerability to environmental stimuli, not only in the controversial clinical condition multiple chemical sensitivity (MCS), but also in the general population. Earlier research has shown overlaps in the characteristics of persons who report noise and air pollutant sensitivities. This study assessed questionnaire responses of 897 young adult college students who reported high versus low frequency of illness from several environmental chemical odors and concomitantly high versus low sensitivity to environmental noise. Subjects who reported increased rates of illness from chemical odors with or without noise sensitivity scored significantly higher (P < 0.0001) on a measure of limbic system symptomatology derived from ictal sensory, somatic, mnemonic, and behavioral manifestations of temporal lobe epilepsy. The group rating high both for illness from chemicals and for noise sensitivity had characteristics predictive of heightened sensitizability from the animal research on time-dependent sensitization (progressive response amplification to repeated, intermittent stimuli over time): i.e., higher female to male ratio (gender risk factor), increased rates of drug abuse problems in blood relatives (genetic risk factor), trait shyness (hyperreactivity to novelty), and increased carbohydrate craving. Despite the increased family histories of drug abuse and levels of personal anxiety and depression, the chemical- and noise-sensitive group reported the lowest rates of current smoking or personal drug abuse problems and the highest frequency of illness from drinking a small amount of alcohol. Taken together, the findings suggest that limbic system dysfunction associates more with chemical than with noise sensitivity; that individuals with both chemical and noise sensitivity may be the most sensitizable subset of the population for prospective studies, and that, in their substance use patterns, young adults with both chemical and noise sensitivity are more similar to MCS patients than are their peers with chemical or noise sensitivity alone.

Mechanical analysis of movement plays an important role in clinical management of neurological and orthopedic conditions. There has been increasing interest in performing movement analysis in real-time, to provide immediate feedback to both therapist and patient. However, such work to date has been limited to single-joint kinematics and kinetics. Here we present a software system, named human body model (HBM), to compute joint kinematics and kinetics for a full body model with 44 degrees of freedom, in real-time, and to estimate length changes and forces in 300 muscle elements. HBM was used to analyze lower extremity function during gait in 12 able-bodied subjects. Processing speed exceeded 120 samples per second on standard PC hardware. Joint angles and moments were consistent within the group, and consistent with other studies in the literature. Estimated muscle force patterns were consistent among subjects and agreed qualitatively with electromyography, to the extent that can be expected from a biomechanical model. The real-time analysis was integrated into the D-Flow system for development of custom real-time feedback applications and into the gait real-time analysis interactive lab system for gait analysis and gait retraining. Electronic supplementary material The online version of this article (doi:10.1007/s11517-013-1076-z) contains supplementary material, which is available to authorized users.

INTRODUCTION Because of improved vehicular safety, acute trauma care, and innovative medical treatments, the percentage of individuals with incomplete versus complete spinal cord injuries (SCIs) is increasing [1]. Partial paralysis from incomplete SCI limits participation in society and adversely affects general health and well-being [2]. These individuals often remain sedentary and exhibit compromised physical endurance, with limited standing and walking capabilities. Fortunately, rehabilitation interventions can enhance physical limitations, elevate activity level, and improve ambulatory function for these individuals. The interventions can be classified into neurotherapeutic interventions that maximize volitional strength, coordination, and locomotor ability, and neuroprosthetic interventions that augment and enhance baseline voluntary function. One aim of neurotherapeutic interventions is improving volitional walking ability via modalities such as strength and endurance exercise, balance training, overground gait training (OGT), body-weight-supported treadmill training (BWSTT), and functional electrical stimulation (FES) assisted gait training. To maximize the potential impact of these interventions, therapists usually prescribe them within weeks or months of injury. One recent study found that lower-limb strength, walking speed, and distance greatly improved after 12 weeks of therapeutic modalities consisting of OGT or BWSTT in the acute injury phase [3]. Subjects were all initially nonambulatory and made measurable volitional gains by the end of rehabilitation that included a 0.8 m/s increase in 15 m walking speed and a 76 m increase in the 6-minute walk distance. Similar outcomes were achieved regardless of the neurotherapeutic intervention because both OGT and BWSTT produced equivalent gains in voluntary function. A crossover study demonstrated that the addition of FES to BWSTT could potentially accelerate gait training in subjects with acute injuries [4]. For ambulatory persons with chronic incomplete SCI, the use of surface stimulation during OGT or BWSTT increased volitional muscle strength [5-6], stride length [5,7-8], and walking speed [6-9]. To eliminate the need to properly place surface electrodes daily, subjects can use implanted FES systems for several functional tasks [10-11]. Additionally, subjects prefer using FES systems versus traditional braces during upright activities [10-11]. Neuroprosthetic interventions employ FES to assist tasks such as standing or walking [12]. Such interventions can be effective for acute or chronic SCI regardless of baseline function. For example, one case study documented the deployment of an FES system in a nonambulatory male with a chronic C6 incomplete SCI (American Spinal Injury Association [ASIA] C). He could stand volitionally, but could not initiate a forward step. He received an eight-channel implanted motor neuroprosthesis to facilitate walking by delivering stimulation bilaterally to the hip flexors, knee extensors, and ankle dorsiflexors to assist his gait during the swing and single-limb stance phases [13]. After 12 weeks of OGT with FES, the subject achieved a maximum walking distance of 309 m and a maximal speed of 0.20 m/s with the neuroprosthesis, but volitional walking function was unchanged. No neurotherapeutic effect occurred after this intensive training, and without stimulation he remained nonambulatory. However, the neuroprosthetic effect of the FES system moved him from a nonambulator to a limited community ambulator. Although neurotherapeutic interventions can produce functional gains, a neuroprosthesis could be a powerful adjunct to traditional physical therapy to further improve ambulatory function above volitional levels. Another reasonable expectation is that an implanted neuroprosthesis could produce changes in maximal volitional function. That is, neuroprosthetic interventions may have neurotherapeutic value. …

Early abstinence in alcohol-dependent subjects is marked by adrenocortical hyporesponsivity. However, it is uncertain whether the blunted response is primarily attributable to a genetic vulnerability or to the chronic abuse of alcohol. In the present study, the authors investigated the influence of a family history (FH) of alcoholism upon suppressed glucocorticoid reactivity.Twenty-two abstinent alcohol-dependent and 14 control men were studied. The cortisol response was assessed in 11 patients following oCRH infusion (.4 ug/kg) and in a separate group of 11 patients following cosyntropin infusion (.01 ug/kg) preceded by high-dose intravenous dexamethasone (8 mg). FH, as determined by self-report, was assessed using two different methods: history of parental alcoholism and number of alcohol-dependent first- and second-degree relatives.Neither a parental history or familial loading of alcoholism had a significant effect upon glucocorticoid responsivity in abstinent alcohol-dependent men.Adrenocorticol responsiveness in recently abstinent alcohol-dependent men does not appear to reflect a preexisting biologic vulnerability to alcoholism.

Prior exposure to social disruption stress (SDR) exacerbates both the acute and chronic phase of Theiler’s murine encephalomyelitis virus infection (TMEV; [Johnson, R.R., Storts, R., Welsh, T.H., Jr., Welsh, C.J., Meagher, M.W., 2004. Social stress alters the severity of acute Theiler’s virus infection. J. Neuroimmunol. 148, 74--85; Johnson, R.R., Prentice, T.W., Bridegam, P., Young, C.R., Steelman, A.J., Welsh, T.H., Welsh, C.J.R., Meagher, M.W., 2006. Social stress alters the severity and onset of the chronic phase of Theiler’s virus infection. J. Neuroimmunol. 175, 39--51]). However, the neuroimmune mechanism(s) mediating this effect have not been determined. The present study examined whether stress-induced increases in the proinflammatory cytokine interleukin-6 (IL-6) contributes to the adverse effects of SDR on acute TMEV infection. Experiment 1 demonstrated that SDR increases central and peripheral levels of IL-6 and that this effect is reversed by intracerebral ventricular infusion of neutralizing antibody to IL-6 prior to each of six SDR sessions. Although SDR reduced the sensitivity of spleen cells to the anti-inflammatory effects of corticosterone, the neutralizing antibody to IL-6 did not alter this effect. To investigate whether stress-induced increases in IL-6 contribute to the exacerbation of acute TMEV infection, Experiment 2 examined whether intracerebral administration of neutralizing antibody to IL-6 during SDR would prevent the subsequent exacerbation of acute TMEV infection. Experiment 3 then replaced the social stress with intracerebral infusion of IL-6 to assess sufficiency. As expected, prior exposure to SDR subsequently increased infection-related sickness behaviors, motor impairment, CNS viral titers, and CNS inflammation. These deleterious effects of SDR were either prevented or significantly attenuated by intracerebral infusion of neutralizing antibody to IL-6 during the stress exposure period. However, infusion of IL-6 alone did not mimic the adverse effects of SDR. We conclude that IL-6 is necessary but not sufficient to exacerbate acute TMEV infection.

BACKGROUND: The purpose of this study was to determine how a driver's foot and ankle forces during a frontal vehicle collision depend on initial lower extremity posture and brake pedal force. METHOD OF APPROACH: A 2D musculoskeletal model with seven segments and six right-side muscle groups was used. A simulation of a three-second braking task found 3647 sets of muscle activation levels that resulted in stable braking postures with realistic pedal force. These activation patterns were then used in impact simulations where vehicle deceleration was applied and driver movements and foot and ankle forces were simulated. Peak rearfoot ground reaction force (F(RF)), peak Achilles tendon force (FAT), peak calcaneal force (F(CF)) and peak ankle joint force (F(AJ)) were calculated. RESULTS: Peak forces during the impact simulation were 476 +/- 687 N (F(RF)), 2934 +/- 944 N (F(CF)) and 2449 +/- 918 N (F(AJ)). Many simulations resulted in force levels that could cause fractures. Multivariate quadratic regression determined that the pre-impact brake pedal force (PF), knee angle (KA) and heel distance (HD) explained 72% of the variance in peak FRF, 62% in peak F(CF) and 73% in peak F(AJ). CONCLUSIONS: Foot and ankle forces during a collision depend on initial posture and pedal force. Braking postures with increased knee flexion, while keeping the seat position fixed, are associated with higher foot and ankle forces during a collision. Language: en

HARDIN, E. C., A. J. VAN DEN BOGERT, and J. HAMILL. Kinematic Adaptations during Running: Effects of Footwear, Surface, and Duration. Med. Sci. Sports Exerc., Vol. 36, No. 5, pp. 838 – 844, 2004. Repetitive impacts encountered during locomotion may be modified by footwear and/or surface. Changes in kinematics may occur either as a direct response to altered mechanical conditions or over time as active adaptations. Purpose: To investigate how midsole hardness, surface stiffness, and running duration influence running kinematics. Methods: In the first of two experiments, 12 males ran at metabolic steady state under six conditions; combinations of midsole hardness (40 Shore A, 70 Shore A), and surface stiffness (100 kN·m 1 , 200 kN·m 1 , and 350 kN·m 1 ). In the second experiment, 10 males ran for 30 min on a 12% downhill grade. In both experiments, subjects ran at 3.4 m·s 1 on a treadmill while 2-D hip, knee, and ankle kinematics were determined using high-speed videography (200 Hz). Oxygen cost and heart rate data were also collected. Kinematic adaptations to midsole, surface, and running time were studied. Results: Stance time, stride cycle time, and maximal knee flexion were invariant across conditions in each experiment. Increased midsole hardness resulted in greater peak ankle dorsiflexion velocity (P 0.0005). Increased surface stiffness resulted in decreased hip and knee flexion at contact, reduced maximal hip flexion, and increased peak angular velocities of the hip, knee, and ankle. Over time, hip flexion at contact decreased, plantarflexion at toe-off increased, and peak dorsiflexion and plantarflexion velocity increased. Conclusion: Lower-extremity kinematics adapted to increased midsole hardness, surface stiffness, and running duration. Changes in limb posture at impact were interpreted as active adaptations that compensate for passive mechanical effects. The adaptations appeared to have the

Muscles have a potentially important effect on lower extremity injuries during an automobile collision. Computational modeling can be a powerful tool to predict these effects and develop protective interventions. Our purpose was to determine how muscles influence peak foot and ankle forces during an automobile collision. A 2-D bilateral musculoskeletal model was constructed with seven segments. Six muscle groups were included in the right lower extremity, each represented by a Hill muscle model. Vehicle deceleration data were applied as input and the resulting movements were simulated. Three models were evaluated: no muscles (NM), minimal muscle activation at a brake pedal force of 400 N (MN), and maximal muscle activation to simulate panic braking (MX). Muscle activation always resulted in large increases in peak joint force. Peak ankle joint force was greatest for MX (10120 N), yet this model also had the lowest peak rearfoot force (629 N). Peak force on the Achilles tendon was 4.5 times greater, during MX (6446 N) compared to MN (1430 N). We conclude that (1) external and internal forces are dependent on muscles, (2) muscle activation level could exacerbate axial loading injuries, (3) external and internal forces can be inversely related once muscle properties are included.

This study (ntotal = 35) compared early life stress ratings, parental relationships, and health status, notably orthostatic blood pressures, of middle-aged women with low-level chemical intolerance (CI group) and depression, depressives without CI (DEP group), and normals. Environmental chemical intolerance is a symptom of several controversial conditions in which women are overrepresented, that is, sick building syndrome, multiple chemical sensitivity, chronic fatigue syndrome, and fibromyalgia. Previous investigators have postulated that people with CI have variants of somatization disorder, depression, posttraumatic stress disorder (PTSD) initiated by childhood abuse or a toxic exposure event. One neurobehavioral model for CI, somatization disorder, recurrent depression, and PTSD is neural sensitization, that is, the progressive amplification of host responses (e.g., behavioral, neurochemical) to repeated intermittent stimuli (e.g., drugs, chemicals, endogenous mediators, stressors). Females are more vulnerable to sensitization than are males. Limbic and mesolimbic pathways mediate central nervous system sensitization. Although both CI and DEP groups had high levels of life stress and past abuse, the CI group had the most distant and weak paternal relationships and highest limbic somatic dysfunction subscale scores. Only the CI group showed sensitization of sitting blood pressures over sessions. Together with prior evidence, these data are consistent with a neural sensitization model for CI in certain women. The findings may have implications for poorer long-term medical as well as neuropsychiatric health outcomes of a subset of women with CI. Subsequent research should test this model in specific clinical diagnostic groups with CI.

The symptom of intolerance to low levels of environmental chemicals (CI, chemical intolerance) is a feature of several controversial polysymptomatic conditions that overlap symptomatically with depression and somatization, i.e., chronic fatigue syndrome, fibromyalgia, multiple chemical sensitivity, and Persian Gulf syndrome. These syndromes can involve many somatic symptoms consistent with possible inflammation. Immunological or neurogenic triggering might account for such inflammation. Serum neopterin, which has an inverse relationship with l-tryptophan availability, may offer a marker of inflammation and macrophage/monocyte activation. This study compared middle-aged women with CI (who had high levels of affective distress; n = 14), depressives without CI (n = 10), and normals (n = 11). Groups did not differ in 4 p.m. resting levels of serum neopterin. However, the CI alone had strong positive correlations between neopterin and all of the scales measuring somatization. These preliminary findings suggest the need for additional research on biological correlates of ‘unexplained’ multiple somatic symptoms in subtypes of apparent somatizing disorders.

Implanted functional electrical stimulation (FES) systems for walking are experimentally available to individuals with incomplete spinal cord injury (SCI); however, data on short-term therapeutic and functional outcomes are limited. The goal of this study was to quantify therapeutic and func- tional effects of an implanted FES system for walking after incomplete cervical SCI. After robotic-assisted treadmill train- ing and overground gait training maximized his voluntary function, an individual with incomplete SCI (American Spinal Injury Association grade C, cervical level 6-7) who could stand volitionally but not step was surgically implanted with an 8-channel receiver stimulator and intramuscular electrodes. Electrodes were implanted bilaterally, recruiting iliopsoas, vas- tus intermedius and lateralis, tensor fasciae latae, tibialis ante- rior, and peroneus longus muscles. Twelve weeks of training followed limited activity post-surgery. Customized stimulation patterns addressed gait deficits via an external control unit. The system was well-tolerated and reliable. After the 12-week training, maximal walking distance increased (from 14 m to 309 m), maximal walking speed was 10 times greater (from 0.02 m/s to 0.20 m/s), and physiological cost index was 5 times less (from 44.4 beats/m to 8.6 beats/m). Voluntary locomotor function was unchanged. The implanted FES system was well- tolerated, reliable, and supplemented function, allowing the participant limited community ambulation. Physiological effort decreased and maximal walking distance increased dramati- cally over 12 weeks.