Cesarean delivery, especially after prolonged labor, may cause the muscles of the uterus to become tired and stop contracting or contraction can be inhibited at the surgical site. Epidemiology
Uterine atony occurs during 1 in 40 births in the United States and is responsible for at least 80% of cases of postpartum hemorrhage. Pathophysiology
The uterus is composed of an interconnected muscle fibers known as the myometrium. The blood vessels that provide the blood supply to the placenta pass through this muscle. After labor it is the contraction of these muscles that physically squeeze the blood vessels so that hemostasis can occur after the delivery of the fetus and the placenta. Local hemostatic factors like tissue factor type-1 plasminogen activator inhibitor and platelets and clotting factors aid in stopping the blood flow.This physiological contraction does not occur if the myometrium becomes atonic. Oxytocin is released continuously during labor to stimulate uterine muscle contraction so the that the fetus can be delivered and it is continued to be released after delivery to stop blood flow. If the oxytocin receptors become desensitized and no longer respond to the hormone then the uterus does not contract. The uterus can also be structurally damaged or distended to prevent contraction. Therefore, as placenta is delivered arteries are damaged and without the muscle contractions hemostasis cannot be reached.Blood loss is an expected part of labor and less than 500 mL is considered normal. Generally, primary PPH is classified as being more than 500 mL of blood lost in the first 24 hours following delivery.
The types of seizures associated with lissencephaly include:

persisting spasms
focal seizures
tonic seizures
atypical seizures
atonic seizures Other possible symptoms of lissencephaly include telecanthus, estropia, hypertelorism, varying levels of mental retardation, cerebellar hypoplasia, corpus callosum aplasia, and decreased muscle tone and tendon reflexes. Over 90% of children affected with lissencephaly have seizures.Patients with subcortical band heterotopia (another disorder associated with pachygyria) typically have milder symptoms and their cognitive function is closely linked to the thickness of the subcortical band and the degree of pachygyria present. Causes
Pachygyria is caused by a breakdown in the fetal neuronal migration process due to genetic or possibly environmental influences. The affected cerebral cortex will typically have only four developed layers instead of the normal six. One of the best known and most common types of neuronal migration disorders is lissencephaly, a diffuse cortical malformation relating directly to agyria and pachygyria. Incomplete neuronal migration during the early fetal brain development is the precursor to lissencephaly. Should neurons follow an abnormal migration during development possible cortical malformations include classical lissencephaly (as stated above) and subcortical band heterotopia with an agyria-pachygyria band spectrum.