Interest in spatial ability has grown over the past few decades following the emergence of correlational evidence associating spatial aptitude with educational performance in the fields of science, technology, engineering, and mathematics. The research field at large and the anatomy education literature on this topic are mixed. In an attempt to generate consensus, a meta‐analysis was performed to objectively summarize the effects of spatial ability on anatomy assessment performance across multiple studies and populations. Relevant studies published within the past 50 years (1969–2019) were retrieved from eight databases. Study eligibility screening was followed by a full‐text review and data extraction. Use of the Mental Rotations Test (MRT) was required for study inclusion. Out of 2,450 screened records, 15 studies were meta‐analyzed. Seventy‐three percent of studies (11 of 15) were from the United States and Canada, and the majority (9 of 15) studied professional students. Across 15 studies and 1,245 participants, spatial ability was weakly associated with anatomy performance (rpooled = 0.240; CI at 95% = 0.09, 0.38; P = 0.002). Performance on spatial and relationship‐based assessments (i.e., practical assessments and drawing tasks) was correlated with spatial ability, while performance on assessments utilizing non‐spatial multiple‐choice items was not correlated with spatial ability. A significant sex difference was also observed, wherein males outperformed females on spatial ability tasks. Given the role of spatial reasoning in learning anatomy, educators are encouraged to consider curriculum delivery modifications and a comprehensive assessment strategy so as not to disadvantage individuals with low spatial ability.

Individuals with spinal cord injury (SCI) have been shown to exhibit systolic, and to a lesser extent, diastolic cardiac dysfunction. However, previous reports of cardiac dysfunction in this population are confounded by the changing loading conditions after SCI and as such, whether cardiac dysfunction per se is present is still unknown. Therefore, our aim was to establish if load-independent cardiac dysfunction is present after SCI, to understand the functional cardiac response to SCI, and to explore the changes within the cellular milieu of the myocardium. Here, we applied in vivo echocardiography and left-ventricular (LV) pressure-volume catheterization with dobutamine infusions to our Wistar rodent model of cardiac dysfunction 5 weeks following high (T2) thoracic contusion SCI, while also examining the morphological and transcriptional alterations of cardiomyocytes. We found that SCI significantly impairs systolic function independent of loading conditions (end-systolic elastance in control: 1.35 ± 0.15; SCI: 0.65 ± 0.19 mm Hg/μL). The reduction in contractile indices is accompanied by a reduction in width and length of cardiomyocytes as well as alterations in the LV extracellular matrix. Importantly, we demonstrate that the reduction in the rate (dP/dt) of LV pressure rise can be offset with beta-adrenergic stimulation, thereby experimentally implicating the loss of descending sympatho-excitatory control of the heart as a principle cause of LV dysfunction in SCI. Our data provide evidence that SCI induces systolic cardiac dysfunction independent of loading conditions and concomitant cardiomyocyte atrophy that may be underpinned by changes in the genes regulating the cardiac extracellular matrix.

Active upper-limb and passive lower-limb exercise are two interventions used in the spinal cord injury (SCI) population. Although the global cardiac responses have been previously studied, it is unclear how either exercise influences contractile cardiac function. Here, the cardiac contractile and volumetric responses to upper-limb (swim) and passive lower-limb exercise were investigated in rodents with a severe high-thoracic SCI. Animals were divided into control (CON), SCI no exercise (NO-EX), SCI passive hindlimb cycling (PHLC), or SCI swim (SWIM) groups. Severe contusion SCI was administered at the T2 level. PHLC and SWIM interventions began on day 8 postinjury and lasted 25 days. Echocardiography and dobutamine stress echocardiography were performed before and after injury. Cardiac contractile indexes were assessed in vivo at study termination via a left ventricular pressure-volume conductance catheter. Stroke volume was reduced after SCI (91 µl in the NO-EX group vs. 188 µl in the CON group, P < 0.05) and was reversed at study termination in the PHLC (167 µl) but not SWIM (90 µl) group. Rates of contraction were reduced in NO-EX versus CON groups (6,079 vs. 9,225 mmHg, respectively, P < 0.05) and were unchanged by PHLC and SWIM training. Similarly, end-systolic elastance was reduced in the NO-EX versus CON groups (0.67 vs. 1.37 mmHg/µl, respectively, P < 0.05) and was unchanged by PHLC or SWIM training. Dobutamine infusion normalized all pressure indexes in each SCI group (all P < 0.05). In conclusion, PHLC improves flow-derived cardiac indexes, whereas SWIM training displayed no cardiobeneficial effect. Pressure-derived deficits were corrected only with dobutamine, suggesting that reduced β-adrenergic stimulation is principally responsible for the impaired cardiac contractile function after SCI. NEW & NOTEWORTHY This is the first direct comparison between the cardiac changes elicited by active upper-limb or passive lower-limb exercise after spinal cord injury. Here, we demonstrate that lower-limb exercise positively influences flow-derived cardiac indexes, whereas upper-limb exercise does not. Furthermore, neither intervention corrects the cardiac contractile dysfunction associated with spinal cord injury.