The  sciatic nerve, also called the ischiadic nerve, is a large nerve in humans and other vertebrate animals which is the largest branch of the sacral plexus and runs alongside the hip joint and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve has no cutaneous branches for the thigh. This nerve provides the connection to the nervous system for the skin of the lateral leg and the whole foot, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus. Structure
In humans, the sciatic nerve is formed from the L4 to S3 segments of the sacral plexus, a collection of nerve fibres that emerge from the sacral part of the spinal cord. The lumbosacral trunk from the L4 and L5 roots descends between the sacral promontory and ala and the S1 to S3 roots emerge from the ventral sacral foramina. These nerve roots unite to form a single nerve in front of the piriformis muscle. The nerve passes beneath piriformis and through the greater sciatic foramen, quitting the pelvis. : 422–4  From here, it travels down the posterior thigh to the popliteal fossa.
Pathophysiology
The progression of heart failure is associated with left ventricular remodeling, which manifests as gradual increases in left ventricular end-diastolic and end-systolic volumes, wall thinning, and a change in chamber geometry to a more spherical, less elongated shape. This process is usually associated with a continuous decline in ejection fraction. The concept of cardiac remodeling was initially developed to describe changes that occur in the days and months following myocardial infarction. Compensation effects
As DCM progresses, two compensatory mechanisms are activated in response to impaired myocyte contractility and reduced stroke volume:
Frank-Starling law
Neurohormonal feedback, via activation of the sympathetic nervous system and the renin-angiotensin system.These responses initially compensate for decreased cardiac output and maintain those with DCM as asymptomatic. Eventually, however, these mechanisms become detrimental, intravascular volume becomes too great, and progressive dilatation leads to heart failure symptoms. Computational models
Cardiac dilatation is a transversely isotropic, irreversible process resulting from excess strains on the myocardium. A computation model of volumetric, isotropic, and cardiac wall growth predicts the relationship between cardiac strains (e.g.