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PubMed1990

Psychiatric consequences of temporal lobectomy for intractable seizures: a 20-30-year follow-up of 14 cases.

Between 1958 and 1968, 14 patients from the epilepsy clinic at the University of Oregon Hospitals and Clinics with a diagnosis of temporal lobe epilepsy (TLE) had a temporal lobectomy for medically intractable seizures. Nine of the 14 patients operated on remained seizure-free over the 20-30-year period of follow-up. Between 6 months and one year following temporal lobectomy, two women, previously healthy from a psychiatric standpoint, developed psychoses, and the previous psychiatric problems of four other patients worsened. Two patients, one with incapacitating paranoid personality disorder and the other with explosive rage attacks preoperatively, had marked improvement in their psychiatric status following temporal lobectomy. The remaining six patients, all psychiatrically healthy prior to surgery, have had no change in psychiatric status following surgery. Development of psychosis or deterioration in psychiatric status after surgery was more common in patients with later age of onset, unreality or déjà vu rather than epigastric aura, pre-operative evidence of bilateral brain damage, and persistence of EEG or clinical seizure activity. Development of a chronic psychosis in psychiatrically healthy individuals many months after temporal lobectomy, even when seizures are arrested or ameliorated, suggests that anomalous synaptic regeneration may follow the surgery in these cases. Careful analysis of histories and outcomes may contribute to better understanding of the pathophysiology and anatomical substrates of psychoses.

Adult↗

PubMed2001

Liquid ammonia mediated metathesis: synthesis of binary metal chalcogenides and pnictides.

Addition of stoichiometric amounts of low valent metal halides to liquid ammonia solutions of disodium chalcogenide (Na(2)E; E = S, Se, Te) afforded a range of both crystalline (PbE (E = S, Se, Te), TlE (E = S, Se), Tl(5)Te(3), Ag(2)E (E = S, Se, Te)) and X-ray amorphous (MS (M = Ni, Cu, Zn, Cd, Hg), M(2)E(3) (M = Ga, In; E = S, Se, Te), HgE (E = Se, Te), CuE (E = S, Se, Te), Cu(2)S) metal chalcogenides in good yield (95%). Reactions between metal halides and sodium pnictides (Na(3)Pn; Pn = As, Sb) in liquid ammonia also afforded X-ray amorphous material (M(3)Pn(2), M = Zn, Cd; MPn, M = Fe, Co, Ni) in good yield (95%). Isolation of the metal chalcogenides and pnictides was achieved through washing with CS(2) and distilled water. All reactions were complete within 36 h. Products were characterized by X-ray powder diffraction (XRD), scanning electron microscopy (SEM), energy-dispersive X-ray analysis (EDXA), electron probe analysis, FT-IR spectroscopy, Raman spectroscopy, microanalysis, and band gap measurements. Annealing amorphous material at 250-300 degrees C for 48 h induced sufficient crystallinity for analysis by X-ray powder diffraction.

Journal Article↗

PubMed1995

Novel deltorphin heptapeptide analogs with potent delta agonist, delta antagonist, or mixed mu antagonist/delta agonist properties.

A series of deltorphin (DLT: Tyr-D-Met-Phe-His-Leu-Met-Asp-NH2) analogs in which Leu5 and/or Met6 were mainly replaced by t-Leu(Tle) and/or N alpha-alkylated glycine were synthesized and examined for their receptor binding properties and in vitro bioactivities by guinea pig ileum (GPI) and mouse vas deferens (MVD) assays. [Tle5]DLT(2) showed a dramatic decrease in the MVD potency when compared to the parent peptide and was found to have a potent delta receptor antagonist activity against various delta agonists with Ke values of 16-311 nM. Interestingly, the antagonist potency of 2 against DPDPE as agonist was 20-fold weaker than that against deltorphins or Leu-enkephalin. Among the analogs in which Met6 was replaced by an N alpha-alkylated Gly residue, [N alpha-isobutyl-Gly6]DLT(5) behaved as a mixed mu antagonist/delta agonist while its isomeric analogs in which the N alpha-alkyl is n-butyl (4) or (R or S) sec-butyl (6a,b) were very potent delta receptor agonists. Analogs 2, 4, 6a, and 6b were highly stable against rat brain and rat plasma enzymes and thus may represent a starting point for the development of novel receptor-specific compounds useful as ligands for studies of opioid receptors.

Amino Acid Sequence↗

PubMed2006

Novel 99mTc-labeled neurotensin analogues with optimized biodistribution properties.

Two new 99mTc-labeled neurotensin(8-13) analogues containing the retro-N(alpha)-carboxymethyl-histidine ((N(alpha)His)Ac) chelator were synthesized as potential radiopharmaceuticals for visualization of pancreatic carcinoma. To improve the pharmacokinetic properties, (N(alpha)His)Ac-Arg-NMeArg-Pro-Tyr-Tle-Leu (NT-XII), which is metabolically stabilized at two positions, was further modified. Shikimic acid (3,4,5-trihydroxy-1-cyclohexene-1-carboxylic acid) was introduced to obtain a more hydrophilic peptide (NT-XVIII), or Tyr11 was replaced by 2,6-dimethyltyrosine (Dmt) resulting in a triple-stabilized NT(8-13) analogue (NT-XIX). The latter has the best biodistribution profile.

Animals↗

PubMed1999

Highly potent cyclic disulfide antagonists of somatostatin.

The search for synthetic analogues of somatostatin (SRIF) which exhibit selective affinities for the five known receptor subtypes (sst1-5) has generated a large number of potent agonist analogues. Many of these agonists display good subtype selectivities and affinities for the subtypes 2, 3, and 5, with very few selective for sst1 or sst4. Until the recent report by Bass and co-workers (Mol. Pharmacol. 1996, 50, 709-715; erratum Mol. Pharmacol. 1997, 51, 170), no true antagonists of somatostatin had been discovered, let alone any displaying differential receptor subtype selectivity. In this present study, we further explore the effect of this putative L,5D6 antagonist motif on somatostatin octapeptide analogues with a cyclic hexapeptide core. The most potent antagonist found to date is H-Cpa-cyclo[DCys-Tyr-DTrp-Lys-Thr-Cys]-Nal-NH2, PRL-2970 (21), which has an IC50 of 1.1 nM in a rat pituitary growth hormone in vitro antagonist assay versus SRIF (1 nM). This analogue bound to cloned human somatostatin subtype 2 receptors with a Ki of 26 nM. The highest hsst2 affinity analogue was H-Cpa-cyclo[DCys-Pal-DTrp-Lys-Tle-Cys]-Nal-NH2, PRL-2915 (15), with a Ki of 12 nM (IC50 = 1.8 nM). This analogue was also selective for hsst2 over hsst3 and hsst5 by factors of 8 and 40, respectively, and had no agonist activity when tested alone at concentrations up to 10 microM. Regression analysis of the binding affinities versus the observed antagonist potencies revealed high correlations for hsst2 (r = 0.65) and hsst3 (r = 0.52) with a less significant correlation to hsst5 (r = 0.40). This is quite different from the somatostatin agonist analogues which show a highly significant correlation to hsst2 (r > 0.9). Receptor-selective somatostatin antagonists should provide valuable tools for characterizing the many important physiological functions of this neuropeptide.

Animals↗

PubMed2005

Squaric acid-based peptidic inhibitors of matrix metalloprotease-1.

[structure: see text] A series of squaric acid-peptide conjugates were synthesized and evaluated as inhibitors of MMP-1. The cyclobut-3-enedione core was substituted at the 3-position with several functional groups, such as -N(alkyl)OH, -NHOH, and -OH, that are designed to bind to the zinc atom in the active site of the metalloprotease. The 4-position of the cyclobut-3-enedione was derivatized with mono- or dipeptides that are designed to bind in the S1' and S2' subsites of the enzyme, and position the metal chelating group appropriately in the active site for binding to zinc. Positional scanning revealed that -N(Me)OH provided the highest level of inhibition among the chelating groups that were tested, and Leu-Tle-NHMe was the preferred amino acid sequence. A combination of these groups yielded an inhibitor with an IC50 value of 95 microM. For one inhibitor, conversion of one of the carbonyl groups on the cyclobut-3-enedione core to a thiocarbonyl group resulted in a 18-fold increase in potency, and yielded a compound with an IC50 value of 15 microM.

Cyclobutanes↗

PubMed2001

Prognostic factors in the surgical treatment of medically intractable epilepsy associated with mesial temporal sclerosis.

OBJECTIVES: To assess the prognostic factors determining seizure remission after temporal lobectomy for intractable epilepsy associated with mesial temporal sclerosis (MTS) at pathology. METHODS: The clinical and investigative features of 116 consecutive patients who had temporal lobe surgery for drug-resistant epilepsy and MTS at pathology were assessed using actuarial statistics and logistic regression analysis. RESULTS: At a median follow-up of 63 months the probability of achieving at least a 1-year period of continuous seizure freedom was 67%. Factors contributing to a favourable outcome were interictal EEG localization to the operated lobe and the absence of secondarily generalized seizures. These were also selected in the multivariate analysis, although at lower statistical significance (P=0.08 and 0.09, respectively). Perinatal complications were associated with a significantly worse outcome but overall, complicated febrile convulsions and congruent neuropsychological deficits were not significantly predictive variables. CONCLUSIONS: The present findings may aid in the non-invasive presurgical assessment of patients with intractable TLE and clinical and neuroimaging evidence of MTS.

Adolescent↗

PubMed2003

Clinical applications of 1H-MR spectroscopy in the evaluation of epilepsies--what do pathological spectra stand for with regard to current results and what answers do they give to common clinical questions concerning the treatment of epilepsies?

Nuclear magnetic resonance spectroscopy (1H-MRS) is a non-invasive method in detecting abnormal spectra of various brain metabolites containing N-acetylaspartate (NAA), Choline (Cho), Creatine (Cr), gamma-Aminobutyric acid (GABA) and Glutamate. Technical processing of the MR-systems, improved automated shimming methods and further development of special shim coils increase the magnetic field homogeneity and lead to a better spectral quality and spectral resolution. The handling of the systems becomes more user-friendly and is more likely to be used in routine diagnostics. The 1H-MRS has become a diagnostic tool for assessing a number of diseases of the central nervous system mainly including epilepsies and brain tumours. The role of 1H-MRS in the assessment of epilepsies will probably increase in future. In the following article, the principles of 1H-MRS and an overview of it in the evaluation and treatment of epilepsies with special regard to temporal lobe epilepsies (TLE) has been illustrated.

Brain↗

PubMed2004

EGFR signaling attenuates Groucho-dependent repression to antagonize Notch transcriptional output.

Crosstalk between signaling pathways is crucial for the generation of complex and varied transcriptional networks. Antagonism between the EGF-receptor (EGFR) and Notch pathways in particular is well documented, although the underlying mechanism is poorly understood. The global corepressor Groucho (Gro) and its transducin-like Enhancer-of-split (TLE) mammalian homologs mediate repression by a myriad of repressors, including effectors of the Notch, Wnt (Wg) and TGF-beta (Dpp) signaling cascades. Given that there are genetic interactions between gro and components of the EGFR pathway (ref. 9 and P.H. et al., unpublished results), we tested whether Gro is at a crossroad between this and other pathways. Here we show that phosphorylation of Gro in response to MAPK activation weakens its repressor capacity, attenuating Gro-dependent transcriptional silencing by the Enhancer-of-split proteins, effectors of the Notch cascade. Thus, Gro is a new junction between signaling pathways, enabling EGFR signaling to antagonize transcriptional output by Notch and potentially other Gro-dependent pathways.

Animals↗

PubMed1997

Central benzodiazepine receptor autoradiography in hippocampal sclerosis.

1. The gamma-aminobutyric acid (GABA)A/central benzodiazepine receptor (cBZR) complex is a major inhibitory receptor in the vertebrate CNS. Binding of [11C]-flumazenil to this complex in vivo is reduced in hippocampal sclerosis (HS). It has been uncertain whether reduced cBZR binding is entirely due to neuronal loss in HS. 2. The objective of this study was to characterize abnormalities of the cBZR in HS with a correlative autoradiographic and quantitative neuropathological study. 3. Saturation autoradiographic studies were performed with [3H]-flumazenil to investigate relationships between neuronal density and receptor availability (Bmax) and affinity (Kd) in HS. Hippocampal tissue was obtained at surgery from 8 patients with intractable temporal lobe epilepsy (TLE) due to HS and autopsies of 6 neurologically normal controls. Neuronal densities were obtained by means of a 3-D counting method. 4. Bmax values for [3H]-flumazenil binding in the subiculum, CA1, CA2, CA3, hilus and dentate gyrus were all found to be significantly reduced in HS compared with controls and significant increases in affinity were observed in the subiculum, hilus and dentate gyrus. In HS, cBZR density in the CA1 region was significantly reduced (P < 0.05) to a greater extent than could be attributable to neurone loss. In other regions, Bmax was reduced in parallel with neuronal density. 5. In HS, there is a loss of cBZR in CA1 over and above loss of neurones. This finding and increases in affinity for flumazenil in subiculum, hilus and dentate gyrus imply a functional abnormality of the GABAA/cBZR complex that may have a role in the pathophysiology of epileptogenicity in HS.

Adult↗

PubMed2003

Mesial temporal sclerosis--a late complication in four allogeneic pediatric recipients with persistent seizures after an acute episode of cyclosporine-A neurotoxicity.

Mesial temporal sclerosis (MTS) is a common finding in patients with intractable temporal lobe epilepsy (TLE). In this report, we retrospectively reviewed the neuroimaging results of four children who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT), and who developed recurrent, partial, intractable seizures following a first event caused by cyclosporine-A (CSA) neurotoxicity. Neuroradiologic findings of MTS were demonstrated in all these patients. We suggest that MTS may be a consequence of CSA neurotoxicity, which induces repeated seizures, associated with other predisposing conditions, as well as being a consequence of the underlying disease and its treatment, and of severe graft-versus-host disease (GvHD).

Child↗

PubMed2001

Bilateral hippocampal granule cell dispersion: autopsy study of 3 infants.

Recent morphologic studies of Ammon's horn sclerosis (AHS) have recorded granule cell dispersion (GCD) in a significant proportion of temporal lobes surgically resected for temporal lobe epilepsy (TLE). We report the first post-mortem descriptions of GCD in three unrelated infants. GCD was bilateral in all three and there were also migrational defects, heterotopias or polymicrogyria. Only one child, a 2.5-year-old boy, presented with a severe seizural disorder and exhibited bilateral AHS. But in the two younger children, deceased at 12 weeks and 5 months, respectively, no seizures were observed and hippocampal neuronal populations were intact. To date, GCD has only been reported in association with epilepsy and has not been observed bilaterally or in neurologically normal individuals. The present observations bring into question the hypothesis that GCD is causally related to seizure activity in early life, suggesting an opposing view that it is an independent developmental disorder.

Cadaver↗

PubMed1996

Inhibition of platelet adhesion to collagen by monoclonal anti-CD36 antibodies.

Monoclonal anti CD36 antibodies capable of inhibiting platelet adhesion to collagen have not previously been identified. We have now prepared two groups of monoclonal antibodies. One group was prepared using, as immunogen, highly purified (99+%) CD36 prepared by a denaturing procedure. These antibodies (Mo series) reacted strongly with CD36 on protein blots but did not immunoprecipitate native CD36 from platelet lysates nor inhibit platelet adhesion to collagen. The second group of monoclonal antibodies (131 series) was prepared using CD36 purified to >95% by a non-denaturing procedure. These antibodies reacted with control platelets, but not Nak(a)-negative platelets which lack CD36, as measured by flow cytometry and immunoprecipitation. Three monoclonal antibodies of this latter group (131.4, 131.5 and 131.7) inhibited platelet adhesion to collagen in static systems under Mg2+ -independent conditions but had lit tle effect in the presence of Mg2+. 131.4 and 131.7 also inhibited adhesion to collagen using citrated whole blood in a parallel plate flow chamber at physiological shear rates (800s-1), whereas 131.5 was without effect. These are the first anti-CD36 monoclonal antibodies shown to be capable of inhibiting platelet adhesion to collagen and provide further evidence that CD36 plays a role in platelet-collagen interaction.

Animals↗

PubMed2001

The relationship between quantitative T2 relaxometry and memory in nonlesional temporal lobe epilepsy.

PURPOSE: We investigated the relationship between preoperative quantitative magnetic resonance imaging (MRI) T2 relaxometry and volumetry of the hippocampi and pre- and postoperative verbal memory in temporal lobectomy patients who had nonlesional temporal lobe epilepsy. METHODS: Pre- and postoperative memory data based on the Logical Memory (LM) subtest of the Wechsler Memory Scale-Revised (WMS-R) and the 30-min delayed recall trial of the Rey Auditory Verbal Learning Test (AVLT) were obtained from 26 left and 15 right temporal lobectomy patients. Coronal MRI T2 maps were generated for these 41 temporal lobectomy patients as well as 61 control patients. Hippocampal T2 relaxation times and hippocampal volumes, converted to z scores using control group data, were correlated with neuropsychological performance in the patients. RESULTS: In left temporal lobe-onset patients, high T2 in the left hippocampal body predicted higher LM performance after surgery. Asymmetrically high T2 in the left hippocampal body (i.e., the right-minus-left difference), compared with the right hippocampal body, also predicted higher LM performance after surgery. In right temporal lobe-onset patients, high T2 in the left hippocampal body predicted relatively lower AVLT performance after surgery. Multiple regression analysis in left temporal-onset patients revealed that high T2 in the left hippocampal body together with higher preoperative LM performance predict higher postoperative LM performance. CONCLUSIONS: Our findings suggest that elevated (i.e., abnormal) hippocampal T2 signal is associated with memory ability (or hippocampal functional capacity) independent of MRI-determined hippocampal atrophy. Therefore, our findings support the use of quantitative T2 relaxometry as an independent predictor of verbal memory outcome in both left and right TLE patients who are candidates for temporal lobectomy.

Adult↗

PubMed2002

Predictive value of cortical injury for the development of temporal lobe epilepsy in 21-day-old rats: an MRI approach using the lithium-pilocarpine model.

PURPOSE: Patients with temporal lobe epilepsy (TLE) usually had an initial precipitating injury in early childhood. However, epilepsy does not develop in all children who have undergone an early insult. As in patients, the consequences of the lithium-pilocarpine-induced status epilepticus (SE) are age dependent, and only a subset of 21-day-old rats will develop epilepsy. Thus with magnetic resonance imaging (MRI), we explored the differences in the evolution of lesions in these two populations of rats. METHODS: SE was induced in 21-day-old rats by the injection of lithium and pilocarpine. T2-weighted images and T2 relaxation-time measurements were used for detection of lesions from 6 h to 4 months after SE. RESULTS: Three populations of rats could be distinguished. The first one had neither MRI anomalies nor modification of the T2 relaxation time, and these rats did not develop epilepsy. In the second one, a hypersignal appeared at the level of the piriform and entorhinal cortices 24 h after SE (increase of 49% of the T2 relaxation time in the piriform cortex) that began to disappear 48-72 h after SE; epilepsy developed in all these animals. The third population of rats showed a more moderate increase of the T2 relaxation time in cortices (14% in the piriform cortex) that could not be seen on T2-weighted images. Epilepsy developed in all these rats. Only in a subpopulation of the 21-day-old rats with epilepsy did hippocampal sclerosis develop. CONCLUSIONS: These results suggest that the injury of the piriform and entorhinal cortices during SE play a critical role for the installation of the epileptic networks and the development of epilepsy.

Age Factors↗

PubMed2003

Cardiac asystole in epilepsy: clinical and neurophysiologic features.

PURPOSE: Cardiac asystole provoked by epileptic seizures is a rare but important complication in epilepsy and is supposed to be relevant to the pathogenesis of sudden unexplained death in epilepsy (SUDEP). We sought to determine the frequency of this complication in a population of patients with medically intractable epilepsy and to analyze the correlation between EEG, electrocardiogram (ECG), and clinical features obtained from long-term video-EEG monitoring. METHODS: Retrospective analysis of the clinical records of hospitalized patients from May 1992 to June 2001 who underwent long-term video-/EEG monitoring. RESULTS: Of a total of 1,244 patients, five patients had cardiac asystole in the course of ictal events. In these patients, 11 asystolic events, between 4 and 60 s long in a total of 19 seizures, were registered. All seizures had a focal origin with simple partial seizures (n = 13), complex partial seizures (n = 4), and secondarily generalized seizures (n = 2). One patient showed the longest asystole ever reported (60 s) because of a seizure. Cardiac asystole occurred in two patients with left-sided temporal lobe epilepsy (TLE) and in three patients with frontal lobe epilepsy (FLE; two left-sided, one bifrontal). Two patients reported previous cardiac disease, but only one had a pathologic ECG by the time of admission. Two patients had a simultaneous central ictal apnea during the asystole. None of the patients had ongoing deficits due to the asystole. CONCLUSIONS: These findings confirm that seizure-induced asystole is a rare complication. The event appeared only in focal epilepsies (frontal and temporal) with a lateralization to the left side. A newly diagnosed or known cardiac disorder could be a risk factor for ictal asystole. Abnormally long postictal periods with altered consciousness might point to reduced cerebral perfusion during the event because of ictal asystole. Central ictal apnea could be a frequent associated phenomenon.

Adolescent↗

PubMed2003

Neocortical temporal FDG-PET hypometabolism correlates with temporal lobe atrophy in hippocampal sclerosis associated with microscopic cortical dysplasia.

PURPOSE: Medically intractable temporal lobe epilepsy (TLE) due to hippocampal sclerosis (HS), with or without cortical dysplasia (CD), is associated with atrophy of the hippocampal formation and regional fluorodeoxyglucose positron-emission tomography (FDG-PET) hypometabolism. The relation between areas of functional and structural abnormalities is not well understood. We investigate the relation between FDG-PET metabolism and temporal lobe (TL) and hippocampal atrophy in patients with histologically proven isolated HS and HS associated with CD. METHODS: Twenty-three patients underwent en bloc resection of the mesial and anterolateral neocortical structures. Ten patients were diagnosed with isolated HS; 13 patients had associated microscopic CD. Temporal lobe volumes (TLVs) and hippocampal volumes were measured. Magnetic resonance imaging (MRI) and PET were co-registered, and regions of interest (ROIs) determined as gray matter of the mesial, lateral, and anterior temporal lobe. RESULTS: All patients (HS with or without CD) had significant ipsilateral PET hypometabolism in all three regions studied (p < 0.0001). In patients with isolated HS, the most prominent hypometabolism was in the anterior and mesial temporal lobe, whereas in dual pathology, it was in the lateral temporal lobe. TLVs and hippocampal volumes were significantly smaller on the epileptogenic side (p < 0.05). The PET asymmetries ipsilateral/contralateral to the epileptogenic zone and TLV asymmetries correlated significantly for the anterior and lateral temporal lobes (p < 0.05) in the HS+CD group, but not in the isolated HS group. Mesial temporal hypometabolism was not significantly different between the two groups. CONCLUSIONS: Temporal neocortical microscopic CD with concurrent HS is associated with more prominent lateral temporal metabolic dysfunction compared with isolated HS in TL atrophy. Further studies are needed to confirm these findings and correlate the PET hypometabolic patterns with outcome data in patients operated on for HS with or without CD.

Adolescent↗

PubMed2003

Neuronal cell death in a rat model for mesial temporal lobe epilepsy is induced by the initial status epilepticus and not by later repeated spontaneous seizures.

PURPOSE: To determine whether repeated seizures contribute to hippocampal sclerosis, we investigated whether cell loss in the (para) hippocampal region was related to the severity of chronic seizure activity in a rat model for temporal lobe epilepsy (TLE). METHODS: Chronic epilepsy developed after status epilepticus (SE) that was electrically induced 3-5 months before. The presence of neuronal damage was assessed by using Fluoro-Jade and dUTP nick end-labeling (TUNEL) of brain sections counterstained with Nissl. RESULTS: We found a negative correlation between the numbers of surviving hilar cells and the duration of the SE (r = -0.66; p < 0.01). In the chronic phase, we could discriminate between rats with occasional seizures (0.15 +/- 0.05 seizures per day) without progression and rats with progressive seizure activity (8.9 +/- 2.8 seizures/day). In both groups, the number of TUNEL-positive cells in parahippocampal regions was similar and higher than in controls. In the hippocampal formation, this was not significantly different from controls. Fluoro-Jade staining showed essentially the same pattern at 1 week and no positive neurons in chronic epileptic rats. CONCLUSIONS: Cell death in this rat model is related to the initial SE rather than to the frequency of spontaneous seizures. These results emphasize that it is of crucial importance to stop the SE as soon as possible to prevent extended cell loss and further progression of the disease. They also suggest that neuroprotectants can be useful during the first week after SE, but will not be very useful in the chronic epileptic phase.

Animals↗