All of the following result in damage to the CNS:
Direct mechanical damage to neural tissue from the worms motion
Toxic byproducts such as nitrogenous waste
Antigens released by dead and living parasites

Eosinophilic meningitis
Although the clinical disease caused by Angiostrongylus invasion into the CNS is commonly referred to as "eosinophilic meningitis", the actual pathophysiology is of a meningoencephalitis with invasion not just of the meninges, or superficial lining of the brain, but also deeper brain tissue. Initial invasion through the lining of the brain, the meninges, may cause a typical inflammation of the meninges and a classic meningitis picture of headache, stiff neck, and often fever. The parasites subsequently invade deeper into the brain tissue, causing specific localizing neurological symptoms depending on where in the brain parenchyma they migrate. Neurologic findings and symptoms wax and wane as initial damage is done by the physical in-migration of the worms and secondary damage is done by the inflammatory response to the presence of dead and dying worms. This inflammation can lead in the short term to paralysis, bladder dysfunction, visual disturbance, and coma and in the long term to permanent nerve damage, mental retardation, nerve damage, permanent brain damage, or death.Eosinophilic meningitis is commonly defined by the increased number of eosinophils in the cerebrospinal fluid (CSF). In most cases, eosinophil levels rise to 10 or more eosinophils per μl in the CSF, accounting for at least 10% of the total CSF leukocyte (white blood cell) count.
The chemical analysis of the CSF typically resembles the findings in "aseptic meningitis" with slightly elevated protein levels, normal glucose levels, and negative bacterial cultures. Presence of a significantly decreased glucose on CSF analysis is an indicator of severe meningoencephalitis and may indicate a poor medical outcome. Initial CSF analysis early in the disease process may occasionally show no increase of eosinophils, only to have classical increases in eosinophils in subsequent CSF analysis. Caution should be advised in using eosinophilic meningitis as the only criterion for diagnosing angiostrongylus infestation in someone with classic symptoms, as the disease evolves with the migration of the worms into the CNS.Eosinophils are specialized white blood cells of the granulocytic cell line, which contain granules in their cytoplasm. These granules contain proteins that are toxic to parasites. When these granules degranulate, or break down, chemicals are released that combat parasites such as A. cantonensis. Eosinophils, which are located throughout the body, are guided to sites of inflammation by chemokines when the body is infested with parasites such as A. cantonensis. Once at the site of inflammation, type 2 cytokines are released from helper T cells, which communicate with the eosinophils, signaling them to activate. Once activated, eosinophils can begin the process of degranulation, releasing their toxic proteins in the fight against the foreign parasite.