Heart rate studies in association with electroencephalography (EEG) as a means of assessing the progress of head injuries.
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In the first six months of 1977 156 patients with craniocerebral injuries underwent computerized tomography. Twelve had severe deficits which led to neurosurgical interventions. Only five had space-occupying haematomas. CT was useful in detecting neurosurgical complications, whereas EEG was useful in staging the severity of the trauma. The two methods, the functional one of EEG and the morphological one of CT, are complementary, especially with regard to the posttraumatic course. The clinical symptoms are reflected by EEG better than by CT.
Electroencephalographic (EEG) investigations were done in 36 patients with intracranial aneurysms, before and after surgery. Thirty five of them suffered from subarachnoid hemorrhage (SAH). Pre-operatively, there was no correlation between patients' age or sex and localisation of the aneurysm or degree of EEG disturbances. The most frequent finding was a generalised slowing, the degree of which depended on the time from bleeding to EEG. Focal abnormalities were due to spasms of the vessels or intracerebral haematomas. There was a high correlation with neurological deficits. Post-operatively, EEG disturbances became worse in 21 cases. Generalised and focal abnormalities increased. These were due to focal oedema and the operative approach. The EEG could be correlated very well with the findings from other investigative methods (CT scanning, angiography). The EEG, as a functional method, showed very well the whole state of the brain after bleeding and after operation.
This work is an attempt to connect the electro-encephalogram (EEG) and monitor of cerebral function (MCF) recordings during the experimental stimulation of the rabbit brain whether this is in the from of direct central stimulation, by stereotaxic location, or in the form of indirect stimulation via a peripheral nerve. These stimulations, performed under alfadione anaesthesia or under the neuroleptanalgesic sedative effect of chlorprothixine, are compared for every animal with the results of the control stimulations. The cardiovascular responses are recorded simultaneously. It has been found that, in simple narcosis induced by alfadione, there is much variation in the EEG recording and even more so in the MCF recording according to the quantity used and the block of responses to stimuli does not appear until there is deep anaesthesia. However, when chlorprothixine is used, the MCF trace is found to be very closely related to the trace of mild anaesthesia with accompanying block to all of the nociceptive stimulations. It would seem, therefore, if we accept the concept of levels of cerebral activity, that the use of the MCF could well open the way to a better understanding of the pure narcotic phenomena and of the neurovegetative response block to aggression.
Accurate diagnosis and progression prediction of Alzheimer's disease (AD) remain challenging due to the heterogeneous nature of the disease, which involves structural brain degeneration, electrophysiological dysfunction, and molecular dysregulation. Most existing deep learning approaches rely on a single modality or limited multimodal combinations, thereby failing to capture the complex cross-domain interactions underlying AD progression. Furthermore, the scarcity of large-scale datasets containing synchronized neuroimaging, electrophysiological, and genomic measurements restricts the development of comprehensive multimodal diagnostic systems. To address these challenges, this study proposes NeuroOmics-Net, a multimodal deep learning framework for Alzheimer's disease analysis that integrates structural magnetic resonance imaging (sMRI), electroencephalography (EEG), and gene expression data. The proposed framework combines a Hierarchical Multi-View Encoder (HME) for modality-specific feature extraction, a Cross-Omics Attention Fusion (CAF) module for adaptive integration of complementary biomarkers, and a Disease Progression Graph Learning (DPGL) module for modeling progression-related relationships across biological domains. To facilitate cross-modal integration from independent cohorts, Regularized Canonical Correlation Analysis (RCCA) is employed to align heterogeneous feature representations within a shared latent space. Experiments were conducted using publicly available datasets from ADNI, PhysioNet, and GEO repositories comprising 1120 diagnosis-aligned samples. The proposed framework achieved 94.3% classification accuracy and an AUC of 0.975 for distinguishing normal controls (NC), mild cognitive impairment (MCI), and Alzheimer's disease subjects, while attaining 93.7% accuracy for predicting conversion from stable mild cognitive impairment (sMCI) to progressive mild cognitive impairment (pMCI). However, a fairness sensitivity analysis using stratified demographic reweighting revealed accuracy ranging from 90.8% (low-education, high-comorbidity proxy subgroup) to 96.1% (low-risk, high-reserve proxy subgroup), a demographic parity gap of 5.3 percentage points, indicating that overall accuracy reflects a performance ceiling in a relatively homogeneous research cohort rather than a realistic estimate for demographically diverse clinical populations. Comparative evaluations demonstrated consistent improvements over state-of-the-art unimodal and multimodal deep learning models. Interpretability analysis further identified clinically relevant biomarkers, including hippocampal and entorhinal atrophy, theta-alpha EEG alterations, and APOE-associated molecular pathways. Because sMRI, EEG, and gene expression data were sourced from separate, unpaired cohorts with no subjects possessing all three synchronized measurements, all reported cross-modal associations reflect population-level statistical correspondence across diagnosis-matched groups rather than within-subject physiological coupling; no claim of intra-individual causal cross-modal interaction is made. These findings demonstrate that NeuroOmics-Net provides an effective computer-aided framework for multimodal biomedical data processing and Alzheimer's disease analysis. By integrating neuroimaging, electrophysiological, and genomic information, the proposed approach enables accurate diagnosis, progression prediction, and biologically interpretable decision support for clinical and translational applications.
The results of the clinical neurological investigation were compared with those of electroencephalography (EEG) and computed tomography (CT) in 64 patients suffering from verified posttraumatic epilepsy. Only 18 patients (28%) showed central neurological features with corresponding focal disorders on CT (15 cases) and EEG (11 cases). The combined application of both methods led to positive results in 94% on the part of at least one accessory examination. The clinical neurological investigation as well as the EEG and CT were normal in only 3 cases, although the traumatic etiology of epilepsy was beyond doubt. In addition to the clinical neurological investigation, EEG and CT are most important accessory examinations for the diagnosis and followup studies in cases of posttraumatic epilepsy.
Nine normal elderly subjects and 81 patients with dementia have been studied by computerised tomography (CT) and electroencephalography (EEG). There was a broad relationship between slowing of the basic frequency of the EEG and the severity of mental impairment. Localised slow-wave activity was found in 19% of those with non-vascular dementia and 72% of those with dementia of vascular origin. The mean size of the ventricles, as determined from CT scans, was larger in the vascular than in the non-vascular group. Within the vascular group it was larger in those without than in those with visible infarcts. There was no relationship in either group between ventricular size and dominant EEG frequency.
Thirty-five elderly patients were investigated because of clinical signs of dementia. The presence or diffuse cerebral atrophy, and its severity, were determined by the use of computed tomography (CT scan). All of the patients were also examined by electroencephalography (EEG), and the presence of diffuse abnormalities, especially diffuse slowing, was noted. Specifically, patients with normal or near-normal EEGs were compared with those with severe diffuse slowing. No correlation between the presence or severity of diffuse EEG abnormalities and the degree of cerebral atrophy as measured by CT scan was found. Though the EEG is clearly identifying physiological dysfunction of nerve cells in demented patients it does not appear to be reliable tool for the prediction of diffuse cerebral atrophy in this population.
The clinical usefulness of non-convulsive responses induced by intermittent photic stimulation (IPS) was studied in 46 patients whose evaluation included both electroencephalography (EEG) and computerized cranial tomography (CT scan). Three patterns of photic responses were identified and related to background EEG activity and type of lesion seen on CT scan. An asymmetry in photic driving manifested only by a consistent amplitude difference greater than 50% was rarely associated with other EEG changes such as focal slowing or significant asymmetry in the alpha rhythm. In contrast, an asymmetry in development of the photic response correlated well with ipsilateral focal slowing and CT scan evidence of parenchymatous brain disease. Bilateral, symmetrical high amplitude single spikes evoked by individual light flashes were seen only in patients with diffuse encephalopathies. In no patient with structural brain disease as judged by CT scan was an abnormality in IPS the only EEG finding. There was also no apparent relationship between the anatomical site of a focal cerebral lesion and the type of response induced by IPS. Photic stimulation is of limited value in non-epileptic patients. Little clinical significance can be attached to nonconculsive responses in the absence of associated EEG changes which by themselves are generally more informative.
The short-term prognostic value of routine electroencephalography (EEG), carried out on the days after cardiac arrest, was evaluated in a consecutive study of 185 patients with acute myocardial infarction together with an episode of clinical cardiac arrest. The individual EEGs were classified on a 5-grade scale. Of the 89 patients who survived, 18 had signs of anoxic brain damage; 96 patients died, 76 as a result of cerebral anoxia. Only 2 patients survived out of the total of 72 for whom the first EEG was classified as grades III--V. The EEGs of both these patients were recorded within a few hours after the cardiac arrest. None of the patients with an EEG of grade I died of cerebral anoxia, while all degrees of brain damage were otherwise observed in connection with EEGs of both grades I and II. It is concluded that an EEG of grades III--V indicates a fatal outcome, provided it has been recorded more than 24 hours after the cardiac arrest. A grade III--V EEG that is recorded within 24 hours after a cardiac arrest should be repeated some days later. It is not possible, on the basis of a single EEG, to predict the extent of the anoxic brain damage.
The variables monitored in intensive care units are generally late indicators of neurologic deterioration. A system based on a LINC-8 computer was therefore developed for on-line monitoring of evoked potentials, electroencephalography (EEG), and transcranial and transthoracic impedances as well as conventional parameters. Somatosensory evoked potentials are recorded at either 30 min or 1 h intervals. One minute epochs of EEG are analyzed every 10 min using a peak-detection algorithm. Impedances and conventional parameters are also monitored at 10 min intervals. In a study of 50 patients, the technical feasibility of this type of monitoring with a small laboratory computer has been demonstrated. In some instances, evoked potentials and EEG show changes prior to detectable neurologic changes. The study suggests that this type of monitoring can provide a valuable adjunct for evaluation of physiologic function in neurosurgical intensive care.
By means of the methods of local cerebral rheoencephalography (REG) and electroencephalography (EEG) the effect of piracetam (1-acetamide-2-pyrrolidone, Pyramem) on cerebral circulation and brain bioelectrical activity was studied in acute experiments on dogs. The following REG parameters were assayed: anacrotic section of the curve and its relative part, amplitude and dicrotic index. The influence of the preparation on the spontaneous EEG was studied by means of surface electrodes, pH, pO2, and pCO2 were determined in blood samples from femoral artery and superior sagittal sinus and arterio-venous differences of O2 (AVD-O2) and CO2 (AVD-CO2) were calculated. The arterial pressure and ECG were followed continuously. The results showed that after piracetam administration (100 mg/kg i.v.) an improvement of the REG parameters is observed: increase of the amplitude and decrease of the values of the relative part and dicrotic index. The changes observed indicated cerebro-vascular resistance decrease and increase of the cerebral blood volume. The AVD-O2 increased and the negative AVD-CO2 decreased. The EEG data indicated an improvement in the functional state of the brain cortex. Suggestions as to mechanism of piracetam effect and the usefulness of the methods were made.
BACKGROUND: Decades before the emergence of precision medicine, psychiatrists raised the question of whether specific seizure characteristics could help optimize electroconvulsive therapy (ECT), as relationships between some of these characteristics and better outcomes were found. From 1990 onward, researchers focused on electroencephalography (EEG) and cardiovascular markers, which were broadly adopted by guidelines worldwide. However, the prognostic value of these markers is still controversial. Here, we provide a systematic summary of the studies on this topic. METHODS: We conducted a literature review on the use of ictal EEG and heart rate as outcome predictors in ECT using the PubMed, EMBASE, Cochrane and PsycINFO databases. RESULTS: Thirty-seven studies addressing more than 100 quality markers fulfilled our inclusion criteria. Single EEG markers were assigned to five categories (postictal inhibition, amplitude, coherence, regularity, and seizure duration). Heart rate and composite markers were considered separately. In contrast to single EEG markers, heart rate and composite markers could be consistently linked to better outcomes in patients with depression. Only a few studies on schizophrenia could be retrieved. CONCLUSION: Multiparametric markers outperformed single markers. Furthermore, changes in heart rate during seizures were related to better outcomes. Although clinical assessment remains the cornerstone of treatment guidance decisions, EEG and cardiac monitoring could help prevent insufficient seizures during the period preceding clinical improvement. Evidence on schizophrenia remains limited. More randomized trials are needed to analyze the role of composite markers as prognostic tools.
Excitation (E)/inhibition (I) imbalance is considered a key mechanism in Autism Spectrum Disorder (ASD). However, E/I imbalance can have different etiologies with increased E relative to I (E > I) and increased I relative to E (E < I). Both neural profiles can be associated with altered clinical phenotype, suggesting "bell"-shape brain-behavior relationships. We derived E/I balance measures from resting-state EEG in a large sex-balanced sample of youths with and without autism (N = 310; 164 youths with ASD and 146 typically developing (TD) youths) to address group discriminative power of neural markers, their relation to social skills, and the potential to define different neural subtypes within the autistic group. We also conducted genome-wide copy number variant (CNV) and gene expression analyses to provide additional insight into distinct neural subtypes in autism. A high-density 128-channel electroencephalography (EEG) was used to register neural activity of participants, blood samples were collected from the ASD youths to obtain genomic DNA, and rich behavioral phenotyping was provided for each participant. The results revealed three subgroups within the autistic cohort with the presence of "typical" E/I, E > I, and E < I neural profiles. The two subgroups with E/I imbalance had altered clinical phenotypes. In addition, these subgroups had different genetic profiles, showing that genes within identified CNVs had distinct expression patterns with the evidence of more prenatal (E < I) vs. postnatal (E > I) gene expression. The study suggests that the proposed clustering approach has relevance for the identification of clinically meaningful neural and genetic subtypes within a heterogeneous autistic cohort.
Effects on the cat central nervous system of water extracts of Zingiber Mioga (ZM) were studied by electroencephalography (EEG). ZM had little effect on the EEG arousal response to electrical stimulation of mid-brain reticular formation. ZM (3 approximately 5 mg/kg, i.v.) suppressed the recruiting response and the augmenting response recorded from the posterior sigmoid gyrus, respectively. ZM (1 approximately 3 mg/kg, i.v.) decreased the photic driving response, while 5 mg/kg, i.v., tended to enhance the response. In the chronic experiments, ZM(1 approximately 3 mg/kg, i.v.) induced a drowsy pattern in the cortex and subcortex, and shortened the lasting time of the EEG arousal response to sonic stimulation. After 5 to 10 minutes, behavior showed a drowsy to light sleeping state, and electromyogram recorded from the platysma showed a decreased amplitude and frequency, but, did not have an inhibitory effect on the motor system, (ataxia). ZM (5 mg/kg, i.v.) induced desynchronization in the cortex and subcortex, arousal wave appeared in hippocampus, midbrain reticular formation, nucl. ventralis postero-lateralis and amygdala, and behavior tended toward the awake stage. After 10 minutes, EEG transferred to a drowsy pattern and behavior showed a drowsy to light sleeping state. The animal could be readily awakened by sonic stimulation, at every time. ZM appears to have an inhibitory effect on the central nervous system.
The behavioral effects of tetrahydroberberine (THB), tetrahydrocoptisine (THC), tetrahydropalmatine (THP) and tetrahydrojateorrhizine (THJ) were compared with those of chlorpromazine (CPZ) and benzodiazepines in mice and rats. Effects of THB were also determined by electroencephalography (EEG) in rabbits. THB was found to pharmacologically exert various actions similar to those of CPZ which is a major tranquilizer, however, the actions of THB were weaker than those of CPZ. Although THB alone did not induce catalepsy, it enhanced the cataleptogenic action of CPZ. At a dose over the effective levels, THB did not lower normal body temperature or induce muscle relaxation and loss of righting reflex. EEG activities in the frontal cortex areas were markedly affected by THB, e.g., fast waves in spontaneous EEG were converted to slow waves. THB and CPZ in a similar manner elicited a sustaining increase in hippocampal afterdischarge, but the action of THB was weaker than that of CPZ. The acute toxicity of THB was lower than that of CPZ and benzodiazepines and the depressant activity of THB almost equalled that of THC and THP, whereas the activity of 1-THB was 1.5 times as great as that of THB. These data indicate that THB, THC and THP may be a new type of tranquilizer.
7 adult cases with petit mal status are described; most of these patients had clinical recurrences of petit mal seizures after time intervals ranging from 15 to 50 years. Electroencephalography (EEG) and computerized transverse axial tomography (CT) findings are described and correlated. All CT studies showed frontal lobe abnormalities. When speaking of absence status in the adult, it is useful to distinguish between such an event within the course of primary generalized epilepsy and its reactivation after a very long seizure-free period at an older age. Such reactivations occur preferentially in women. CT supplies more structural information on the living brain and thus we could identify a dysplastic configuration of the skull and hemispheres in a 28-year-old patient and frontocortical and moderate subcortical lesions in the older age-group. The role of the frontal lobe in releasing spike-and-wave discharges of different degrees of generalization appears to be a new aspect worthy of further investigation.
BACKGROUND: Sleep and epilepsy interact through complex bidirectional mechanisms. Although NREM sleep facilitates interictal epileptiform discharges (IED), the diagnostic contribution of individual sleep stages remains uncertain. In particular, it is unclear whether deeper sleep stages such as N3 provide an advantage over N2 for spike detection or localization in clinical (electroencephalography) EEG practice. METHODS: This systematic review followed PRISMA 2020 guidelines. PubMed and Web of Science were searched for studies reporting quantitative IED measures across sleep stages in patients with epilepsy. Eligible studies included scalp EEG, video-EEG, polysomnography, or intracranial recordings. Mean IED rates per minute were derived when possible. Comparisons between NREM and REM sleep and between N2 and N3 stages were performed using study level non-parametric tests. Risk of bias was assessed with the ROBINS-I tool. RESULTS: Ten observational studies including 266 patients (mean age 30.1 years) were analyzed. IED rates were significantly higher during NREM than REM sleep (Wilcoxon signed-rank test, W = 0, p = 0.0019, r = 0.87). No significant difference was observed between N2 and N3 sleep, although median spike rates were slightly higher during N3 than N2 (0.99 vs 0.86 IED/min). REM showed the lowest activity. CONCLUSIONS: NREM sleep consistently exhibited higher IED rates than REM sleep, reinforcing the neurophysiological association between sleep stage and epileptiform activity without establishing diagnostic superiority.