Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebrovascular permeability to protein (CVP-p) was assessed during limbic seizures by injecting unrestrained rats intraperitoneally with kainic acid followed by intravenous horseradish peroxidase (HRP); animals survived approximately 1 h after seizure onset. Brains were processed for the blue HRP reaction product followed by light microscopic examination of sequential sagittal sections. In all cases kainate-induced seizures caused increased CVP-p within the thalamus, temporal hippocampal formation, and neocortex. Somewhat less frequently other limbic structures and the striatum were HRP-positive. A lamina-specific extravasation occurred in the dorsal hippocampus; reaction product occupied the mossy fiber zone of field CA3, a likely focus of kainate action. Extravasation of HRP also occurred within, or juxtaposed to, certain myelinated fiber bundles. Brains from animals treated as blanks (kainate but no HRP) were devoid of peroxidase activity, and in nonseizing animals HRP gained access only to circumventricular organs. Although regions of increased CVP-p partially covary with areas of increased electrical activity and glucose metabolism, neuronal activation occurs over a much greater volume of brain tissue than does CVP-p. A close relationship may exist between these circumscribed areas of protein extravasation and seizure foci. Both vasogenic and cytotoxic edema appear to be simultaneously present during kainate seizures.
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PMID:Increased cerebrovascular permeability to protein during systemic kainic acid seizures. 670 55

Unstimulated and stimulated whole and unstimulated and stimulated parotid saliva were collected from subjected in three groups: I, control; II, seizure subjects ingesting phenytoin and without gingival overgrowth; III, seizure subjects receiving phenytoin and with grades 1 and 2 gingival overgrowth. Unstimulated whole saliva was obtained from mentally retarded donors with grade 3 phenytoin associated gingival overgrowth. The samples were analyzed for protein, lysozyme, lactoperoxidase, lactoferrin and aggregation capacity towards Streptococcus sanguis. Differences occurred in the salivary composition of patients ingesting phenytoin. No deficiencies of flow rate, protein or the specific proteins were found in subjects ingesting phenytoin. Instead, the only changes in these parameters were greater concentrations or secretion rates. Several differences occurred only in subjects with gingival overgrowth. These latter differences were prominent in unstimulated whole saliva. The data demonstrate changes in the oral cavity environment of patients ingesting phenytoin. These differences, however, do not have an obvious relationship to development of phenytoin associated gingival overgrowth. Some of the salivary changes occurred in patients undergoing therapy for seizures both with phenytoin and with other drugs. Increased amounts of unstimulated whole saliva components likely are due to excess tissue rather than a phenytoin effect on salivary gland secretions. In addition, most of the changes in salivary composition would not be expected to produce an environment the encourages plaque accumulation.
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PMID:Salivary composition, phenytoin ingestion and gingival overgrowth. 694 8

The effects of hypoglycemia on cerebrovascular permeability to a protein, horseradish peroxidase (HRP), were studied in mice given 3 or 8 units of crytalline zinc insulin intraperitoneally. HRP (10 mg in 0.1 ml saline) was injected intravenously 15 to 20 minutes prior to sacrifice. Both mildly and severely hypoglycemic groups of mice showed a drastic reduction in the normal transit of HRP across cerebral arterioles. The number of normally-stained vessel segments and of HRP-filled endothelial vesicles decreased in insulin-treated mice. In the brains of severely hypoglycemic mice, however, increased parenchymal HRP accumulation occurred. A ruptured blood vessel was found in the center of one-fourth of the focal exudates examined. Electron microscopic examination revealed thrombin, sometimes extending through the vessel wall, and hemorrhage, yet inter-endothelial tight junctions remained intact. Seizures were associated with severe hypoglycemia in 6 out of 10 mice with serum glucose levels below 40 mg/100 ml following 8 units of insulin, but the number of focal exudates per brain was similar in all 10 mice. We conclude that insulin-induced hypoglycemia is associated with decreased HRP transit across cerebral arterioles, and that severe insulin shock is also accompanied by actual rupture of vessel walls and extravasation of blood and HRP into the parenchyma of the brain.
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PMID:Effects of insulin-induced hypoglycemia on cerebrovascular permeability to horseradish peroxidase. 698 50

Light and electron microscopy and quantitative estimates of pinocytotic activity in cerebral arterioles and capillaries were performed in two different rat models of altered blood-brain barrier permeability in order to determine the side of initially increased vesicular transport. Seizures were produced by 20 consecutive electroshocks, and ischemic neuronal damage was produced by a 30-minute period of combined right common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase was used to evaluate blood-brain barrier permeability. Serial 1micronm.sections showed an ateriole within most foci of horseradish peroxidase extravasation. There were areas of brain in both experimental groups in which the only permeable vessels were arterioles, and in one ischemic animal, the only permeable vessels were arterioles. Pinocytotic activity was determined in capillaries and arterioles and expressed as the number of horseradish peroxidase-containing pinocytotic vesicles per square millimeter of endothelial cytoplasmic area +/- standard error. The pinocytotic activity in capillaries and arterioles, respectively, was 12.2 +/- 5.4 and 6.7 +/- 3.0 in normal rats, 86.7 +/- 22.1 and 267 +/- 46.1 after seizures, and 52.7 +/- 10.6 and 91.2 +/- 33.2 following cerebral ischemia. These results indicate the importance of the arterioles in maintaining and altering the blood-brain barrier and suggest that abnormal blood-brain barrier permeability occurs first within the arteriole.
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PMID:The importance of cerebral arterioles in alterations of the blood-brain barrier. 740 36

Activation of the dorsal midbrain has a powerful anticonvulsant effect in the maximal electroshock model of epilepsy. The suppression of tonic seizures can be obtained most reliably from an area centred on the intercollicular nucleus overlapping into the deep layers of the superior colliculus and adjacent mesencephalic reticular formation. As part of a series of investigations to identify neural mechanisms responsible for mediating the anticonvulsant properties of the dorsal midbrain, the present study provides an anatomical description of the efferent projections of this region. Small amounts of wheatgerm agglutinin-horseradish peroxidase (10-30 nl of a 1% solution) were injected into the intercollicular nucleus and surrounding tissue. The resulting anterograde transport of the tracer was plotted on a set of standard atlas sections. Four major output pathways were identified: (i) an ipsilateral descending projection which had terminations in the microcellular tegmental nucleus, lateral and ventral pontine reticular nucleus pars oralis, ventrolateral tegmental nucleus, ventral and caudal pontine reticular nucleus pars caudalis, raphe magnus nucleus and the gigantocellular nucleus; (ii) a contralateral descending projection which for the most part targeted the same brainstem structures but with weaker terminal labelling; (iii) a projection to the contralateral dorsal midbrain with comparatively weak terminal label in the contralateral superior colliculus, intercollicular nucleus, periaqueductal gray, mesencephalic reticular formation and cuneiform area; (iv) ipsilateral ascending pathway with terminations in the red nucleus, zona incerta, peripeduncular area, parafascicular nucleus, lateral hypothalamus, parts of the pretectum and caudal thalamus. At a general level the dorsal midbrain anticonvulsant zone shares its major output projections and efferent targets with at least one of its near neighbours, including the superior colliculus, periaqueductal gray, the cuneiform nucleus and pedunculopontine nucleus. The possibility that anticonvulsant properties of the intercollicular area can simply be attributed to a unique set of efferent projections is therefore not supported by the anatomy.
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PMID:The dorsal midbrain anticonvulsant zone--II. Efferent connections revealed by the anterograde transport of wheatgerm agglutinin-horseradish peroxidase from injections centred on the intercollicular area in the rat. 754 3

Wheatgerm agglutinin-horseradish peroxidase (WGA-HRP) histochemistry was combined with post-embedding immunogold cytochemistry in order to establish whether the subthalamic nucleus (STN) gives origin to glutamate (Glu)-enriched nerve terminals in substantia nigra, pars reticulata (SNr). Two adult cats served as normal controls and in two other animals crystalline WGA-HRP had been implanted bilaterally in STN. In all four animals ultrathin sections from SN were subjected to an immunogold procedure using antiserum raised against either Glu or gamma-aminobutyric acid (GABA). In some experiments the sections were subjected to consecutive incubations with both GABA and Glu antisera. These two antisera label two morphologically distinct types of boutons in SNr. The GABA antiserum labels boutons with pleomorphic vesicles, and they establish symmetrical synaptic contacts, mainly with dendritic shafts and spines, and occasionally with cell bodies. The Glu antiserum labels boutons with vesicles which are smaller and more uniform with regard to size and shape than those seen in the GABA-labelled boutons. The Glu-labelled boutons are engaged in asymmetrical synaptic contacts mainly with dendritic shafts and more rarely with cell bodies. The number of GABA-labelled boutons in SNr greatly exceeds the number of Glu-labelled ones. In the experimental material a considerable number of boutons in SNr are labelled with WGA-HRP reaction product. Several of these boutons are enriched in Glu-like immunoreactivity (Glu-LI), but not in GABA-LI. It is concluded that the subthalamonigral projection in the cat is likely to use Glu as a transmitter. The findings are briefly discussed with respect to the role played by STN in movement disorders and the involvement of excitatory amino acids in SN for the propagation of epileptic seizures and development of neurotoxicity.
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PMID:Terminals of subthalamonigral fibres are enriched with glutamate-like immunoreactivity: an electron microscopic, immunogold analysis in the cat. 767 8

Previous studies showed that the inferior colliculus (IC) and the pontine reticular nucleus (RPO) are involved in the initiation and propagation of seizure activity in genetically epilepsy-prone rats (GEPR-9s), respectively. Bilateral knife cuts in the coronal plane were made in the midbrain to determine what effect the disruption of efferent fibers of the IC would have on seizure activity. In addition, some lesions were injected with horseradish peroxidase (HRP) to trace the interrupted fibers and identify the neurons of origin. Consistent with previous results, lesions that involved the central nucleus of the IC or the lateral lemniscus blocked audiogenic seizures. Seizures were also blocked with lesions located between the external and central nuclei of the IC. In contrast, lesions located between the IC and superior colliculus and those within the superior colliculus reduced the audiogenic response score, but did not completely block audiogenic seizures. In the cases with intercollicular lesions, HRP-labeled axons were observed to arise from neurons in both the external nucleus and dorsal cortex of the IC, but not the central nucleus, and they entered the deep layers of the superior colliculus. These results indicate that the projection from the central nucleus to the external nucleus of the IC is important for the propagation of seizure activity in GEPR-9s. Also, these data show that projections from the IC to the superior colliculus play a role in seizure propagation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of midbrain collicular knife cuts on audiogenic seizure severity in the genetically epilepsy-prone rat. 806 44

The authors report the case of a female newborn infant, who had seizures and vesicles at the nose and inferior lip since the fifth day of life. CSF changes suggested an encephalitis. Signs of neurologic and respiratory deterioration were followed by death. Partial cranial autopsy showed a necrohemorrhagic temporal encephalitis without intranuclear inclusions. Immunohistochemical examination by the avidin-biotin-peroxidase technique with polyclonal antibodies against Herpes simplex type 1 and type 2 was positive to type 2 Herpes simplex virus.
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PMID:[Neonatal encephalitis caused by herpes simplex: immunohistochemical diagnosis of a case]. 829 44

Status epilepticus was induced in rats by injecting a combination of dibutyryl-cAMP (db-cAMP) and ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM), and the effect of phenytoin (PHT), entrapped in liposomes (PHT-L) and given intravenously at 40 mg/kg, on the spiking activity of the AM epileptogenic focus was examined. Electroencephalograms were recorded from the db-cAMP/EDTA-injected AM and the bilateral sensorimotor cortices. One dose of PHT-L, given 30 min after intra-AM db-cAMP, produced immediate and transient seizure suppression, but did not suppress the sequential spiking activity, which lasted for more than 5 h. In contrast, two doses of PHT-L, given 30 and 60 min after intra-AM db-cAMP/EDTA, produced delayed and local suppression of AM discharges, and immediate and transient seizure suppression was also observed. The AM discharges began to be suppressed about 100 min after the second injection of PHT-L injection, with no overt change occurring in cortical spiking activity. This was followed by total seizure suppression about 170 min after the second PHT-L injection. This effect was not observed after one or two injections of PHT alone. When horseradish peroxidase (HRP), to which the blood-brain barrier is impermeable, was entrapped in liposomes (HRP-L) and given intravenously 30 min after intra-AM db-cAMP/EDTA, an accumulation of HRP was found in the db-cAMP/EDTA-injected AM in 2 of the 5 animals tested. With 2 doses of HRP-L given 30 and 60 min after intra-AM db-cAMP/EDTA, the local augmentation of HRP in the AM was found in all 5 of the 5 animals tested. Our findings suggest that: (1) the AM epileptogenic focus created by db-cAMP/EDTA has a high affinity for liposomes, and this factor participates in the local suppression of AM discharges by PHT-L, and (2) two injections of PHT-L are required for the AM to gather an effective amount of PHT-L.
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PMID:Liposome-entrapped phenytoin locally suppresses amygdaloid epileptogenic focus created by db-cAMP/EDTA in rats. 871 31

We report a case of a reversible posterior leukoencephalopathy syndrome (RPLS). A 57-year-old male had classical polyarteritis nodosa with mononeuritis multiplex, renal insufficiency, and a high titer of p-ANCA (MPO). He was normotensive. He was treated with high dose methylprednisolone and then with oral prednisolone and cyclophosphamide. Despite the treatment, his renal function rapidly deteriorated and hypertension progressed. He had two generalized seizures; at that time his blood pressure was 200/140 mmHg. CT scan revealed bilaterally symmetric hypodensities in the thalamus, the occipital white matter, and the brainstem. T2-weighted MRI showed increased signal intensities in the temporo-occipital white matter, the thalamus, the posterior limbs of the internal capsules, the external capsules, the midbrain, the pons, and the middle cerebellar peduncles. T1-weighted images showed hypointensities in these areas. Treatment with nifedipine improved his blood pressure; 5 days later he was only moderately disoriented. Follow-up CT demonstrated an ill-defined hypodense area only in the left parietal lobe. To our knowledge, there are only two reported cases of RPLS associated with systemic vasculitides. Interestingly, thalamic lesions are outstanding also in these cases. Under these circumstances, treatment of hypertension is of primary importance, and steroid therapy should not be withdrawn or reduced.
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PMID:[A reversible posterior leukoencephalopathy syndrome in a patient with classical polyarteritis nodosa]. 914 79


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