Obstructive sleep apnea in children with epilepsy: prospective pilot trial.

BACKGROUND: Obstructive sleep apnea (OSA) is prevalent in adults with epilepsy, especially refractory, but limited data exist in children with epilepsy. AIMS: We conducted a prospective pilot study in children with epilepsy to identify the prevalence of OSA and its relationship to the use of antiepileptic drugs (AEDs) and epilepsy types. METHODS: We used Michigan Pediatric Sleep Questionnaire (PSQ) in children with epilepsy. Patients were classified by seizures frequency as mild (0-1 seizure/month) or severe, refractory epilepsy (> 1 seizures/month). We used PSQ ≥ 0.33 as a cutoff point to assess the risk of OSA. RESULTS: Of 84 children, 52 were classified as mild and 32 as severe. Prevalence of OSA was significantly higher in the severe (43.8%) vs the mild group (30.7%, P < 0.05). Children on >1 AED had significantly higher prevalence of OSA (45.8%) than children on ≤1 AED (30.6%, P < 0.05). There was no significant correlation between the prevalence of OSA and seizure types. CONCLUSIONS: OSA is more prevalent in refractory epilepsy and in children who are on multiple AEDs. While further studies are needed to confirm these findings and to assess the consequences of OSA, we believe it is important to screen the children with epilepsy for OSA.

Clinical report from the pilot USA Kernicterus Registry (1992 to 2004).

To identify antecedent clinical and health services events in infants (>/=35 weeks gestational age (GA)) who were discharged as healthy from their place of birth and subsequently sustained kernicterus. We conducted a root-cause analysis of a convenience sample of 125 infants >/=35 weeks GA cared for in US healthcare facilities (including off-shore US military bases). These cases were voluntarily reported to the Pilot USA Kernicterus Registry (1992 to 2004) and met the eligibility criteria of acute bilirubin encephalopathy (ABE) and/or post-icteric sequelae. Multiple providers at multiple sites managed this cohort of infants for their newborn jaundice and progressive hyperbilirubinemia. Clinical signs of ABE, verbalized by parents, were often inadequately elicited or recorded and often not recognized as an emergency. Clinical signs of ABE were reported in 7 of 125 infants with a subsequent diagnosis of kernicterus who were not re-evaluated or treated for hyperbilirubinemia, although jaundice was noted at outpatient visits. The remaining infants (n=118) had total serum bilirubin (TSB) levels >20 mg per 100 ml (342 micromol l(-1); range: 20.7 to 59.9 mg per 100 ml). No specific TSB threshold coincided with onset of ABE. Of infants <37 weeks GA with kernicterus, 34.9% were LGA (large for gestational age) as compared with 24.7% of term infants (>37 weeks GA). Although >90% mothers initiated breast-feeding, assessment of milk transfer and lactation support was suboptimal in most. Mortality was 4% (5 of 125) in infants readmitted at age 0.2 mg per 100 ml per hour), contributing factors, alone or in combination, included undiagnosed hemolytic disease, excessive bilirubin production related to extra-vascular hemolysis and delayed bilirubin elimination (including increased enterohepatic circulation, diagnosed and undiagnosed genetic disorders) in the context of known late prematurity (<37 weeks), glucose 6-phosphate-dehydrogenase deficiency, infection and dehydration. Readmission was at age 35 mg per 100 ml had post-icteric sequelae (n=73). There was a narrow margin of safety between birthing hospital discharge or home birth and readmission to a tertiary neonatal/pediatric facility. Progression of hyperbilirubinemia to hazardous levels and onset of neurological signs were often not identified as infant's care and medical supervision transitioned during the first week after birth. The major underlying root cause for kernicterus was systems failure of services by multiple providers at multiple sites and inability to identify the at-risk infant and manage severe hyperbilirubinemia in a timely manner.

Observation of a continuous phase transition in a shape-memory alloy.

Elastic neutron-scattering, inelastic x-ray scattering, specific-heat, and pressure-dependent electrical transport measurements have been made on single crystals of AuZn and Au0.52Zn0.48. Elastic neutron scattering detects new commensurate Bragg peaks (modulation) appearing at Q =(1.33,0.67,0) at temperatures corresponding to each sample's transition temperature (TM = 64 and 45 K, respectively). Although the new Bragg peaks appear in a discontinuous manner in the Au0.52Zn0.48 sample, they appear in a continuous manner in AuZn. Surprising us, the temperature dependence of the AuZn Bragg peak intensity and the specific-heat jump near TM are in favorable accord with a continuous transition. A fit to the pressure dependence of TM suggests the presence of a critical end point in the AuZn phase diagram located at TM* = 2.7 K and p* = 3.1 GPa.

Energy gaps and Kohn anomalies in elemental superconductors.

The momentum and temperature dependence of the lifetimes of acoustic phonons in the elemental superconductors lead and niobium were determined by resonant spin-echo spectroscopy with neutrons. In both elements, the superconducting energy gap extracted from these measurements was found to converge with sharp anomalies originating from Fermi-surface nesting (Kohn anomalies) at low temperatures. The results indicate electron many-body correlations beyond the standard theoretical framework for conventional superconductivity. A possible mechanism is the interplay between superconductivity and spin- or charge-density-wave fluctuations, which may induce dynamical nesting of the Fermi surface.

Strain phase diagram and domain orientation in SrTiO3 thin films.

SrTiO3 thin films were used as a model system to study the effects of strain and epitaxial constraint on structural phase transitions of perovskite films. The basic phenomena revealed will apply to a variety of important structural transitions including the ferroelectric transition. Highly strained SrTiO3 films were grown on different substrates, providing both compressive and tensile strain. The measured strain-temperature phase diagram is qualitatively consistent with theory; however, the increase in the phase transition temperature is much larger than predicted. Because of the epitaxial strain and substrate clamping, the SrTiO3 lattice is tetragonal at all temperatures. The phase transitions involve only changes in internal symmetry. The low temperature phase under tensile strain has a unique structure with orthorhombic Cmcm space group but a tetragonal lattice, an interesting consequence of epitaxial constraint.

New concepts in bilirubin encephalopathy.

Revised concepts of bilirubin encephalopathy have been revealed by studies of bilirubin toxicity in cultured CNS cells and in congenitally jaundiced Gunn rats. Bilirubin neurotoxicity is related to the unbound (free) fraction of unconjugated bilirubin (Bf), of which the dominant species at physiological pH is the protonated diacid, which can passively diffuse across cell membranes. As the binding affinity of plasma albumin for bilirubin decreases strikingly as albumin concentration increases, previously reported Bf values were underestimated. Newer diagnostic tests can detect reversible neurotoxicity before permanent damage occurs from precipitation of bilirubin (kernicterus). Early toxicity can occur at Bf only modestly above aqueous saturation and affects astrocytes and neurons, causing mitochondrial damage, resulting in impaired energy metabolism and apoptosis, plus cell-membrane perturbation, which causes enzyme leakage and hampers transport of neurotransmitters. The concentrations of unbound bilirubin in the cerebro-spinal fluid and CNS cells are probably limited mainly by active export of bilirubin back into plasma, mediated by ABC transporters present in the brain capillary endothelium and choroid plexus epithelium. Intracellular bilirubin levels may be diminished also by oxidation, conjugation and binding to cytosolic proteins. These new concepts may explain the varied susceptibility of neonates to develop encephalopathy at any given plasma bilirubin level and the selective distribution of CNS lesions in bilirubin encephalopathy. They also can suggest better strategies for predicting, preventing and treating this syndrome.

Quasielastic neutron scattering in the high-field phase of a Haldane antiferromagnet.

Inelastic neutron scattering experiments on the Haldane-gap quantum antiferromagnet Ni(C5D14N2)2-N3(PF6) are performed in magnetic fields below and above the critical field H(c) at which the gap closes. Quasielastic neutron scattering is found for H>H(c), indicating topological excitations in the high-field phase.

Auditory brainstem response and unbound bilirubin in jaundiced (jj) Gunn rat pups.

The role of plasma bilirubin-albumin binding in the pathogenesis of kernicterus in human newborns is controversial. Kernicterus in the jaundiced (jj) Gunn rat pup, an animal model for kernicterus, prolongs interwave intervals and decreases wave amplitude in the auditory brainstem response (ABR). Plasma total bilirubin concentration (TBC), albumin concentration, and unbound bilirubin concentration (UBC), a measure of bilirubin-albumin binding, were measured in 16-day-old jj Gunn rat pups (n = 21) and compared with ABR wave latencies, interwave intervals, and wave amplitudes by linear correlation. The UBC, but not the TBC or TBC/albumin ratio, correlated positively and significantly with ABR I-II and I-III interwave intervals (r = 0.55, p = 0.009, and r = 0.60, p = 0.004, respectively). The UBC, but not the TBC or TBC/albumin ratio, predicts bilirubin toxicity, as measured by bilirubin-induced ABR changes in jj Gunn rat pups.

Optical response of high-dielectric-constant perovskite-related oxide.

Optical conductivity measurements on the perovskite-related oxide CaCu3Ti4O12 provide a hint of the physics underlying the observed giant dielectric effect in this material. A low-frequency vibration displays anomalous behavior, implying that there is a redistribution of charge within the unit cell at low temperature. At infrared frequencies (terahertz), the value for the dielectric constant is approximately 80 at room temperature, which is far smaller than the value of approximately 10(5) obtained at lower radio frequencies (kilohertz). This discrepancy implies the presence of a strong absorption at very low frequencies due to dipole relaxation. At room temperature, the characteristic relaxation times are fast (less than or approximately 500 nanoseconds) but increase dramatically at low temperature, suggesting that the large change in dielectric constant may be due to a relaxor-like dynamical slowing down of dipolar fluctuations in nanosize domains.

Field-induced three- and two-dimensional freezing in a quantum spin liquid.

Field-induced commensurate transverse magnetic ordering is observed in the Haldane-gap compound Ni(C(5)D(14)N(2))2N(3)(PF(6)) by means of neutron diffraction. Depending on the direction of applied field, the high-field phase is shown to be either a three-dimensional ordered Néel state or a short-range ordered state with dominant two-dimensional spin correlations. The structure of the high-field phase is determined, and properties of the observed quantum phase transition are discussed.

Bilirubin and the auditory system.

The auditory system is highly sensitive to bilirubin toxicity. Damage to the auditory nervous system includes auditory neuropathy or auditory dyssynchrony and auditory processing problems which may occur with or without deafness, hearing loss. Auditory dysfunction may occur in children with or without other signs of classical kernicterus. Bilirubin selectively damages the brainstem auditory nuclei, and may also damage the auditory nerve and spiral ganglion containing cell bodies of primary auditory neurons. The inner ear, thalamic and cortical auditory pathways appear to be spared. Noninvasive auditory neurophysiological tests such as the auditory brainstem response (ABR) or brainstem auditory response (BAER) play an important role in the early detection of bilirubin-induced auditory and central nervous system dysfunction in the neonate.

Responses to constant work rate bicycle ergometry exercise in primary pulmonary hypertension: the effect of inhaled nitric oxide.

OBJECTIVES: The purpose of this study was to investigate the responses of patients with primary pulmonary hypertension (PPH) to constant work rate exercise and to examine the effect of nitric oxide (NO) inhalation. BACKGROUND: Maximal exercise tolerance is reduced in PPH, but gas exchange responses to constant work rate exercise have not been defined. We hypothesized that increased pulmonary vascular resistance in PPH would reduce the rate of rise of minute oxygen consumption in response to a given work rate. Because NO may lower pulmonary vascular pressures in PPH, we also postulated that inhaled NO might ameliorate gas exchange abnormalities. METHODS: Nine PPH patients and nine matched normal subjects performed 6-min duration constant work rate cycle ergometry exercise (33.9+/-13.4 W). Patients performed two experiments: breathing air and breathing air with NO (20 ppm). Preexercise right ventricular systolic pressure was assessed by Doppler echocardiography. Normal subjects performed the air experiment only. Gas exchange and heart rate responses were characterized by fitting monoexponential curves. RESULTS: In PPH patients, resting right ventricular systolic pressure fell after NO inhalation (from 83.8+/-16.9 to 73.9+/-21.6 mm Hg, p<0.01, analysis of variance with Tukey correction), but not after breathing air alone (from 88.0+/-20.8 to 86.7+/-20.6 mm Hg, p = NS). Nitric oxide did not affect any of the gas exchange responses. Minute oxygen consumption was similar by the end of exercise in patients and normals, but increased more slowly in patients (mean response time [MRT]: air, 63.17+/-14.99 s; NO, 61.60+/-15.45 s) than normals (MRT, 32.73+/-14.79, p<0.01, analysis of variance, Tukey test). Minute oxygen consumption kinetics during recovery were slower in patients (MRT air: 82.50+/-29.94 s; NO, 73.36+/-15.87 s) than in normals (MRT, 34.59+/-7.11 s, p<0.01). Heart rate kinetics during exercise and recovery were significantly slower in patients than in normals. CONCLUSIONS: The cardiac output response is impaired in PPH. Nitric oxide lowered pulmonary artery pressure at rest, but failed to improve exercise gas exchange responses.

Expression of the alpha and beta subunits of Ca2+/calmodulin kinase II in the cerebellum of jaundiced Gunn rats during development: a quantitative light microscopic analysis.

The homozygous (jj) jaundiced Gunn rat model for hyperbilirubinemia displays pronounced cerebellar hypoplasia. To examine the cellular mechanisms involved in bilirubin toxicity, this study focused on the effect of hyperbilirubinemia on calcium/calmodulin-dependent kinase II (CaM kinase II). CaM kinase II is a neuronally enriched enzyme which performs several important functions. Immunohistochemical analysis of alternating serial sections were performed using monoclonal antibodies for the alpha and beta subunits of CaM kinase II. Measurements were made of the total numbers of stained cells in each of the deep cerebellar nuclei and of Purkinje and granule cell densities in cerebellar lobules II, VI, and IX. The beta subunit was present in Purkinje cells and deep cerebellar nuclei of both groups at all ages, but only granule cells which had migrated through the Purkinje cell layer showed staining for beta subunit; external granule cells were completely negative. Many Purkinje cells had degenerated in the older animals, and the percent of granule cells stained for beta subunit was significantly reduced. The alpha subunit was found exclusively in Purkinje cells, although its appearance was delayed in the jaundiced animals. Sulfadimethoxine was administered to some jj rats 24 h or 15 days prior to sacrifice to increase brain bilirubin concentration. Results showed that bilirubin exposure modulated both alpha and beta CaM kinase II subunit expression in selective neuronal populations, but sulfadimethoxine had no acute effect on enzyme immunoreactivity. Thus, developmental expression of the alpha and beta subunits of CaM kinase II was affected by chronic bilirubin exposure during early postnatal development of jaundiced Gunn rats.

Nitrate-enhanced thallium 201 single-photon emission computed tomography imaging in hibernating myocardium.

OBJECTIVES: This study tested the usefulness of nitrate-enhanced thallium 201 imaging for detecting myocardial viability. BACKGROUND: Previous work suggests that nitrates enhance the ability of (201)Tl imaging to detect viable myocardium. METHODS: Eighteen patients with coronary artery disease underwent (201)Tl imaging at rest, after 4 hours of redistribution, and during intravenous nitroglycerine infusion (mean dose = 5.96 +/- 5.37 microgram/kg/min). Twelve patients had their echocardiograms repeated after revascularization. Perfusion and wall motion were scored from 0 to 2 (absent to normal). RESULTS: All the regions identified as viable by the rest/redistribution pair of scans were identified as viable by the rest/nitroglycerine pair of scans. Ninety-one percent of these regions were identified as viable by the single nitroglycerine scan alone. In patients who underwent revascularization, the total (201)Tl perfusion score improved from 193 to 214 after revascularization (P =.009). Wall motion score improved from 151 to 168 after revascularization (P =.09). Both the rest/nitroglycerine and rest/redistribution studies correctly predicted 14 (88%) of 16 regions that improved after revascularization. Most importantly, the rest/nitroglycerine and rest/redistribution studies were able to predict postrevascularization myocardial viability (absence of akinesis or dyskinesis after revascularization), with a sensitivity of 95% and 92%, respectively, and a predictive accuracy of 84.4%. CONCLUSIONS: Nitroglycerine infusion during (201)Tl imaging is a useful technique for detecting underperfused, viable myocardium, requires less time to perform than rest/redistribution imaging, and may allow detection of viable myocardium with a single (201)Tl single-photon emission computed tomographic study.

Acetylsalicylic acid reduces vegetation bacterial density, hematogenous bacterial dissemination, and frequency of embolic events in experimental Staphylococcus aureus endocarditis through antiplatelet and antibacterial effects.

BACKGROUND: Platelets are integral to cardiac vegetations that evolve in infectious endocarditis. It has been postulated that the antiplatelet aggregation effect of aspirin (ASA) might diminish vegetation evolution and embolic rates. METHODS AND RESULTS: Rabbits with Staphylococcus aureus endocarditis were given either no ASA (controls) or ASA at 4, 8, or 12 mg. kg-1. d-1 IV for 3 days beginning 1 day after infection. Vegetation weights and serial echocardiographic vegetation size, vegetation and kidney bacterial densities, and extent of renal embolization were evaluated. In addition, the effect of ASA on early S aureus adherence to sterile vegetations was assessed. In vitro, bacterial adherence to platelets, fibrin matrices, or fibrin-platelet matrices was quantified with either platelets exposed to ASA or S aureus preexposed to salicylic acid (SAL). ASA at 8 mg. kg-1. d-1 (but not at 4 or 12 mg. kg-1. d-1) was associated with substantial decreases in vegetation weight (P<0.05), echocardiographic vegetation growth (P<0.001), vegetation (P<0.05) and renal bacterial densities and renal embolic lesions (P<0.05) versus controls. Diminished aggregation resulted when platelets were preexposed to ASA or when S aureus was preexposed to SAL (P<0.05). S aureus adherence to sterile vegetations (P<0.05) or to platelets in suspension (P<0.05), fibrin matrices (P<0.05), or fibrin-platelet matrices (P<0.05) was significantly reduced when bacteria were preexposed to SAL. CONCLUSIONS: ASA reduces several principal indicators of severity and metastatic events in experimental S aureus endocarditis. These benefits involve ASA effects on both the platelet and the microbe.

Role of glutamate receptor-mediated excitotoxicity in bilirubin-induced brain injury in the Gunn rat model.

Severe hyperbilirubinemia in neonates with prematurity and/or systemic illnesses such as hemolytic disease, acidosis, and hypoxemia enhances their risk for developing cerebral palsy, paralysis of ocular upgaze, and deafness. This neurologic syndrome has been associated with selective neuronal vulnerability in the basal ganglia, certain brainstem nuclei, and Purkinje cells. However, the mechanism by which bilirubin damages neurons remains unclear. In these studies, we found that intracerebral injection of N-methyl-D-aspartate (NMDA), an excitotoxic analogue of glutamate, caused greater injury in jaundiced 7-day-old Gunn (jj) rat pups than in nonjaundiced heterozygous (Nj) littermate controls. NMDA injection caused even greater injury when protein-bound bilirubin was displaced with the sulfonamide drug sulfadimethoxine in jaundiced homozygous pups. In additional experiments, the acute signs of bilirubin-mediated neuronal injury, induced in homozygous (jj) Gunn rats by treatment with sulfonamide, were reduced by concurrent treatment with the NMDA-type glutamate channel antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohept-5,10-imine (MK-801, dizocilpine). The results suggest that bilirubin may cause encephalopathy and neuronal injury, at least in part, through an NMDA receptor-mediated excitotoxic mechanism. This conclusion is consistent with clinical observations that bilirubin encephalopathy is synergistically worsened by hypoxemia, which also shares an excitotoxic mechanism of neuronal injury.

Primary pulmonary hypertension: improved long-term effects and survival with continuous intravenous epoprostenol infusion.

OBJECTIVES: This study sought to determine the long-term effects of continuous infusion of epoprostenol (epo) therapy on survival and pulmonary artery pressure in patients with primary pulmonary hypertension (PPH). BACKGROUND: PPH is a progressive disease for which there are few effective therapies. METHODS: Patients with PPH and New York Heart Association functional class III or IV symptoms of congestive heart failure underwent right heart catheterization and Doppler-echocardiography to measure the maximal systolic pressure gradient between the right ventricle and right atrium (delta P) and cardiac output (CO). Doppler-echocardiography and catheterization data were compared. Patients were followed up long term with Doppler-echocardiography. RESULTS: Of 69 patients who went on to receive epo, 18 were followed up for > 330 days (range 330 to 700). During long-term follow-up, there was a significant reduction in delta P, which decreased from 84.1 +/- 24.1 to 62.7 +/- 18.2 (mean +/- SD, p < 0.01). A Kaplan-Meier plot of survival of our study patients demonstrated improved survival compared with that of historical control subjects. The 1-, 2- and 3-year survival rates for our patients were 80% (n = 36), 76% (n = 22) and 49% (n = 6) compared with 10- (88%, n = 31), 20- (56%, n = 27) and 30-month (47%, n = 17) survival rates in historical control subjects. CONCLUSIONS: Patients receiving continuous infusion of epo for treatment of PPH experience a decrease in pulmonary artery pressure. Long-term follow-up of this single-center patient group demonstrated improved long-term survival during epo therapy compared with that in historical control subjects and confirms predicted improved outcomes based on shorter follow-up periods.

Development of cerebellar hypoplasia in jaundiced Gunn rats: a quantitative light microscopic analysis.

The homozygous (ii) Gunn rat provides a model for hyperbilirubinemia which includes prominent cerebellar hypoplasia. Development of the Gunn rat cerebellum was examined with and without the additional effects of elevating brain bilirubin concentration to still higher levels via sulfadimethoxine (sulfa) administration. Homozygous (jj) Gunn rats and heterozygous (Nj) littermate controls (n = 32 each) were given 100 mg/kg sulfa or saline at postnatal days 3, 7, 17, and 30, and most were sacrificed 24 h later (n = 4 for each genotype at each age). Cerebellar volume, total volume and cell number for each deep cerebellar nucleus, densities for Purkinje and granule cells in the cerebellar cortex of lobules II, VI and IX, and the density of vacuolated Purkinje cells were all measured quantitatively. Cytoplasmic vacuolation provided an indication of bilirubin toxicity and was never observed in the Nj control rats. Vacuolated Purkinje cells were first observed in jj-saline rats at 18 days and were found only in the more anterior lobules of the cerebellum (II and VI). By contrast, vacuolated Purkinje cells were observed in jj-sulfa rats at both 4 and 8 days, but only in the most posterior cerebellar lobule (IX). In all older jj rats, the decline in vacuolation was accompanied by significant necrosis and resorption of the Purkinje cells in the anterior lobules. Since the Purkinje cells in the posterior lobules are the first to differentiate in the cerebellum and are resistant to bilirubin toxicity in jj-saline rats, the results support the presence of a critical period when elevated brain bilirubin may be most toxic to neuronal development. The findings suggest that neurons undergoing differentiation at the time of bilirubin exposure are most susceptible to cell death, while cells that are slightly more or slightly less mature may show only transient changes.

Estimation of regional end-systolic wall stress during exercise in coronary artery disease.

Estimating left ventricular wall stress has recognized applications, but formulae for global stress cannot be applied to ischemic ventricles. A mathematic method for estimating regional stress in infarcted ventricles has been described. The hypothesis tested was that exercise-induced ischemia increases end-systolic wall stress. Subcostal four-chamber echocardiograms were recorded at rest and during peak symptom-limited exercise in 19 controls and 41 patients with chest pain undergoing coronary arteriography. Centerline regional wall motion and regional end-systolic wall stress were measured at rest and at peak exercise. The normal controls had increased wall motion with exercise, but wall stress remained low. All 32 of the patients with coronary artery disease (> or = 50% diameter narrowing) had wall motion abnormalities with exercise, but the sensitivity of identifying right coronary artery obstructions was poor. Patients with coronary disease had higher regional stress at peak exercise than did the controls. The sensitivity of identifying lesions in all three coronary arteries (0.95 to 1.0) was better than that for wall motion (p < 0.04). The specificity of wall stress needs to be tested in a larger population. Exercise-induced ischemia causes increased regional end-systolic wall stress that reflects its distribution in patients with coronary artery disease. These changes can be measured non-invasively during exercise echocardiography.

Long-lasting reduction of inhibitory function and gamma-aminobutyric acid type A receptor subunit mRNA expression in a model of temporal lobe epilepsy.

This study evaluated hippocampal inhibitory function and the level of expression of gamma-aminobutyric acid type A (GABAA) receptor mRNA in an in vivo model of epilepsy. Chronic recurrent limbic seizures were induced in rats using injections of pilocarpine. Electrophysiological studies performed on hippocampal slices prepared from control and epileptic animals 1 to 2 months after pilocarpine injections demonstrated a significant hyperexcitability in the epileptic animals. Reduced levels of mRNA expression for the alpha 2 and alpha 5 subunits of the GABAA receptors were evident in the CA1, CA2, and CA3 regions of the hippocampus of epileptic animals. No decrease in mRNA encoding alpha 1, beta 2, or gamma 2 GABAA receptor subunits was observed. In addition, no change in the mRNA levels of alpha CaM kinase II was seen. Selective decreases in mRNA expression did not correlate with neuronal cell loss. The results indicate that selective, long-lasting reduction of GABAA subunit mRNA expression and increased excitability, possibly reflecting loss of GABAergic inhibition, occur in an in vivo model of partial complex epilepsy.