Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcineurin plays an important role in the development of neuronal excitability, modulation of receptor's function and induction of apoptosis in neurons. It has been established in kindling models that status epilepticus induces brain focal edema and astrocyte activation. However, the role of calcineurin in brain focal edema and astrocyte activation in status epilepticus has not been fully understood. In this study, we employed a model of lithium-pilocarpine-induced status epilepticus and detected calcineurin expression in hippocampus by immunoblotting, brain focal edema by non-invasive magnetic resonance imaging (MRI-7T) and astrocyte expression by immunohistochemistry. We found that the brain focal edema was seen at 24 h after status epilepticus, and astrocyte expression was obviously seen at 7 d after status epilepticus. Meanwhile, calcineurin expression was seen at24 h and retained to 7 d after status epilepticus. A FK506, a calcineurin inhibitor, remarkably suppressed the status epilepticus-induced brain focal edema and astrocyte expression. Our data suggested that calcineurin overexpression plays a very important role in brain focal edema and astrocyte expression. Therefore, calcineurin may be a novel candidate for brain focal edema occurring and intracellular trigger of astrogliosis in status epilepticus.
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PMID:Increased calcineurin expression after pilocarpine-induced status epilepticus is associated with brain focal edema and astrogliosis. 2600 Sep 33

BACKGROUND Central nervous system complications after transplantation occur in up to 40% of recipients and these complications are associated with increased length of hospital stay and mortality. Catatonia is a neuropsychiatric clinical syndrome which has been described in case reports and in a small case series as occurring in the immediate post-solid organ transplantation (SOT) period, and it has been attributed to calcineurin inhibitor neurotoxicity, psychological vulnerability, and depression. Among transplant recipients, the incidence of catatonia is unknown; it may be under diagnosed in part due to a broad differential diagnosis in the post-transplantation setting, which includes hypoactive delirium, non-convulsive status epilepticus, drug toxicity, conversion disorder, and volitional uncooperativeness. CASE REPORT We present 2 cases of catatonia diagnosed in liver allograft recipients. We also reviewed current literature for cases of catatonia among SOT recipients. We provide provisional evaluation and management strategies of recipients with clinical concern for catatonia. Catatonia generally occurs within the few first days after liver transplantation, and presents with staring, immobility, or mutism, but is also associated with other neurological and psychiatric symptoms. Catatonia can be successfully treated with intravenous lorazepam, and thus, modifying immunosuppressive regimens may be avoidable. Medications to treat catatonia are generally tapered over weeks to months, and psychiatric follow-up is indicated. The early post-liver transplantation period may be a state of relative deficiency in GABA (gamma-aminobutyric acid) signaling, predisposing liver transplant recipients in particular to post-transplantation catatonia. CONCLUSIONS Despite difficulties in establishing the diagnosis, catatonia after liver transplantation was rapidly responsive to intravenous lorazepam, indicating that changing immunosuppressants may be avoidable.
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PMID:Catatonia After Liver Transplantation. 3015 Jun 6