Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cases presented here, along with a preliminary body of clinical literature, suggest that, in conjunction with other factors, cyclosporine has an etiologic role in the production of a variety of organic mental disorders, including delirium, generalized anxiety disorder, hallucinosis, and organic mood disorder-depressed. The cases in this report were chosen in part because they illustrate definable organic syndromes. Other transplant recipients may experience less severe or isolated symptoms, such as sleep-wake reversal, insomnia, anxiety, lethargy, or mild confusional states that do meet full criteria for organic mental syndrome but that appear to be related to cyclosporine. Persecutory delusions may also occur in both floridly delirious patients and in patients with only minimal disorientation. Mental state aberrations most commonly begin within 2 weeks of treatment with cyclosporine, and, frequently, most acute symptoms resolve within a few weeks of onset. However, in more severely delirious patients or in patients with medical courses complicated by other problems, symptoms may continue longer. In particular, difficulties with memory and with the acquisition of new information may persist for several weeks. Less commonly, mental syndromes may also occur following longer periods of treatment with cyclosporine. Individual vulnerability appears to vary widely, and many patients demonstrate mental complications at cyclosporine levels that are in the moderate therapeutic range for immunosuppression. In addition, patients who have recently been started on cyclosporine and who demonstrate high therapeutic, rapidly rising, or toxic serum levels may be at greatest risk. Other risk factors may include intravenous administration, hypomagnesemia, hypocholesterolemia, and concurrent methylprednisolone bolus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporine-associated organic mental disorders in liver transplant recipients. 200 44

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11