A Rare Anatomical Variant of Unilateral Piriformis Muscle Agenesis: A Case Report.

Anatomical variation of neuromuscular structures of the gluteal region is common. The piriformis muscle, in particular, has an important relationship with the sciatic nerve and may be associated with distinct clinical conditions. We report an incidental finding of unilateral piriformis muscle agenesis diagnosed on computed tomography and magnetic resonance imaging, a rare anatomical variant of the gluteal region.

Can We Discriminate Symptomatic Hip Patients From Asymptomatic Volunteers Based on Anatomic Predictors? A 3-Dimensional Magnetic Resonance Study on Cam, Pincer, and Spinopelvic Parameters.

BACKGROUND: Given the high prevalence of patients with hip deformities and no ongoing hip dysfunction, understanding the anatomic factors predicting the symptomatic state is critical. One such variable is how the spinopelvic parameters (SPPs) may interplay with hip anatomic factors. HYPOTHESIS/PURPOSE: SPPs and femoral- and acetabular-specific parameters may predict which patients will become symptomatic. The purpose was to determine which anatomic characteristics with specific cutoffs were associated with hip symptom development and how these parameters relate to each other. STUDY DESIGN: Cohort study (Diagnosis); Level of evidence, 2. METHODS: 548 participants were designated either symptomatic patients (n = 176, scheduled for surgery with hip pain and/or functional limitation) or asymptomatic volunteers (n = 372, no pain) and underwent 3-dimensional magnetic resonance imaging. Multiple femoral (α angle, Ω angle, neck angle, torsion), acetabular (version, coverage), and spinopelvic (pelvic tilt, sacral slope [SS], pelvic incidence) parameters were measured semiautomatically. Normative values, optimal differentiating thresholds, and a logistic regression analysis were computed. RESULTS: Symptomatic patients had larger cam deformities (defined by increased Ω angle and α angle), smaller acetabular coverage, and larger pelvic incidence and SS angles compared with the asymptomatic volunteers. Discriminant receiver operating characteristic analysis confirmed that radial 2-o'clock α angle (threshold 58°-60°, sensitivity 75%-60%, specificity 80%-84%; area under the curve [AUC] = 0.831), Ω angle (threshold 43°, sensitivity 72%, specificity 70%; AUC = 0.830), acetabular inclination (threshold 6°, sensitivity 65%, specificity 70%; AUC = 0.709), and SS (threshold 44°, sensitivity 72%, specificity 75%; AUC = 0.801) ( P < .005) were the best parameters to classify participants. When parameters were entered into a logistic regression, significant positive predictors for the symptomatic patients were achieved for SS, acetabular inclination, Ω angle, and α angle at 2-o'clock, correctly classifying 85% of cases (model sensitivity 72%, specificity 91%; AUC = 0.919). CONCLUSION: Complex dynamic interplay exists between the hip and SPPs. A cam deformity, acetabular undercoverage, and increased SPP angles are predictive of a hip symptomatic state. SPPs were significant to discriminate between participants and were important in combination with other hip deformities. Symptomatic patients can be effectively differentiated from asymptomatic volunteers based on predictive anatomic factors.

Dysregulation of TrkB Receptors and BDNF Function by Amyloid-ß Peptide is Mediated by Calpain.

Brain-derived neurotrophic factor (BDNF) and its high-affinity full-length (FL) receptor, TrkB-FL, play a central role in the nervous system by providing trophic support to neurons and regulating synaptic plasticity and memory. TrkB and BDNF signaling are impaired in Alzheimer's disease (AD), a neurodegenerative disease involving accumulation of amyloid-ß (Aß) peptide. We recently showed that Aß leads to a decrease of TrkB-FL receptor and to an increase of truncated TrkB receptors by an unknown mechanism. In the present study, we found that (1) Aß selectively increases mRNA levels for the truncated TrkB isoforms without affecting TrkB-FL mRNA levels, (2) Aß induces a calpain-mediated cleavage on TrkB-FL receptors, downstream of Shc-binding site, originating a new truncated TrkB receptor (TrkB-T') and an intracellular fragment (TrkB-ICD), which is also detected in postmortem human brain samples, (3) Aß impairs BDNF function in a calpain-dependent way, as assessed by the inability of BDNF to modulate neurotransmitter (GABA and glutamate) release from hippocampal nerve terminals, and long-term potentiation in hippocampal slices. It is concluded that Aß-induced calpain activation leads to TrkB cleavage and impairment of BDNF neuromodulatory actions.