The forces responsible for the movement of the lateral body wall folds are poorly understood, and a better understanding of these forces would help to explain why gastroschisis occurs mostly to the right of the umbilicus, while other ventral body wall defects occur in the midline.At least six hypotheses have been proposed for the pathophysiology:

Failure of mesoderm to form in the body wall
Rupture of the amnion around the umbilical ring with subsequent herniation of bowel
Abnormal involution of the right umbilical vein leading to weakening of the body wall and gut herniation
Disruption of the right vitelline (yolk sac) artery with subsequent body wall damage and gut herniation
Abnormal folding of the body wall results in a ventral body wall defect through which the gut herniates
Failure to incorporate the yolk sac and related vitelline structures into the umbilical stalkThe first hypothesis does not explain why the mesoderm defect would occur in such a specific small area. The second hypothesis does not explain the low percentage of associated abnormality compared with omphalocele. The third hypothesis was criticized due to no vascular supplement of anterior abdominal wall by umbilical vein. The fourth hypothesis was commonly accepted, but it was later shown that the right vitelline artery (right omphalomesenteric artery) did not supply the anterior abdominal wall in this area. More evidence is needed to support the fifth hypothesis.
The motor output is amplified due to the missing limb; therefore, the patient may experience the overflow of information as pain. The patient contains repressed memories from previous motor commands of clenching the hand and sensory information from digging their nails into their palm. These memories remain due to previous neural connections in the brain. Phantom limb syndrome
The term "phantom limb" was coined by physician Silas Weir Mitchell in 1871. For many years, the dominant hypothesis for the cause of phantom limbs was irritation in the peripheral nervous system at the amputation site (neuroma). By the late 1980s, Ronald Melzack had recognized that the peripheral neuroma account could not be correct, because many people born without limbs also experienced phantom limbs. According to Melzack the experience of the body is created by a wide network of interconnecting neural structures, which he called the "neuromatrix".Pons and colleagues (1991) at the National Institutes of Health (NIH) showed that the primary somatosensory cortex in macaque monkeys undergoes substantial reorganization after the loss of sensory input.Hearing about these results, Vilayanur S. Ramachandran hypothesized that phantom limb sensations in humans could be due to reorganization in the human brains somatosensory cortex. Ramachandran and colleagues illustrated this hypothesis by showing that stroking different parts of the face led to perceptions of being touched on different parts of the missing limb. Later brain scans of amputees showed the same kind of cortical reorganization that Pons had observed in monkeys.Maladaptive changes in the cortex may account for some but not all phantom limb pain.