Pathophysiology
Two distinct but related processes are considered to be involved in the development of obesity: sustained positive energy balance (energy intake exceeding energy expenditure) and the resetting of the body weight "set point" at an increased value. The second process explains why finding effective obesity treatments has been difficult. While the underlying biology of this process still remains uncertain, research is beginning to clarify the mechanisms.At a biological level, there are many possible pathophysiological mechanisms involved in the development and maintenance of obesity. This field of research had been almost unapproached until the leptin gene was discovered in 1994 by J. M. Friedmans laboratory. While leptin and ghrelin are produced peripherally, they control appetite through their actions on the central nervous system. In particular, they and other appetite-related hormones act on the hypothalamus, a region of the brain central to the regulation of food intake and energy expenditure. There are several circuits within the hypothalamus that contribute to its role in integrating appetite, the melanocortin pathway being the most well understood. The circuit begins with an area of the hypothalamus, the arcuate nucleus, that has outputs to the lateral hypothalamus (LH) and ventromedial hypothalamus (VMH), the brains feeding and satiety centers, respectively.The arcuate nucleus contains two distinct groups of neurons. The first group coexpresses neuropeptide Y (NPY) and agouti-related peptide (AgRP) and has stimulatory inputs to the LH and inhibitory inputs to the VMH.
To compensate, the large torque producing global muscles are used to stabilize the spine.In one study, patients are taught to train the co-contraction of deep abdominal muscles and lumbar multifidus in static postures, functional tasks and aerobic activities. This technique was shown to reduce pain and functional disability when compared to other conservative treatments. These results also had a long- term effect in reducing levels of pain and functional disability. This is because motor programming eventually became automatic, and conscious control was no longer needed to contract the deep abdominal muscles during activities. Activity restriction
Activity restriction of spondylolysis is advised for a short period of time once the patient becomes symptomatic, followed by a guided physical therapy program. Once spondylolysis has been diagnosed, treatment often consists of a short rest period of two to three days, followed by a physical therapy program. There should be restriction of heavy lifting, excessive bending, twisting and avoidance of any work, recreational activities or participation in sport that causes stress to the lumbar spine. Activity restriction can help eliminate and control a patients symptoms so they are able to resume their normal activities. Activity restriction is most commonly used in conjunction with other rehabilitation techniques including bracing. Bracing
Acute spondylolysis is most commonly treated through the use of an antilordotic brace (Boston brace) to control and limit spinal movement, and reduce stress on the injured spinal segment. Bracing immobilizes the spine in a flexed position for a short period to allow healing of the bony defect in the pars interarticularis.