Biomechanical modelling of the facet joints: a review of methods and validation processes in finite element analysis

There is an increased interest in studying the biomechanics of the facet joints. For in silico studies, it is therefore important to understand the level of reliability of models for outputs of interest related to the facet joints. In this work, a systematic review of finite element models of multi-level spinal section with facet joints output of interest was performed. The review focused on the methodology used to model the facet joints and its associated validation. From the 110 papers analysed, 18 presented some validation of the facet joints outputs. Validation was done by comparing outputs to literature data, either computational or experimental values; with the major drawback that, when comparing to computational values, the baseline data was rarely validated. Analysis of the modelling methodology showed that there seems to be a compromise made between accuracy of the geometry and nonlinearity of the cartilage behaviour in compression. Most models either used a soft contact representation of the cartilage layer at the joint or included a cartilage layer which was linear elastic. Most concerning, soft contact models usually did not contain much information on the pressure-overclosure law. This review shows that to increase the reliability of in silico model of the spine for facet joints outputs, more needs to be done regarding the description of the methods used to model the facet joints, and the validation for specific outputs of interest needs to be more thorough, with recommendation to systematically share input and output data of validation studies.

Re-expression of Locomotor Function After Partial Spinal Cord Injury

After a complete spinal section, quadruped mammals (cats, rats, and mice) can generally regain hindlimb locomotion on a treadmill because the spinal cord below the lesion can express locomotion through a neural circuitry termed the central pattern generator (CPG). In this review, we propose that the spinal CPG also plays a crucial role in the locomotor recovery after incomplete spinal cord injury.

Locomotor and Reflex Adaptation After Partial Denervation of Ankle Extensors in Chronic Spinal Cats

This work investigates the capacity of the spinal cord to generate locomotion after a complete spinal section and its ability to adapt its locomotor pattern after a peripheral nerve lesion. To study this intrinsic adaptive capacity, the left lateral gastrocnemius-soleus (LGS) nerve was sectioned in three cats that expressed a stable locomotion following a complete spinal transection. The electromyograph (EMG) of multiple hindlimb muscles and reflexes, evoked by stimulating the left tibial (Tib) nerve at the ankle, were recorded before and after denervation during treadmill locomotion. Following denervation, the mean amplitude of EMG bursts of multiple hindlimb muscles increased during locomotion, similar to what is found after an identical denervation in otherwise intact cats. Reflex changes were noted in ipsilateral flexors, such as semitendinosus and tibialis anterior, but not in the ipsilateral knee extensor vastus lateralis following denervation. The present results demonstrate that the spinal cord possesses the circuitry necessary to mediate increased EMG activity in multiple hindlimb muscles and also to produce changes in reflex pathways after a muscle denervation. The similarity of changes following LGS denervation in cats with an intact and transected spinal cord suggests that spinal mechanisms play a major role in the locomotor adaptation.

Adaptive changes of locomotion after central and peripheral lesions

This paper reviews findings on the adaptive changes of locomotion in cats after spinal cord or peripheral nerve lesions. From the results obtained after lesions of the ventral/ventrolateral pathways or the dorsal/dorsolateral pathways, we conclude that with extensive but partial spinal lesions, cats can regain voluntary quadrupedal locomotion on a treadmill. Although tract-specific deficits remain after such lesions, intact descending tracts can compensate for the lesioned tracts and access the spinal network to generate voluntary locomotion. Such neuroplasticity of locomotor control mechanisms is also demonstrated after peripheral nerve lesions in cats with intact or lesioned spinal cords. Some models have shown that recovery from such peripheral nerve lesions probably involves changes at the supra spinal and spinal levels. In the case of somesthesic denervation of the hindpaws, we demonstrated that cats with a complete spinal section need some cutaneous inputs to walk with a plantigrade locomotion, and that even in this spinal state, cats can adapt their locomotion to partial cutaneous denervation. Altogether, these results suggest that there is significant plasticity in spinal and supraspinal locomotor controls to justify the beneficial effects of early proactive and sustained locomotor training after central (Rossignol and Barbeau 1995; Barbeau et al. 1998) or peripheral lesions.Key words: spinal lesions, nerve lesions, locomotion, neuroplisticity, locomotor training.

Nitric oxide mediates sympathetic vasoconstriction at supraspinal, spinal, and synaptic levels

The purposes of this study were to investigate the level of the sympathetic nervous system in which nitric oxide (NO) mediates regional sympathetic vasoconstriction and to determine whether neural mechanisms are involved in vasoconstriction after NO inhibition. Ganglionic blockade (hexamethonium), α1-receptor blockade (prazosin), and spinal section at T1 were used to study sympathetic involvement. NO was blocked with N ω-nitro-l-arginine methyl ester (l-NAME). Regional blood flow in the mesenteric and renal arteries and terminal aorta was monitored by electromagnetic flowmetry in conscious rats.l-NAME (3–5 mg/kg iv) increased arterial pressure and peripheral resistance. Ganglionic blockade (25 mg/kg iv) significantly reduced the increase in resistance in the mesentery and kidney in intact and spinal-sectioned rats. Ganglionic blockade significantly decreased hindquarter resistance in intact rats but not in spinal-sectioned rats. Prazosin (200 μg/kg iv) significantly reduced the increased hindquarter resistance. We concluded that NO suppresses sympathetic vasoconstriction in the mesentery and kidney at the spinal level, whereas hindquarter tone is mediated at supraspinal and synaptic levels.

Initiation of rat vasopressin cell responses to simulated hypotensive hemorrhage

Hypotensive hemorrhage is a major stimulus for vasopressin (VP) release, but in rats it is uncertain which receptors initiate this response. We have investigated this issue using transient occlusion of the inferior vena cava to simulate hypotensive hemorrhage. Single-unit recording experiments done in the supraoptic nucleus of pentobarbital-anesthetized rats demonstrated that severe caval occlusion, sufficient to drop mean arterial pressure (MAP) below 30 mmHg, excited 88% of putative VP neurosecretory cells and a similar proportion of putative oxytocin (OT) cells. Responsive VP cells increased their firing by 8.5 +/- 0.6 spikes/s within 11.2 +/- 0.8 s of the fall in MAP. This response was unrelated to the size of the fall in MAP and was unchanged by combined sinoaortic denervation (SAD) and vagal denervation, by T1 spinal section, or by administration of the angiotensin-converting enzyme inhibitor captopril, except that spinal section decreased the response latency. Moderate caval occlusion, sufficient to drop MAP to approximately 50 mmHg, did not excite any of the OT cells tested but did excite 65% of VP cells, causing a 3.8 +/- 0.3 spikes/s increase in firing after a delay of 9.0 +/- 1.3 s. This response was proportional to the size of the preceding fall in MAP, and after combined SAD and vagal denervation only 20% of VP cells still responded. Elimination of sinoaortic or vagal afferents alone had no effect on VP cell responses to moderate caval occlusion, except that SAD significantly increased the response latency. These data suggest that in rat the mechanisms that initiate the VP response to hypotensive hemorrhage depend on stimulus intensity.(ABSTRACT TRUNCATED AT 250 WORDS)