Acta Neuropathol (1988) 76:101 - 106 Ar Neuropatholoslca 9 Springer-Verlag1988 Case report Cytomembranous inclusions in the brain of a patient with the acquired immunodeficiency syndrome S. Lee 1, C. Harris 2, A. Hirsehfelda, and D. W. Dickson 1 Departments of ~ Pathology (Neuropathology) and The Rose F. Kennedy for Research in Mental Retardation and Human Development, 2 Internal Medicine (Division of Infectious Diseases), and 3 Neurosurgery, Albert Einstein College of Medicine and The Bronx Municipal Hospital Center, 1300 Morris Park Avenue, Bronx, NY 10461, USA Summary. Ultrastructural studies c f cells and tissues in the acquired immunodeficiency syndrome (AIDS) have revealed two distinct cytomembranous inclusions referred to as "tubuloreticular inclusions" (TRI) and "confronting cylindrical cisterns" (CCC). TRI are found most often in leukocytes and endothelial cells in conditions with elevated levels of' alpha-interferon, such as viral infections, autoimmune diseases and cer- tain neoplasms. On the other hand, CCC are detected almost exclusively in mononuclear inflammatory cells and are limited to a few conditions, of which AIDS is the most common. CCC have been proposed as an ultrastructural marker for human immunodeficiency virus (HIV) infection. We describe CCC in mononu- clear inflammatory ceils in the brain of a patient with AIDS. Finding CCC in brain tissue with no other specific feature such as multinucleated giant cells, nevertheless, should alert the neuropathologist to the possibility that the patient might have AIDS. Key words: AIDS - Confronting cylindrical cis- terns - Cytomembranous inclusions - Tubuloretic- ular inclusions - Ultrastructure Central nervous system (CSN) manifestations are fre- quent in acquired immunodeficiency syndrome (AIDS) [1, 2, 4, 15, 19, 21, 25, 30, 31, 33]. Patients often develop signs and symptoms of progressive neurological deterioration along with radiological evi- dence of diffuse brain atrophy and atl;enuation of deep cerebral white matter [20]. The mechanism of CNS involvement is unknown since the CD4 molecule, which acts as the viral receptor for HIV [12, 16, 18], has not been reported in intrinsic cells of the CNS; however, messenger RNA for CD4 has been detected Offprint requests to: D. W. Dickson (address see above) in brain [35]. There is increasing evidence that mono- cyte-macrophages may be the mediators of some of the pathology of AIDS [8, 9], and that they may be instrumental in CNS manifestations [7, 8, 34, 36]. The most frequent pathological finding in patients with subacute encephalitis of AIDS is a nonspecific leukoencephalopathy [13], often associated with mononuclear inflammatory cell infiltrates and multi- nucleated giant cells [3, 5, 29]. We describe ultra- structural findings of mononuclear inflammatory cells in the white matter of a patient with AIDS that may be of diagnostic utility in future cases. Case history This 41-year-old Hispanic, homosexual man had a 2-month his- tory of Pneumocystic carinii pneumonia before transfer to the Bronx Municipal Hospital Center from another hospital where he was being evaluated for brain lesions. He originally presented with fever and headache. Computed tomography (CT) of the head showed a right occipital lesion. He did not respond to initial therapy with pyrimethamine and triple sulfa. Approximately 1 week prior to transfer, he developed generalized seizures. A CT at that time revealed increased size of the fight occipital lesion and a new right parietal lesion; both lesions were contrast- enhancing with edema. On admission he had a temperature of 105~ generalized lymphadenopathy, mild left hemiparesis, and left homonymous hemianopsia. Pertinent laboratory findings included hemoglobin 10.2 g/100 ml, hematocrit 28.2%, white blood cell count 1800/ram3 and platelet count 129,000/mm3. Lumbar puncture revealed an opening pressure of 200 cm. The CSF glucose was 59 mg/100 ml, and the protein was 30 mg/100 ml. There were 119 erythrocytes and no leukocytes. The India ink preparation and cryptococcal antigen were negative. All cultures were negative. Serum and CSF anti-toxoplasma IgG immunofluorescent antibody titers were negative. The patient was treated empirically with anti-toxoplasma medication; however, he remained febrile and leukopenic. Blood cultures a week following admission were positive for Cryptococcus neoformans: however, repeat lumbar puncture failed to reveal cryptococcal organisms or antigen. CSF cultures were also negative. Anti-toxoplasma medication was stopped and amphotericin was started. Two weeks later a CT scan