Cues to land softly and quietly result in acute reductions in ground reaction force loading rates in runners.

BACKGROUND: A common gait retraining goal for runners is reducing vertical ground reaction force (GRF) loading rates (LRs), which have been associated with injury. Many gait retraining programs prioritize an internal focus of attention, despite evidence supporting an external focus of attention when a specific outcome is desired (e.g., LR reduction). RESEARCH QUESTION: Does an external focus of attention (using cues for quiet, soft landings) result in comparable reductions in LRs to those achieved using a common internal focus (forefoot striking while barefoot)? METHODS: This observational study included 37 injured runners (18 male; mean age 36 (14) years) at the OMITTED Running Center. Runners wore inertial measurement units over the distal-medial tibia while running on an instrumented treadmill at a self-selected speed. Data were collected for three conditions: 1) Shod-Control (wearing shoes, without cues); 2) Shod-Quiet (wearing shoes, cues for quiet, soft landings); and 3) Barefoot-FFS (barefoot, cues for forefoot strike (FFS)). Within-subject variables were compared across conditions: vertical instantaneous loading rate (LR, primary outcome); vertical stiffness during initial loading; peak vertical GRF; peak vertical tibial acceleration (TA); and cadence. RESULTS: Vertical LR, stiffness, and TA were lower in the Shod-Quiet compared to Shod-Control p < 0.001). Peak vertical GRF and cadence were not different between Shod-Quiet and Shod-Control. Reductions in stiffness and LR were similar between Shod-Quiet and Barefoot-FFS, and GRF in Barefoot-FFS remained similar to both shod conditions. However, runners demonstrated additional reductions in TA and increased cadence when transitioning from Shod-Quiet to the Barefoot-FFS condition (p < 0.05). SIGNIFICANCE: These results suggests that a focus on quiet, soft landings may be an effective gait retraining method for future research.

Clinical Application of Gait Retraining in the Injured Runner.

Despite its positive influence on physical and mental wellbeing, running is associated with a high incidence of musculoskeletal injury. Potential modifiable risk factors for running-related injury have been identified, including running biomechanics. Gait retraining is used to address these biomechanical risk factors in injured runners. While recent systematic reviews of biomechanical risk factors for running-related injury and gait retraining have been conducted, there is a lack of information surrounding the translation of gait retraining for injured runners into clinical settings. Gait retraining studies in patients with patellofemoral pain syndrome have shown a decrease in pain and increase in functionality through increasing cadence, decreasing hip adduction, transitioning to a non-rearfoot strike pattern, increasing forward trunk lean, or a combination of some of these techniques. This literature suggests that gait retraining could be applied to the treatment of other injuries in runners, although there is limited evidence to support this specific to other running-related injuries. Components of successful gait retraining to treat injured runners with running-related injuries are presented.

Nonsurgical Approach in Management of Tibialis Posterior Tendinopathy With Combined Radial Shockwave and Foot Core Exercises: A Case Series.

Tibialis posterior tendinopathy is a common debilitating condition seen by foot and ankle providers. Non-operative management is difficult as patients often present in later stages of the disease. This case series evaluated the combination of radial shockwave therapy and a foot core progression exercise regimen on 10 patients who had failed standard conservative treatment techniques. Median follow-up time was 4 months. Clinically important differences in the Foot and Ankle Ability Measure were met in 9 (90%) and 8 (80%) of patients for activities of daily living and sport sub-scores, respectively. No adverse effects were observed.

Intact visual latent inhibition in schizophrenia patients in a within-subject paradigm.

People are normally slower to learn a CS-UCS association if they first experience the CS without the UCS. This normal slowing, termed "latent inhibition" (LI), is reported by some to be absent in schizophrenia patients. Our previous studies detected generalized learning deficits but not LI deficits in schizophrenia patients, using between-subject auditory and visual LI paradigms. To understand our divergent results, we developed a within-subject visual LI paradigm that detects LI in normal male subjects that we previously reported to be disrupted by acute treatment with dopamine agonists. In the present study, we verified the ability of this dopamine-sensitive within-subject LI paradigm to detect LI among both male and female normal control subjects, and then used this paradigm to assess LI in schizophrenia patients. Among normals, LI exhibited no sex differences or menstrual cyclicity. Compared to normals, schizophrenia patients exhibited learning deficits with both preexposed (PE) and non-preexposed (NPE) stimuli. Despite these generalized deficits, both acutely hospitalized patients and stable outpatients with schizophrenia exhibited robust LI, as evidenced by significantly faster learning with NPE than PE stimuli. LI deficits in schizophrenia may be paradigm-specific and are not detected by a paradigm that we previously reported to be sensitive to disruption by dopamine agonists.

Dopamine agonists disrupt visual latent inhibition in normal males using a within-subject paradigm.

Latent inhibition (LI) is the delayed learning of an association when the conditioned stimulus has previously been experienced out of the context of that association. LI can be measured across species and has been used to understand the neurobiology of schizophrenia, since some reports suggest that schizophrenia patients exhibit LI deficits. One challenge of LI studies in humans has resulted from the fact that LI paradigms have almost uniformly involved between-subject comparisons. We now report a new within-subject paradigm that detected LI in normal adult male subjects after ingestion of a placebo. After amphetamine (20 mg p.o.) or bromocriptine (1.25 mg p.o.), LI was not evident, suggesting that the LI detected by this paradigm is sensitive to disruption by dopamine agonists. The apparent advantages and limitations of this paradigm are discussed with regard to its future use in understanding the neural basis of reported LI deficits in schizophrenia.

Amphetamine effects on prepulse inhibition across-species: replication and parametric extension.

Despite the similarities of prepulse inhibition (PPI) of the startle reflex and its apparent neural regulation in rodents and humans, it has been difficult to demonstrate cross-species homology in the sensitivity of PPI to pharmacologic challenges. PPI is disrupted in rats by the indirect dopamine (DA) agonist amphetamine, and while studies in humans have suggested similar effects of amphetamine, these effects have been limited to populations characterized by smoking status and specific personality features. In the context of a study assessing the time course of several DA agonist effects on physiological variables, we failed to detect PPI-disruptive effects of amphetamine in a small group of normal males. The present study was designed to reexamine this issue, using a larger sample and a paradigm that should be more sensitive for detecting drug effects. PPI in rats was shown to be disrupted by the highest dose of amphetamine (3.0 mg/kg) at relatively longer prepulse intervals (>30 ms). In humans, between-subject comparisons of placebo (n=15) vs 20 mg amphetamine (n=15) failed to detect significant PPI-disruptive effects of amphetamine, but significant PPI-disruptive effects at short (10-20 ms) prepulse intervals were detected using within-subject analyses of postdrug PPI levels relative to each subject's baseline PPI. Post hoc comparisons failed to detect greater sensitivity to amphetamine among subjects characterized by different personality and physiological traits. Bioactivity of amphetamine was verified by autonomic and subjective changes. These results provide modest support for cross-species homology in the PPI-disruptive effects of amphetamine, but suggest that these effects in humans at the present dose are subtle and may be best detected using within-subject designs and specific stimulus characteristics.

Prestimulus modification of the startle reflex: relationship to personality and physiological markers of dopamine function.

Prepulse inhibition (PPI), a measure of sensorimotor gating, is regulated by dopamine (DA) in rodents. We examined the relationship of PPI in humans to putative markers of brain DA function: (1) novelty seeking (NS; Cloninger's Tridimensional Personality Questionnaire (TPQ)), which is associated with specific DA receptor subtypes, and is reduced in Parkinson's Disease; (2) blink rate, which is increased in primates by DA agonists, and is reduced in Parkinson's Disease. PPI, TPQ and blink rate were measured in 79 normal adult males. A significant negative correlation was observed between resting blink rate and mean PPI, but not between NS and PPI. Blink rate correlated positively with resting EMG level, but this did not account for the relationship between blink rate and PPI. In normal male humans, PPI is inversely related to a physiological marker of resting DA tone (blink rate), but not to a putatively DA-linked personality trait (high NS).

Effects of amantadine and bromocriptine on startle and sensorimotor gating: parametric studies and cross-species comparisons.

BACKGROUND: We recently reported that prepulse inhibition (PPI) in humans was increased by the dopamine (DA) agonist/ N-methyl- D-aspartate (NMDA) antagonist amantadine (200 mg), but was not significantly altered by the DA agonist bromocriptine (1.25-2.5 mg). PPI-enhancing effects of DA agonists occur in rats under specific stimulus conditions, including short prepulse intervals (<30 ms). We characterized the effects of amantadine and bromocriptine on PPI across species, assessing: (1) dose-response effects on PPI in rats over 10- to 120-ms prepulse intervals; (2) drug effects on PPI in humans, using this same range of prepulse intervals; and (3) drug effects on measures related to PPI, including PPI of perceived stimulus intensity (PPIPSI), and startle habituation. METHODS: Drug effects on PPI were assessed in male Sprague Dawley rats ( n=90) and humans ( n=49); startle habituation and PPIPSI were also studied in humans. RESULTS: Amantadine and bromocriptine exhibited dose- and stimulus-dependent effects on PPI in rats, increasing PPI with short (10-20 ms) prepulse intervals, and decreasing PPI with long (60-120 ms) prepulse intervals. In humans, amantadine increased PPI with both short (20 ms) and long (120 ms) prepulse intervals. Bromocriptine had no significant effect on PPI in humans, but tended to increase PPI at short (20 ms) intervals. Amantadine eliminated PPIPSI. CONCLUSIONS: Amantadine modifies prepulse effects on startle in rats and humans, and disrupts prepulse effects on perceived stimulus intensity in humans; bromocriptine has clear effects on PPI in rats, but not in humans. The divergent effects of amantadine on sensorimotor and sensory effects of prepulses may reflect a divergence of brain circuitry regulating these processes.

Prestimulus effects on startle magnitude: sensory or motor?

Startle may be inhibited when the startling event is preceded by a stimulus; this is called prepulse inhibition (PPI) when the prestimulus is weak and nonstartling (s) and paired pulse inhibition when the prestimulus elicits startle (S1). The authors examined the relationship of these measures across species and tested whether paired pulse inhibition--like PPI--is independent of the startling effects of the prestimulus. PPI (s-S1 configuration) and paired pulse inhibition (S1-S2 configuration) were elicited in 1 test, using similar stimulus parameters in rats and humans. The amount of PPI and paired pulse inhibition was significantly correlated within subjects in both rats and humans. Paired pulse inhibition was not diminished when the startling effects of S1 were eliminated by a weak prepulse (s-S1-S2 configuration), nor was it enhanced when these prepulse effects were eliminated by the dopamine agonist apomorphine (in rats). Despite apparent differences in the inhibitory processes mediating PPI and paired pulse inhibition, both are independent of the motoric response to the prestimulus.