The main clinical challenge in reference to toxoplasmosis with HIV is its differentiation from cerebral lymphoma as also discussed in Chap. 30. In a series from Johns Hopkins in the pre-antiretroviral era (see Johnson, 1998), approximately 11 percent of AIDS patients developed a primary CNS lymphoma. In a patient with a cerebral nodule, if there has been no response to antibiotics (see below), stereotaxic brain biopsy may be necessary for diagnosis of lymphoma. There is an association of this type of CNS lymphoma with Epstein-Barr virus in AIDS patients. The prognosis of cerebral lymphoma in AIDS is considerably less favorable than in non-AIDS patients; the response to radiation therapy, methotrexate, and corticosteroids is short-lived, and survival is usually measured in months.
Antibody tests for toxoplasmosis may be obtained; the absence of IgG antibodies makes infection unlikely and raises the consideration of brain lymphoma. Also, if antitoxoplasmal therapy with pyrimethamine and sulfadiazine fails to reduce the size of the lesions within several weeks, another cause should be sought, again mainly lymphoma. In those patients who cannot tolerate the frequent side effects of pyrimethamine or sulfonamides (rash or thrombocytopenia), clindamycin may be of value. Recently, it has been suggested that positron emission tomography (PET) and other metabolic imaging techniques can identify lymphoma as the cause of a mass lesion in the HIV patient. The less frequent possibilities of tuberculous or bacterial brain abscess should be kept in mind if none of these avenues allow a confident diagnosis.
Progressive multifocal leukoencephalopathy This important brain infection with the JC virus appears regularly in patients with HIV, generally when CD4+ counts are below 50 cells/μL. In the past, the disorder had been closely associated with iatrogenic immunosuppression, mainly for hematologic malignancy and solid organ transplantation and ironically, this is now increasingly the case. As the name implies, there are areas of cerebral demyelination with characteristic changes in the oligodendrocytes. This disease is discussed further on in this chapter.
Cytomegalovirus Among the nonfocal neurologic complications of AIDS, the most common are CMV and cryptococcal infections. At autopsy, about one-third of HIV patients are found to be infected with CMV. However, the contribution of this infection to the total clinical picture is often uncertain. Despite this ambiguity, certain features have emerged as typical of CMV encephalitis in the HIV patient. According to Holland and colleagues, late in the course of AIDS and usually concurrent with CMV retinitis, the encephalopathy evolves over 3 to 4 weeks. Its clinical features include an acute confusional state or delirium combined in a small proportion of cases with cranial nerve signs including ophthalmoparesis, nystagmus, ptosis, facial nerve palsy, or deafness. In one of our patients, there were progressive oculomotor palsies that began with light-fixed pupils.
Pathologic specimens and MRI show the process to be concentrated in the ventricular borders, especially evident as T2 signal hyperintensity in these regions. The lesions may extend more diffusely through the adjacent white matter and be accompanied by meningeal enhancement by gadolinium in a few cases. Extensive destructive lesions have also been reported; this has been true in two of our own cases. Such lesions may be associated with hemorrhagic changes in the CSF in addition to showing an inflammatory response. CMV may also produce a painful lumbosacral polyradiculitis in AIDS (Chap. 43).