Multidirectional instability of the shoulder: pathophysiology, diagnosis, and management.

Multidirectional instability of the shoulder is a complex entity. Relatively few series of patients with this condition have been reported. Affected patients have global (anterior, inferior, and posterior) excessive laxity of the glenohumeral joint capsule and a rotator interval capsule defect. The onset of symptoms is frequently related to atraumatic events. The chief complaint is more often related to pain than to instability per se. Symptoms are mostly experienced within the midrange of glenohumeral motion. Because the contralateral shoulder is often equally lax and asymptomatic, it appears that factors in addition to excessive capsular laxity play a pathophysiologic role. These factors may include subtle losses of strength and/or neuromotor coordination of the rotator cuff and scapular stabilizing muscles, defective proprioceptive responses, and the absence of a limited joint volume. Most patients can be successfully treated nonoperatively with a specific exercise program. If a 6-month trial of nonoperative management fails, the patient is a candidate for surgical reconstruction. The most time-honored procedure is an open inferior capsular shift, which corrects excessive global laxity of the capsule and the rotator interval defect.

Selective coral mortality associated with outbreaks of Acanthaster planci L. in Bootless Bay, Papua New Guinea.

Population outbreaks of crown-of-thorns sea star (Acanthaster planci L.) remain one of the most significant biological disturbances on tropical coral reefs although the increasing attention given to other threats has greatly limited recent progress in understanding the cause and consequences of this phenomenon. In September 2005 dramatic increases in the abundance of A. planci were observed on reefs within Bootless Bay, Central Province, Papua New Guinea, where few crown-of-thorns have previously been reported. Densities of A. planci peaked at 162 sea stars per hectare and caused extensive coral mortality. This outbreak killed upwards of 55% of live corals, reducing overall coral cover from 42.4% in 2005 down to just 19.1% in March 2006. Declines in coral cover were largely driven by widespread mortality of Acropora spp. which dominated reef assemblages prior to the outbreak. The extensive depletion of Acropora spp. greatly altered the coral composition as well as the physical structure of reef habitats. In the absence of any other major disturbances these coral communities are likely to quickly recover, but this outbreak highlights the ongoing contribution of A. planci to degradation of coral reef environments.