Seizures and treatment for cerebral cysticercosis.
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Biomedical subjects
Publications and source records attributed to A C White.
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Neurocysticercosis due to parenchymal cysts carries a good prognosis regardless of therapy. Extraparenchymal neurocysticercosis (including ventricular, spinal, and subarachnoid types) carries a poorer prognosis. Most extraparenchymal cases present with hydrocephalus. Medical treatment alone in doses and schedules developed for parenchymal disease is frequently unsuccessful. For ventricular disease, most cases can be managed with shunting procedures either alone or together with the administration of antiparasitic agents (e.g., praziquantel or albendazole), without extirpation of the cysts. Subarachnoid disease was formerly associated with a case fatality rate of about 50%. However, with the combination of shunting procedures for hydrocephalus, antiparasitic agents, and, in some cases, surgical extirpation of the cysts, the prognosis is much improved. Spinal cysticercosis can be either leptomeningeal (which responds like subarachnoid disease) or intramedullary. For all forms of neurocysticercosis, the role of antiparasitic agents needs to be better defined.
Early passaged bovine pulmonary artery endothelial cells exposed to 0.1-2.0 ng/ml transforming growth factor-beta 1 (TGF-beta 1) showed concentration-dependent growth inhibition, as assessed by [3H]thymidine labeling and cell counts, over a 96-h interval. Most of the inhibition of [3H]thymidine labeling measured at 96 h persisted when the medium was replaced with TGF-beta 1-free medium after 24 h, but the inhibition of labeling was prevented by the presence of anti-TGF-beta 1 antibody in the replacement medium. Additions of 2 mM cysteine, 1 mM cystine, or 2 mM N-acetylcysteine at the time of the initial addition of TGF-beta 1 blocked the inhibitory effect of TGF-beta 1 on [3H]-thymidine labeling when this was assessed after 72-96 h, but not at earlier times. Prevention of the inhibitory effect on cellular proliferation produced by cysteine, cystine and N-acetylcysteine was associated with elevation of cellular glutathione that was present at 48-96 h. There was no evidence for direct inactivation of TGF-beta 1 by the thiol-amino acids. Conditioned medium from TGF-beta 1-treated endothelial cells inhibited proliferation of mink lung carcinoma (CCL64) cells, supporting a previously reported concept of autocrine production of TGF-beta 1 by the endothelial cells. The inhibitory action of the conditioned medium was partially prevented when 1 mM cysteine was added during conditioning. Thus, TGF-beta 1 treatment of endothelial cells appears to set off autocrine production by these cells of TGF-beta 1 that perpetuates the inhibition of cellular proliferation. Replenishment of cellular glutathione with thiol-amino acids counteracts the growth-inhibitory effect of TGF-beta 1 through a currently undefined mechanism.
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Human neurocysticercosis results from infestation of the central nervous system with the metacestode form (tissue cyst) of Taenia solium. Cysticercosis is being increasingly recognized as a cause of neurologic symptoms in residents and emigrants from developing countries. Taeniid parasites have developed elaborate mechanisms to persist in the tissues of their intermediate hosts. The invasive larvae, termed oncospheres, are susceptible to antibody and complement. However, by the time that the host has generated an antibody response, the parasites have begun to transform to the more resistant metacestode form. The metacestodes also have means of evading complement-mediated destruction, including paramyosin, which inhibits C1q; taeniaestatin, which inhibits both classical and alternate pathways (likely by inhibiting factor D and C3 esterase); and sulfated polysaccharides, which activate complement away from the parasite. Similarly, antibody does not seem to be able to kill the mature metacestode. The parasites may even stimulate the host to produce antibody, which could be bound via Fc receptors, and used as a source of protein. Finally, taeniaestatin and other parasite molecules may interfere with lymphocyte proliferation and macrophage function, thus paralyzing the cellular immune response. Because the symptoms of neurocysticercosis are typically associated with a brisk inflammatory response, we hypothesize that disease is primarily the result of injured or dying parasites. This hypothesis raises important questions in assessing the role of chemotherapy in the management of neurocysticercosis as well as in evaluation of clinical trials, most of which have been uncontrolled.
Acquisition of autoanalgesia (behaviorally activated antinociception) was assessed across 7 consecutive days by shocking rats 10 sec after the determination of their tail-flick latencies. Thus the effect of conditioned fear on antinociception was being investigated, since each shock preceded the subsequent tail-flick test by 24 h. Autoanalgesia was acquired by the second fear-conditioning trial. Although pretreatment with naltrexone or diazepam had no effect, spinal cord transection at the thoracic level effectively obviated autoanalgesia. Investigations of opiate and opioid binding indicated significantly less binding in the fear-conditioned rats as well as an inverse relationship between binding and antinociception. These changes in binding are suggestive of partial mediation of autoanalgesia by an endogenous opiate peptide that is released by the fear-conditioning procedure.
A review of the literature suggests that body temperature may rise when a person is under emotional stress. The term "psychogenic fever" has been applied to this phenomenon. A study of temperature and pulse rate of psychiatric patients diagnosed predominantly as neurotic in a university teaching hospital was undertaken. Changes in pulse rate indicated that the period before ward rounds was more stressful than other times of the day. However, psychogenic fever in these patients was not found. One case of factitious fever was uncovered during the study.
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Infection with Histoplasma capsulatum in 58 patients whose immune responses were suppressed (Immunosuppressed patients) (16 from the present series and 42 described previously) was analyzed. The most common underlying diseases were Hodgkin's disease (29 per cent), chronic lymphocytic leukemia (19 per cent) and acute lymphocytic leukemia (17 per cent). Sixty-three per cent of the patients had received cytotoxic drugs, and 57 per cent had taken corticosteroids. Widely disseminated infection occurred in 88 per cent of the patients, with predominant involvement of lungs and organs of the reticuloendothelial system. Localized pulmonary infection was present in the remaining patients. The most useful diagnostic method was bone marrow biopsy with microscopic examination for the intracellular yeast form of H. capsulatum. Biopsy of oral lesions, lung, liver and lymph node also proved diagnostically helpful. Growth of H. capsulatum in culture was frequently too slow to be beneficial in diagnosing histoplasmosis in ill patients. Serologic methods were of little diagnostic help in this population of immunosuppressed patients. The response to amphotericin B therapy was excellent (6.7 per cent mortality rate) in those patients in whom the diagnosis was established early and in whom a full course of antifungal therapy could be given. In contrast, the mortality rate in patients who received no antifungal therapy or less than 1 g of amphotericin B was 100 per cent.
An enzyme-linked immunosorbent assay was developed to detect rabbit immunoglobulin G antibodies against purified lipopolysaccharide of the rough Re mutant of Salmonella minnesota. The time necessary for each step was investigated, and this resulted in a test that could be completed in 1 working day. Serial dilutions of rabbit sera drawn throughout immunization with the Re mutant revealed an elimination of the prozone effect upon prolonged immunization. We interpret this to demonstrate an increase in immunoglobulin G affinity for the lipopolysaccharide on prolonged immunization. We propose that the enzyme-linked immunosorbent assay prozone effect be investigated for use as a measure of antibody affinity.
The correlation between serum and saliva lithium levels in patients undergoing lithium prophylaxis therapy is discussed. Although a high correlation can be obtained, there is an unacceptably high individual variation of paired results. Two strategies were used in an attempt to improve the reliability of saliva as a predictor of serum levels. A naturally occurring marker in saliva and serum was used. This showed high correlation but still did not prevent large sporadic differences. Serially paired results in individual patients also showed occasional excessive variation. Although saliva lithium has been used for monitoring when serum assessment is impracticable, it is considered that it is, as yet, an unreliable technique.
An epidural abscess caused by Aspergillus fumigatus occurred in a recipient of a cadaveric, renal allograft. The patient had persistent back pain and a peripheral neuropathy that involved the lower extremities. Signs of spinal cord compression evolved. No definite portal of entry was found. Diagnosis was made by histologic examination and culture of a biopsy specimen. Therapy, consisting of aggressive surgical debridement, intravenous amphotericin B, and oral flucytosine was unsuccessful in eradicating the organism. At postmortem examination, Aspergillus was identified at the abscess site. To our knowledge, aspergillosis presenting as an epidural abscess in the immunosuppressed, renal transplant recipient has not previously been reported and should be considered in the differential diagnosis of back pain and peripheral neuropathy in such a patient.
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