BackgroundDuring pregnancy, women are at risk of developing persistent symptomatic diastasis recti abdominis (DRA), which may have a detrimental effect on their physical function and quality of life (QoL). The aim of this prospective cohort study was to determine the effect of surgical repair of DRA on abdominal trunk function, urinary incontinence and QoL in postpartum women with trunk instability symptoms resistant to training.MethodsPostpartum women with diagnosed DRA and training‐resistant symptoms underwent double‐row plication of the linea alba. Abdominal trunk function was evaluated as the primary endpoint using a multimodal examination tool, the Abdominal Trunk Function Protocol. Recurrence was assessed by CT, urinary incontinence was evaluated using the Urogenital Distress Inventory (UDI‐6) and Incontinence Impact Questionnaire (IIQ‐7), and QoL was assessed with the Short Form 36 (SF‐36®) questionnaire. All subjects were examined before and 1 year after surgery.ResultsSixty women were recruited. There was no DRA recurrence at the 1‐year follow‐up. Self‐reported abdominal trunk function had improved in 98 per cent of patients, with a mean score improvement of 79·1 per cent. In the physiological tests monitored by a physiotherapist, 76 per cent performed better and endured exercise tests longer than before surgery. All SF‐36® subscales improved significantly compared with preoperative scores and reached levels similar to, or higher than, the normative Swedish female population. For the UDI‐6 and IIQ‐7, 47 and 37 per cent respectively reported fewer symptoms at follow‐up than before surgery, and 13 and 8 per cent respectively reported more symptoms.ConclusionIn this series of postpartum women presenting with DRA and symptoms of trunk instability resistant to training, surgical reconstruction resulted in a significant improvement in abdominal trunk function, urinary incontinence and QoL.
BackgroundDiffuse traumatic axonal injury (TAI), a common consequence of traumatic brain injury, is associated with high morbidity and mortality. Inflammatory processes may play an important role in the pathophysiology of TAI. In the central fluid percussion injury (cFPI) TAI model in mice, the neuroinflammatory and astroglial response and behavioral changes are unknown.MethodsTwenty cFPI-injured and nine sham-injured mice were used, and the neuroinflammatory and astroglial response was evaluated by immunohistochemistry at 1, 3 and 7 days post-injury. The multivariate concentric square field test (MCSF) was used to compare complex behavioral changes in mice subjected to cFPI (n = 16) or sham injury (n = 10). Data was analyzed using non-parametric statistics and principal component analysis (MCSF data).ResultsAt all post-injury time points, β-amyloid precursor protein (β-APP) immunoreactivity revealed widespread bilateral axonal injury and IgG immunostaining showed increased blood–brain barrier permeability. Using vimentin and glial fibrillary acidic protein (GFAP) immunohistochemistry, glial cell reactivity was observed in cortical regions and important white matter tracts peaking at three days post-injury. Only vimentin was increased post-injury in the internal capsule and only GFAP in the thalamus. Compared to sham-injured controls, an increased number of activated microglia (MAC-2), infiltrating neutrophils (GR-1) and T-cells (CD3) appearing one day after TAI (P<0.05 for all cell types) was observed in subcortical white matter. In the MCSF, the behavioral patterns including general activity and exploratory behavior differed between cFPI mice and sham-injured controls.ConclusionsTraumatic axonal injury TAI resulted in marked bilateral astroglial and neuroinflammatory responses and complex behavioral changes. The cFPI model in mice appears suitable for the study of injury mechanisms, including neuroinflammation, and the development of treatments targeting TAI.
Widespread traumatic axonal injury (TAI) results in brain network dysfunction, which commonly leads to persisting cognitive and behavioural impairments following traumatic brain injury (TBI). TBI induces a complex neuroinflammatory response, frequently located at sites of axonal pathology. The role of the pro-inflammatory cytokine interleukin (IL)-1β has not been established in TAI. An IL-1β-neutralizing or a control antibody was administered intraperitoneally at 30 min following central fluid percussion injury (cFPI), a mouse model of widespread TAI. Mice subjected to moderate cFPI (n = 41) were compared with sham-injured controls (n = 20) and untreated, naive mice (n = 9). The anti-IL-1β antibody reached the target brain regions in adequate therapeutic concentrations (up to ~30 μg/brain tissue) at 24 h post-injury in both cFPI (n = 5) and sham-injured (n = 3) mice, with lower concentrations at 72 h post-injury (up to ~18 μg/g brain tissue in three cFPI mice). Functional outcome was analysed with the multivariate concentric square field (MCSF) test at 2 and 9 days post-injury, and the Morris water maze (MWM) at 14-21 days post-injury. Following TAI, the IL-1β-neutralizing antibody resulted in an improved behavioural outcome, including normalized behavioural profiles in the MCSF test. The performance in the MWM probe (memory) trial was improved, although not in the learning trials. The IL-1β-neutralizing treatment did not influence cerebral ventricle size or the number of microglia/macrophages. These findings support the hypothesis that IL-1β is an important contributor to the processes causing complex cognitive and behavioural disturbances following TAI.
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