The condition was first described between 1888 and 1891. Signs and symptoms
The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth (i.e., the earlier a baby is born, the later signs of NEC are typically seen).Initial symptoms include feeding intolerance and failure to thrive, increased gastric residuals, abdominal distension, and bloody stools. Symptoms may progress rapidly to abdominal discoloration with intestinal perforation and peritonitis and systemic hypotension requiring intensive medical support. Cause
The exact cause is unclear. Several risk factors have been implicated:

Maternal factors
Acid-suppressing medications
Chorioamnionitis
Cocaine abuse
In utero growth restriction
Increased body mass index
Intrahepatic cholestasis during pregnancy
Lack of prenatal steroids
Mode of delivery
Placental abruption
Pre-eclampsia
Smoking

Main risk factors
Low birth weight
Prematurity
Formula feeding (bovine based)
Intestinal dysbiosis

Other risk factors
Acute hypoxia
Antibiotic exposure
Blood transfusions
Cardiac anomalies
Neonatal anemia
Poor intestinal perfusion
Prolonged use of indomethacin for patent  ductus arteriosus closure

Diagnosis
Diagnosis is usually suspected clinically, but often requires the aid of diagnostic imaging, most commonly radiography, which can show the intestines and may show areas with death tissue or a bowel perforation.
CNTF has numerous trophic roles in motor neurons in the peripheral nervous system including the prevention of atrophy of dennervated tissue and the prevention of degeneration and death of motor neurons after nerve injury. (frostick)  In sciatic motor neurons both CNTF receptor mRNA expression and CNTF receptor is increased after injury for a prolonged time frame compared to the short time frame in the central nervous system suggesting a role for CNTF in nerve regeneration.Insulin-like growth factors (IGFs) have been shown to increase the rate of peripheral nervous system axon regeneration. IGF-I and IGF-II mRNA levels are significantly increased distal to the site of crush injury in rat sciatic nerves. At the site of nerve repair, locally delivered IGF-I can significantly increase the rate of axon regeneration within a nerve graft and help expedite functional recovery of a paralyzed muscle. Role of neurite-promoting factors
Neurite promoting factors include many extracellular matrix proteins produced by Schwann cells at the distal stump including fibronectin and laminin. Fibronectin are components of the basal lamina and promote neurite growth and adhesion of the growth cone to the basal lamina. In regenerating neural cells, neurite promoting factors play a role in adhesion of the axon and include neural cell adhesion molecule (N-CAM) and N-cadherin. Treatment
Unless otherwise demonstrated, nerve injuries are commonly irreversible, and therefore complete treatment is rather difficult, though still possible and hence lifelong management of disabilities arising due to nerve injuries is necessary. Nerve regeneration therapies
Electrical stimulation can promote nerve regeneration.