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)

The adenosine A3 receptor is expressed in brain, but the consequences of activation of this receptor on electrophysiological activity are unknown. We have characterized the actions of a selective adenosine A3 receptor agonist, 2-chloro-N6-(3-lodobenzyl)-adenosine-5'-N-methyluronamide (Cl-IB-MECA), and a selective A3 receptor antagonist, 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1, 4-(+/-)-dihydropyridine-3,5-dicarboxylate (MRS 1191), in brain slices from rat hippocampus. In the CA1 region, activation of A3 receptors had no direct effects on synaptically evoked excitatory responses, long-term potentiation, or synaptic facilitation. However, activation of A3 receptors with Cl-IB-MECA antagonized the adenosine A1 receptor-mediated inhibition of excitatory neurotransmission. The effects of Cl-IB-MECA were blocked by pretreatment with MRS 1191, which by itself had no effect on A1 receptor-mediated responses. The presynaptic inhibitory effects of baclofen and carbachol, mediated via GABA(B) and muscarinic receptors, respectively, were unaffected by Cl-IB-MECA. The maximal response to adenosine was unchanged, suggesting that the primary effect of Cl-IB-MECA was to reduce the affinity of adenosine for the receptor rather than to uncouple it. Similar effects could be demonstrated after brief superfusion with high concentrations of adenosine itself. Under normal conditions, endogenous adenosine in brain is unlikely to affect the sensitivity of A1 receptors via this mechanism. However, when brain concentrations of adenosine are elevated (e.g., during hypoxia, ischemia, or seizures), activation of A3 receptors and subsequent heterologous desensitization of A1 receptors could occur, which might limit the cerebroprotective effects of adenosine under these conditions.
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PMID:Activation of hippocampal adenosine A3 receptors produces a desensitization of A1 receptor-mediated responses in rat hippocampus. 898 83

We studied two epileptic patients with arachnoid brain cysts by proton magnetic resonance spectroscopy (1H MRS). In addition, histochemical analyses of surgical specimens, cerebrospinal fluid, and cystic fluid were performed in one of the patients. In both patients, greatly increased levels of excitatory amino acids (EAAs) glutamate and aspartate were present in the cystic fluid, while there was only a moderate increase of glutamate in the epileptogenic brain tissue adjacent to the cyst in one of the patients. In non epileptic brain regions, no elevations of the EAAs were present. Since EAAs are involved in induction and maintenance of epileptogenesis, their extremely high concentrations in the cystic fluid may explain seizures in some patients with such brain cysts. Our findings may have therapeutical consequences for patients with drug resistant epilepsy, in whom elevated concentrations of EAAs in the cysts can be verified. Surgery with the aim to create a communication between the cyst and the subarachnoidal space may prevent an accumulation of the EAAs and thus result in a relief of seizures.
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PMID:Increased excitatory amino acid levels in brain cysts of epileptic patients. 933 89

An association between complex febrile convulsions and the development of hippocampal atrophy, which is characterized by neuron loss and gliosis, has been suggested but is still controversial. In proton magnetic resonance spectroscopy (1H-MRS) a reduction in N-acetylaspartate (NAA), a neuron marker, or in its ratio to other metabolites, that is, creatine and phospocreatine (Cr) and choline-containing compounds (Cho), is considered a sensitive method for detecting neuron loss. We performed 1H-MRS of mesial temporal regions, including hippocampi, in two different groups of children with epilepsy: in children with a history of complex febrile convulsions (CFCs) (n = 7; mean age 7.1 years) and in children without any history of CFCs, referred to herein as the non-CFC group (n = 6; mean age 7.6 years). Changes in the metabolite ratios were detected in 57% of children in the CFC group and in 67% of children in the non-CFC group. In both groups, NAA/(Cho + Cr), NAA/Cho, and NAA/Cr were significantly decreased ipsilaterally to the seizure focus when compared with the control group, but no significant differences were detected between the CFC and non-CFC groups. Also on the contralateral side, NAA/(Cho + Cr) and NAA/Cr were significantly decreased in both patient groups, but the differences were not significant between the CFC and non-CFC groups. Metabolite abnormalities in the mesial temporal region were detected in children with intractable epilepsy and in children whose epilepsy is well controlled by antiepileptic medication. The noninvasive 1H-MRS can be considered an additional diagnostic method to promote early detection of mesial temporal abnormalities that, in the light of this study, seem to be underdiagnosed in children with either temporal lobe epilepsy or other seizure types.
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PMID:Proton spectroscopy in children with epilepsy and febrile convulsions. 974 26

Hippocampal metabolite concentrations were determined by localized in vivo proton magnetic resonance spectroscopy (1H MRS) in eleven patients suffering from refractory mesial temporal lobe epilepsy (MTLE), as well as in eleven age-matched healthy volunteers, and compared with patient history, postoperative outcome and histopathology. Main results are: 1) In patients, the decrease in N-acetylaspartate (NAA) concentrations was highly significant ipsilateral, and less but still significant contralateral to the electroencephalogram-defined focus, as compared to controls. 2) The decrease in ipsilateral NAA measured preoperatively correlates with the degree of hippocampal sclerosis but 3) does not reliably predict postoperative outcome, although there is a trend toward better outcome in patients with a marked decrease of NAA. 4) Hippocampal NAA decrease (ipsi- and contralateral) is highly correlated with early onset age of epileptic seizures. 5) Among patients with similar onset age in early childhood, there is a strong association between duration of the disease and contralateral (and, though less clear-cut, ipsilateral) NAA loss. These results are concordant with the notion of a generally progressive worsening and complicating course of symptoms in poorly controlled MTLE.
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PMID:Quantitative 1H MRS in the evaluation of mesial temporal lobe epilepsy in vivo. 981 80

A 55-year-old woman, who had two episodes of difficulty in putting a key into a keyhole probably due to optic ataxia at age 52 and 54 years old, developed speaking errors and was admitted to our hospital. She was 152.5 cm in height and 52.5 kg in weight. Neurological examination revealed right homonymous hemianopsia and sensory aphasia. A CSF examination revealed lymphocytic pleocytosis of 88/microliter. Serum lactate and pyruvate were remarkably increased after an aerobic exercise test. A few ragged-red fibers were present in the biopsied brachial biceps muscle. Brain MRI by FLAIR method showed scattered high signal lesions in the left temporal lobe, bilateral parieto-occipital lobes, left insular cortex and left thalamus. The left superficial temporal lesion was enhanced by gadolinium-DTPA. The proton MRS demonstrated the lactic acid peak as well as the decrease of NAA/choline ratio (0.38) in the left parieto-occipital region. Thus, she was diagnosed as a case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and successfully treated with ubidecarenone (150 mg/day). Six months later, she again developed seizure, right hemiparesis and deterioration of aphasia and presented again CSF lymphocytic pleocytoses of 15/microliter. Brain MRI demonstrated new lesions in the left temporoparietal lobes, left insular cortex and left corona radiata. Therefore, CSF pleocytosis appeared to be associated with stroke-like episodes in this case. Although the mechanism of CSF pleocytosis remains to be elucidated, it may involve the breakdown of blood-brain barrier caused by mitochondrial dysfunction. Otherwise, an inflammatory process similar to that in cases of Leber disease, who developed multiple sclerosis-like additional lesions in the central nervous system, may also take place in MELAS.
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PMID:[A case of MELAS showing CSF pleocytosis associated with stroke-like episodes]. 986 8

The study provides a review of the basic examination procedures and results of proton magnetic resonance spectroscopy (1H MRS) in patients suffering from mesial temporal lobe epilepsy (MTLE). The source of seizures in MTLE is most often an epileptogenic focus secondary to hippocampal sclerosis. 1H MRS currently plays an important role in the non-invasive diagnosis of this type of epileptogenic lesion. The decisive 1H MRS parameter characterizing an epileptogenic lesion is a statistically significantly decreased value of N-acetylaspartate levels compared with control values, most often associated with a decrease in the ratios of the intensities of NAA/Cr, NAA/Cho and NAA/(Cr + Cho) signals. Moreover, MRS makes it possible to distinguish bilateral involvement of mesial temporal structures typically associated with a bilateral decrease in the levels of metabolites and/or their ratios. As regards other metabolic compounds which play an important role in the pathobiochemistry of epilepsy, MRS is employed to study the action of gamma-aminobutyric acid (GABA), inositol, lactate, glutamine, and glutamate, the clinical function of which has not been fully clarified as yet. It is in this context that one should consider the application of 1H MRS in evaluating the action of some new anti-epileptic agents affecting excitatory and inhibitory amino acids. There is no doubt that in vivo 1H MRS, along with other imaging methods, has made a significant contribution to the clinical and biochemical description of epileptic seizures and has assumed a prominent position among the techniques of pre-operative examination in epileptic surgery.
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PMID:1H MR spectroscopy in patients with mesial temporal epilepsy. 995 70

Single-voxel proton magnetic resonance spectroscopy (1H MRS) has shown abnormalities in patients with temporal lobe epilepsy (TLE) and hippocampal sclerosis (HS). Many TLE patients, however, do not have HS or other lesions on quantitative magnetic resonance imaging (MRI) (MRI-negative). Fifteen control subjects, 15 patients with unilateral HS, and 15 MRI-negative TLE patients underwent 1H MRS at an echo time of 30 msec on a 1.5-T GE Signa scanner. Voxels were tailored to the individual hippocampi. N-Acetylaspartate (NAA), creatine, choline, total glutamate plus glutamine (Glx), and myo-inositol (Ins) were quantitated by using an external standard and LCModel, a user-independent quantitation method. Normal ranges were defined as the control mean +/- 2.5 SD. In HS patients, 12 of 15 had abnormally low NAA in sclerotic hippocampi; 3 of these 12 also had abnormally low NAA contralaterally. Abnormally low NAA/Ins ratios lateralized the side affected by HS in 7 of 15 patients, without any bilateral abnormalities. In 15 MRI-negative TLE patients, 4 had abnormally low hippocampal NAA ipsilateral to seizure onset, 1 of whom had abnormally low NAA bilaterally. Analysis of groups of subjects showed a bilateral decrease in NAA, most marked in patients with HS and on the side of seizure onset. The mean NAA/Ins ratio was lower in patients with HS than in control subjects and in MRI-negative patients. The concentration of Glx was higher ipsilateral to seizure onset in MRI-negative patients than in HS patients. Quantitative short echo time 1H MRS identified abnormalities in 87% of patients with HS and 27% of MRI-negative TLE patients in concordance with other lateralizing data. In individual and group comparisons, 1H MRS described a metabolite profile in the hippocampi of MRI-negative TLE patients that was different from patients with HS, with an increase in Glx and a less marked decrease in NAA than was seen in HS.
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PMID:Short echo time single-voxel 1H magnetic resonance spectroscopy in magnetic resonance imaging-negative temporal lobe epilepsy: different biochemical profile compared with hippocampal sclerosis. 1007 52

Ketogenic diet (KD) is highly effective in controlling epileptic seizures in children. One of the mechanisms postulated, the accumulation of ketone bodies, acetoacetate (AcAc) and/or betahydroxybutyrate (beta-OHB) in the brain, would be detectable by non-invasive proton magnetic resonance spectroscopy (1H-MRS). 1H-MRS was performed in occipital cortical grey matter in 14 epileptics (E); ages 3.8-48.3 years), seven KD and seven without, and 16 healthy age-matched subjects. One E was examined before and after KD. A singlet resonance (sigma = 2.22 ppm), distinct from AcAc (sigma = 2.26 and 3.46 ppm), and identified as acetone was present in all spectra of children on KD (nine spectra in five children; concentration 0.7 +/- 0.2 mM). This resonance was absent from Control and E without diet. AcAc and beta-OHB, which were not detectable in KD brain, were found in urine or blood of all KD. Seizures were well controlled in all E in whom acetone was detected. Two of seven E, both adults, were seizure-free without detectable acetone. Cerebral acetone may contribute to seizure control in KD, but is unlikely to be the sole mechanism.
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PMID:Identification of cerebral acetone by 1H-MRS in patients with epilepsy controlled by ketogenic diet. 1038 91

A 35-year-old man presented with partial seizures 10 years after resection of a left-sided glioblastoma multiforme. At the old operative site MRI demonstrated extensive cortical and white matter gadolinium enhancement, and PET showed hypermetabolism. Biopsy of the area was postponed when MRS showed a normal biochemical spectrum. MRI and PET abnormalities resolved after control of the seizures. MRS is noninvasive and can provide essential information in the management of patients with seizures and previously treated cerebral neoplasms.
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PMID:Transient MRI enhancement in a patient with seizures and previously resected glioma: use of MRS. 1040 62

Proton magnetic resonance spectroscopy ((1)H-MRS) was performed in seven healthy volunteers and 17 patients with temporal lobe epilepsy (TLE) to clarify the correlation of the severity of epilepsy with bilateral temporal changes in N-acetylaspartate (NAA), choline-containing compounds (Cho) and creatine + phosphocreatine (Cr). Despite unilateral EEG focus, bilateral temporal reduction in NAA /(Cho + Cr) was revealed in patients with intractable seizures. The potential for seizure generation correlated with the NAA /(Cho + Cr) reduction not only on the ipsilateral side but also on the contralateral side. Proton MRS proved to be a useful measurement for obtaining important information about the neuronal changes as well as the lateralization of the epileptogenic focus in TLE patients.
Seizure 2000 Jun
PMID:Seizure frequency and bilateral temporal abnormalities: a proton magnetic resonance spectroscopy of temporal lobe epilepsy. 1088 Feb 88


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