Effect of lumbar fasciae on the stability of the lower lumbar spine

The biomechanical effect of tensioning the lumbar fasciae (LF) on the stability of the spine during sagittal plane motion was analysed using a validated finite element model of the normal lumbosacral spine (L4-S1). To apply the tension in the LF along the direction of the fibres, a local coordinate was allocated using dummy rigid beam elements that originated from the spinous process. Up to 10 Nm of flexion and 7.5 Nm of extension moment was applied with and without 20 N of lateral tension in the LF. A follower load of 400 N was additionally applied along the curvature of the spine. To identify how the magnitude of LF tension related to the stability of the spine, the tensioning on the fasciae was increased up to 40 N with an interval of 10 N under 7.5 Nm of flexion/extension moment. A fascial tension of 20 N produced a 59% decrease in angular motion at 2.5 Nm of flexion moment while there was a 12.3% decrease at 10 Nm in the L5-S1 segment. Its decrement was 53 and 9.6% at 2.5 Nm and 10 Nm, respectively, in the L4-L5 segment. Anterior translation was reduced by 12.1 and 39.0% at the L4-L5 and L5-S1 segments under 10 Nm of flexion moment, respectively. The flexion stiffness shows an almost linear increment with the increase in fascial tension. The results of this study showed that the effect of the LF on the stability of the spine is significant.     

A review of methods to assess coactivation in the spine

Coactivation is an important component for understanding the physiological cost of muscular and spinal loads and their associations with spinal pathology and potentially myofascial pain. However, due to the complex and dynamic nature of most activities of daily living, it can be difficult to capture a quantifiable measure of coactivation. Many methods exist to assess coactivation, but most are limited to two-muscle systems, isometric/complex analyses, or dynamic/uniplanar analyses. Hence, a void exists in that coactivation has not been documented or assessed as a multiple-muscle system under realistic complex dynamic loading. Overall, no coactivation index has been capable of assessing coactivation during complex dynamic exertions. The aim of this review is to provide an understanding of the factors that may influence coactivation, document the metrics used to assess coactivity, assess the feasibility of those metrics, and define the necessary variables for a coactivation index that can be used for a variety of tasks. It may also be clinically and practically relevant in the understanding of rehabilitation effectiveness, efficiency during task performance, human-task interactions, and possibly the etiology for a multitude of musculoskeletal conditions.     

ApoE4 delays dendritic spine formation during neuron development and accelerates loss of mature spines in?vitro

The ε4 allele of the gene that encodes apolipoprotein E (APOE4) is the greatest genetic risk factor for Alzheimer''s disease (AD), while APOE2 reduces AD risk, compared to APOE3. The mechanism(s) underlying the effects of APOE on AD pathology remains unclear. In vivo, dendritic spine density is lower in APOE4-targeted replacement (APOE-TR) mice compared with APOE2- and APOE3-TR mice. To investigate whether this apoE4-induced decrease in spine density results from alterations in the formation or the loss of dendritic spines, the effects of neuron age and apoE isoform on the total number and subclasses of spines were examined in long-term wild-type neurons co-cultured with glia from APOE2-, APOE3- and APOE4-TR mice. Dendritic spine density and maturation were evaluated by immunocytochemistry via the presence of drebrin (an actin-binding protein) with GluN1 (NMDA receptor subunit) and GluA2 (AMPA receptor subunit) clusters. ApoE isoform effects were analyzed via a method previously established that identifies phases of spine formation (day-in-vitro, DIV10–18), maintenance (DIV18–21) and loss (DIV21–26). In the formation phase, apoE4 delayed total spine formation. During the maintenance phase, the density of GluN1+GluA2 spines did not change with apoE2, while the density of these spines decreased with apoE4 compared to apoE3, primarily due to the loss of GluA2 in spines. During the loss phase, total spine density was lower in neurons with apoE4 compared to apoE3. Thus, apoE4 delays total spine formation and may induce early synaptic dysfunction via impaired regulation of GluA2 in spines.     

Altered spinal kinematics and muscle recruitment pattern of the cervical and thoracic spine in people with chronic neck pain during functional task

Knowledge on the spinal kinematics and muscle activation of the cervical and thoracic spine during functional task would add to our understanding of the performance and interplay of these spinal regions during dynamic condition. The purpose of this study was to examine the influence of chronic neck pain on the three-dimensional kinematics and muscle recruitment pattern of the cervical and thoracic spine during an overhead reaching task involving a light weight transfer by the upper limb. Synchronized measurements of the three-dimensional spinal kinematics and electromyographic activities of cervical and thoracic spine were acquired in thirty individuals with chronic neck pain and thirty age- and gender-matched asymptomatic controls. Neck pain group showed a significantly decreased cervical velocity and acceleration while performing the task. They also displayed with a predominantly prolonged coactivation of cervical and thoracic muscles throughout the task cycle. The current findings highlighted the importance to examine differential kinematic variables of the spine which are associated with changes in the muscle recruitment in people with chronic neck pain. The results also provide an insight to the appropriate clinical intervention to promote the recovery of the functional disability commonly reported in patients with neck pain disorders.     

Neuromuscular response of the trunk to inertial based sudden perturbations following whole body vibration exposure

The effects of whole body vibration exposure on the neuromuscular responses following inertial-based trunk perturbations were examined. Kinematic and surface EMG (sEMG) data were collected while subjects were securely seated on a robotic platform. Participants were either exposed to 10 min of vibration or not, which was followed by sudden inertial trunk perturbations with and without timing and direction knowledge. Amplitude of sEMG was analyzed for data collected during the vibration protocol, whereas the onset of sEMG activity and lumbar spine angle were analyzed for the perturbation protocol. Data from the vibration protocol did not show a difference in amplitude of sEMG for participants exposed to vibration and those not. The perturbation protocol data showed that those not exposed to vibration had a 14% faster muscle onset, despite data showing no difference in fatigue level.     

The role of trunk muscles in sitting balance control in people with low back pain

The purpose of this study was to examine the muscular activities and kinetics of the trunk during unstable sitting in healthy and LBP subjects. Thirty-one healthy subjects and twenty-three LBP subjects were recruited. They were sat on a custom-made chair mounted on a force plate. Each subject was asked to regain balance after the chair was tilted backward at 20°, and then released. The motions of the trunk and trunk muscle activity were examined. The internal muscle moment and power at the hip and lumbar spine joints were calculated using the force plate and motion data. No significant differences were found in muscle moment and power between healthy and LBP subjects (p > 0.05). The duration of contraction of various trunk muscles and co-contraction were significantly longer in the LBP subjects (p < 0.05) when compared to healthy subjects, and the reaction times of the muscles were also significantly reduced in LBP subjects (p < 0.05). LBP subjects altered their muscle strategies to maintain balance during unstable sitting, but these active mechanisms appear to be effective as trunk balance was not compromised and the internal moment pattern remained similar. The changes in muscle strategies may be the causes of LBP or the result of LBP with an attempt to protect the spine.     

Reproducible reference frame for in vitro testing of the human vertebrae

Definition of an anatomical reference frame is necessary for in vitro biomechanical testing. Nevertheless, there is neither a clear recommendation, nor consensus in the literature concerning an anatomical reference frame for in vitro testing of the human vertebrae. The scope of this work is to define a reference frame for the human vertebrae for in vitro applications. The proposed anatomical reference frame relies on alignment of well-defined points on the endplates, and on two landmarks on the posterior wall. The repeatability of the proposed alignment procedure has been tested in vitro by 5 operators, on 7 specimens. Furthermore, the feasibility and repeatability of the proposed procedure was assessed in silico, using CT-scans of the same specimens.     

Damage accumulation location under cyclic loading in the lumbar disc shifts from inner annulus lamellae to peripheral annulus with increasing disc degeneration

It is difficult to study the breakdown of lumbar disc tissue over several years of exposure to bending and lifting by experimental methods. In our earlier published study we have shown how a finite element model of a healthy lumbar motion segment was used to predict the damage accumulation location and number of cyclic to failure under different loading conditions. The aim of the current study was to extend the continuum damage mechanics formulation to the degenerated discs and investigate the initiation and progression of mechanical damage. Healthy disc model was modified to represent degenerative discs (Thompson grade III and IV) by incorporating both geometrical and biochemical changes due to degeneration. Analyses predicted decrease in the number of cycles to failure with increasing severity of disc degeneration. The study showed that the damage initiated at the posterior inner annulus adjacent to the endplates and propagated outwards towards its periphery in healthy and grade III degenerated discs. The damage accumulated preferentially in the posterior region of the annulus. However in grade IV degenerated disc damage initiated at the posterior outer periphery of the annulus and propagated circumferentially. The finite element model predictions were consistent with the infrequent occurrence of rim lesions at early age but a much higher incidence in severely degenerated discs.     

Nicotine induces dendritic spine remodeling in cultured hippocampal neurons

Cholinergic neurons in the CNS are involved in synaptic plasticity and cognition. Both muscarinic and nicotinic acetylcholine receptors (nAChRs) influence plasticity and cognitive function. The mechanism underlying nAChR‐induced plasticity, however, has remained elusive. Here, we demonstrate morphological changes in dendritic spines following activation of α4β2* nAChRs, which are expressed on glutamatergic pre‐synaptic termini of cultured hippocampal neurons. Exposure of the neurons to nicotine resulted in a lateral enlargement of spine heads. This was abolished by dihydro‐β‐erythroidine, an antagonist of α4β2* nAChRs, but not by α‐bungarotoxin, an antagonist of α7 nAChRs. Tetanus toxin or a mixture of 2‐amino‐5‐phosphonovaleric acid and 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione, antagonists of NMDA‐ and AMPA‐type glutamate receptors, blocked the nicotine‐induced spine remodeling. In addition, nicotine exerted full spine‐enlarging response in the post‐synaptic neuron whose β2 nAChR expression was knocked down. Finally, pre‐treatment with nicotine enhanced the Ca²⁺‐response of the neurons to glutamate. These data suggest that nicotine influences the activity of glutamatergic neurotransmission through the activation of pre‐synaptic α4β2 nAChRs, resulting in the modulation of spinal architecture and responsiveness. The present findings may represent one of the cellular mechanisms underlying cholinergic tuning of brain function.