Seizure frequency and bioelectric brain activity in epileptic patients in stable and unstable atmospheric pressure and temperature in different seasons of the year--a preliminary report

Background and purposeAn epileptic seizure is a sum of exogenous and endogenous factors affecting an epileptic focus. The aim of the study was to examine the influence of changes in atmospheric pressure and temperature on the increase in the frequency of seizures and changes in EEG in epileptic patients.Material and methodsThe study included 30 epileptic patients (aged 19–54) reporting the influence of changes in weather conditions on the increase in the frequency of seizures for at least 2 years. EEG was performed twice each season at the time of stable and unstable weather conditions.ResultsIn stable and unstable weather conditions, epileptic changes in EEG were most often found in winter (in 43.3% and 63.3% of patients, respectively). Unstable weather conditions increased the proportion of patients with epileptic changes in EEG also in the other seasons. Unstable weather conditions caused an increase in the frequency of seizures in 40% of patients in spring, 43.3% in autumn, 40% in winter and in approximately 7% in summer.ConclusionsIn spring, autumn and winter, unstable weather conditions cause an increase in the frequency of seizures in almost half of the epileptic patients but only in 7% in summer. The increase in frequency of seizures in unstable weather conditions did not correspond in all patients with increase of changes in EEG. The higher proportion of epileptic patients with changes in EEG in unstable weather conditions in all seasons suggests an impact of these conditions on subclinical seizure discharges in this period.     

Effect of diet on tissue protease activity

Rats 1,3,12, and 24 months old were fed diets low in protein (8% casein), and proteolytic activity in tissue from brain, liver, and lung was determined. After a low-protein diet was fed for 4 weeks to 1-month-old rats, there was a significant increase in cathepsin D activity in liver, and calpain activity was increased in lung. Little change was seen in proteolytic activity in brain. In 12-month-old rats, there was an increase in cathepsin D activity in brain and liver. In 24-month-old rats, cathepsin D activity in the liver and calpain activity in lung were increased. There was no change in proteolytic activity in the brain. When animals were fed diets supplemented with fatty acids or antioxidants for 2 months, in 3-month-old rats calpain activity was increased in brain but decreased in lung. Cathepsin D activity was significantly increased in young and adult animals in brain and in liver. These observations suggest that diet changes result in significant alteration in tissue calpain and cathepsin D levels, and possibly activity, in vivo. Generally, changes are greater for cathepsin D than for calpain, and are smaller in brain than in other tissues. © 1995 Wiley-Liss, Inc.     

Neuronal hemoglobin is reduced in Alzheimer's disease, argyrophilic grain disease, Parkinson's disease, and dementia with Lewy bodies

Previous studies have demonstrated the presence of hemoglobin α-chain and β-chain in neurons of the rodent and human brain thus indicating that hemoglobin is a normal component of nerve cells and that hemoglobin may play a role in intraneuronal oxygen homeostasis. Progressing with these studies, hemoglobin expression has been examined in selected cell population in the brains of Alzheimer's disease (AD), argyrophilic grain disease (AGD), Parkinson's disease (PD) and Dementia with Lewy bodies (DLB). Double labeling immunofluorescence and confocal microscopy revealed reduced hemoglobin α-chain and β-chain in practically all neurons with small amounts of granular or punctuate hyperphosphorylated tau deposits and in neurons with tangles in the hippocampus and frontal cortex in AD and in the hippocampus in AGD; in ballooned neurons containing αB-crystallin in the amygdala in AD and AGD; and in about 80% of neurons with punctuate α-synuclein deposits and in neurons with Lewy bodies in the substantia nigra pars compacta and in vulnerable neurons of the medulla oblongata in PD and DLB; and in neurons with Lewy bodies in the frontal cortex in DLB. Hemoglobin immunoreactivity was also observed in the core of neuritic plaques and in diffuse plaques, but not in dystrophic neurites. Loss of hemoglobin was specific as neuroglobin was present equally in neurons with and without abnormal protein inclusions, and erythropoietin receptor was expressed equally in neurons without and in neurons with abnormal protein aggregates in AD, AGD, PD, and DLB.     

Classification of neurons in the ectosylvian auditory cortex of the dog

The rapid Golgi method was used to classify the neurons in the MES and PES auditory areas of the dog. Small pyramids were found in layer II with percentages of 12% in the MES area and 8.1% in the PES area. Medium sized pyramids possessed a bimodal distribution, the first in layer IV and the second in V, with 58% in MES and 62% in PES. Large pyramids were found in layer V with a proportion of 12.5% in MES and 17% in PES. The star neurons were found in layer III with proportions of 5.9% in MES and 4.0% in PES. The double bouquet neurons in layer III had a proportion of 1.5% in MES and 1.7% in PES. Fusiform neurons in layers V and VI were in proportions of 2.2% in MES and 6.4% in PES. The principal finding was a special auditory cell occurring in layers V and VI of the MES area with a proportion of 8% and from 14.8 to 34.8% in the strata between 1 and 2 mm. Less than 1% of neurons in the PES area were identified as special cells. Its appearance was an inverted pyramidal cell with a large dendrite extending toward the white matter from which the axon arose.     

Localization and pharmacological modulation of GABA-B receptors in the globus pallidus of parkinsonian monkeys

Changes in GABAergic transmission in the external and internal segments of the globus pallidus (GPe and GPi) contribute to the pathophysiology of the basal ganglia network in Parkinson's disease. Because GABA-B receptors are involved in the modulation of GABAergic transmission in GPe and GPi, it is possible that changes in the functions or localization of these receptors contribute to the changes in GABAergic transmission. To further examine this question, we investigated the anatomical localization of GABA-B receptors and the electrophysiologic effects of microinjections of GABA-B receptor ligands in GPe and GPi of MPTP-treated (parkinsonian) monkeys. We found that the pattern of cellular and ultrastructural localization of the GABA-BR1 subunit of the GABA-B receptor in GPe and GPi was not significantly altered in parkinsonian monkeys. However, the magnitude of reduction in firing rate of GPe and GPi neurons produced by microinjections of the GABA-B receptor agonist baclofen was larger in MPTP-treated animals than in normal monkeys. Injections of the GABA-B receptor antagonist CGP55845A were more effective in reducing the firing rate of GPi neurons in parkinsonian monkeys than in normal animals. In addition, the injections of baclofen in GPe and GPi, or of CGP55845A in GPi lead to a significant increase in the proportion of spikes in rebound bursts in parkinsonian animals, but not in normal monkeys. Thus, despite the lack of changes in the localization of GABA-BR1 subunits in the pallidum, GABA-B receptor-mediated effects are altered in the GPe and GPi of parkinsonian monkeys. These changes in GABA-B receptor function may contribute to bursting activities in the parkinsonian state.     

Roles of neurotransmitter amino acids in seizure severity and experience in the genetically epilepsy-prone rat

This investigation was designed to compare seizure-naive and seizure-experienced genetically epilepsy-prone rats (GEPRs) in order to distinguish transmitter amino acid changes related to seizure severity from those associated with seizure experience. Moderate (GEPR-3) and severe (GEPR-9) seizure male GEPRs were divided into seizure-naive and seizure-experienced groups based on whether seizure-inducing acoustical stimuli had been presented between 45 and 60 days of age, and then were sacrificed at76 ± 3 days. γ-Aminobutyric acid (GABA) concentrations were lower in both GEPR-3s and GEPR-9s compared to non-epileptic controls in each brain region examined. Aspartate content was elevated in 5 of 6 brain areas in GEPR-9s compared to non-epileptic controls, and in 3 regions was higher in GEPR-9s than in GEPR-3s. In contrast, taurine concentrations were higher in GEPR-3s than in non-epileptic controls in each region, and in 4 areas were higher in GEPR-3s than in GEPR-9s. Changes resulting from seizure experience consisted of increases in aspartate, glutamate and glycine in seizure-experienced compared to seizure-naive groups in inferior colliculus and in motor-sensory and frontal cortices. These findings suggest that the high levels of taurine in GEPR-3s and the elevated content of aspartate in GEPR-9s have roles as determinants of seizure severity. The low concentrations of GABA in both types of GEPRs are consistent with a role for this amino acid in determination of seizure susceptibility. Furthermore, the seizure-induced changes in aspartate and glutamate in both types of GEPRs support the concept that these excitatory amino acids mediate changes in seizure predisposition. The current results are in agreement with previous studies indicating that imbalances in neurotransmitter amino acids are important factors in determinig seizure behavior in the GEPR.     

The spontaneous firing pattern of forebrain neurons. I. The effects of dopamine and non-dopamine depleting lesions on caudate unit firing patterns

Unilateral lesions in and around the course of the nigrostriatal pathway (in the substantia nigra, in the supranigral region and more rostrally in the area of the medial forebrain bundle) in cats produced a marked slowing of single unit firing in the caudate nucleus contralateral to the lesion. In addition, the medial forebrain bundle lesion produced a tendency for an increase in unit firing rates in the caudate nucleus ipsilateral to the lesion. Lesions in the supranigral region in monkeys produced indications of a slowing in the firing rate of single units in the contralateral caudate and an increase in the firing rate of units in the caudate ipsilateral to the lesion. These alterations in spontaneous unit firing were independent of lesion-induced changes in concentrations of striatal dopamine or the activities of tyrosine hydroxylase and DOPA decarboxylase.     

Age-related alterations in immunoreactivity of the midsized neurofilament subunit in the brainstem reticular formation of the cat

In the present study, we compared the immunoreactivity of the midsized subunit of neurofilaments (NF-M) in the brainstem reticular formation of adult and old cats. There was a dramatic decrease in immunoreactivity in most reticular nuclei in the old cats. The most obvious reduction in these regions occurred in dendritic arborizations. In contrast, a small number of nuclei showed a slight increase in immunoreactivity in the aged animals. The age-related changes in immunoreactivity indicate that there is an alteration of NF-M content in reticular neurons and their processes in old age. Such changes in NF-M content may be the basis for the alterations in the morphology of reticular neurons in aged animals.     

Altered Cholinergic Mechanisms and Blood Pressure Regulation in the Rostral Ventrolateral Medulla of DOCA-Salt Hypertensive Rats

We examined whether cholinergic transmission in the rostral ventrolateral medulla (RVLM) of deoxycorticosterone acetate-salt hypertensive rats (DHR) is enhanced and the enhancement is involved in the maintenance of hypertension in DHR, and whether cholineacetyltransferase (ChAT) activities and ChAT mRNA expression are enhanced in neurons intrinsic to the RVLM of DHR. Rats were anesthetized, paralyzed, and artificially ventilated. Unilateral microinjection of cholinergic agents into the RVLM produced a pressor response. The pressor response to physostigmine was greater in DHR than in control rats, whereas the response to carbachol was the same in both sets of rats. Bilateral microinjection of scopolamine into the RVLM produced a decrease in blood pressure. The depressor response was greater in DHR than in control rats. The number of ChAT-activity-detected neurons in the RVLM was greater in DHR than in control rats. The number of ChAT mRNA-expressing neurons in the RVLM was also clearly greater in DHR than in control rats. These results demonstrate that cholinergic transmission in the RVLM is enhanced in DHR, and this enhancement may play a role in the maintenance of hypertension in DHR. It is probable that enhanced activity of cholinergic neurons intrinsic to the RVLM is at least in part, responsible for the enhanced cholinergic transmission in the RVLM of DHR.     

CT、MRI引导立体定向脑活检术的临床研究

目的评价CT或MRI引导立体定向活检术在确定脑深部病变的病理组织学诊断及选择适宜的治疗方法中的作用.方法采用计算机体层摄影(CT)或磁共振成像(MRI)引导立体定向技术对420例脑深部或脑主要功能区病灶进行了活检手术.其中男252例,女168例,年龄4.5～71岁,平均40.3岁.病变位于脑深部104例,鞍区82例,基底节区78例,三脑室后部50例,多发病灶48例,脑室内23例,小脑半球19例,脑干内14例,斜坡2例.CT引导手术386例,MRI引导手术34例.结果共有405例作出了病理诊断,活检总阳性率为96.43%,其中肿瘤359例(85.48%),炎性病变33例(7.86%),其他病变13例(3.10%).未作出病理诊断者15例(3.57%).共发生手术并发症7例(1.67%)出血5例(1.2%),癫痫1例,意识障碍1例.结论 CT或MRI引导的立体定向脑深部病变活检术是一种明确颅内占位病变的组织学诊断的可靠方法,并能为临床治疗方法的选择提供依据.     

经鼻蝶垂体腺瘤切除术出血并发症的原因分析及处理

目的探讨经鼻蝶垂体腺瘤切除手术出血并发症的原因及处理方法。方法回顾性研究104例经鼻蝶垂体腺瘤切除手术发生出血并发症病人的临床资料，出血后保守治疗82例，再次手术治疗22例。结果鞍上远隔部出血8例，痊愈3例，长期昏迷1例，死亡4例；颈内动脉出血5例，痊愈4例，死亡1例；瘤腔内出血38例，痊愈25例，视力下降7例，动眼神经麻痹2例，长期昏迷1例，死亡3例；鼻腔出血53例，均获得满意止血。结论出血是经鼻蝶垂体腺瘤手术的常见并发症，大多预后良好，少数严重出血可危及生命；提高显微手术技巧和总结经验教训可减少和避免手术出血并发症。     

Age-dependent loss of PTP and LTP in the hippocampus of PrP-null mice

We have investigated synaptic function in the hippocampus in mice of different ages carrying a null mutation in the PrP gene. Experiments carried out in vivo and in vitro in two laboratories revealed no differences in the ability of juvenile and young adult control and PrP-null mice to express long-term potentiation, paired-pulse facilitation, or posttetanic potentiation in either the dentate gyrus or in the CA1 region. However, we found a significant reduction in the level of posttetanic potentiation and long-term potentiation in the CA1 region of aged PrP-null mice. These results are discussed in relationship to reported increased levels of oxidative stress in older PrP-null mice.     

Perception of pain in the minimally conscious state with PET activation: an observational study

BACKGROUND: Patients in a minimally conscious state (MCS) show restricted self or environment awareness but are unable to communicate consistently and reliably. Therefore, better understanding of cerebral noxious processing in these patients is of clinical, therapeutic, and ethical relevance. METHODS: We studied brain activation induced by bilateral electrical stimulation of the median nerve in five patients in MCS (aged 18-74 years) compared with 15 controls (19-64 years) and 15 patients (19-75 years) in a persistent vegetative state (PVS) with (15)O-radiolabelled water PET. By way of psychophysiological interaction analysis, we also investigated the functional connectivity of the primary somatosensory cortex (S1) in patients and controls. Patients in MCS were scanned 57 (SD 33) days after admission, and patients in PVS 36 (9) days after admission. Stimulation intensities were 8.6 (SD 6.7) mA in patients in MCS, 7.4 (5.9) mA in controls, and 14.2 (8.7) mA in patients in PVS. Significant results were thresholded at p values of less than 0.05 and corrected for multiple comparisons. FINDINGS: In patients in MCS and in controls, noxious stimulation activated the thalamus, S1, and the secondary somatosensory or insular, frontoparietal, and anterior cingulate cortices (known as the pain matrix). No area was less activated in the patients in MCS than in the controls. All areas of the cortical pain matrix showed greater activation in patients in MCS than in those in PVS. Finally, in contrast with patients in PVS, those in MCS had preserved functional connectivity between S1 and a widespread cortical network that includes the frontoparietal associative cortices. INTERPRETATION: Cerebral correlates of pain processing are found in a similar network in controls and patients in MCS but are much more widespread than in patients in PVS. These findings might be objective evidence of a potential pain perception capacity in patients in MCS, which supports the idea that these patients need analgesic treatment.     

Regional and cellular differences in rat brain protein synthesis in vivo and in slices during development

We compared the rate of protein synthesis in immature and adult rat brain in vivo to that in brain slices. After the incorporation of a flooding dose of [14C]valine, in vivo and in brain slices, the label in proteins was measured in CNS regions and in neuron- and glia-enriched fractions. In regions in vivo in the adult, incorporation rates in corpus callosum were lower than in other regions, which were similar; in the young, cerebellum showed the highest rates and hypothalamus and cord the lowest. Since hypothalamus and cord were low in the young, there was no change during development in these two areas; in other areas incorporation rates in young were 2-3 times higher than in adult brain proteins. Incorporation rates in slices were lower than in vivo. In the young, cerebellum, olfactory bulb, and cord were close to in vivo, and other areas in slices from young incorporated at 60-90% of in vivo rates. In adult slices incorporation was 5-15% of that in vivo except in olfactory bulb, where it was 30%. In the cellular fractions, incorporation in vivo in young was close in the neuronal and glial fractions; in adults incorporation rates in neurons were higher, as the decrease in development was less in neurons than astrocytes. In slices in young, astrocytes incorporated amino acids at 100% of the in vivo rates, neurons at 60%; in adult slices, incorporation was at only 4-7% of the in vivo rate. The results show that developmental changes in protein metabolism occur in all brain areas and brain cells, with metabolic rates in young 2-3 times that in adult.(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in central cholinergic neurons in the spontaneously hypertensive rat

The activity of choline acetyltransferase (ChAT) was measured in discrete areas of the brain in 4-, 8- and 12-week-old spontaneously hypertensive rats (SH rats) and age matched Wistar Kyoto (WKY rats) controls. The concentration of acetylcholine (ACh) was also measured in certain hindbrain nuclei of 12 week SH and WKY rats. An increase in the ChAT activity and ACh concentration in the locus coeruleus was detected in 12-week-old SH rats. Decreases in the ChAT activity were found in several hypothalamic nuclei of SH rats, specially in the paraventricular nucleus of 4-week-old rats, in the dorsomedial nucleus at 8 and 12 weeks and in the posterior hypothalamic nucleus at 12 weeks. Changes in ChAT activity were also detected in 4- and 8-week-old SH rats in the anterior ventral thalamus and in the nucleus giganto-cellularis.These results suggest that cholinergic nerve activity in certain rat brain areas, several of which play a role in cardiovascular control, is altered in spontaneously hypertensive rats.     

Alteration of midkine expression in the ischemic brain of humans

Midkine (MK) is a heparin-binding growth factor that occurs as a product of the retinoic acid-inducible gene. Alteration of MK expression in ischemic brain lesions was examined in humans immunohistochemically in nine patients and in two control subjects without neurological disorders. Some neurons were MK-immunopositive, but no evident MK-immunoreactivity was observed in astrocytes in brains of control subjects. In the ischemic lesions, significant elevation of MK-immunoreactivity in the astrocytes and depletion of the reactivity in neurons were seen, especially in the early period, where edema and eosinophilic neurons were prominent. On the other hand, MK-immunoreactivity was not observed in hypertrophic and fibrillary astrocytes in the later period. These findings suggest that the MK in astrocytes play some role in the repair process in the early period of the ischemic brain lesions in humans.     

Proteolytic enzyme activities in mononuclear cells and granulocytes of patients with various neurological disorders

Our studies showed a significantly increased neutral protease activity in mononuclear cells in patients with MS in relapse, active neuro-Behçet's disease, acute disseminated encephalomyelitis (ADEM) and polymyositis. Furthermore, in patients with ADEM there was a significant increase in the activities of neutral and acid proteases in granulocytes, while a significant decrease of acid protease activity was found in both mononuclear cells and granulocytes of cases of polymyositis. No change in lysosomal enzyme activities of any of the cell preparations was observed in MS in remission, inactive neuro-Behçet's disease, cerebrovascular diseases, polyneuropathy and non-inflammatory myopathy. A significant decrease of acid protease activity in mononuclear cells was found in myotonic dystrophy. A significant decrease in neutral and acid protease activities in granulocytes was found in Duchenne type muscular dystrophy and myasthenia gravis, while only the neutral protease activity in granulocytes was decreased in nonpurulent meningitis.These results suggest that abnormal protease activities in mononuclear cells may be related to the immune or chronic inflammatory processes and that abnormal protease activities in granulocytes may be related to more acute inflammatory processes.     

Tissue levels of leu-enkephalin in rats with adjuvant arthritis

To study the level of leu-enkephalin in bone and joint tissues and in the spinal cord of rats with adjuvant arthritis, arthritis was induced in Lewis rats by the injection of Mycobacterium butyricum in Freund's incomplete adjuvant (FIA). Immunoelectron microscopy (IEM) was used to monitor the cellular distribution of leu-enkephalin in control and arthritis groups, and radioimmunoassay (RIA) was used to measure the concentration in the tissues. The results of IEM showed increased levels of leu-enkephalin in the matrix of the sciatic nerve, in nerve fibres in the synovial membrane and periosteum, as well as in fibroblasts and endothelial cells of the periosteum in arthritic groups. In macrophage-like cells of the synovial membrane as well as monocyte and polymorphonuclear lineage cells in the bone marrow, the level of leu-enkephalin was decreased in the arthritic group. The results of RIA showed that the concentration of leu-enkephalin was lower in the ankle and increased in the spinal cord of arthritic animals compared with controls. In conclusion, leu-enkephalin levels were decreased in joints and in bone marrow, but increased in nerve tissues in the group with arthritis. Further studies are needed to show whether leu-enkephalin is involved in a process that serves to limit the effect of immunisation.