Non-Invasive Vagal Nerve Stimulation Pre-Treatment Reduces Neurological Dysfunction After Closed Head Injury in Mice.

Non-invasive vagus nerve stimulation (nVNS) has recently been suggested as a potential therapy for traumatic brain injury (TBI). We previously demonstrated that nVNS inhibits cortical spreading depolarization, the electrophysiological event underlying migraine aura, and is relevant to TBI. Our past work also suggests a role for interleukin-1 beta (IL-1ß) in cognitive deficits after closed head injury (CHI) in mice. We show that nVNS pre-treatment suppresses CHI-associated spatial learning and memory impairment and prevents IL-1ß activation in injured neurons, but not endothelial cells. In contrast, nVNS administered 10 min after CHI was ineffective. These data suggest that nVNS prophylaxis might ameliorate neuronal dysfunction associated with CHI in populations at high risk for concussive TBI.

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue in Participants With Primary Sjögren's Syndrome.

OBJECTIVES: Fatigue is one of the most important symptoms needing improvement in Primary Sjögren's syndrome (PSS). Previous data from our group suggest that noninvasive stimulation of the vagus nerve (nVNS) may improve symptoms of fatigue. This experimental medicine study uses the gammaCore device (electroCore) and a sham device to investigate the relationship between nVNS and fatigue in PSS, and to explore potential mechanisms involved. MATERIALS AND METHODS: Forty participants with PSS were randomly assigned to use active (n = 20) or sham (n = 20) nVNS devices twice daily for 54 days in a double-blind manner. Patient-reported measures of fatigue were collected at baseline and day 56: Profile of Fatigue (PRO-F)-Physical, PRO-F-Mental and Visual Analogue Scale of abnormal fatigue (fVAS). Neurocognitive tests, immunologic responses, electroencephalography alpha reactivity, muscle acidosis, and heart rate variability were compared between devices from baseline to day 56 using analysis of covariance. RESULTS: PRO-F-Physical, PRO-F-Mental, and fVAS scores were significantly reduced at day 56 in the active group only (p = 0.02, 0.02, and 0.04, respectively). Muscle bioenergetics and heart rate variability showed no change between arms. There were significant improvements in digit span and a neurocognitive test (p = 0.03), and upon acute nVNS stimulation, frontal region alpha reactivity showed a significant negative relationship with fatigue scores in the active group (p < 0.01). CONCLUSIONS: We observed significant improvements in three measures of fatigue at day 56 with the active device but not the sham device. Directly after device use, fatigue levels correlate with measures of alpha reactivity, suggesting modulation of cholinergic system integrity as a mechanism of action for nVNS.

Optimizing the Porohyperelastic Response of a Layered Compliance Matched Vascular Graft to Promote Luminal Self-Cleaning.

Thrombosis and intimal hyperplasia have remained the major failure mechanisms of small-diameter vascular grafts used in bypass procedures. While most efforts to reduce thrombogenicity have used a biochemical surface modification approach, the use of local mechanical phenomena to aid in this goal has received somewhat less attention. In this work, the mechanical, fluid transport, and geometrical properties of a layered and porous vascular graft are optimized within a porohyperelastic finite element framework to maximize self-cleaning via luminal reversal fluid velocity (into the lumen). This is expected to repel platelets as well as inhibit the formation of and/or destabilize adsorbed protein layers thereby reducing thrombogenic potential. A particle swarm optimization algorithm was utilized to maximize luminal reversal fluid velocity while also compliance matching our graft to a target artery (rat aorta). The maximum achievable luminal reversal fluid velocity was approximately 246 µm/s without simultaneously optimizing for host compliance. Simultaneous optimization of reversal flow and compliance resulted in a luminal reversal fluid velocity of 59 µm/s. Results indicate that a thick highly permeable compressible inner layer and a thin low permeability incompressible outer layer promote intraluminal reversal fluid velocity. Future research is needed to determine the feasibility of fabricating such a layered and optimized graft and verify its ability to improve hemocompatibility.

An assessment of burnout in New Zealand orthopaedic resident medical officers.

AIMS: Burnout and fatigue are common in the medical profession. The primary aim was to assess rates of burnout in trainee and non-trainee orthopaedic registrars in New Zealand. A secondary aim was to establish which specific factors are associated with burnout. METHODS: In 2021, a 53-question online survey was sent to New Zealand trainee and non-trainee orthopaedic registrars. The survey included questions addressing demographics, modifiable factors known to lead to burnout, information on respective orthopaedic departments, and how respondents had fared with COVID-19. Registrars also completed the Maslach Burnout Inventory-Human Services Survey for Medical Personnel (MBI-HSS MP), a 22-question validated survey that is designed to assess the frequency and intensity of perceived burnout among medical personnel. RESULTS: Fifty of 62 (80.6%) trainees and 66 of 70 (estimated number) (94.3%) of non-trainees completed the survey. Trainees and non-trainees both exhibited moderate levels of burnout. The trainee mean score emotional exhaustion (EE) 22.5, depersonalisation (DP) 8.8, personal achievement (PA) 35.9; non-trainee mean score EE 22.4, DP 8.9, PA 35.9. Fifty-two point two percent of trainees and 50% of non-trainees scored in the severe range for at least one of EE or DP. Factors shown to reduce burnout are the presence of a senior colleague (P<0.001), participation in professional assistance (P=0.049), working in a department with a full complement of staff (P=0.020) and being able to attend health maintenance appointments (P=0.050). CONCLUSION: Our study shows that approximately half of both trainee and non-trainee orthopaedic registrars are exhibiting signs of burnout. This is comparable to other developed nations with a similar healthcare system.

Neuromodulation Strategies to Reduce Inflammation and Improve Lung Complications in COVID-19 Patients.

Since the outbreak of the COVID-19 pandemic, races across academia and industry have been initiated to identify and develop disease modifying or preventative therapeutic strategies has been initiated. The primary focus has been on pharmacological treatment of the immune and respiratory system and the development of a vaccine. The hyperinflammatory state ("cytokine storm") observed in many cases of COVID-19 indicates a prognostically negative disease progression that may lead to respiratory distress, multiple organ failure, shock, and death. Many critically ill patients continue to be at risk for significant, long-lasting morbidity or mortality. The human immune and respiratory systems are heavily regulated by the central nervous system, and intervention in the signaling of these neural pathways may permit targeted therapeutic control of excessive inflammation and pulmonary bronchoconstriction. Several technologies, both invasive and non-invasive, are available and approved for clinical use, but have not been extensively studied in treatment of the cytokine storm in COVID-19 patients. This manuscript provides an overview of the role of the nervous system in inflammation and respiration, the current understanding of neuromodulatory techniques from preclinical and clinical studies and provides a rationale for testing non-invasive neuromodulation to modulate acute systemic inflammation and respiratory dysfunction caused by SARS-CoV-2 and potentially other pathogens. The authors of this manuscript have co-founded the International Consortium on Neuromodulation for COVID-19 to advocate for and support studies of these technologies in the current coronavirus pandemic.

Efficacy profile of noninvasive vagus nerve stimulation on cortical spreading depression susceptibility and the tissue response in a rat model.

BACKGROUND: Noninvasive vagus nerve stimulation (nVNS) has recently emerged as a promising therapy for migraine. We previously demonstrated that vagus nerve stimulation inhibits cortical spreading depression (CSD), the electrophysiological event underlying migraine aura and triggering headache; however, the optimal nVNS paradigm has not been defined. METHODS: Various intensities and doses of nVNS were tested to improve efficacy on KCl-evoked CSD frequency and electrical threshold of CSD in a validated rat model. Chronic efficacy was evaluated by daily nVNS delivery for four weeks. We also examined the effects of nVNS on neuroinflammation and trigeminovascular activation by western blot and immunohistochemistry. RESULTS: nVNS suppressed susceptibility to CSD in an intensity-dependent manner. Two 2-minute nVNS 5 min apart afforded the highest efficacy on electrical CSD threshold and frequency of KCl-evoked CSD. Daily nVNS for four weeks did not further enhance efficacy over a single nVNS 20 min prior to CSD. The optimal nVNS also attenuated CSD-induced upregulation of cortical cyclooxygenase-2, calcitonin gene-related peptide in trigeminal ganglia, and c-Fos expression in trigeminal nucleus caudalis. CONCLUSIONS: Our study provides insight on optimal nVNS parameters to suppress CSD and suggests its benefit on CSD-induced neuroinflammation and trigeminovascular activation in migraine treatment.

Traumatic Injury Under COVID-19 Stay-at-Home Advisory: Experience of a New England Trauma Center.

BACKGROUND: With the onset of the COVID-19 pandemic and subsequent widespread stay-at-home advisories throughout early 2020, hospitals have noticed a decrease in illnesses unrelated to COVID-19. However, the impact on traumatic injury is relatively unknown. This study aims to characterize patterns of trauma during the COVID-19 pandemic at a Level I Trauma Center. MATERIALS & METHODS: A retrospective review was performed of adult trauma patients from March to June, in the years 2018 through 2020. Primary outcome was the number of trauma activations (volume). Secondary outcomes included activation level, mechanism of injury, mortality rate, and length of stay, and other demographic background. Trauma patterns of the 2018 and 2019 periods were combined as historical control, and compared to patterns of the biweekly-matched period of 2020. RESULTS: A total of 2,187 patients were included in analysis (Pre-COVID n = 1,572; COVID n = 615). Results were significant for decreased trauma volume but longer length of stay during COVID cohort, and for an increased proportion of males. No significant difference was found for other demographic variables, trauma mechanisms, or severity. Trauma volume patterns mirrored COVID rates in the state. CONCLUSIONS: Despite a decline in trauma volume, other trauma patterns including severity and mechanism remained unchanged during the COVID-19 period. The decreased volume was not associated with a markedly lower clinical workload, change in team structure, or provider coverage re-distribution. Our data suggests that trauma volume and severity remained high enough during COVID-19 peak to necessitate full staffing, which may provide guidance in the event of a pandemic resurgence.

Initial Seronegative West Nile Virus Encephalitis in an Immunocompromised Child.

We present a case of initial seronegative West Nile virus encephalitis in an immunocompromised child due to B-cell acute lymphoblastic leukemia. Although diagnostic guidelines for West Nile virus infection exist, we highlight that these may not be met in immunocompromised patients who may have a delayed immune response.

Single-Cut Single-Screw Capitate-Shortening Osteotomy for Kienbock's Disease.

Background Kienbock's disease, in spite of an uncertain natural history, is known to cause lunate compromise, leading to central column collapse, carpal instability, and degenerative arthritis of the wrist. Joint leveling procedures are performed in the early stages of Kienbock's disease to "unload" the lunate. Capitate shortening is the preferred procedure in Kienbock's patients with positive ulnar variance. Description of Technique We describe the rationale and a simplified technique of capitate shortening in early Kienbock's disease. This is a single-cut osteotomy with single-screw stabilization. Patients and Methods We have performed this technique in three cases. We present a case of a 26-year-old male who presented with a 1-year history of pain in his right wrist. Radiology performed demonstrated lunate sclerosis. Diagnostic arthroscopy revealed healthy articular surfaces. Single osteotomy capitate shortening was performed with an oscillating saw and fixed with a single cannulated compression screw. A shortening of 1.5mm was obtained with this technique. Results At 1- to 2-year follow-up, all three patients had considerable pain relief but did not have a complete resolution of pain. There was a significant improvement in function and grip strength. There have been no cases with infection, nonunion, avascular necrosis or a need for a salvage procedure. Conclusion The simplified technique of capitate shortening is easy to perform, less traumatic to the capitate vascularity, and leads to good short-term functional results.

Vagus nerve stimulation reduces spreading depolarization burden and cortical infarct volume in a rat model of stroke.

Cortical spreading depolarization (SD) waves negatively affect neuronal survival and outcome after ischemic stroke. We here aimed to investigate the effects of vagus nerve stimulation (VNS) on SDs in a rat model of focal ischemia. To this end, we delivered non-invasive VNS (nVNS) or invasive VNS (iVNS) during permanent middle cerebral artery occlusion (MCAO), and found that both interventions significantly reduced the frequency of SDs in the cortical peri-infarct area compared to sham VNS, without affecting relative blood flow changes, blood pressure, heart rate or breathing rate. In separate groups of rats subjected to transient MCAO, we found that cortical stroke volume was reduced 72 h after transient MCAO, whereas stroke volume in the basal ganglia remained unchanged. In rats treated with nVNS, motor outcome was improved 2 days after transient MCAO, but was similar to sham VNS animals 3 days after ischemia. We postulate that VNS may be a safe and efficient intervention to reduce the clinical burden of SD waves in stroke and other conditions.

Vagus nerve stimulation inhibits cortical spreading depression exclusively through central mechanisms.

Experimental and clinical data strongly support vagus nerve stimulation (VNS) as a novel treatment in migraine. Vagus nerve stimulation acutely suppresses cortical spreading depression (CSD) susceptibility, an experimental model that has been used to screen for migraine therapies. However, mechanisms underlying VNS efficacy on CSD are unknown. Here, we interrogated the central and peripheral mechanisms using VNS delivered either invasively (iVNS) or noninvasively (nVNS) in male Sprague-Dawley rats. Cortical spreading depression susceptibility was evaluated 40 minutes after the stimulation. iVNS elevated the electrical CSD threshold more than 2-fold and decreased KCl-induced CSD frequency by 22% when delivered to intact vagus nerve. Distal vagotomy did not alter iVNS efficacy (2-fold higher threshold and 19% lower frequency in iVNS vs sham). By contrast, proximal vagotomy completely abolished iVNS effect on CSD. Pharmacological blockade of nucleus tractus solitarius, the main relay for vagal afferents, by lidocaine or glutamate receptor antagonist CNQX also prevented CSD suppression by nVNS. Supporting a role for both norepinephrine and serotonin, CSD suppression by nVNS was inhibited by more than 50% after abrogating norepinephrinergic or serotonergic neurotransmission alone using specific neurotoxins; abrogating both completely blocked the nVNS effect. Our results suggest that VNS inhibits CSD through central afferents relaying in nucleus tractus solitarius and projecting to subcortical neuromodulatory centers providing serotonergic and norepinephrinergic innervation to the cortex.

Noninvasive vagus nerve stimulation alters neural response and physiological autonomic tone to noxious thermal challenge.

The mechanisms by which noninvasive vagal nerve stimulation (nVNS) affect central and peripheral neural circuits that subserve pain and autonomic physiology are not clear, and thus remain an area of intense investigation. Effects of nVNS vs sham stimulation on subject responses to five noxious thermal stimuli (applied to left lower extremity), were measured in 30 healthy subjects (n = 15 sham and n = 15 nVNS), with fMRI and physiological galvanic skin response (GSR). With repeated noxious thermal stimuli a group × time analysis showed a significantly (p < .001) decreased response with nVNS in bilateral primary and secondary somatosensory cortices (SI and SII), left dorsoposterior insular cortex, bilateral paracentral lobule, bilateral medial dorsal thalamus, right anterior cingulate cortex, and right orbitofrontal cortex. A group × time × GSR analysis showed a significantly decreased response in the nVNS group (p < .0005) bilaterally in SI, lower and mid medullary brainstem, and inferior occipital cortex. Finally, nVNS treatment showed decreased activity in pronociceptive brainstem nuclei (e.g. the reticular nucleus and rostral ventromedial medulla) and key autonomic integration nuclei (e.g. the rostroventrolateral medulla, nucleus ambiguous, and dorsal motor nucleus of the vagus nerve). In aggregate, noninvasive vagal nerve stimulation reduced the physiological response to noxious thermal stimuli and impacted neural circuits important for pain processing and autonomic output.

The Effects of Noninvasive Vagus Nerve Stimulation on Fatigue and Immune Responses in Patients With Primary Sjögren's Syndrome.

OBJECTIVES: Primary Sjögren's syndrome (pSS) sufferers have rated chronic fatigue as the most important symptom needing improvement. Emerging data suggest that stimulation of the vagus nerve can modulate immunological responses. The gammaCore device (electroCore), developed to stimulate the cervical vagus nerve noninvasively, was used to assess the effects of vagus nerve activation on immune responses and clinical symptoms of pSS. MATERIALS AND METHODS: Fifteen female pSS subjects used the nVNS device twice daily a 26-day period. At baseline, blood was drawn before and after application of the gammaCore device for 90 sec over each carotid artery. The following fatigue-related outcome measures were collected at baseline, day 7 and day 28: EULAR patient reported outcome index, profile of fatigue (Pro-F), visual analogue scale of abnormal fatigue, and Epworth sleepiness scale (ESS). Whole blood samples were stimulated with 2 ng/mL lipopolysaccharide (LPS) and the supernatant levels of IFNγ, IL12-p70, TNFα, MIP-1α, IFNα, IL-10, IL-1ß, IL-6, and IP-10 were measured at 24 hours. In addition, clinical hematology and flow cytometric profiles of whole blood immune cells were analyzed. RESULTS: Pro-F and ESS scores were significantly reduced across all three visits. LPS-stimulated production of IL-6, IL-1ß, IP-10, MIP-1α, and TNFα were significantly reduced over the study period. Patterns of NK- and T-cell subsets also altered significantly over the study period. Interestingly, lymphocyte counts at baseline visit correlated to the reduction in fatigue score. CONCLUSION: The vagus nerve may play a role in the regulation of fatigue and immune responses in pSS and nVNS may reduce clinical symptoms of fatigue and sleepiness. However, a sham-controlled follow-up study with a larger sample size is required to confirm the findings.

Exploration of the Impact of Brief Noninvasive Vagal Nerve Stimulation on EEG and Event-Related Potentials.

OBJECTIVES: The primary objective of this study was to explore the impact of noninvasive Vagal Nerve Stimulation (nVNS) on brain electrophysiology, as assessed through spontaneous resting-state EEG and stimulus-driven event-related potentials (ERPs). METHODS: A hand-held transcutaneous stimulator was placed on the neck over the main branch of the left vagus (active condition) or more laterally over neck muscles (sham condition), with two 120-sec long bursts of stimulation applied over a five-minute period. For each of eight neurotypical subjects, prior to stimulation, and then again beginning at 15, 120, and 240 min post-stimulation, ten minutes of background EEG data were collected, along with a series of ERPs-N100 auditory sensory-gating; the N1/P2 loudness dependent auditory evoked responses (LDAER); mismatch negativity; P300a; and P300b. Each subject participated in active and sham stimulation sessions. RESULTS: Brief nVNS had a significant (p < 0.05), and in some cases prolonged (>2 hours), impact on the spontaneous EEG (decreased theta and alpha, and increased beta and gamma), and on sensory gating, LDAER, and P300b evoked responses. Based on prior literature, these specific observations may reflect nVNS-induced modulation of particular neurotransmitter systems including those for GABA (gamma power and frequency); acetylcholine (sensory gating); serotonin (LDAER); and noradrenaline (P300b). CONCLUSIONS: Brief nVNS leads to changes in a sub-set of resting-state and event-related electrophysiologic indices of brain activity. These changes are believed to be mediated by vagal afferent projections to the nucleus of the solitary tract, which in turn regulates several neurotransmitter systems through known direct and indirect neuroanatomic pathways.

Non-invasive vagus nerve stimulation reduces blood-brain barrier disruption in a rat model of ischemic stroke.

BACKGROUND: Vagus nerve stimulation (VNS) significantly reduces infarct volume in rat models of cerebral ischemia, but the mechanism of this protective effect remains open. HYPOTHESIS: This study tested the hypothesis that non-invasive VNS (nVNS), during transient middle cerebral artery occlusion (MCAO), protects the blood-brain barrier (BBB), leading to reduced infarct size in ischemic brain. METHODS: Spontaneous hypertensive rats (SHRs) were subjected to a 90 min MCAO. nVNS treated rats received 5 stimulations (duration: 2 min; every 10 min) on the skin overlying the cervical vagus nerve in the neck beginning 30 min after MCAO onset. Control rats received the same stimulations on the quadriceps femoris muscle. Twenty-four hours after MCAO onset, MRI and immunohistochemistry (IHC) were performed for analyses of infarct size and BBB leakage. RESULTS: Compared with the control group, anatomic MRI T2-weighted images showed significantly smaller infarct sizes in the nVNS group. Dynamic contrast-enhanced (DCE)-MRI showed a significantly decreased BBB transfer rate (Ki map) in the lesion area in the nVNS group, which was spatially correlated with the attenuation of the infarct size. Furthermore, significantly lower serum IgG leakage, visualized by IHC, was seen in the ischemic hemisphere in nVNS treated rats. nVNS also protected vascular tight junction proteins from disruption in microvessels, and reduced expression of matrix metalloproteinases-2/9 in reactive astrocytes surrounding the compromised vessels in the ischemic hemispheres. CONCLUSION: Our data suggest that the neuroprotective role of a series of nVNS administrations during MCA occlusion, spatially correlates with protection of BBB integrity from damage and reduction of infarct extent induced by ischemic stroke.

High-Resolution Multi-Scale Computational Model for Non-Invasive Cervical Vagus Nerve Stimulation.

OBJECTIVES: To develop the first high-resolution, multi-scale model of cervical non-invasive vagus nerve stimulation (nVNS) and to predict vagus fiber type activation, given clinically relevant rheobase thresholds. METHODS: An MRI-derived Finite Element Method (FEM) model was developed to accurately simulate key macroscopic (e.g., skin, soft tissue, muscle) and mesoscopic (cervical enlargement, vertebral arch and foramen, cerebral spinal fluid [CSF], nerve sheath) tissue components to predict extracellular potential, electric field (E-Field), and activating function along the vagus nerve. Microscopic scale biophysical models of axons were developed to compare axons of varying size (Aα-, Aß- and Aδ-, B-, and C-fibers). Rheobase threshold estimates were based on a step function waveform. RESULTS: Macro-scale accuracy was found to determine E-Field magnitudes around the vagus nerve, while meso-scale precision determined E-field changes (activating function). Mesoscopic anatomical details that capture vagus nerve passage through a changing tissue environment (e.g., bone to soft tissue) profoundly enhanced predicted axon sensitivity while encapsulation in homogenous tissue (e.g., nerve sheath) dulled axon sensitivity to nVNS. CONCLUSIONS: These findings indicate that realistic and precise modeling at both macroscopic and mesoscopic scales are needed for quantitative predictions of vagus nerve activation. Based on this approach, we predict conventional cervical nVNS protocols can activate A- and B- but not C-fibers. Our state-of-the-art implementation across scales is equally valuable for models of spinal cord stimulation, cortex/deep brain stimulation, and other peripheral/cranial nerve models.

Microglia modulation through external vagus nerve stimulation in a murine model of Alzheimer's disease.

Chronically activated microglia contribute to the development of neurodegenerative diseases such as Alzheimer's disease (AD) by the release of pro-inflammatory mediators that compromise neuronal function and structure. Modulating microglia functions could be instrumental to interfere with disease pathogenesis. Previous studies have shown anti-inflammatory effects of acetylcholine (ACh) or norepinephrine (NE), which mainly activates the ß-receptors on microglial cells. Non-invasive vagus nerve stimulation (nVNS) is used in treatment of drug-resistant depression, which is a risk factor for developing AD. The vagus nerve projects to the brainstem's locus coeruleus from which noradrenergic fibers reach to the Nucleus Basalis of Meynert (NBM) and widely throughout the brain. Pilot studies showed first signs of cognitive-enhancing effects of nVNS in AD patients. In this study, the effects of nVNS on mouse microglia cell morphology were analyzed over a period of 280 min by 2-photon laser scanning in vivo microscopy. Total branch length, average branch order and number of branches, which are commonly used indicators for the microglial activation state were determined and compared between young and old wild-type and amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice. Overall, these experiments show strong morphological changes in microglia, from a neurodestructive to a neuroprotective phenotype, following a brief nVNS in aged animals, especially in APP/PS1 animals, whereas microglia from young animals were morphologically unaffected.

Mechanism of action of non-invasive cervical vagus nerve stimulation for the treatment of primary headaches.

Stimulation of the cervical vagus nerve with implanted vagus nerve stimulation (iVNS) has been used clinically for more than 20 years to treat patients with epilepsy. More recently, a non-invasive cervical vagus nerve stimulation (nVNS), gammaCore, was developed, which has been purported to also stimulate the vagus nerve without the cost and morbidity associated with an iVNS system. gammaCore has been used to acutely treat various types of primary headaches, including migraine and cluster headaches (CH), and for the prevention of episodic, chronic, and menstrual migraines and CH. The gammaCore device was cleared by the FDA for the acute treatment of pain in episodic CH patients. In this review, we summarize the clinical work that has been published in the use of gammaCore for treating primary headache disorders, present an overview of studies demonstrating that nVNS does indeed stimulate similar vagus nerve fibers as the implantable VNS system, and then present several animal headache-related studies that address the mechanism of action of nVNS.

Microstructure of the Distal Radius and Its Relevance to Distal Radius Fractures.

Background There is a paucity of information on the microstructure of the distal radius, and how this relates to its morphology and function. Purpose This study aims to assess the microanatomical structure of the distal radius, and relate this to its morphology, function, and modes of failure. Methods Six dry adult skeletal distal radii were examined with microcomputed tomography scan and analyzed with specialist computer software. From 3D and 2D images, the subchondral, cortical, and medullary trabecular were assessed and interpreted based on the overall morphology of the radius. Results The expanded distal radial metaphysis provides a wide articular surface for distributing the articular load. The extrinsic wrist ligaments are positioned around the articular perimeter, except on the dorsal radial corner. The subchondral bone plate is a 2 mm multilaminar lattice structure, which is thicker below the areas of the maximal articular load. There are spherical voids distally, which become ovoid proximally, which assist in absorbing articular impact. It does not have Haversian canals. From the volar aspect of the lunate facet, there are thick trabecular columns that insert into the volar cortex of the radius at the metaphyseal-diaphyseal junction. For the remainder of the subchondral bone plate, there is an intermediate trabecular network, which transmits the load to the intermediate trabeculae and then to the trabecular arches. The arches pass proximally and coalesce with the ridges of the diaphyseal cortex. Conclusion The distal radius morphology is similar to an arch bridge. The subchondral bone plate resembles the smooth deck of the bridge that interacts with the mobile load. The load is transmitted to the rim, intermediate struts, and arches. The metaphyseal arches allow the joint loading forces to be transmitted proximally and laterally, providing compression at all levels and avoiding tension. The arches have a natural ability to absorb the impact which protects the articular surface. The distal radius absorbs and transmits the articular impact to the medullary cortex and intermediate trabeculae. The medullary arches are positioned to transmit the load from the intermediate trabeculae to the diaphysis. Clinical Relevance The microstructure of the distal radius is likely to be important for physiological loading of the radius. The subchondral bone plate is a unique structure that is different to the cancellous and cortical bone. All three bone types have different functions. The unique morphology and microstructure of the distal radius allow it to transmit load and protect the articular cartilage.