| Stage 1 |
Closely fits original racemose NCC description Base of brain and Sylvian fissure involvement common Fluid filled cystic masses involving one or more subarachnoid spaces Frequently untreated, first presentation, or remotely treated with regrowth Symptoms and signs often related to mass effect Inflammation (arachnoiditis) usually present but does not the predominate the disease pathophysiology. It may be contributing to symptoms and disease at this point. CSF shows high cestode antigen and T. solium DNA, pleocytos is usually lymphocytic predominance, sometimes with increased eosinophils |
| Stage 2 |
Inflammation dominates the pathophysiologic mechanisms Cyst degeneration from treatment or natural evolution generates arachnoiditis directed to sites of degenerating (ed) cysts The overall picture is one of inflammation in the presence of unaffected, partially affected, or fully degenerated cysts. At times, there may be an unexplained, localized or diffuse arachnoiditis without the presence of cysts Lacunar infarcts are a major cause of morbidity Hydrocephalus is frequent complication as is the development of localized signs and symptoms at sites of involvement Decreased parasite mass leads to lower but still detectable cestode antigen and DNA levels; pleocytosis present sometimes with increased eosinophils |
| Stage 3 |
Resolving or resolved disease, residual but decreasing inflammation as judged by decreased or no enhancement or decreased or no CSF pleocytosis Sequelae of prior inflammation includes hydrocephalus, brain atrophy, residual of stroke, nerve entrapment, arachnoid cyst, calcifications within cisterns or following the middle cerebral arteries |
