Femoroacetabular impingement in 45 professional athletes: associated pathologies and return to sport following arthroscopic decompression

Femoroacetabular impingement (FAI) occurs when an osseous abnormality of the proximal femur (cam) or acetabulum (pincer) triggers damage to the acetabular labrum and articular cartilage in the hip. Although the precise etiology of FAI is not well understood, both types of FAI are common in athletes presenting with hip pain, loss of range-of-motion, and disability in athletics. An open surgical approach to decompressing FAI has shown good clinical outcomes; however, this highly invasive approach inherently may delay or preclude a high level athlete’s return to play. The purpose of this study was to define associated pathologies and determine if an arthroscopic approach to treating FAI can allow professional athletes to return to high-level sport. Hip arthroscopy for the treatment of FAI allows professional athletes to return to professional sport. Between October 2000 and September 2005, 45 professional athletes underwent hip arthroscopy for the decompression of FAI. Operative and return-to-play data were obtained from patient records. Average time to follow-up was 1.6 years (range: 6 months to 5.5 years). Forty two (93%) athletes returned to professional competition following arthroscopic decompression of FAI. Three athletes did not return to play; however, all had diffuse osteoarthritis at the time of arthroscopy. Thirty-five athletes (78%) remain active in professional sport at an average follow-up of 1.6 years. Arthroscopic treatment of FAI allows professional athletes to return to professional sport.     

Glial S100B Positive Vacuoles In Purkinje Cells: Earliest Morphological Abnormality In SCA1 Transgenic Mice

Spinocerebellar ataxia-1 (SCA1) is caused by the expansion of a polyglutamine repeat within the disease protein, ataxin-1. The overexpression of mutant ataxin-1 in SCA1 transgenic mice results in the formation of cytoplasmic vacuoles in Purkinje neurons (PKN) of the cerebellum. PKN are closely associated with neighboring Bergmann glia. To elucidate the role of Bergmann glia in SCA1 pathogenesis, cerebellar tissue from 7 days to 6 wks old SCA1 transgenic and wildtype mice were used. We observed that Bergmann glial S100B protein is localized to the cytoplasmic vacuoles in SCA1 PKN. These S100B positive cytoplasmic vacuoles began appearing much before the onset of behavioral abnormalities, and were negative for other glial and PKN marker proteins. Electron micrographs revealed that vacuoles have a double membrane. In the vacuoles, S100B colocalized with receptors of advanced glycation end-products (RAGE), and S100B co-immunoprecipated with cerebellar RAGE. In SCA1 PKN cultures, exogenous S100B protein interacted with the PKN membranes and was internalized. These data suggest that glial S100B though extrinsic to PKN is sequestered into cytoplasmic vacuoles in SCA1 mice at early postnatal ages. Further, S100B may be binding to RAGE on Purkinje cell membranes before these membranes are internalized.     

Cognitive profiles of individual patients with Parkinson's disease and dementia: comparison with dementia with lewy bodies and Alzheimer's disease.

We describe the pattern of cognitive profiles within a community-based sample of patients with Parkinson's disease (PD) and dementia (PDD) using cluster analyses, and compare the results with data from patients with Alzheimer's disease (AD) and dementia with Lewy bodies (DLB). Fifty patients with PDD and 39 with AD from Stavanger, Norway, and 62 patients with DLB from San Diego, CA, USA were diagnosed by either standardized clinical procedures or criteria (all PDD and all AD cases) or necropsy (all DLB cases). Four subgroups were identified: two subgroups with a subcortical cognitive profile (one with mild and one with moderate dementia severity), one subgroup with global impairment and severe dementia, and one subgroup with a cortical cognitive profile and moderate dementia. Of the patients with PDD and with DLB, 56% and 55%, respectively, had a subcortical cognitive profile, compared with only 33% of the AD patients. Conversely, 30% of the patients with PDD and 26% of those with DLB had a cortical cognitive profile, compared with 67% of the patients with AD. These findings suggest that in some patients with PDD, frontosubcortical changes are the main contributing factor to dementia, whereas in other patients, cortical and hippocampal changes are more important.     

Facilitated percutaneous coronary intervention.

The goal of the initial treatment for ST-segment elevation myocardial infarction is rapid and effective reperfusion. Randomized trials have demonstrated that primary angioplasty is preferred over thrombolysis if done in a timely manner and by an experienced team. However, due to many factors, performance of primary angioplasty within the goal of 90 min is often not possible. A combined strategy of immediate thrombolysis in the emergency room or in the ambulance followed by angioplasty theoretically could provide early reperfusion with subsequent angioplasty to insure complete reperfusion. Over 17 clinical trials have been reported. Compared with thrombolysis, facilitated angioplasty in the most recent trials has been shown to have a more favorable long-term outcome. Trials comparing facilitated angioplasty with full- or half-dose thrombolysis versus primary angioplasty have been far less favorable with the largest trial to date, the ASSENT (Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention)-4 trial, demonstrating a worse outcome in the primary end point of death, congestive heart failure, or shock at 90 days. Pending the results of the FINESSE (Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events) trial, current data suggest that facilitated angioplasty does not offer any advantage over primary angioplasty and may be harmful.     

Importance of spatiotemporal heterogeneity of cellular restitution in mechanism of arrhythmogenic discordant alternans

BACKGROUND: Spatially discordant cellular alternans form a substrate for development of unidirectional block and ventricular fibrillation. However, the mechanisms responsible for discordant alternans remain poorly understood. Previous work suggests electrical restitution is critical to the development of alternans in single cells. OBJECTIVES: The purpose of this study was to investigate the hypothesis that spatial and temporal heterogeneities of restitution underlie the mechanism eliciting discordant alternans. METHODS: Steady-state pacing was used to elicit concordant cellular alternans in nine Langendorff-perfused guinea pig hearts. A single extrastimulus (S2) was applied every 51st beat following either the even or the odd beat of alternans. The cellular response to S2 was determined using optical mapping to generate action potential duration (APD) restitution curves from 256 ventricular sites for both the even and the odd beats. RESULTS: Restitution kinetics were temporally heterogeneous during alternans, as restitution curves between the even and the odd beats differed significantly. Temporal heterogeneity was quantified by the average separation of restitution between the two curves, or Delta-restitution. Delta-Restitution was spatially heterogeneous and proportional to the amount of alternans at a given ventricular site. A computer simulation based on the experimental results showed the mechanism of discordant alternans was dependent on both spatial and temporal heterogeneities of restitution. CONCLUSION: Both temporal and spatial heterogeneities of restitution exist during cellular alternans in the intact heart. Temporal heterogeneities of restitution, quantified by Delta-restitution, are proportional to the magnitude of cellular alternans. The combination of spatial and temporal heterogeneities of restitution may underlie the genesis of discordant alternans.