Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients who had cerebral aspergillosis with massive intracerebral hemorrhage were presented. Case I was a 59-year-old woman who had slight mental retardation. There was swelling in the left forehead, from which mucosal cysts of frontal sinus had been removed 2 years before her admission. She had a diagnosis of subdural abscess and radical operation was performed. Aspergillus was found in the abscess histologically. Three months after the operation, CT scan revealed multiple abscess in bilateral frontal lobe. When she lost consciousness suddenly 4 months after the operation, CT scan showed a huge intracerebral hematoma. Case 2 was a 16-year-old girl who suffered from immunological dysfunction caused by more than 6 months antibiotics-steroid treatment for pneumonitis. She lost her consciousness after complaints of severe headache. CT scan showed a heterogeneous high density area with severe brain edema in the left temporal lobe. The removal of hematoma was performed immediately. The level of her consciousness improved, but she died of the complication of DIC and renal failure 14 days after the hemorrhage. Autopsy revealed a number of aspergillomas in lungs, kidneys, gastrointestinal tract, liver and pancreas. Marked necrosis and a number of aspergillus hyphae which invaded and penetrated the wall of cerebral vessels were found in the brain tissue. It was presumed that such a huge intracerebral hematoma was caused by direct invasion and penetration into the brain of aspergillus from the blood vessels. The diagnosis of cerebral aspergillosis is made mainly by the pathological examination of the tissue obtained at surgery or autopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of cerebral aspergillosis with intracerebral hemorrhage]. 322 71

Neuronal migration disorders (NMDs) can be associated with neurological dysfunction such as mental retardation, and clusters of disorganized cells (heterotopias) often act as seizure foci in medically intractable partial epilepsies. Methylazoxymethanol (MAM) treatment of pregnant rats results in neuronal heterotopias in offspring, especially in hippocampal area CA1. Although the neurons in dysplastic areas in this model are frequently hyperexcitable, the precise mechanisms controlling excitability remain unclear. Here, we used IR-DIC videomicroscopy and whole cell voltage-clamp techniques to test whether the potent anti-excitatory actions of neuropeptide Y (NPY) affected synaptic excitation of heterotopic neurons. We also compared several synaptic and intrinsic properties of heterotopic, layer 2-3 cortical, and CA1 pyramidal neurons, to further characterize heterotopic cells. NPY powerfully inhibited synaptic excitation onto normal and normotopic CA1 cells but was nearly ineffective on responses evoked in heterotopic cells from stimulation sites within the heterotopia. Glutamatergic synaptic responses on heterotopic cells exhibited a comparatively small, D-2-amino-5-phosphopentanoic acid-sensitive, N-methyl-D-aspartate component. Heterotopic neurons also differed from normal CA1 cells in postsynaptic membrane currents, possessing a prominent inwardly rectifying K(+) current sensitive to Cs(+) and Ba(2+), similar to neocortical layer 2-3 pyramidal cells. CA1 cells instead had a prominent Cs(+)- and 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyrimidinium chloride-sensitive I(h) and negligible inward rectification, unlike heterotopic cells. Thus heterotopic CA1 cells appear to share numerous physiological similarities with neocortical neurons. The lack of NPY's effects on intra-heterotopic inputs, the small contribution of I(h), and abnormal glutamate receptor function, may all contribute to the lowered threshold for epileptiform activity observed in hippocampal heterotopias and could be important factors in epilepsies associated with NMDs.
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PMID:NPY sensitivity and postsynaptic properties of heterotopic neurons in the MAM model of malformation-associated epilepsy. 1242 9

A 12-year-old boy with mental retardation and cerebral palsy developed hyperthermia during dental treatment performed while he was conscious. During the treatment, he was highly excited, and shortly after completion of the procedure, general muscular spasms occurred. His axillary temperature was 41.6 degrees C then. He was transferred to another general hospital and there he was judged to have become afebrile and was discharged. His condition deteriorated during the night, and he was readmitted to the same hospital the following morning. The patient did not respond to the therapy and died from multiple organ failure on the 13th day. It was thought that hyperthermia had led to rhabdomyolysis and DIC. The cause of death is discussed. Hyperthermia in a handicapped patient is not always transient or benign, and can be life threatening.
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PMID:Fatal hyperthermia due to dental treatment. 1650 53