Postural Rigidity Research Articles

The Complexity of Center of Pressure Positions During Quiet Stance and Its Relationship to Cognition, Aging, and Falls.

In a secondary analysis of data taken from a publicly available database, we examined cognitive performance, postural sway, and relations between them for 4 groups: younger and older individuals with versus without a recent history of falls. Our objective was to compare linear versus nonlinear measures of postural activity as post hoc predictors of cognitive performance and falling. We evaluated standing body sway in 147 participants (18-85-years old) over 60 seconds, separately with eyes-open and with eyes-closed. We evaluated cognitive performance using portions of the Trail Making Test. We evaluated postural activity in terms of standard deviation, velocity, and amplitude of the Center of Pressure (CoP). Separately, we used detrended fluctuation analysis (DFA) to examine the complexity of CoP displacements. Using analysis of variance, we conducted separate analyses of cognitive performance and postural activity comparing Younger and Older Adults and Non-fallers and Fallers, taking into account Vision (eyes-closed vs open) and the direction of postural movements (Anteroposterior vs Mediolateral) while also controlling for participants' characteristics. We used moderation analyses to evaluate whether relationships between Trail Making Test scores and the linear and nonlinear outcomes were moderated by Age group or Fall status. For postural activity, only DFA differed between Non-fallers and Fallers. Older adults exhibited increased complexity associated with better processing speed function, while fallers show an opposite association, relying on processing speed to increase postural rigidity instead of facilitating adaptive control of balance. We conclude that DFA can provide information regarding postural activity and cognitive performance that cannot be obtained from more traditional, linear measures of postural activity and that DFA may be a valuable tool for assessing fall risk.

Responses to balance challenges in persons with panic disorder: A pilot study of computerized static and dynamic balance measurements

IntroductionSeveral studies have shown an association between panic disorder (PD) and reduced balance abilities, mainly based on functional balance scales.This pilot study aims to demonstrate the feasibility of studying balance abilities of persons with PD (PwPD) using computerized static and, for the first time, dynamic balance measurements in order to characterize balance control strategies employed by PwPD.MethodsTwelve PwPD and 11 healthy controls were recruited. PD diagnosis was confirmed using the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM‐IV), and the severity of symptoms was evaluated using the Hamilton Anxiety Scale (HAM‐A), PD Severity Scales (PDSS), and Panic and Agoraphobia Scale (PAS). Balance was clinically assessed using the Activities‐Specific Balance Confidence (ABC) scale and physically by the Mini‐Balance Evaluation Systems Test (Mini‐BESTest). Dizziness was evaluated using the Dizziness Handicap Inventory (DHI) scale. Postural control was evaluated statically by measuring body sway and dynamically by measuring body responses to rapid unexpected physical perturbations.ResultsPwPD had higher scores on the HAM‐A (17.6 ± 10.3 vs. 3.0 ± 2.9; p < .001), PDSS (11.3 ± 5.1 vs. 0; p < .001), and PAS (20.3 ± 8.7 vs. 0; p < .001) questionnaires and lower scores on the balance scales compared to the controls (ABC scale: 156.2 ± 5.9 vs. 160 ± 0.0, p = .016; Mini‐BESTest: 29.4 ± 2.1 vs. 31.4 ± 0.9, p = .014; DHI: 5.3 ± 4.4 vs. 0.09 ± 0.3, p < .001). In the static balance tests, PwPD showed a not‐significantly smaller ellipse area of center of pressure trajectory (p = .36) and higher body sway velocity (p = .46), whereas in the dynamic balance tests, PwPD had shorter recovery time from physical perturbations in comparison to controls (2.1 ± 1.2s vs. 1.6 ± 0.9 s, p = .018).ConclusionThe computerized balance tests results point to an adoption of a ‘‘postural rigidity’’ strategy by the PwPD, that is, reduced dynamic adaptations in the face of postural challenges. This may reflect a nonsecure compensatory behavior. Further research is needed to delineate this strategy.

Long-Term Intravitreal Ranibizumab as a Potential Additional Risk Factor for Neurodegeneration in Parkinson's Disease: A Case Report.

In November 2012, a 72-year old patient was diagnosed with left eye wet age-related macular degeneration. The patient received three monthly intravitreal injections of ranibizumab, with complete resolution of retinal hemorrhage and edema and reinstatement of visual acuity. In May 2015, symptomatic relapse was detected. The patient was again treated with intravitreal ranibizumab, with overall six injections till the end of February 2016. In May 2016, the patient complained of left hand resting tremor, bradykinesia, and postural rigidity of head and trunk. A diagnosis of clinically established PD was made based on new criteria of the Movement Disorders Society. Single Photon Emission Computerized Tomography of the Dopamine Transporter with (123I) ioflupane documented a low Dopamine Transporter (DAT) uptake mostly in the right striatum. Due to the documented protective role of vascular endothelial growth factor (VEGF) on the dopaminergic neurons, intensive intravitreal injections of the anti-VEGF agent ranibizumab may have played as an additional risk factor accelerating the neurodegeneration process related to PD and the onset of the related clinical signs and symptoms.

Does Postural Rigidity Decrease during REM Sleep without Atonia in Parkinson Disease?

Rigidity is a muscle hypertonia typical of Parkinson disease (PD), whereas rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by abnormally increased muscle tone during REM sleep (REM sleep without atonia) and enacting dream behaviors. Because movements are not bradykinetic during RBD in patients with PD, we investigated whether the background, wake postural rigidity is attenuated during REM sleep without atonia, in absence of movement. The amplitude of levator menti (postural muscle) electromyographic activity during relaxed evening wakefulness (considered as reference) and sleep (N2, N3, atonic REM sleep, and quiet REM sleep without atonia) was measured in 20 patients with PD (with and without RBD), 10 patients with idiopathic RBD patients and 10 healthy subjects. The chin tone amplitude progressively decreased from wake to N2, N3, and atonic REM sleep in the four groups, but the highest amplitude was observed in PD patients with RBD during atonic REM sleep. Furthermore, chin muscle tone amplitude did not attenuate from wake to REM sleep without atonia in patients with both PD and RBD but dramatically attenuated (by 40% on average) in patients with idiopathic RBD. The high amplitude of chin muscle tone in PD with RBD (but not in idiopathic RBD) during REM sleep with and without atonia suggests that both PD-related hypertonia and RBD-related enhanced muscle tone coexist during REM sleep, together affecting chin muscle tone. Consequently, some rapid RBD movements likely start against a rigid postural tone.

Changes in Balance Strategy and Neuromuscular Control during a Fatiguing Balance Task-A Study in Perturbed Unilateral Stance.

Fatigue impairs sensorimotor performance, reduces spinal reflexes and affects the interaction of antagonistic muscles in complex motor tasks. Although there is literature dealing with the interference of fatigue and postural control, the interpretation is confounded by the variety of paradigms used to study it. This study aimed to evaluate the effects of postural fatigue on balance control and strategy, as well as on neuromuscular modulation, in response to postural perturbation (PERT) during a fatiguing balance task. A fatigue protocol consisting of continuous exposure to perturbations until exhaustion was executed in 24 subjects. Number of failed attempts, paths of center of pressure displacement (COP), ankle, knee, and hip joint kinematics, electromyographic activity of the soleus (SOL), tibialis anterior (TA), rectus femoris (RF), vastus lateralis (VL), biceps femoris (BF), and gluteus maximus muscles (GM) and spinal excitability of SOL at the peak of the short-latency responses (SLR) were recorded after posterior PERT. The co-contraction index (CCI) was calculated for TA_SOL, VL_BF and RF_GM. (1) The number of failed attempts significantly increased while COP amplitude and velocity, as well as angular excursion at the ankle, knee and hip joints, decreased with fatigue (P < 0.05). (2) Concomitantly, CCI of SOL_TA, VL_BF and RF_GM increased and spinal excitability in SOL declined. (3) Adaptations progressively augmented with progressing exhaustion and occurred in the distal prior to proximal segment. Distinctly deteriorated balance ability was accompanied by a modified neuromuscular control—the increase in co-contraction reflected by simultaneously activated antagonists is accompanied by smaller knee and hip joint excursions, indicating an elevated level of articular stiffness. These changes may be associated with an exaggerated postural rigidity and could have caused the delayed and reduced postural reactions that are reflected in the changes in COP displacement when compensating for sudden PERT. The reduction in spinal excitability may either be caused by fatigue itself or by an increase in reciprocal inhibition due to augmented TA activity.

Deception effects on standing center of pressure

Accurate deception detection is a desirable goal with many applications including credibility assessment, security screening, counter-terrorism, and homeland security. However, many deception detection methodologies involve intrusive sensors or other limitations that preclude their use in a covert manner. Posturography may overcome these limitations by using minimally invasive force platform technology. In this study, we tested the hypothesis that posturography would reveal deception-related increases in postural rigidity similar to those observed with previous methodologies. Participants were randomly assigned to a control (CG) or experimental group (EG), and interviewed about the contents of a backpack in their possession while standing on a force platform. EG participants were asked to conceal the presence of several “prohibited” items in the backpack from the interviewer. Center of pressure (COP) measures from the force platform were used to characterize postural sway during participants’ verbal responses. We observed a significant deception-related increase in sway frequency, an effect primarily occurring during longer responses that is likely related to increased cognitive load. These findings suggest deception-related increases in postural rigidity as reported in previous work, and demonstrate the feasibility of using posturography as a deception detection tool.

Acute alcohol intoxication impairs segmental body alignment in upright standing.

Balance control when standing upright is a complex process requiring input from several partly independent mechanisms such as coordination, feedback and feedforward control, and adaptation. Acute alcohol intoxication from ethanol is recognized as a major contributor to accidental falls requiring medical care. This study aimed to investigate if intoxication at 0.06 and 0.10% blood alcohol concentration affected body alignment. Mean angular positions of the head, shoulder, hip, and knee were measured with 3D-motion analysis and compared with the ankle position in 25 healthy adults during standing with or without perturbations, and with eyes open or closed. Alcohol intoxication had significant effects on body alignment during perturbed and unperturbed stance, and on adaptation to perturbations. It induced a significantly more posterior alignment of the knees and shoulders, and a tendency for a more posterior and left deviated head alignment in perturbed stance than when sober. The impact of alcohol intoxication was most apparent on the knee alignment, where availability of visual information deteriorated the adaptation to perturbations. Thus, acute alcohol intoxication resulted in inadequate balance control strategies with increased postural rigidity and impaired adaptation to perturbations. These factors probably contribute to the increased risk of falling when intoxicated with alcohol.

TRANSLATIONAL IMPACT

Parkinson’s disease (PD) is the second most common neurodegenerative disease, affecting at least one out of every 100 people over the age of 60. PD is characterized by postural rigidity, resting tremors, and slowing of movements and thought processes. To date, the existing treatments for PD alleviate some symptoms, but neither affect its underlying pathology nor delay its progression. The pathologic hallmark of PD is the formation of Lewy bodies (LBs) within degenerating neurons. A major component of LBs is α-synuclein (α-syn), a small synaptic lipid-interacting protein of unknown function. α-Syn is implicated in dominantly inherited forms of PD and the closely related diseases dementia with Lewy bodies and multiple systems atrophy. These diseases also feature profound mitochondrial dysfunction and oxidative stress resulting from exposure to either metals or environmental toxins. Despite a decade of research, the mechanisms by which α-syn mediates neurotoxicity remain poorly understood and it is still unclear how α-syn toxicity is related to mitochondrial dysfunction.In this study, the authors report a slightly higher toxicity α-syn strain (HiTox), which exhibits strong mitochondrial defects in addition to the ER-to-Golgi trafficking defects they had previously described in their yeast model system. Transcriptional profiling revealed that many genes involved in mitochondrial function were significantly altered in cells overexpressing α-syn well before cells began to die. These yeast cells had abnormal mitochondrial morphology and exhibited oxidative stress.Chemical screening of the HiTox strain identified a family of compounds that are potent suppressors of α-syn toxicity. These molecules reversed the adverse cellular features associated with α-syn toxicity, including ER-to-Golgi trafficking defects, abnormal mitochondrial morphology and oxidative stress. Moreover, these compounds antagonized α-syn toxicity in dopaminergic neurons of C. elegans and in rat primary neuronal cultures. These compounds also rescued rat primary neurons from rotenone toxicity, which has been used to model mitochondrial dysfunction in PD.This work establishes a direct link between α-syn, ER-to-Golgi trafficking defects and mitochondrial dysfunction. This suggests that α-syn acts on a deeply rooted biological process crucial to neuronal viability. Moreover, the identification of novel compounds capable of antagonizing α-syn toxicity in different model systems spanning a billion years of evolution from yeast to mammals highlights the strength of using the simple model organism S. cerevisiae to investigate complex biological questions about human disease.

Mice expressing mutant parkin exhibit hallmark features of Parkinson's disease.

Parkinson's disease (PD) is the second most prevalent late-onset neurodegenerative disorder and affects ∼1% of the population older than 65 years. PD manifests as a movement disorder clinically characterized by resting tremor, bradykinesia, and postural rigidity. Hypokinetic movements, along with

Steele-Richardson-Olszewski-Syndrom - Darstellung eines selten erkannten Krankheitsbildes anhand zweier Fallberichte

Steele-Richardson-Olszewski syndrome (SROS), which is also known as supranuclear palsy, is a neurodegenerative disorder and belongs to the atypical Parkinsonian syndrome family. Its typical symptoms consist of the triad vertical gaze palsy, slowing or absence of vertical saccades and a recent history of postural instability with otherwise unexplained falls. The reason for neurodegeneration in SROS is a genetically determined structural abnormality of the intracellular tau protein. Unless the expression of abnormal tau protein can be stopped by medication, there is no cure for SROS. Within the past 2 years, the results of neuro-ophthalmological and strabismological examinations in our department have lead to the diagnosis of SROS in 2 patients. In patient #1, a 64-year-old man with an exophoria of 1 degree at far and near gaze, upgaze was limited to 15 degrees. Neither horizontal nor vertical saccades could be performed. No optokinetic nystagm response could be obtained in either direction. Additionally, the patient showed a staring facial expression, a slowing down in speech velocity and body movements and a postural rigidity. Patient #2 is a 67-year-old woman in whom the cover test revealed 4 degrees of esophoria at far and 4 degrees of exophoria at near gaze. Upgaze was limited to 10 15 degrees in both eyes. Saccades were slowed down in horizontal and vertical directions. Smooth pursuit movements were interrupted by spontaneous saccadic oscillations. In addition, the patient complained of a history of frequent falls and difficulties in writing and verbal articulation. In both patients the clinical findings pointed to the diagnosis of probable SROS. A definitive diagnosis requires the histological proof of neurofibrillary degeneration with neuropil threads in a characteristic distribution in the brainstem and in the basal ganglia. Due to the similarity of symptoms to those of Parkinson's disease and atypical Parkinsonian syndromes, SROS may be misdiagnosed as such and presumably the true prevalence of SROS lies far above today's estimations.

Visceral and postural reflexes evoked by genital stimulation in urethane-anesthetized female rats

The present study describes several muscular reflexes produced by genital stimulation, the nerves that subserve them, and the visceral and postural effects induced by these reflexes. Electrical stimulation of the iliococcygeus (ic) and pubococcygeus (pc) (striated) muscles produced movement of the vaginal orifice and wall, membranous urethra, tail and pelvis. Electrical stimulation of the psoas major (pm) or iliacus (i) (striated) muscles produced movements of the lumbar vertebrae and extension of the ipsilateral hindlimb. Sensory mechanostimulation elicited responses of these muscles as follows: stimulation of the perineal skin, clitoral sheath or distal vagina produced reflex contraction of the ic and pc muscles. Stimulation of the cervix produced reflex contraction of the pm and i muscles and also blocked the above reflex contraction of the ic and pc muscles. Both the cervical stimulation-induced blockage of the ic and pc reflex response, and the cervical stimulation-induced activation of pm and i muscles was prevented by bilateral transection of the viscerocutaneous branch of the pelvic nerve. Based on the above observations, it is proposed that stimulation of the vaginal surface of the cervix resulting from penile intromission and/or seminal plug deposition during mating behavior in the rat may reflexively active pm and i, thereby contributing to the hindleg postural rigidity and lordotic dorsiflexion that are characteristic of the normal mating posture in female rats.

Tonic inhibitory influences of locus coeruleus on the response gain of limb extensors to sinusoidal labyrinth and neck stimulations.

Previous experiments had shown that in decerebrate cats activation of limb extensor motoneurons during side-down roll tilt of the animal or side-up neck rotation depends on both an increased discharge of excitatory vestibulospinal (VS) neurons and a reduced discharge of inhibitory reticulospinal (RS) neurons of the medulla, thus leading to disinhibition of limb extensor motoneurons. The present experiments were performed to find out whether the locus coeruleus (LC) complex keeps under its tonic inhibitory control the medullary inhibitory RS neurons and, if so, whether this structure intervenes in the gain regulation of the vestibular and neck reflexes acting on the limb extensor musculature. In precollicular decerebrate cats with good postural rigidity of the four limbs, the amplitude of modulation and thus the response gain of the first harmonic component of multiunit EMG responses of limb extensors to sinusoidal stimulation of labyrinth and neck receptors (at 0.15 Hz, +/- 10 degrees) were quite small in forelimb muscles (triceps brachii) and almost negligible or absent in hindlimb muscles (triceps surae). Electrolytic lesion limited to the LC complex decreased the tonic contraction of limb extensors, but greatly increased in the forelimbs (and brought to the light in the hindlimbs) the response modulation of extensor muscles to the same parameters of labyrinth or neck stimulation. Correspondingly, the response gain increased, but no change in the phase angle of the responses was observed. Both changes in posture, as well as in response gain of the limb extensors to labyrinth and neck stimulation, fully developed some time after the LC lesion. This increase in response gain of the vestibular and neck reflexes acting on the limb extensor muscles did not depend on the decrease in postural activity following the LC lesion, since it was still obtained when an increased static stretch of the extensor muscle following passive flexion of the limb compensated for the reduced EMG activity. Moreover, the slope of the regression line relating the gain of the multiunit EMG response of the triceps brachii to animal tilt with the base frequency greatly increased following lesioning of the LC, thus indicating that for the same background discharge of the muscle the amplitude of modulation, and thus the response gain, increased significantly. The effects described above involved mainly, but not exclusively, the limbs ipsilateral to the side of the lesion.(ABSTRACT TRUNCATED AT 400 WORDS)

Open-field freezing as a stable parameter of wildness in Mus musculus

Wild mice show a characteristic postural rigidity (freezing) which clearly differentiates them from domestic mice. The behavior is typically elicited under conditions such as those present in a novel open field. Differences between randombred laboratory-maintained wilds and domestics are stable despite variation in availability of escape from the field, level of illumination during testing, and age of animals at testing. In contrast to measures of escape latency and activity, freezing alone differentiates wilds from two strains of domestics across all testing conditions. Freezing is a distinctive, stable behavior differentiating wilds from their domestic counterparts.