Gestational CMV infection also produces PVL in neonates. Injury pathway
Two major factors appear to be involved in the development of PVL:  (1) decreased blood or oxygen flow to the periventricular region (the white matter near the cerebral ventricles) and (2) damage to glial cells, the cells that support neurons throughout the nervous system. These factors are especially likely to interact in premature infants, resulting in a sequence of events that leads to the development of white matter lesions. The initial hypoxia (decreased oxygen flow) or ischemia (decreased blood flow) can occur for a number of reasons. Fetal blood vessels are thin-walled structures, and it is likely that the vessels providing nutrients to the periventricular region cannot maintain a sufficient blood flow during episodes of decreased oxygenation during development. Additionally, hypotension resulting from fetal distress or cesarean section births can lead to decreased blood and oxygen flow to the developing brain. These hypoxic-ischemic incidents can cause damage to the blood brain barrier (BBB), a system of endothelial cells and glial cells that regulates the flow of nutrients to the brain. A damaged BBB can contribute to even greater levels of hypoxia. Alternatively, damage to the BBB can occur due to maternal infection during fetal development, fetal infections, or infection of the newly delivered infant. Because their cardiovascular and immune systems are not fully developed, premature infants are especially at risk for these initial insults. Damage caused to the BBB by hypoxic-ischemic injury or infection sets off a sequence of responses called the inflammatory response.
Tumor extension
Extension of the tumor to the base of tongue reduces the chances of cure drastically. It also increases the chances of recurrence after treatment. Metastasis
Spread of cancer cells to local structures like tissues, vessels, large nerves and lymphatics worsens a patients prognosis.A study that analyzed the survival rate in HPV-related oropharynx carcinoma to that in HPV-unrelated oropharynx carcinoma. The study revealed that based on the HPV status of the patient, for STAGE III and STAGE IV oropharynx carcinoma, there was a discrepancy in survival after three years. The survival was 82% in HPV positive and then also 57% in HPV negative cancers. References


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