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EEG Patterns and Imaging Correlations in Encephalopathy: Encephalopathy Part II
Abstract
The EEG patterns seen with encephalopathies can be correlated to cerebral imaging findings including head computerized tomography and MRI. Background slowing without slow-wave intrusion is seen with acute and chronic cortical impairments that spare subcortical white matter. Subcortical/white matter structural abnormalities or hydrocephalus may produce projected slow-wave activity, while clinical entities involving both cortical and subcortical regions (diffuse cerebral abnormalities) engender both background slowing and slow-wave activity. Triphasic waves are seen with hepatic and renal insufficiency or medication toxicities (e.g., lithium, baclofen) in the absence of a significant cerebral imaging abnormality, Conversely, subcortical/white matter abnormalities may facilitate the appearance of triphasic waves without significant hepatic, renal, or toxic comorbidities. More specific syndromes, such as Jakob-Creutzfeldt disease, autoimmune limbic encephalitis, autoimmune corticosteroid-responsive encephalopathy with thyroid autoimmunity, sepsis-associated encephalopathy, and acute disseminated encephalomyelitis, have imaging/EEG changes that are variable but which may include slowing and epileptiform activity. This overview highlighting EEG-imaging correlations may help the treating physician in the diagnosis, and hence the appropriate treatment, of patients with encephalopathy.
... Encephalopathy is an acute/subacute consciousness disorder which may result from a variety of causes, including metabolic (see Figure 6), toxic, infective or structural brain dysfunction [65]. Despite the poor specificity of slow wave EEG, is well known that selective cortical damage is associated to slowing of the resting background in the theta frequency, while subcortical white matter damage produces polymorphic delta activity [66]. ...
... Slower delta activity is seen with more severe manifestations of encephalopathy. Patients with polymorphic delta activity have large areas of subcortical white matter dysfunction [66] or severe metabolic or infectious derangements [70]. Delta EEG may be also associated with posterior reversible encephalopathy. ...
... Intermittent rhythmic delta activity, which is usually frontally predominant, is a nonspecific pattern that may be seen in a variety of causes, including metabolic encephalopathies, increased third ventricle pressure, hemispheric lesions, or widespread dysfunction of the cortical and subcortical structures [66,96]. Burst suppression or Suppression burst pattern is commonly seen following severe hypoxic-ischemic injury, though it may evolve or transition later to alpha or theta coma, and then to electro-cerebral inactivity [93]. ...
Introduction: Some neurologic conditions that can quickly and with low costs be recognized, classified and treated thanks to the availability of an EEG recording in an emergency setting. However, although considered a cheap, not invasive, highly accurate diagnostic investigation, still today, an EEG recording in emergency, in real time during the event paroxysmal ictal phase, is not yet been become a routine.
Areas covered: This review will cover the role and utility of EEG recording in the emergency setting, both in emergency department and intensive care unit, in adult and pediatric age, in people admitted for status epilepticus (convulsive or non-convulsive), paroxysmal non-epileptic events, or other conditions/diseases presenting with mental status changes.
Expert opinion: The prompt recognition of some specific EEG-patterns can permit an immediate and appropriate therapeutic choice with the resolution of dramatic clinical pictures, which, if not recognized, sometimes could result in severe prognostic events with high mortality or neuropsychiatric disability. It is important in the next future, to improve the availability of these EEG digital continuous monitoring, which should be widely used in emergency settings, developing moreover tools and techniques permitting also review, analysis and EEG-reporting by experts who can work away from the hospital.
... HE is clinically manifested as disorientation, confusion, inappropriate behavior, agitation, somnolence, stupor, and/or frank coma. A wide range of motor dysfunctions has been described in HE, including asterixis, hypertonia, hyperreflexia, and/or extrapyramidal manifestations [2]. ...
... HE is associated with a poor survival outcome and a high risk of in-hospital mortality [2]. This necessitated the development of a number of prognostic scoring systems to estimate the clinical outcome of HE in clinical practice. ...
Background
Hepatic encephalopathy (HE) is a serious condition associated with high rates of mortality. Many scoring systems are used to predict the outcome of HE in patients admitted to the intensive care unit (ICU). The most used scores are Child-Turcotte-Pugh (CTP), Model for End-stage Liver Disease (MELD), Chronic Liver Failure-Sequential Organ Failure Assessment (CLIF-SOFA), and Acute Physiology and Chronic Health Evaluation II (APACHE II). These scores were thoroughly investigated in HE associated with acute liver failure (type A). In the present study, we aimed to evaluate the prognostic value of these scores in patients with HE on a background of liver cirrhosis (type C). Two hundred cirrhotic patients hospitalized with HE were included in the study. Diagnosis and classification of HE were based on the West Haven criteria. APACHE II, CLIF-SOFA, MELD, MELD-Na, and CTP scores were calculated for all patients within the first 24 h after admission. According to survival outcomes, patients were categorized into either improved or deceased. Demographic, clinical, and laboratory data as well as prognostic scores were compared in both deceased and improved groups. The receiver operating characteristic (ROC) curve was plotted, and the area under the ROC curve (AUROC) was calculated for each score. Backward logistic regression analysis was used to identify the predictors of mortality.
Results
60.5% of patients were males. The mean age was 61.09 ± 8.94 years. The main precipitating factors of HE was infections predominantly spontaneous bacterial peritonitis ( n = 108, 54.0%) followed by variceal bleeding ( n = 39, 19.5%). All scores were significantly higher in the deceased patients. AUROC were 0.734 (CI95% 0.666–0.803), 0.717 (CI95% 0.647–0.787), 0.663 (CI95% 0.589–0.738), 0.626 (CI95% 0.549–0.704), and 0.609 (CI95% 0.531–0.686) for CLIF-SOFA, MELD-Na, MELD, APACHE II, and CTP scores, respectively. MELD, MELD-Na, and CLIF-SOFA scores were the independent predictors of mortality. Among these scores, CLIF-SOFA was the strongest independent predictor of mortality (OR = 1.142, CI95% = 0.888–1.467, p = 0.001).
Conclusions
CLIF-SOFA score was superior to other prognostic scores in predicting mortality in hospitalized patients with HE type C.
... For each subject, the PSD was averaged in the canonical frequency bands (i.e., delta 0.5-3; theta 4-7; alpha 8-12; low beta 13-17; high beta 18-30) by averaging across all electrodes and for all frequency bins. Our analysis was restricted to frequencies up to 30 Hz due to the lower quality of the EEG above that frequency (50 Hz line noise and other artefacts). ...
... The occurrence of ic-IED was demonstrated to be associated with increased delta power on scalp EEG, in particular for frequencies equal to or higher than 1. Focal delta slow waves have generally been considered the classic sign of a brain lesion, in particular located at the level of the deep white matter [26][27][28] or thalamus [29], but studies also demonstrated that they do not have a specific nature and are present in a large range of brain lesions (for instance tumoural lesions [27] or cortical-subcortical abnormalities [30]) and encephalopathic conditions [31]. ...
Background
To evaluate whether interictal epileptiform discharges (IEDs) that are not visible on the scalp are associated with changes in frequency spectrum on scalp EEG.
Methods
We recorded simultaneous scalp high-density EEG and intracranial EEG recordings in 9 patients undergoing presurgical invasive recordings for pharmaco-resistant temporal lobe epilepsy. We selected epochs with hippocampal IED visible on intracranial EEG (ic-IED) but not on scalp EEG, as well as control epochs without intracranial EEG IED. We computed Welch’s power spectral density (PSD) for each scalp electrode and for each subject, the PSD was further averaged across the canonical frequency bands and compared between the two conditions with and without ic-IED. For each patient we determined the peak frequency in the delta band (the significantly strongest frequency band in all patients) during periods of ic-IED. We also determined the five electrodes showing strongest power at the peak frequency.
Results
We found that IEDs are associated with an increase in delta power on scalp EEG, in particular at frequency ≥ 1.4Hz. Electrodes showing slow frequency power changes associated with IEDs were consistent with the hemispheric lateralization of IED. Electrodes with maximum power of slow activity were not limited to temporal regions but also involved frontal (bilateral or unilateral) regions.
Conclusions
In patient with clinical picture suggestive of temporal lobe epilepsy, the presence of delta slowing ≥1.4Hz in anterior-temporal regions can represent a scalp marker of hippocampal IEDs. To our best knowledge this is the first study that demonstrates the co-occurrence of intracranial IED and increased delta power.
... Low voltage or generalized suppression patterns is often associated with extensive cortical and subcortical lesions such as anoxic encephalopathy or severe head trauma. This pattern was related to an unfavorable prognosis (score 4 qualitative classification of EEG alteration: Amodio et al., 1999) [40][41][42] or irreversible character as at ischemic encephalopathy 39,[42][43][44][45] with the exception of hypothyroid encephalopathy, which is reversible except for cretinism. 39,42,43,[45][46][47] , but in our series we found a good evolution in 60% of the patients. ...
... EEG patterns we observe has findings like those observed in ischemic encephalopathy described in the literature (low voltage and unreactive to external stimuli). 39,40,[42][43][44][45] However, by performing follow-up EEGs, we have been able to document how our patients present a reversible picture both in the clinic and in the EEG. So, we also believe that ischemia does not appear to be the cause of these EEG findings, in addition to the fact that the respiratory and hemodynamic status of patients does not suggest it (some patients did not even need oxygen). ...
Background. Interest in electroencephalographic (EEG) coronavirus disease 2019 (COVID-19) findings has been growing, especially in the search for a specific-features EEG of encephalopathy. Methods. We made a retrospective analysis of 29 EEGs recorded in 15 patients with COVID-19 and neurological symptoms. We classified the EEGs as “Acute EEG” and “follow-up EEG.” We did a statistical analysis between voltage and respiratory status of the patient, stay or not in the intensive care unit (ICU), days of stay in the ICU, sedative drugs, pharmacological treatment, type of symptoms predominating, and outcome. Results. We found EEG abnormalities in all patients studied. We observed the amplitude of background <20 µV at 93% of “acute EEG,” versus only 21.4% of “follow-up EEG.” The average voltage went from 12.33 ± 5.09 µV in the acute EEGs to 32.8 ± 20.13 µV in the follow-up EEGs. A total of 60% of acute EEGs showed an intermittent focal rhythmic. We have not found a statistically significant association between voltage of acute EEG and nonneurological clinical status (including respiratory) that may interfere with the EEG findings. Conclusions. Nonspecific diffuse slowing EEG pattern in COVID-19 is the most common finding reported, but we found in addition to that, as a distinctive finding, low voltage EEG, that could explain the low prevalence of epileptic activity published in these patients. A metabolic/hypoxic mechanism seems unlikely on the basis of our EEG findings. This pattern in other etiologies is reminiscent of severe encephalopathy states associated with poor prognosis. However, an unreactive low voltage pattern in COVID-19 patients is not necessarily related to poor prognosis.
... As alpha frequencies are supposed to originate from cortical layers, cortical impairment due to stroke lesions may weaken alpha activity. Studies of combined EEG, MRI, CT research reflected alpha attenuation as a sign of brain injury [19,25]. Beta activity is higher in the stroke group than the control group in the working and cognitive tasks. ...
... Delta activity may suggest hyperpolarization and curbing of cortical nerve cells, hampering neural activity. An increase in abnormal delta is often associated with brain injury (lesion) location [25]. Previous studies revealed higher delta power in the electrodes of the cortical positions in post-stroke recording [7,31,32]. ...
Electroencephalography (EEG) can access ischemic stroke-derived cortical impairment and is believed to be a prospective predictive method for acute stroke prognostics, neurological outcome, and post-stroke rehabilitation management. This study aims to quantify EEG features to understand task-induced neurological declines due to stroke and evaluate the biomarkers to distinguish the ischemic stroke group and the healthy adult group. We investigated forty-eight stroke patients (average age 72.2 years, 62% male) admitted to the rehabilitation center and seventy-five healthy adults (average age 77 years, 31% male) with no history of known neurological diseases. EEG was recorded through frontal, central, temporal, and occipital cortical electrodes (Fz, C1, C2, T7, T8, Oz) using wireless EEG devices and a newly developed data acquisition platform within three months after the appearance of symptoms of ischemic stroke (clinically confirmed). Continuous EEG data were recorded during the consecutive resting, motor (walking and working activities), and cognitive reading tasks. The statistical results showed that alpha, theta, and delta activities are biomarkers classifying the stroke patients and the healthy adults in the motor and cognitive states. DAR and DTR of the stroke group differed significantly from those of the healthy control group during the resting, motor, and cognitive tasks. Using the machine-learning approach, the C5.0 model showed 78% accuracy for the resting state, 89% accuracy in the functional motor walking condition, 84% accuracy in the working condition, and 85% accuracy in the cognitive reading state for classification the stroke group and the control group. This study is expected to be helpful for post-stroke treatment and post-stroke recovery.
... L'IRM serait un outil complémentaire de l'EEG pour la recherche de diagnostics différentiels mais non contributif pour le diagnostic d'encéphalopathie spécifique du lithium [32]. Cependant, grâce aux dernières avancées technologiques, l'IRM 9,5 Tesla permet la détection d'éléments de plus petite taille dans le cerveau, comme l'acide ascorbique, et pourrait donc apporter une plus-value dans le diagnostic d'encéphalopathies métaboliques [32]. ...
... L'IRM serait un outil complémentaire de l'EEG pour la recherche de diagnostics différentiels mais non contributif pour le diagnostic d'encéphalopathie spécifique du lithium [32]. Cependant, grâce aux dernières avancées technologiques, l'IRM 9,5 Tesla permet la détection d'éléments de plus petite taille dans le cerveau, comme l'acide ascorbique, et pourrait donc apporter une plus-value dans le diagnostic d'encéphalopathies métaboliques [32]. Les patients traités par lithium au long cours présenteraient un volume de matière grise significativement plus important que les individus non exposés [33], avec une augmentation significative de la taille des structures limbiques (amygdale, hippocampe, thalamus) comparativement aux sujets non exposés [34]. ...
L'intoxication au lithium peut entraîner des complications neurologiques graves comme une altération de la conscience et un tableau d'encéphalopathie, avec un risque de décès ou de séquelles au long cours. Avec une présentation parfois atypique, voire même sans hyperlithiémie plasmatique initiale, le retard au repérage de ces complications peut être important. De plus, aucune recommandation spécifique de ces complications n'est disponible dans la littérature. L'objectif de cet article est de proposer une mise au point concernant la prise en charge diagnostique et thérapeutique des complications neurologiques, telles que l'encéphalopathie, imputables au lithium.
Lithium intoxication may induce neurological complications, initially characterised by a conscience alteration and an encephalopathy clinical picture with a risk of death or sever long-term consequences. With an occurrence sometimes atypical and possibly without initial hyperlitemia, the diagnosis delay of these complications might be important. Moreover, no specific guidelines focused on these complications are available. The aim of this article is to propose an update on diagnosis and treatment of neurological complications attributable to lithium, as encephalopathy.
... 3.5. Electroencephalographers should have a solid knowledge of EEG patterns seen in the ICU, e.g., anoxic (post-cardiac arrest syndrome), toxic, metabolic, sepsis, and hypercapnic/hypoxic encephalopathies (Kaplan and Rossetti, 2011;Bauer et al., 2013;Stern, 2015;Gélisse et al., 2019;Kaplan et al., 2020). Etiologies may be mixed (Fig. 1 Infectious encephalitides may show LPDs with periodicity of less of four seconds (so called "short periods") (Gaches, 1971;Dunand and Jallon 2002). ...
... Acute disseminated encephalomyelitis (ADEM) is an inflammatory disorder, typically occurring a few days after a viral or bacterial infection, and is more common in children. The EEG may show bilateral slow-wave activity, more or less symmetrically (Dale et al., 2000;Hollinger et al., 2002;Kaplan and Rossetti, 2011), sometimes with focal slowing and less frequently, with epileptiform discharges (Dale et al., 2000;Hollinger et al., 2002). In children, anterior, bilateral, high-voltage and sometimes asymmetric complexes have been reported (Fig. 4). ...
There are questions and challenges regarding neurologic complications in COVID-19 patients. EEG is a safe and efficient tool for the evaluation of brain function, even in the context of COVID-19. However, EEG technologists should not be put in danger if obtaining an EEG does not significantly advance diagnosis or change management in the patient. Not every neurologic problem stems from a primary brain injury: confusion, impaired consciousness that evolves to stupor and coma, and headaches are frequent in hypercapnic/hypoxic encephalopathies. In patients with chronic pulmonary disorders, acute symptomatic seizures have been reported in acute respiratory failure in 6%. The clinician should be aware of the various EEG patterns in hypercapnic/hypoxic and anoxic (post-cardiac arrest syndrome) encephalopathies as well as encephalitides. In this emerging pandemic of infectious disease, single-use subdermal EEG needle electrodes may be used in comatose patients. Full EEG montages using the 10-20 system, including a derivation for ECG, are strongly recommended so as to cover relevant temporal lobe regions. We recommend noting whether the patient is undergoing or has been placed prone, as well as noting the body and head position during the EEG recording (supine versus prone) to avoid overinterpretation of respiratory, head movement, electrode, muscle or other artifacts. There is slight elevation of intracranial pressure in the prone position. In non-comatose patients, the hyperventilation procedure should be avoided. At present, non-specific EEG findings and abnormalities should not be considered as being specific for COVID-19 related encephalopathy.
... Bilateral tonic-clonic seizures are an uncommon manifestation of MIE and the EEG findings associated with this condition are considered unspecific [19]. In general, EEG has been successfully applied to identify epileptic states or interictal pattern or whether an altered mental status derives from lateralized focal dysfunction or significant metabolic alterations; however, the correlation between EEG patterns, imaging findings and specific clinical diagnoses such as MIE are underrecognized, and much of our understanding of these correlations come from isolated case reports [20]. Investigations with electro-clinical-neuroimaging correlations would expedite appropriate diagnosis and clinical management of patients in the ICU and neurological ward, improving patients' care and shortening the duration of patients' stay in the hospital [20,21]. ...
... In general, EEG has been successfully applied to identify epileptic states or interictal pattern or whether an altered mental status derives from lateralized focal dysfunction or significant metabolic alterations; however, the correlation between EEG patterns, imaging findings and specific clinical diagnoses such as MIE are underrecognized, and much of our understanding of these correlations come from isolated case reports [20]. Investigations with electro-clinical-neuroimaging correlations would expedite appropriate diagnosis and clinical management of patients in the ICU and neurological ward, improving patients' care and shortening the duration of patients' stay in the hospital [20,21]. ...
Metronidazole-induced encephalopathy (MIE) is a rare and often under-recognized iatrogenic condition. The diagnosis should be considered in metronidazole-treated patients presenting with acute encephalopathy, unprovoked seizures and cerebellar signs. While typical magnetic resonance imaging (MRI) findings strongly support the diagnosis, electroencephalography (EEG) features have been rarely reported and poorly described. We present a longitudinal EEG assessment in one patient with encephalopathy due to metronidazole toxicity who presented a peculiar EEG pattern presentation and evolution. During the acute phase of encephalopathy, the EEG showed a monomorphic, sharply contoured theta activity symmetrically represented over frontal regions with an anterior-posterior progression which evolved in parallel with clinical worsening. Together with a systematic review of the literature, we discuss whether this EEG activity may represent a distinct neurophysiological correlate of 'cerebellar encephalopathy'.
... Delta wave may indicate hyperpolarization and curbing of cortical nerve cells, hindering neural activity. Abnormal delta activity is often associated with brain injury (lesion) location [36]. Several studies revealed higher delta power in the electrodes of the cortical positions in post-stroke EEG [5,6]. ...
State-of-the-art healthcare technologies are incorporating advanced Artificial Intelligence (AI) models, allowing for rapid and easy disease diagnosis. However, most AI models are considered “black boxes,” because there is no explanation for the decisions made by these models. Users may find it challenging to comprehend and interpret the results. Explainable AI (XAI) can explain the machine learning (ML) outputs and contribution of features in disease prediction models. Electroencephalography (EEG) is a potential predictive tool for understanding cortical impairment caused by an ischemic stroke and can be utilized for acute stroke prediction, neurologic prognosis, and post-stroke treatment. This study aims to utilize ML models to classify the ischemic stroke group and the healthy control group for acute stroke prediction in active states. Moreover, XAI tools (Eli5 and LIME) were utilized to explain the behavior of the model and determine the significant features that contribute to stroke prediction models. In this work, we studied 48 patients admitted to a hospital with acute ischemic stroke and 75 healthy adults who had no history of identified other neurological illnesses. EEG was obtained within three months following the onset of ischemic stroke symptoms using frontal, central, temporal, and occipital cortical electrodes (Fz, C1, T7, Oz). EEG data were collected in an active state (walking, working, and reading tasks). In the results of the ML approach, the Adaptive Gradient Boosting models showed around 80% accuracy for the classification of the control group and the stroke group. Eli5 and LIME were utilized to explain the behavior of the stroke prediction model and interpret the model locally around the prediction. The Eli5 and LIME interpretable models emphasized the spectral delta and theta features as local contributors to stroke prediction. From the findings of this explainable AI research, it is expected that the stroke-prediction XAI model will help with post-stroke treatment and recovery, as well as help healthcare professionals, make their diagnostic decisions more explainable.
... Alternatively, there remains the possibility that structural damage disrupting coordination between brain regions could be responsible for the steepening of the aperiodic slope. For instance, disruption of thalamocortical connections via white matter lesions has been associated with increased power in the delta band and suppression of fast activity (Kaplan and Rossetti, 2011) an effect which may in fact reflect a rotation of the aperiodic power spectrum, as demonstrated here. ...
Decades of electrophysiological work have demonstrated the presence of “spectral slowing” in stroke patients – a prominent shift in the power spectrum towards lower frequencies, most evident in the vicinity of the lesion itself. Despite the reliability of this slowing as a marker of dysfunctional tissue across patient groups as well as animal models, it has yet to be explained in terms of the pathophysiological processes of stroke. To do so requires clear understanding of the neural dynamics that these differences represent, acknowledging the often overlooked fact that spectral power reflects more than just the amplitude of neural oscillations. To accomplish this, we used a combination of frequency domain and time domain measures to disambiguate and quantify periodic (oscillatory) and aperiodic (non-oscillatory) neural dynamics in resting state magnetoencephalography (MEG) recordings from chronic stroke patients. We found that abnormally elevated low frequency power in these patients was best explained by a steepening of the aperiodic component of the power spectrum, rather than an enhancement of low frequency oscillations, as is often assumed. However, genuine oscillatory activity at higher frequencies was also found to be abnormal, with patients showing alpha slowing and diminished oscillatory activity in the beta band. These aperiodic and periodic abnormalities were found to covary, and could be detected even in the un-lesioned hemisphere, however they were most prominent in perilesional tissue, where their magnitude was predictive of cognitive impairment. This work redefines spectral slowing as a pattern of changes involving both aperiodic and periodic neural dynamics and narrows the gap in understanding between non-invasive markers of dysfunctional tissue and disease processes responsible for altered neural dynamics.
... The occurrence of isolated delta and theta waves in the wake EEG of septic patients suggests that they are at least in part related to oscillations. 17,53,54 Unfortunately, most of the discussed papers limit their spectrum analysis to only one vigilance state, or in some cases to a single frequency band of interest. Where oscillatory activity is discussed, spectra were typically not decomposed into periodic and aperiodic components. ...
Sepsis-associated encephalopathy (SAE) is a frequent severe complication of sepsis and the systemic inflammatory response syndrome, associated with high mortality and long-term neurological consequences in surviving patients. One of the main clinical sings of SAE are discontinuous sleep periods that are fragmented by frequent awakening. Even though this brain state fragmentation strongly impacts the functionality of the nervous- as well as other systems, its underlying network mechanisms are still poorly understood. In this work, we therefore aim at characterizing the properties and dynamics of brain oscillatory states in response to SAE in an acute rat model of sepsis induced by high dose LPS (10 mg/kg). To focus on intrinsically generated brain state dynamics, we used a urethane model that spares oscillatory activity in REM- and NREM-like sleep states. Intraperitoneal LPS injection led to a robust instability of both oscillatory states resulting in several folds more state transitions. Using power spectra analysis we identified opposing shifts in low frequency oscillations (1–9 Hz) in REM and NREM-like states under influence of LPS. This resulted in increased similarity between both states. Moreover, the state-space jitter in both states increased as well, pointing to higher within-state instability. The reduction of inter-state spectral distances in 2-D state space, combined with increased within-state jitter might represent a key factor in changing the energy landscape of brain oscillatory state attractors, and hence lead to altered sleep architecture. Their emergence during sepsis might point to a mechanism underlying severe sleep fragmentation as described both in sepsis patients and SAE animal models.
... Циррозы печени в структуре гастроэнтерологической патологии занимают особое место, связанное не только с клиническими проявлениями терминальной стадии патологии печени, но и с системными эффектами функциональной неполноценности печени [7,8]. Вместе с тем, связь патологии печени и заболеваний пародонта изучена недостаточно, а диагно-стика пародонтитов зачастую носит отсроченный характер [9,10,11]. При циррозах печени заболевания пародонта могут возникать как самостоятельно существующие, так и способствовать ускорению терминальной фазы течения заболевания с возникновением системных инфекций [12,13,14]. ...
The frequency and clinical course of chronic generalized periodontitis against the background of liver cirrhosis of various etiologies were studied. 70 patients with chronic generalized periodontitis of varying degrees in combination with liver cirrhosis were examined (23 patients (32.9%) had liver cirrhosis class A, 25 (35.7%) — class B, 22 (31.4%) — class C. Comparison group — 17 patients with periodontitis without somatic pathology. Control group — 20 practically healthy volunteers. A signifi cantly reduced level of oral hygiene was revealed in patients with liver cirrhosis of classes B and C. Periodontal pathogenic microorganisms were signifi cantly more common in the contents of periodontal pockets with cirrhosis. With an increase in the class of CP, the frequency of bacterial expansion increased. The severity of periodontal damage in patients with liver cirrhosis is associated with a loss of bone mineral density by the type of osteopenia (47.2%) or osteoporosis (31.4%), increasing according to the class of liver cirrhosis and the severity of periodontal disease The degree of resorption of the alveolar process is associated with a systemic decrease in bone mineral density. The eff ects of generalized osteopenic syndrome and resorption of the alveolar processes are characteristic of patients with alcoholic liver damage and liver cirrhosis with cholestasis syndrome.
... The increase of alpha oscillations and decrease of delta oscillations may also indicate a relief of subcortical and cortical injury by XNKQ acupuncture, since the abnormal delta activity has been found to reflect cortical deafferentation due to subcortical injury, whereas the alpha activity disturbances, such as attenuation or slowing, are generally indicative of cortical injury. 34 It should be noted that the decrease in the relative delta power and the increase in the relative alpha power were regionally distinct between the first 0-14 days and in the latter 15-30 days. Both changes in the delta and alpha bands occurred initially in the intact hemisphere and later partly transferred to the peri-infarct cortex. ...
Objectives: In China, Xingnao Kaiqiao (XNKQ) acupuncture has been widely used for stroke treatment. However, its electrophysiological mechanism remains unclear. Hence, this study aims to study how XNKQ acupuncture modulates brain rhythm oscillations of stroke patients, and investigate its correlation with stroke recovery. Design: Randomized control trial. Subjects: Twenty (sub)acute ischemic stroke patients were enrolled and randomly assigned to two groups (an acupuncture group [AG] [n = 10] and a control group [CG] [n = 10]), and four patients (two patients in each group) dropped out of the study. Interventions: All patients received conventional treatments, and the patients in AG received additional XNKQ acupuncture treatment once a day for 10 consecutive days. Outcome measures: Before treatment, 14 days after, and 30 days after treatment onset, their movement impairments and neurologic deficits were measured using the National Institute of Health Stroke Scale (NIHSS), the Fugl-Meyer (FM) Scale, the Modified Rankin Scale (mRS), and the Modified Barthel Index (MBI), and their electroencephalogram data were recorded. Results: Compared with the CG, the AG showed more improvement in FM scores (p = 0.02), as well as decreased relative delta power and increased relative alpha power after 2 weeks' treatment. The decrease of the relative delta power and the increase of the relative alpha power in the ipsilesional frontal area were significantly correlated with the FM improvement (F5, F7, FC1, and Fz electrodes, all |r| > 0.517, p < 0.040). Conclusions: The curative effect of XNKQ acupuncture related to its electrophysiological modulation. This study was registered at the Chinese Clinical Trial Registry (ChiCTR2000038560).
... is not clear how much the previously described power spectrum changes are due to altered background spectrum or specific oscillatory activity, as the peak frequencies within spectral power bands were typically not analyzed. The occurrence of isolated delta and theta waves in the wake EEG of septic patients suggests that they are at least in part related to oscillations (Bolton, 1987;Kaplan and Rossetti, 2011;Oddo et al., 2009). ...
Sepsis-associated brain dysfunction (SABD) is a frequent severe complication of sepsis and the systemic inflammatory response syndrome. It is associated with high mortality and a majority of survivors suffer long-term neurological consequences. Here, we studied the effects of SABD on oscillatory brain states in an acute rat model of sepsis induced by high dose LPS (10 mg/kg). To focus on intrinsically generated brain state dynamics, we used a urethane model that spares oscillatory activity in REM- and NREM-like sleep states. Soon after the intraperitoneal LPS injection we observed a robust fragmentation of both oscillatory states resulting in a three-fold increase in the number of state transitions that lasted for several hours, although the overall time spent in either state did not change. Analysis of power spectra showed opposing shifts in low frequency oscillations (1-9 Hz) that resulted in increased similarity between both states in 2-D state space. The described spectral characteristics of sepsis-induced EEG state instability might point to a mechanism underlying severe sleep fragmentation as described both in sepsis patients and in SABD animal models.
... Потенциал Р300 регистрировали в рамках вероятностной парадигмы появления значимого стимула (тон 2000 Гц) и незначимого стимула (тон 1000 Гц). Вероятность появления значимого стимула составила 30%, незначимого -70%, длительность стимула была 50 мс интенсивность -70 Дб SPL, использовались наушники [9,10]. ...
Study Objective: To identify the differences in physiological parameters in groups of patients in an acute period of haemorrhagic parenchymatous stroke (supratentorial hemisphere hematomas) with favourable outcome and fatality. Study Design: prospective study. Materials and Methods. We have examined 96 patients with supratentorial haemorrhagic stroke. Haemorrhagic stroke was diagnosed on the basis of neuroimaging results, clinical symptoms and medical history, as well as clinical and laboratory data. A cluster analysis and expert examinations made it possible to divide patients into two groups: 49 patients who died of the acute haemorrhagic stroke and 47 patients with a favourable outcome. We evaluated the level of consciousness, cognitive functions, neurophysiological parameters: electroencephalography (EEG), cognitive evoked potentials Р300, heart rate variability (HRV). Study Results. In patients with a favourable outcome, an overall amplitude of the EEG spectrum was higher vs. patients with lethal outcome (statistically significant results were noted in all leads). A significant increase in the mean frequency of theta waves was seen in both groups, especially in the group with lethal outcomes. When Р300 in patients with lethal outcome was evaluated, a significantly lower P2N2 amplitude in Fz was noted vs favourable outcome group: 5.1 (2.6; 9.1) μV vs 8.9 (5.6; 20.4) μV (U = 148; p = 0.021). A comparative analysis of HRV revealed significant differences only in heart rate (mean R-R): it was lower in patients who died in the acute period of haemorrhagic stroke: 696 (608; 836) ms vs 806 (743; 911) ms (U = 181; p = 0.033). In patients with lethal outcomes, there is an increase in the number of linear correlations in physiological parameters vs. favourable outcome group. Conclusion. Deaths from acute haemorrhagic stroke are preceded by reduction in the basic cortical rhythm, growth in slow waves activity, reduction in the stimuli recognition mechanism activation (according to cognitive evoked potentials Р300). An analysis of the rate of correlation in physiological mechanisms of brain activity regulation (EEG), neurophysiological correlates in stimuli recognition and decisionmaking (Р300), as well as autonomic regulation mechanisms (HRV) shows limited functional reserves in patients with lethal outcomes. Keywords: haemorrhagic stroke, event-associated potential, heart rate variability, correlation analysis.
... Although HE is a reversible syndrome of impaired brain functions accompanying advanced liver failure, it is not a single clinical entity and its diagnosis mainly depends on the exclusion and suspicion with no specific diagnostic test (Ferenci, 2017;Swaminathan et al., 2018). However, liver dysfunction can be treated successfully, HE is associated with poor survival and a high risk of recurrence and changes from covert HE to overt HE (Kaplan and Rossetti, 2011). ...
... Electroencephalography (EEG) is known to be a reliable tool for evaluation and diagnosis of HE [6,7]. It provides vital information about the cortical postsynaptic activity that is modulated by both physiological and pathological diencephalic and brain-stem influences. ...
Background and aim:
Hepatic encephalopathy is a serious complication that entails liver cirrhosis with a high mortality rate. The Child- Turcotte-Pugh class (CTP class) and model for end-stage liver disease (MELD) score are two important prognostic indicators for cirrhosis, while sequential organ failure assessment (SOFA) is a dynamic score for the assessment of critically ill patients. Patients with liver disease with advanced CTP class and higher MELD scores have poor prognosis. The aim of this study was to evaluate the role of electroencephalography (EEG) in cirrhotic patients requiring ventilator support for hepatic encephalopathy Grade III-IV.
Methods:
A retrospective study was conducted on patients admitted to the liver intensive care unit (ICU) of a tertiary teaching institute. EEG records of 92 patients with Grade III-IV hepatic encephalopathy who were admitted between April 2015 and May 2017 to the liver ICU were analyzed. The correlation between EEG findings and 28-day mortality, ICU length of stay, and the number of days on mechanical ventilation was determined.
Results:
Seventy-eight of 92 patients (85%) exhibited bilateral slowing EEG pattern, suggestive of encephalopathy. A triphasic pattern was the most common EEG abnormality in 40% (31 of 78) of the patients. Patients with abnormal EEG had a significantly higher MELD score compared to those with a normal EEG (P=0.02). There were no significant differences in length of mechanical ventilation between both groups, but an increasing trend was observed in those with abnormal EEG (P=0.09).
Conclusion:
EEG findings correlate well with severity of disease in critically ill patients with liver disease.
Relevance for patients:
EEG has a role in monitoring and prognostication of hepatic encephalopathy in critically ill patients with liver disease.
... These are similar to the cerebral complications of ESRD (Cai et al., 2011;Rayi and Mandalaneni, 2020). In particular, encephalopathy, usually referred to as diffuse cerebral dysfunction, was suggested to be associated with a slowing of background activity in both delta and theta frequency bands on an electroencephalogram (EEG) (Kaplan and Rossetti, 2011;Sutter et al., 2013;Demir et al., 2014;Rayi and Mandalaneni, 2020). The EEG background activity can be observed in both the time domain and frequency domain. ...
Renal failure and diabetes can induce cerebral complications, including encephalopathy, for which attentional and cognitive impairment are common symptoms. It is possible that renal failure with comorbid diabetes may induce more severe encephalopathy due to multiple pathogenic mechanisms. This concept was supported by the main findings of this study, which showed that EEG background activity between end-stage renal disease with and without comorbid diabetes was significantly different in relative power of delta in the eyes-open condition in frontoparietal regions; theta in the eyes-closed condition in all regions; beta in the parieto-occipital regions in both eye conditions; the delta/theta ratio in both eye conditions in frontoparietal regions; and the theta/beta ratio in all regions in the eyes-closed condition. These findings may increase awareness of comorbid cerebral complications in clinical practice. Moreover, the delta/theta ratio is recommended as an optimal feature to possibly determine the severity of encephalopathy.
... In the early stage of onset, the patient developed myoclonic seizure of the left hand, and EEG showed periodic triphasic waves in the bilateral occipital regions, which is similar to the seizure and EEG changes seen in Creutzfeldt-Jakob disease (CJD). Studies have revealed that the EEG patterns are correlated to cerebral imaging findings, and similar EEG changes can occur with different cerebral abnormalities according to the rate of encephalopathy progression, the duration, and so on (9). Therefore, the periodic triphasic waves similar to CJD in this patient may be related to the restricted diffusion of DWI in the cerebral cortex similar to CJD. ...
Background: There are few reported cases of posterior reversible encephalopathy syndrome (PRES) combined with essential thrombocythemia (ET). We report a case of PRES-like syndrome in ET.
Case Report: A 60-year-old man with a history of hypertension and thrombocythemia presented with progressive visual loss after waking up; and neurological examination showed pupils were 3 mm and equally reactive to light, which suggested cortical blindness. Brain magnetic resonance imaging (MRI) revealed restricted diffusion in diffusion-weighted imaging (DWI) in the bilateral parietal and occipital lobes. Routine blood tests revealed a platelet count of 1,044 × 10 ⁹ /L. ET was diagnosed after exclusion of other causes. Electroencephalography (EEG) showed periodic triphasic waves in the occipital region. The lesions of the parietal and occipital lobes on MRI and periodic triphasic waves of EEG disappeared quickly, and patient's vision returned to normal after the treatment with hydroxyurea and sodium bicarbonate. The patient experienced hallucinatory palinopsia during the recovery of vision.
Conclusion: ET may be a risk factor for PRES.
... In addition, nonspecific neurological and psychiatric manifestations ranging from attention, working memory, psychomotor speed, and visuospatial ability alteration to disorientation to time and space, inappropriate behavior, and acute confusional state with agitation or somnolence have also been documented in patients suffering from HE (4,5). A poor survival and a high risk of recurrence strongly characterize HE if liver disease is not successfully treated (6). Nevertheless, also the mildest form is correlated to a reduced quality of life as well as to the increased risk to develop severe HE (1, 7). ...
Objective: Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by liver failure and by an impaired neurotransmission and neurological function caused hyperammonemia (HA). HE, in turn, decreases the phosphorylation of Protein kinase Cε (PKCε) contributing to the impairment of neuronal functions. Dehydroepiandrosterone (DHEA) exerts a neuroprotective effect by increasing the GABAergic tone through a GABAA receptors stimulation. Therefore, we investigated the protective effect of DHEA in an animal model of HE, and the possible modulation of PKCε expression in different brain area.
Methods: Fulminant hepatic failure was induced in 18 male, Sprague Dawley rats by i.p. administration of 3 g/kg D-Galactosamine and after 30 minutes a group of animals received a subcutaneous injection of 25 mg/Kg (DHEA) repeated twice a day (3 days). Exploratory behavior and general activity were evaluated 24 h and 48 h after the treatments by open field test. Then, brain cortex and cerebellum were used for immunoblotting analysis of PKCε level.
Results: DHEA administration showed a significant improvement of locomotor activity both 24 and 48 h after D-Galactosamine treatment (****P < 0.0001) but did not ameliorate the liver parenchymal degeneration. Western blot analysis revealed a reduced immunoreactivity of PKCe (*P < 0.05) following D-galactosamine treatment in rat cortex and cerebellum. After the addition of DHEA, PKCε increased in the cortex in comparison with D-galactosamine-treated (***P < 0.001) and control group (*P < 0.05), while in the cerebellum only decreased (*P < 0.05) with respect to the control group. PKCε decreased after treatment with NH4Cl alone and in combination with DHEA both in cerebellum and cortex (****P < 0.0001). MTS assay demonstrated the synergistic neurotoxic action of NH4Cl and glutamate pretreatment in cerebellum and cortex along with an increased cell survival after DHEA pretreatment, which resulted significant only in the cerebellum (*P < 0.05).
Conclusion: An association between the DHEA-mediated increase of PKCε expression and the improvement of comatose symptoms was observed. PKCε activation and expression in the brain could inhibit GABA-ergic tone counteracting HE symptoms. In addition, DHEA seemed to ameliorate the symptoms of HE and to increase the expression of PKCε in cortex and cerebellum.
... Some evidence from joint EEG and neuroimaging observations and animal studies indicate that alpha activity disorders (e.g., amplitude attenuation, slowing) usually indicate cortical damage, while abnormal delta frequencies reflect subcortical and/or white matter damage the cortex goes in [15,16]. However, this is just a conjecture, and we need more evidence to assess these possibilities finally. ...
A growing number of studies have demonstrated the role of quantitative
electroencephalography in assessing brain function in neuro-intensive care
units. Still, few studies have examined patients with large hemisphere infarction. Thirty patients with large hemisphere infarction were included
in this preliminary study, and the patients were divided into the death group (twelve
patients) and survival group (eighteen patients). Electroencephalography monitored the patients, and
a computerized tomography inspection was performed. The quantitative electroencephalography of
the alpha-beta/delta-theta ratio change index was calculated and used to
predict the prognosis of early large hemisphere infarction patients. The relationship between three months
modified Rankin Scale, and alpha-beta/delta-theta ratio change
index was analyzed. The death group had negative changes for alpha-beta/delta-theta ratio
change index (-0.0140 ± 0.0193), while there was an opposite trend in the
survival group, the median is 0.004 (-0.0067, 0.0137). The death group’s brain
function decreased more severely and rapidly than the survival group (P
= 0.004). The highest diagnostic value (AUC value 0.815, P < 0.001)
was observed when the alpha-beta/delta-theta ratio change index dropped and exceeded -0.008. The area
under the GCS curve was 0.674, but its predictive ability was low (P =
0.094). The correlation analysis result showed that the 3-month modified Rankin Scale was
negatively correlated with the alpha-beta/delta-theta ratio change index (r = -0.489, P =
0.006). The alpha-beta/delta-theta ratio change index is considered an indicator for predicting the prognosis of large hemisphere infarction. Therefore, the alpha-beta/delta-theta ratio change index may be a reliable quantitative EEG parameter that predicts the early prognosis of patients with acute large hemispheric infarction.
... The alteration of brain functioning, which can produce behavioral, cognitive and motor effects were termed porto systemic encephalopathy and later included in the term Hepatic Encephalopathy. Unless the underlying liver diseases is successfully treated, Hepatic Encephalopathy is associated with poor survival and 1 high risk of recurrences .The incidence and prevalence of hepatic encephalopathy are related to the severity of the underlying liver 2 insufciency .In patients with cirrhosis, fully symptomatic overt hepatic encephalopathy is an event that denes the decompensated 3 phase of the disease ,also variceal bleeding or ascites .The manifestation of hepatic encephalopathy may not be an obvious clinical nding and there are multiple tools used for its detection, which inuences the variation in the reported incidence and prevalence rates. The prevalence of overt hepatic encephalopathy at the time of diagnosis of cirrhosis is 10%-14% in general, 16%-21% in those with decompensated cirrhosis, and 10% to 50% in patients with trans jugular intrahepatic portosystemic shunt. ...
Introduction: Hepatic encephalopathy is a frequent complication and one of the most debilitating manifestations of liver diseases, severely affecting the lives of patients. Aims and objective: i. To study the precipitating factors of hepatic encephalopathy. ii. To observe the clinical manifestation at the time of presentation of hepatic encephalopathy. iii. To observe the seasonal variation of hepatic encephalopathy in cirrhotic patient. Materials and method: General Medicine, Murshidabad Medical college and R. G. Kar Medical college in West Bengal. All adult cirrhotic Patients admitted with encephalopathy in the medicine ward within the study period. One year starting from 1st Nov 2019 to 31st October 2020. Conclusion: This study found that most common precipitating factors of hepatic encephalopathy in our patients are infection, constipation electrolyte imbalance and Variceal Haemorrhage bleeding. These are potentially preventable and reversible.
... Acute encephalopathy is a non-specific term used to describe the acute impairment of brain function which presents clinically as alteration in the level of consciousness [74]. It is mostly triggered by infections, especially those caused by viruses [75]. ...
Coronavirus disease 2019 (COVID-19) is an emerging global health emergency caused by the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The global outbreak of SARS-CoV-2 infection has been declared a global pandemic by the World Health Organization (WHO). The clinical presentation of SARS-CoV-2 infection depends on the severity of the disease and may range from an asymptomatic infection to a severe and lethal illness. Fever, cough, and shortness of breath are among the most common symptoms associated with SARS-CoV-2 infection. Accumulating evidence indicates that COVID-19 patients commonly develop neurological symptoms, such as headache, altered mental status, anosmia, and myalgia. In this comprehensive literature review, we have summarized the most common neurological complications and reported neurological case studies associated with COVID-19, and neurological side effects associated with COVID-19 treatments. Additionally, the post-acute COVID-19 syndrome and long-term neurological complications were discussed. We also explained the proposed mechanisms that are involved in the pathogenesis of these neurological complications.
... [25] Neuroimaging with brain CT and MRI can be performed with various specificity as they do not reveal specific abnormalities in most sepsis cases but combined with EEG may provide helpful patterns for diagnosis. [26] Somatosensitive Evoked Potentials have also been used as they could be sensitive markers of sepsis-associated cerebral dysfunction. [4,8,10] Electroencephalography has been trialed for many years as a diagnostic and monitoring tool in SAE. ...
Sepsis-associated encephalopathy (SAE) is the term used to define brain dysfunction related to infections that are principally located outside the central nervous system (CNS). A number of published studies report that electroencephalography (EEG) has been used in the evaluation of patients with sepsis, alone or usually in combination, to evoked potentials and neuroimaging. This was in an effort to assess if EEG can be a tool in the diagnosis and monitoring of the neurological status in sepsis patients. Although there is no specific test for the diagnosis and prognosis of sepsis related encephalopathy, our literature review suggests that EEG has a role in the assessment of this clinical entity. Due to its low cost and simplicity in its performance, EEG could be a potential aid in the assessment of sepsis neurological complications even in the early, subclinical stages of the syndrome. The aim of this review is to summarize the published literature regarding the application and utility of electroencephalography in adult patients with sepsis.
... A wide spectrum of motor disorders can be observed in HE, including asterixis, hypertonia, hyperreflexia, and extrapyramidal dysfunction [1]. Unless the underlying liver disease is successfully treated, HE is associated with poor survival and a high risk of recurrence [3,4]. e spectrum of HE ranges from minimal brain function deficits, known as minimal HE, to hepatic coma [5][6][7]. ...
Background. Hepatic encephalopathy (HE) is one of the most debilitating complications of cirrhosis leading to death. Decrease in HE mortality and recurrence has been linked with timely identification and early treatment. There is a need to document the burden, predictors, and treatment outcomes of HE in an adult population with liver cirrhosis in our setting as only reports from resource-endowed countries abound in the literature. This study aimed therefore to determine the prevalence, predictors, and treatment outcomes of patients with liver cirrhosis admitted at St. Dominic Hospital (SDH) in Akwatia, Ghana. Materials and Methods. A prospective study was conducted involving one hundred and sixty-seven (167) patients admitted at the medical wards in SDH with liver cirrhosis from January 1st, 2018, to March 24th, 2020. The demographic and clinical features of the patients were collected using a standardized questionnaire. Biochemical, haematological, and abdominal ultrasound scans were done for all patients. Patients were then followed up until discharge or death. Results. There were 109 (65.3%) males out of the 167 patients with a mean age of 45.8 and 47.5 years for those with and without HE, respectively. The prevalence of HE was 31.7% (53/167). Out of 53 participants with HE, 75.5% (40/53) died. There was a strong association between HE and death (p
... The present study did not reveal any age-dependent changes in delta power (Figures 1-3). This could be explained by the fact that delta oscillatory power is mainly related with pathological conditions [71], such as stroke [72,73] and Alzheimer's disease [74]; therefore, we did not find specific regions which showed age-dependent changes in delta oscillatory power in our healthy volunteers. That enhanced slow oscillatory power could be explained by pathological conditions rather than physiological aging is a useful information for clinical practice. ...
Aging and gender influence regional brain activities. Although these biases should be considered during the clinical examinations using magnetoencephalography, they have yet to be standardized. In the present study, resting-state magnetoencephalography data were recorded from 54 healthy females and 48 males aged 22 to 75 years, who were controlled for cognitive performance. The regional oscillatory power was estimated for each frequency band (delta, theta, alpha, beta, low-gamma, and high-gamma) using the sLORETA-like algorithm and the biases of age and gender were evaluated, respectively. The results showed that faster oscillatory powers increased with age in the rostral regions and decreased in the caudal regions, while few slower oscillatory powers changed with age. Gender differences in oscillatory powers were found in a broad frequency range, mostly in the caudal brain regions. The present study characterized the effects of healthy aging and gender asymmetricity on the regional resting-state brain activity, with the aim to facilitate the accurate and efficient use of magnetoencephalography in clinical practice.
... It is associated with alternate periods of agitation and lethargy, along with periods of sleep cycle impairment. 1 In hospitalized patients, encephalopathy reflects a diffuse disturbance of cerebral function of any origin, and is associated with poor outcomes, especially in the elderly. 2 EEG may assist in determining the underlying brain dysfunction and its severity in these patients, 3 given ample body of empirical evidence suggesting that different grades of background activity slowdown correlate with the functional severity of clinical encephalopathy. 4 However, when considering the prognostic correlation of an increasing background slowing, it is always important to perform activation procedures to test the reactivity, including eye opening, as well as response to sounds and painful stimulations. ...
Objective
The objective of this work was to study the electroencephalographic (EEG) grading of neuronal dysfunction in encephalopathy of various etiologies and assess their association with clinical outcomes.
Subjects and Methods
This retrospective cross-sectional study was performed between June and November 2018 at the Neurology Department of King Fahd Hospital of University, Kingdom of Saudi Arabia (KSA) and involved a review and analysis of EEG and medical records pertaining to 222 patients in whom encephalopathy was diagnosed.
Results
In patients suffering from encephalopathy, advanced age ( P = .01), low Glasgow Coma Scale (GCS) scores ( P = .00), and certain etiologies, namely hypoxic-ischemic encephalopathy (HIE) ( P = .00), septic encephalopathy ( P = .01), and other illnesses ( P = .00), were significantly associated with unfavorable clinical outcomes, whereas traumatic brain injury (TBI) ( P = .01) and GCS >7 ( P = .00) were associated with favorable outcomes. Among different etiologies, EEG grade I ( P = .02) and grade IV ( P = .04) neuronal dysfunction was significantly associated with TBI while grade III ( P = .05) and grade V ( P = .02) neuronal dysfunction was significantly associated with HIE. Grade I ( P = .03) neuronal dysfunction was mostly observed in septic encephalopathy cases, while patients suffering from other illnesses were also found to have grade I ( P = .04) and grade IV ( P = .05) neuronal dysfunction based on their EEG.
Conclusion
EEG is being conducted routinely to determine the course and severity of various forms of encephalopathy. However, the clinical implications of EEG grading for neuronal dysfunction are largely dependent on underlying etiology and other clinical parameters, such as age and GCS score. Further larger prospective cohort studies involving other important prognostic parameters and continuous EEG monitoring are thus needed.
... It is associated with alternate periods of agitation and lethargy, along with periods of sleep cycle impairment. 1 In hospitalized patients, encephalopathy reflects a diffuse disturbance of cerebral function of any origin, and is associated with poor outcomes, especially in the elderly. 2 EEG may assist in determining the underlying brain dysfunction and its severity in these patients, 3 given ample body of empirical evidence suggesting that different grades of background activity slowdown correlate with the functional severity of clinical encephalopathy. 4 However, when considering the prognostic correlation of an increasing background slowing, it is always important to perform activation procedures to test the reactivity, including eye opening, as well as response to sounds and painful stimulations. ...
Abstract Objective: The objective of this work was to study the electroencephalographic (EEG) grading of neuronal dysfunction in encephalopathy of various etiologies and assess their association with clinical outcomes. Subjects and Methods: This retrospective cross-sectional study was performed between June and November 2018 at the Neurology Department of King Fahd Hospital of University, Kingdom of Saudi Arabia (KSA) and involved a review and analysis of EEG and medical records pertaining to 222 patients in whom encephalopathy was diagnosed. Results: In patients suffering from encephalopathy, advanced age (P ¼ .01), low Glasgow Coma Scale (GCS) scores (P ¼ .00), and certain etiologies, namely hypoxic-ischemic encephalopathy (HIE) (P ¼ .00), septic encephalopathy (P ¼ .01), and other illnesses (P ¼ .00), were significantly associated with unfavorable clinical outcomes, whereas traumatic brain injury (TBI) (P ¼ .01) and GCS >7 (P ¼ .00) were associated with favorable outcomes. Among different etiologies, EEG grade I (P ¼ .02) and grade IV (P ¼ .04) neuronal dysfunction was significantly associated with TBI while grade III (P ¼.05) and grade V (P ¼ .02) neuronal dysfunction was significantly associated with HIE. Grade I (P ¼ .03) neuronal dysfunction was mostly observed in septic encephalopathy cases, while patients suffering from other illnesses were also found to have grade I (P ¼ .04) and grade IV (P ¼ .05) neuronal dysfunction based on their EEG. Conclusion: EEG is being conducted routinely to determine the course and severity of various forms of encephalopathy. However, the clinical implications of EEG grading for neuronal dysfunction are largely dependent on underlying etiology and other clinical parameters, such as age and GCS score. Further larger prospective cohort studies involving other important prognostic parameters and continuous EEG monitoring are thus needed.
... Cognitive disabilities and changes in bioelectrical brain activity are the most often causes for stroke [8,12,13,20,22]. Neurofeedback can be used as rehabilitation method for people after stroke. ...
Background: Stroke patients develop the ability to perform higher levels of functional activity on basis of concentrated rehabilitative training which affects sensory, motor and cognitive functions. Objective: The main aim of our work was to show the usefullness of neurofeedback therapy in rehabilitation of stroke patients. Design: 27 stroke patients with severe disabilitis were included in the pilot study (men aged 32 to 68 years, mean age 52.4 ± 3.29 years, median 57 years). They all underwent complex study of brain bioelectrical activity EEG and 15 trainings of neurofeedback. Results: By the end of the rehabilitation (after 17 sessions) recollection of psychotrauma led to an increase in the power of the alpha rhythm in both left and right hemispheres. Atthe endpoint of the study differences in the power of the alpha rhythm in the left hemisphere were 1.47 times greater, and in the right hemisphere, 1.95 times greater than at the first visit. The regress of theta rhythm (1.25 times in the left, 1.11 times in the right hemisphere) decreased considerable, which affected the alpha / thetaratio - decreased 1.04 times in the left, 1.18 times in the right hemisphere, and also the coefficient (alpha + theta) / beta - decreased 1.17 times in the left and 1.21 times in the right. Differences in the saturation of blood vessels index at the last visit were 1.69 times greater than at the first visit. Neurophysiological changes correlated with an improvement in the emotional shpere. By the time of discharge, the indicators on the Beck depression scale decreased by 1.4 times, on the Spielberger-Khanin scale, situational anxiety decreased by 1.63 times, personal anxiety - by 1.4 times; regression of indicators in the hospital scale of anxiety and depression (HADS) was observed in 1.89 times. Conclusion: The data presented indicate that the use of the neurofeedbackmethod leads to a reduction of anxiety-depressive disorders, which positively affects the usefulness of combine rehabilitation. Keywords: stroke, neurofeedback, electroencephalogram, alpha rhythm, rehabilitation.
... We visually analyzed the EEGs according to the definitions of the American Clinical Neurophysiology Society's Standardized EEG Terminology [20,21]. Visually analyzed encephalopathy patterns have been categorized in 4 grades: (i) grade I, excess of slow posterior activity; (ii) grade II, predominant theta activity in more than 50% of recording; (iii) grade III, predominant delta activity in more than 50% of recording; and (iv) grade IV, burst-suppression pattern [10,22]. ...
We used quantified electroencephalography (qEEG) to define the features of encephalopathy in patients released from the intensive care unit after severe illness from COVID-19. Artifact-free 120–300 s epoch lengths were visually identified and divided into 1 s windows with 10% overlap. Differential channels were grouped by frontal, parieto-occipital, and temporal lobes. For every channel and window, the power spectrum was calculated and used to compute the area for delta (0–4 Hz), theta (4–8 Hz), alpha (8–13 Hz), and beta (13–30 Hz) bands. Furthermore, Shannon’s spectral entropy (SSE) and synchronization by Pearson’s correlation coefficient () were computed; cases of patients diagnosed with either infectious toxic encephalopathy (ENC) or post-cardiorespiratory arrest (CRA) encephalopathy were used for comparison. Visual inspection of EEGs of COVID patients showed a near-physiological pattern with scarce anomalies. The distribution of EEG bands was different for the three groups, with COVID midway between distributions of ENC and CRA; specifically, temporal lobes showed different distribution for EEG bands in COVID patients. Besides, SSE was higher and hemispheric connectivity lower for COVID. We objectively identified some numerical EEG features in severely ill COVID patients that can allow positive diagnosis of this encephalopathy.
... Similarly, pathologies affecting both cortical and subcortical brain regions can lead to SWA along with background slowing. 7 In the histology and EEG study of patients with diffuse encephalopathy, paroxysmal synchronous discharges (PSDs) with either (spikes, spike and wave complexes, sharp waves [SWs] or SWA that emerged from the background and then returned to lower voltage activity), as well as continuous, irregular, and asynchronous polymorphic delta activity (PDA) in EEG, were associated with combined cortical and subcortical gray matter pathology, or with white matter pathology. 8 Therefore, the aim of the present study was to determine the correlations between different EEG patterns and underlying structural brain abnormalities in 910559E EGXXX10.1177/1550059420910559Clinical ...
Objective. The present study aimed to determine the clinical and radiological correlates of different electroencephalographic (EEG) patterns in hospitalized patients. Subjects and Methods. In this retrospective study performed at the Neurology Department, King Fahd University Hospital, Kingdom of Saudi Arabia (KSA), data of 374 patients who underwent EEG were reviewed and analyzed. Results. Presence of focal spike and wave or sharp wave (SW) ( P = .00), generalized theta activity ( P = .00), generalized delta activity ( P = .04), persistent focal slow wave activity (SWA) ( P = .003) and asymmetric background ( P = .01) in the EEG record was significantly associated with abnormal imaging findings. Specifically, generalized theta delta activity ( P = .01) and markedly attenuated EEG activity ( P = .007) were associated with presence of cortical lesions; whereas, triphasic waves (TWs) ( P = .009), and generalized theta activity ( P = .001) were found to be related with presence of subcortical lesions. While, generalized delta activity ( P = .01) was the only correlate with extra-axial lesions. Conclusion. At present, certain EEG patterns cannot be precisely correlated with imaging findings, suggesting that intercurrent metabolic, infectious, and/or toxic contributors could be the confounding factors. Nonetheless, when EEG patterns are examined alongside magnetic resonance imaging findings and other clinically relevant data, these might be indicative of a group of diseases in some pertinent situations. Thus, further larger prospective clinical studies that incorporate continuous EEG monitoring, advanced radiology techniques, and laboratory analyses would be beneficial to elucidate their interplay for better firm up the correlations.
Foreign bodies of the nose are frequently encountered among children, although in adults are rare. Longstanding foreign body may cause congestion, mucosa swelling, ulcers, bone structure destruction and severe exocranial and endocranial complications. Still, foreign bodies are often asymptomatic and consequently may remain undetected for many years. We describe a case of a 58 years old female patient who was admitted to our clinic. She complained of unilateral nasal seromucous discharge and she said that she had a bullet in her nose since preschool period. She did not remember any circumstances in which the foreign body could have been introduced into her nasal cavity. CT scan revealed
metal opacity foreign body in left nasal cavum. The foreign body – bullet, was removed endoscopically. This case report points that foreign body may be asymptomatic even for a few decades.
Key words: rhinorrhea, foreign body, bullet
Olfactory dysfunction is an increasingly recognized affliction that carries with it significant social, psychological, and safety implications. The three most common causes are sinonasal disease, upper respiratory infection, and head trauma. A certain number of working-age, clinically healthy people have initial problems in terms of olfactive dysfunction that can be registered for specific olfactory tests. The aim of this
study is to examine olfactory function and whether dysfunction is associated with sex, age and smoking. The study is conducted over 38 healthy adults employed at Clinical-hospital Center „Zemun” by olfactory discs (Zurcher-Geruchs Test). Seven patients out of 38 (18.42%) demonstrated hyposmia or anosmia. Our study found no significant correlation of sex and smoking with olfactory dysfunction.
The reduction or loss of olfactive function is not uncommon in a population of clinically healthy subjects.
Key words: sense of smell, olfactometry results, healthy adults
Introduction: Triphasic waves (TW) constitute an electroencephalographic pattern associated with certain kinds of encephalopathy. Brain atrophy may be a predisposing factor linked with TW.
Objective: To compare the degree of brain atrophy and white matter disease between patients with acute encephalopathy with and without TW.
Methods: A retrospective observational study including adult patients with encephalopathy, with and without TW, hospitalized between 2016 and 2017. The degree of brain atrophy and white matter lesion were defined using the Global Cortical Atrophy and Age Related White Matter Changes (ARWMC) scales, respectively. Scores were compared between groups. Mortality rates were registered.
Results: Sixteen patients with TW were identified matched by age and sex with 30 patients without TW. The mean age was 80 years in the TW group. Women represented 87.5%. Multifactorial encephalopathy was the most frequent diagnosis followed by metabolic encephalopathy. Patients with TW had more brain atrophy (10.43 vs 6.9, p= 0.03). Mean ARWMC was 9.43±6.5 and 8.5 ±7.89 in patients with and without TW respectively (p= 0.5). Mortality rate was higher in the TW group (31.25 vs 6.66% p= 0.02).
Conclusions: Patients with acute encephalopathy and TW had higher degree of cerebral atrophy. It is possible that this structural alteration predisposes to the appearance of TW. There was no significant difference in white matter lesion degree. The mortality of the TW group was high, so future studies are necessary to determine their prognostic value.
INTRODUCCIÓN:
La covid-19 afecta principalmente al aparato respiratorio, sin embargo, también se ha descrito afectación tanto directa como indirecta en el sistema nervioso central y periférico, lo cual ocasiona una gran variedad de manifestaciones neurológicas, siendo la encefalopatía una de las más frecuentemente observadas.
OBJETIVO:
Se busca mostrar la utilidad del video-electroencefalograma (vEEG) en el diagnóstico de encefalopatía en pacientes ingresados por covid-19, así como su valor para determinar el pronóstico de estos pacientes.
MÉTODOS:
Estudio observacional retrospectivo con 76 vEEG de 41 pacientes con covid-19 confirmada. Los estudios se han realizado entre los meses de marzo del 2020 y junio del 2021. Se estudió la gravedad de la enfermedad, así como sus características clínicas y neurológicas, el tratamiento farmacológico y los hallazgos electroencefalográficos según el grado de disfunción de la encefalopatía que desarrollaron estos pacientes.
RESULTADOS:
De los 41 pacientes, 12 (29 %) presentaron signos electroencefalográficos de disfunción cerebral leve, 15 (37 %) disfunción cerebral moderada y 14 (34 %) disfunción cerebral severa, los cuales se asociaron con una mayor mortalidad.
CONCLUSIONES:
En los 76 vEEG realizados a los 41 pacientes ingresados con encefalopatías asociadas con infección por covid-19, no se observó un patrón distinto a los descritos en encefalopatías de otras etiologías. El vEEG fue útil para confirmar la sospecha clínica de una disfunción cerebral en pacientes con encefalopatías asociadas con infección por covid-19 y para asignarle un grado de severidad, confirmando su beneficio como biomarcador diagnóstico y pronóstico.
Background
Sepsis-associated brain dysfunction (SABD) is a frequent severe complication of sepsis and the systemic inflammatory response syndrome. It is associated with high mortality and a majority of survivors suffer long-term neurological consequences. Sleep is commonly affected in sepsis and there is a strong correlation between its impairment and development of other complications or increased mortality in sepsis patients. Here, we investigate the effects of sepsis on brain activity patterns in order to better understand possible sources of sleep-wake disturbances associated with severe systemic inflammation.
Methods
We studied the effects of high LPS doses (10mg/kg) on oscillatory brain states in an acute rat model of sepsis under urethane anaesthesia, which maintains REM- and NREM sleep-like states. Twelve Long-Evans rats (6 LPS, 6 controls) were implanted with eight independently movable tetrodes in the dorsal hippocampus. Baseline LFP activity was recorded for 3 hours after saline injection, followed by another 3 hours after LPS or saline injection. REM and NREM were automatically classified based on LFP activity and quantified. Within- and between-state dynamics were analysed using a 2-D state space approach based on spectral power ratios. Aperiodic and periodic components of the power spectrum were quantified for each state. Blood serum samples and brains were collected for IL-1β quantification and histological verification of electrode placement.
Results
Soon after LPS injection we observed a robust fragmentation of both oscillatory states resulting in a three-fold increase in the number of state transitions that lasted for several hours, although the overall time spent in either state did not change. Analysis of power spectra showed opposing shifts in low frequency oscillations (1–9 Hz) in REM and NREM that resulted in increased similarity between both states in 2-D state space.
Conclusions
The observed increased spectral similarity between REM and NREM and increased instability within the states may point to a mechanism underlying the severe sleep fragmentation described both in sepsis patients and in SABD animal models.
Background
Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is a common type of acute encephalopathy in Japan; the condition is clinically characterized by prolonged seizures as the initial neurological symptom, followed by late seizures 4–6 days later. It is difficult to differentiate AESD from prolonged febrile seizures (PFSs). Here, we explored the use of electroencephalography to differentiate AESD from PFSs.
Methods
We studied the electroencephalograms (EEGs) of children <6 years of age diagnosed with AESD or PFSs; all EEGs were recorded within 48 h of seizure onset (i.e., before the late seizures of AESD). Two pediatric neurologists evaluated all EEGs, focusing on the basic rhythm, slowing during wakefulness/arousal by stimuli, spindles, fast waves, and slowing during sleep.
Results
The EEGs of 14 children with AESD and 31 children with PFSs were evaluated. Spindles were more commonly reduced or absent in children with AESD than in those with PFSs (71% vs. 31%, p = 0.021). Fast waves were also more commonly reduced or absent in children with AESD (21% vs. 0%, p = 0.030). The rates of all types of slowing did not differ between children with AESD and those with PFSs, but continuous or frequent slowing during sleep was more common in the former (50% vs. 17%, p = 0.035).
Conclusions
EEG findings may usefully differentiate AESD from PFSs. Reduced or absent spindles/fast waves and continuous or frequent slowing during sleep are suggestive of AESD in children with prolonged seizures associated with fever.
The COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV- 2) is causing a worldwide pandemic of COVID-19 within a short span of time. Although patients with COVID-19 primarily present with fever and respiratory illness; a wide range of symptoms involving different systems have been described. While the neurological sequelae of the virus remain poorly understood, there are a growing number of reports of neurological manifestation of COVID-19.The neurological manifestation including both central and peripheral nervous system are increasingly reported in a very subset of COVID-19 patients. The SARS-CoV-2 enters the body mainly via the ACE- 2 receptors within the respiratory system, which causes the body to initiate an immunologic response against potential damage to non-renewable cells. There’s increasing evidence of accumulating that COVID-19, particularly in severe cases, can have neurological consequences although respiratory symptoms nearly always develop before neurological ones. Patients with pre-existing neurological conditions could also be at elevated risk for COVID-19 associated neurological symptoms. The neurological presentations of COVID-19 patients maybe acute and post-acute state. The acute presentations are classified into specific (such as stroke, encephalitis, acute polyneuropathy, etc.) and nonspecific (such as delirium, headache, dizziness, etc.) symptoms with anatomical involvement of either central nervous system including brain or spinal cord, and/or peripheral nervous system, neuromuscular junctions or muscles. Several neurological symptoms have also been demonstrated in post-acute or long covid-19 syndrome. There is a possibility to overlook or misinterpretation of, neurological symptoms in some COVID-19 patients. In infants and young children, the foremost common CNS phenomena are febrile seizures; in adults, non-focal abnormalities will be either neurological or constitutional. To date, neurological manifestations of COVID-19 are described largely within the disease trajectory, and also the long-term effects of such manifestations still remain unexplored and unfolded. This article is intended to review the possible neuro-invasive routes of SARS-CoV-2 and its mechanisms which initiate the neurological damage with neurological presentations of COVID-19 patients. Bangladesh J Medicine July 2021; 32(2) : 120-137
Triphasic waves are EEG phenomena typically seen in patients with acute encephalopathy and have importance in diagnosis and prognosis in these cases. The underlying metabolic disturbances associated with their incidence have been described previously, but neuroimaging characteristics are not well delineated. There are a few small studies that define neuroimaging results in patients with triphasic waves. This review highlights the most common neuroimaging findings in these patients, including subcortical white matter disease, which itself may be a risk factor for triphasic waves.
Triphasic waves can be seen in a wide range of medical conditions, particularly in metabolic encephalopathies. Neuroimaging studies provide valuable diagnostic information for neurological conditions and can also help in our understanding of anatomical substrates for these conditions. Because of practical challenges and the fact that most encephalopathies with triphasic waves are presumed to be metabolic in etiology, large studies of imaging findings associated with triphasic waves are limited. We present a summary of studies that are currently available and a discussion of insights that these studies provide.
Dyspnea or breathlessness is a symptom occurring in multiple acute and chronic illnesses, however, the understanding of the neural mechanisms underlying its subjective experience is limited. In this topical review, we propose neural oscillatory dynamics and cross-frequency coupling as viable candidates for a neural mechanism underlying respiratory perception, and a technique warranting more attention in respiration research. With the evidence for the potential of neural oscillations in the study of normal and disordered breathing coming from disparate research fields with a limited history of interdisciplinary collaboration, the main objective of the review was to converge the existing research and suggest future directions. The existing findings show that distinct limbic and cortical activations, as measured by hemodynamic responses, underlie dyspnea, however, the time-scale of these activations is not well understood. The recent findings of oscillatory neural activity coupled with the respiratory rhythm could provide the solution to this problem, however, more research with a focus on dyspnea is needed. We also touch on the findings of distinct spectral patterns underlying the changes in breathing due to experimental manipulations, meditation and disease. Subsequently, we suggest general research directions and specific research designs to supplement the current knowledge using neural oscillation techniques. We argue for the benefits of interdisciplinary collaboration and the converging of neuroimaging and behavioral methods to best explain the emergence of the subjective and aversive individual experience of dyspnea.
Purpose:
Triphasic waves (TWs), a common EEG pattern, are considered a subtype of generalized periodic discharges. Most patients with TWs present with an altered level of consciousness, and the TW pattern is believed to represent thalamocortical dysfunction. However, the exact meaning and mechanism of TWs remain unclear. The objective of the current study was to evaluate the source of TWs using EEG source imaging and computerized tomography.
Methods:
Twenty-eight patients with TWs were investigated. Source analysis was performed on the averaged TWs for each individual, and source maps were extracted. Normalization and automatic segmentation of gray matter were performed on computerized tomography scans before analysis. Finally, voxelwise correlation analyses were conducted between EEG source maps and gray matter volumes.
Results:
Source analyses showed that the anterior cingulate cortex was mainly involved in TWs (16/28 patients, 57%). Correlation analyses showed moderate positive and negative correlations between source location and gray matter volumes for the posterior cingulate (T = 2.85; volume = 6,533 mm3; r = 0.53; P = 0.002) and the superior frontal gyrus (T = 2.54; volume = 18,167 mm3; r = -0.48; P < 0.0001), respectively.
Conclusions:
The results suggest that the anterior cingulate is involved in the origin of TWs. Furthermore, the volumes of posterior brain regions were positively correlated with TWs, indicating a possible preservation of these structures. Conversely, the volumes of anterior regions were negatively correlated with TWs. These findings may indicate a structural pattern necessary for the generation of the abnormal network responsible for TWs.
Objective
Many intensive care unit (ICU) survivors suffer disabling long-term cognitive impairment (LTCI) after critical illness. We compared EEG characteristics during critical illness with patients’ 1-year neuropsychological outcomes.
Methods
We performed a post hoc analysis of patients in the BRAIN-ICU study who had undergone EEG for clinical purposes during admission (n = 10). All survivors underwent formal cognitive assessments at 12-month follow-up. We evaluated EEGs by conventional visual inspection and computed 10 quantitative features. We explored associations between EEG and patterns of LTCI using Wilcoxon rank-sum tests and Spearman’s rank correlations.
Results
Of 521 Vanderbilt patients enrolled in the parent study, 24 had EEG recordings during admission. Ten survivors had EEG tracings available and completed follow-up cognitive testing. All but one inpatient EEG showed generalized background slowing. All patients demonstrated cognitive impairment in at least one domain at follow-up. The most common deficits occurred in delayed memory (DM—median index 62) and visuospatial/constructional (VC—median index 69) domains. Relative alpha power correlated with VC score (ρ = 0.78, P = .008). Peak interhemispheric coherence correlated negatively with DM (ρ = −0.81, P = .018).
Conclusions
Quantitative EEG features during critical illness correlated with domain-specific cognitive performance in our small cohort of ICU survivors. Further study in larger prospective cohorts is required to determine whether these relationships hold.
Significance
EEG may serve as a prognostic biomarker predicting patterns of long-term cognitive impairment.
The two main problems in the daily clinical practice of EEG are i) its under-use dedicated mainly to epilepsy and ii) subjectivity in de visu analysis. However, both problems can be overcome by using numerical tools in clinical practice that broaden the scope and introduce real objectivity to bioelectrical measurements. We have developed a method for quantitative EEG (qEEG) for daily use based on the homeostatic foundation of EEG. This method is robust, easy, and not time consuming and is arranged in two branches: the analysis of the spectral composition in each channel and synchronization. Notably, channels are arranged in differential mode. Since 2016, we have used this method for more than 4100 EEGs from scalp recordings in outpatients, epilepsy evaluation, and evaluation and monitoring in the intensive care unit (ICU). We have been able to identify numerical properties that are not visually evident in several pathologies, including COVID-19 in patients suffering encephalopathy, and have performed diagnosis in ICU patients and differentiation between epileptic and non-epileptic spells or minimum cognitive states. The use of numerical variables across successive recordings in the same patient has proven to be of great utility. We propose that qEEG use should be expanded globally for daily clinical practice.
Immune checkpoint inhibitors (ICI) have transformed the prognosis of cancers previously considered lethal (e.g., melanoma). The spectrum of therapeutic indications is rapidly expanding, including the vast majority of thoracic malignancies. By enhancing immune responses against cancer, ICI treatments lead to the development of immune-related adverse events that may affect any organ. Severity varies from mild to fatal clinical manifestations. Neurologic involvement is relatively rare and highly heterogeneous, including central and peripheral nervous system diseases associated with neural specific autoantibodies or not, central nervous system vasculitis, granulomatous and demyelinating disorders. Symptoms often manifest within the first 4 cycles of treatment and can develop regardless of the class of ICI used. An unfavorable outcome is seen in up to one third of patients and is generally associated to the patients’ clinical characteristics (e.g., age, coexistence systemic adverse events), cancer type (e.g., lung cancer vs other), and specific clinical setting (e.g., ICI treatment in patients with pre-existing paraneoplastic neurological autoimmunity, ICI re-challenge after a first neurological immune-related adverse event). Diagnosis should be suspected in patients with new onset neurological symptoms while on ICI treatment that are not explained by metastatic disease or other metabolic/infectious disorders. Recommended treatment is based on clinical severity and consists of ICI discontinuation with or without immunosuppressive therapy, although alternative approaches are reasonable depending on cancer status (e.g., aggressive immunotherapy without discontinuing ICI in patients with initial cancer response). Early recognition and appropriate treatment of these neurological immune-related adverse events is crucial for improved patient outcomes and therapeutic planning.
Compressed sensing, also known as compressive sampling is a new technique being rapidly developed over the last few years. The theory states that when some prior information about the signal is available and appropriately incorporated into the signal reconstruction procedure, a signal can be accurately reconstructed even if the Shannon/ Nyquest sampling requirement is violated. The key idea of compressed sensing is to recover a sparse signal from very few non-adaptive, linear measurements by optimization technique. Following the discovery by Donoho in (2006), that sparsity could enable exact solution of ill-posed problems under certain conditions, there has been a tremendous growth on efficient application of sparsity constraints for solving ill-posed problems. The theoretical foundation of compressed sensing has already become a key concept in various areas of applied mathematics, computer science, and electrical engineering. In this chapter we will detail the application of compressed sensing in X-ray computed tomography (CT) and Electroencephalography. Starting from the very basic principles we will provide theoretical justifications on why and how sparsity prior is used in CT and in EEG.
Purpose:
Triphasic waves (TWs) have been associated with multiple conditions and adverse outcomes. This study explores the role of white matter disease (WMD) in the generation of TWs when other common causes associated with these discharges are absent.
Methods:
This is a retrospective case series performed at Johns Hopkins Bayview Medical Center from January 2016 to May 2018, which screened for patients with severe WMD, who had TWs on EEG without the presence of commonly cited provoking factors, including (1) hepatic disease; (2) severe uremia over baseline; (3) the drugs cefepime, ifosfamide, lithium, and baclofen; or (4) global hypoxic-ischemic injury. A control population with no WMD or abnormal electrographic findings outside of theta-delta slowing was also identified.
Results:
Eleven patients were identified. The most common comorbid condition was infection, occurring in 82% of patients. Infections were urinary tract infection (36%), respiratory (27%), and central nervous system (18%). Metabolic abnormalities included glucose aberrations (36%), calcium derangements (18%), and hypernatremia (9%). Structural abnormalities included acute stroke (9%) and chronic central nervous system abscess (9%). All except one patient had one or more structural, metabolic, or infectious abnormalities in addition to WMD. Comorbidities were not statistically different in the control population.
Conclusions:
This is the first series to demonstrate convincingly the presence of TWs in patients with WMD in the absence of commonly cited risk factors. The authors hypothesize that less recognized risk factors of WMD and mild metabolic or infectious abnormalities may be drivers of TWs. With a growing elderly population, the presence of WMD will increase, and treating physicians need to look beyond the common causes of TWs.
To investigate the clinical correlates of frontal intermittent rhythmic delta activity (FIRDA).
we prospectively assessed all EEG studies recorded in our center over 3 months for the presence of frontal intermittent rhythmic delta activity (FIRDA). The FIRDA group was compared with a randomly selected control group from among EEGs recorded during the same period. Comparisons among FIRDA and non-FIRDA groups were performed using uni- and multi-variate analyses.
We found 36 patients with FIRDA among 559 EEG recordings (6%); the control group consisted of 80 subjects. While epilepsy was more frequent in the control group, structural brain lesions and encephalopathy were independently associated with the occurrence of FIRDA, but we could not identify any specific etiology. Asymmetric FIRDA was associated with an underlying brain lesion. Occasionally, FIRDA was recorded in otherwise healthy subjects during hyperventilation.
FIRDA appears more common than previously reported, and is associated with a wide range of lesions and encephalopathic conditions.
FIRDA occurrence should prompt investigations for toxic-metabolic disturbances and for structural lesions (particularly if asymmetric), but does not suggest an epileptic predilection.
Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) presents with focal or diffuse nonenhancing MR imaging abnormalities in 50% of patients with SREAT during subacute exacerbation. Vasculitic changes in biopsy studies as well as the elevation of antithyroid antibodies and CSF protein suggests an inflammatory cause. We report the case of a patient with SREAT with changes on diffusion-weighted MR imaging, which improved with corticosteroid therapy and plasmapheresis, supporting the theory of inflammatory changes in exacerbation of presumptive SREAT.
Excellent early work on stupor and coma can be found (particularly with regard to anoxia) in the work of Fischgold and Mathis (1959) in France, and Pamela Prior in England (1973a). These workers correlated deepening levels of coma with particular EEG patterns, and the suppression of EEG reactivity. Alpha frequency patterns in coma (alpha coma), spindle-like sleep patterns in coma (spindle coma) and "triphasic waves" are among the wide variety of endocrine disorders discussed in case reports and series leading to identification of particular EEG patterns. EEG correlations with prognosis are most reliable with cardiorespiratory arrest (CRA) with its consequent anoxic-ischemic insult. If etiology is known, EEG can often be a reliable predictor of outcome. EEG usually has little specificity with regards to etiology, but some patterns do favor particular diagnoses: for example, triphasic waves (TWs) are frequently seen with hepatic and renal insufficiency in young adults; spindle coma patterns are believed to indicate dysfunction at the brainstem level (Chatrian, 1990). EEG is most useful in differentiating organic from psychiatric conditions, in excluding nonconvulsive status epilepticus (NCSE), and in providing a rough guide as to the degree of cortical and subcortical dysfunction.
Abnormalities on diffusion-weighted images (DWIs) and fluid-attenuated inversion recovery (FLAIR) images are reported in Creutzfeldt-Jakob disease (CJD). To our knowledge, no large study has been conducted to determine the sensitivity and specificity of DWI and FLAIR imaging for diagnosing CJD.
Two neuroradiologists, blinded to diagnosis, retrospectively evaluated DWI and FLAIR images from 40 patients with probable or definite CJD and 53 control subjects with other forms of dementia and rated the likelihood of CJD on the basis of the imaging findings.
DWI and FLAIR imaging was 91% sensitive, 95% specific, and 94% accurate for CJD. Interrater reliability was high (kappa = 0.93). Sensitivity was higher for DWI than FLAIR imaging. Abnormalities involved cortex and deep gray matter (striatum and/or thalamus) in 68% of patients with CJD, cortex alone in 24%, and deep gray matter alone in 5%. The most typical and specific patterns were corresponding hyperintensity on both FLAIR images and DWIs confined to the gray matter in the cortex, striatum, medial and/or posterior thalamus, or a combination of these areas. Narrow-window soft-copy review of artifact-free DWIs and FLAIR images and recognition of the normal variation in cortical signal intensity proved critical for successful differentiation of CJD from other dementias.
Because specific patterns of abnormality on DWI and FLAIR images are highly sensitive and specific for CJD, these sequences should be performed whenever CJD is suspected.
Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT), often termed Hashimoto encephalopathy, is a poorly understood and often misdiagnosed entity.
To characterize the clinical, laboratory, and radiologic findings in patients with SREAT to potentially improve recognition of this treatable entity.
Retrospective analysis of clinical features and diagnostic test data.
Two affiliated tertiary care referral institutions.
Twenty consecutive (6 male) patients diagnosed as having SREAT from 1995 to 2003.
Clinical features and ancillary test findings associated with SREAT.
The median age at disease onset was 56 years (range, 27-84 years). The most frequent clinical features were tremor in 16 (80%), transient aphasia in 16 (80%), myoclonus in 13 (65%), gait ataxia in 13 (65%), seizures in 12 (60%), and sleep abnormalities in 11 (55%). All patients were assigned an alternative misdiagnosis at presentation, most commonly viral encephalitis (n = 5), Creutzfeldt-Jakob disease (n = 3), or a degenerative dementia (n = 4). The most frequent laboratory abnormalities were increased liver enzyme levels in 11, increased serum sensitive thyroid-stimulating hormone levels in 11, and increased erythrocyte sedimentation rate in 5. In only 5 patients (25%) did cerebrospinal fluid abnormalities suggest an inflammatory process. Magnetic resonance imaging abnormalities believed to be related to the encephalopathy were present in 5 patients (26%).
The clinical, laboratory, and radiologic findings associated with SREAT are more varied than previously reported. Misdiagnosis at presentation is common. This treatable syndrome should be considered even if the serum sensitive thyroid-stimulating hormone level and erythrocyte sedimentation rate are normal, the cerebrospinal fluid profile does not suggest an inflammatory process, and neuroimaging results are normal. Until the pathophysiologic mechanism of this and other autoimmune encephalopathies is better characterized, we believe that descriptive terms that reflect an association rather than causation are most appropriate for this syndrome.
The cause of "posterior reversible encephalopathy syndrome" (PRES) is not established. We recently encountered several patients who developed PRES in the setting of severe infection. In this study, we comprehensively reviewed the clinical and imaging features in a large cohort of patients who developed PRES, with particular attention to those with isolated infection, sepsis, or shock (I/S/S).
The clinical/imaging features of 106 patients who developed PRES were comprehensively evaluated. In 25 of these patients, PRES occurred in association with severe I/S/S separate from transplantation. The clinical/imaging features (computer tomography, MR imaging, and MR angiography [MRA]) of the patients with I/S/S were further evaluated, including organ/tissue/blood culture results, mean arterial blood pressure (MAP) at toxicity, extent of cerebral edema, and presence of vasospasm.
PRES occurred in association with I/S/S in 25 of 106 patients (23.6%), in addition to 4 other major clinical settings, including cyclosporine/FK-506 (post-transplant) neurotoxicity (46.2%), autoimmune disease (10.4%), postchemotherapy (3.7%), and eclampsia (10.4%). In the 25 patients with I/S/S, available cultures demonstrated a predominance of gram-positive organisms (84%). Blood pressure was "normal" at toxicity in 10 patients (MAP, 95 mm Hg); "severe" hypertension was present in 15 patients (MAP, 137 mm Hg). Extent of brain edema graded on imaging studies was greater in the normal MAP group compared with the severe hypertension group (P < .05). MRA demonstrated vasospasm in patients with severe hypertension and vessel "pruning" in the normal MAP group.
Infection/sepsis/shock may be an important cause of PRES, particularly in relation to infection with gram-positive organisms.
Purpose:
The study reviewed emergent cases of nonconvulsive status epilepticus (NCSE) to evaluate causes of diagnostic and management delay and examined frequent diagnostic features suggestive of NCSE.
Methods:
In a retrospective study, we assessed the clinical presentation of 23 patients with one or more NCSE episodes, their medical history, EEG, and antiepileptic drug (AED) treatment. We also evaluated causes of diagnostic delay in patients referred to the emergency room (ER) in confusional states.
Results:
There was considerable overlap in clinical features of patients with complex partial SE (CPSE) and generalized nonconvulsive SE (GNSE). Delays in seeking medical attention were common. Diagnosis was significantly delayed in 10 patients. Three cases illustrate the possible markedly different presentations of NCSE.
Conclusions:
NCSE often goes unrecognized or is mistaken for behavioral or psychiatric disturbance. The pleomorphic clinical presentation of NCSE indicates that EEG and a therapeutic trial of AEDs afford the best diagnostic measures in acute waxing and waning confusional states associated with agitation, bizarre behavior, staring, increased tone, mutism, or subtle myoclonus.
Measurement of amino acids in brain tissue obtained at autopsy from cirrhotic patients dying in hepatic coma revealed a threefold
increase in glutamine and a concomitant decrease in brain glutamate. The GABA levels were found to be unaltered. Studies using
an animal model of portal-systemic encephalopathy gave similar results. Glutamic acid decarboxylase (GAD) activities were
within normal limits, both in the brains of cirrhotic patients and portocaval-shunted rats. A previous study reported normal
[3H]GABA binding to synaptic membrane preparations from cerebral cortex in these animals. Taken together, these findings suggest
that cerebral GABA function is not impaired in hepatic encephalopathy associated with chronic liver disease and portal-systemic
shunting. On the other hand, there is evidence to suggest that the releasable pool ofglutamate may be depleted in brain in hepatic encephalopathy. Data consistent with this hypothesis include: (i) Reduction in the evoked
release of endogenous glutamate by superfusion of hippocampal slices with pathophysiological levels of ammonia; (ii) ammonia-induced
reduction of glutamatergic neurotransmission; and (iii) an increase in the number of [3H]glutamate binding sites in synaptic membrane preparations from hyperammonemia rats and from rats with portocaval shunts.
Such neurochemical changes may be of pathophysiological significance in hepatic encephalopathy.
Sepsis is often complicated by an acute and reversible deterioration of mental status, which is associated with increased mortality and is consistent with delirium but can also be revealed by a focal neurologic sign. Sepsis-associated encephalopathy is accompanied by abnormalities of electroencephalogram and somatosensory-evoked potentials, increased in biomarkers of brain injury (i.e., neuron-specific enolase, S-100 beta-protein) and, frequently, by neuroradiological abnormalities, notably leukoencephalopathy. Its mechanism is highly complex, resulting from both inflammatory and noninflammatory processes that affect all brain cells and induce blood-brain barrier breakdown, dysfunction of intracellular metabolism, brain cell death, and brain injuries. Its diagnosis relies essentially on neurologic examination that can lead one to perform specific neurologic tests. Electroencephalography is required in the presence of seizure; neuroimaging in the presence of seizure, focal neurologic signs or suspicion of cerebral infection; and both when encephalopathy remains unexplained. In practice, cerebrospinal fluid analysis should be performed if there is any doubt of meningitis. Hepatic, uremic, or respiratory encephalopathy, metabolic disturbances, drug overdose, withdrawal of sedatives or opioids, alcohol withdrawal delirium, and Wernicke's encephalopathy are the main differential diagnoses of sepsis-associated encephalopathy. Patient management is based mainly on controlling infection, organ system failure, and metabolic homeostasis, at the same time avoiding neurotoxic drugs.
Voltage-gated potassium channels are thought to be the target of antibodies associated with limbic encephalitis. However, antibody testing using cells expressing voltage-gated potassium channels is negative; hence, we aimed to identify the real autoantigen associated with limbic encephalitis.
We analysed sera and CSF of 57 patients with limbic encephalitis and antibodies attributed to voltage-gated potassium channels and 148 control individuals who had other disorders with or without antibodies against voltage-gated potassium channels. Immunohistochemistry, immunoprecipitation, and mass spectrometry were used to characterise the antigen. An assay with HEK293 cells transfected with leucine-rich, glioma-inactivated 1 (LGI1) and disintegrin and metalloproteinase domain-containing protein 22 (ADAM22) or ADAM23 was used as a serological test. The identity of the autoantigen was confirmed by immunoabsorption studies and immunostaining of Lgi1-null mice.
Immunoprecipitation and mass spectrometry analyses showed that antibodies from patients with limbic encephalitis previously attributed to voltage-gated potassium channels recognise LGI1, a neuronal secreted protein that interacts with presynaptic ADAM23 and postsynaptic ADAM22. Immunostaining of HEK293 cells transfected with LGI1 showed that sera or CSF from patients, but not those from control individuals, recognised LGI1. Co-transfection of LGI1 with its receptors, ADAM22 or ADAM23, changed the pattern of reactivity and improved detection. LGI1 was confirmed as the autoantigen by specific abrogation of reactivity of sera and CSF from patients after immunoabsorption with LGI1-expressing cells and by comparative immunostaining of wild-type and Lgi1-null mice, which showed selective lack of reactivity in brains of Lgi1-null mice. One patient with limbic encephalitis and antibodies against LGI1 also had antibodies against CASPR2, an autoantigen we identified in some patients with encephalitis and seizures, Morvan's syndrome, and neuromyotonia.
LGI1 is the autoantigen associated with limbic encephalitis previously attributed to voltage-gated potassium channels. The term limbic encephalitis associated with antibodies against voltage-gated potassium channels should be changed to limbic encephalitis associated with LGI1 antibodies, and this disorder should be classed as an autoimmune synaptic encephalopathy.
National Institutes of Health, National Cancer Institute, and Euroimmun.
Current American Academy of Neurology (AAN) guidelines for outcome prediction in comatose survivors of cardiac arrest (CA) have been validated before the therapeutic hypothermia era (TH). We undertook this study to verify the prognostic value of clinical and electrophysiological variables in the TH setting.
A total of 111 consecutive comatose survivors of CA treated with TH were prospectively studied over a 3-year period. Neurological examination, electroencephalography (EEG), and somatosensory evoked potentials (SSEP) were performed immediately after TH, at normothermia and off sedation. Neurological recovery was assessed at 3 to 6 months, using Cerebral Performance Categories (CPC).
Three clinical variables, assessed within 72 hours after CA, showed higher false-positive mortality predictions as compared with the AAN guidelines: incomplete brainstem reflexes recovery (4% vs 0%), myoclonus (7% vs 0%), and absent motor response to pain (24% vs 0%). Furthermore, unreactive EEG background was incompatible with good long-term neurological recovery (CPC 1-2) and strongly associated with in-hospital mortality (adjusted odds ratio for death, 15.4; 95% confidence interval, 3.3-71.9). The presence of at least 2 independent predictors out of 4 (incomplete brainstem reflexes, myoclonus, unreactive EEG, and absent cortical SSEP) accurately predicted poor long-term neurological recovery (positive predictive value = 1.00); EEG reactivity significantly improved the prognostication.
Our data show that TH may modify outcome prediction after CA, implying that some clinical features should be interpreted with more caution in this setting as compared with the AAN guidelines. EEG background reactivity is useful in determining the prognosis after CA treated with TH.
To review recent clinical data and summarize actual recommendations for the management of electrographic seizures and status epilepticus in neuro-ICU patients.
Electrographic, 'nonconvulsive', seizures are frequent in neuro-ICU patients including traumatic brain injury, subarachnoid hemorrhage, intracerebral hemorrhage and hypoxic-ischemic encephalopathy. Continuous electroencephalography monitoring is thus of great potential utility. The impact of electrographic seizures on outcome however is not entirely established and it is also unclear what type of electroencephalography paroxysms require treatment and when and how exactly to treat them. Evidence from randomized studies is lacking and will not be available in the near future. Given robust animal and human evidence showing the potential negative impact of seizures on secondary cerebral damage and outcome, treatment of seizures appears reasonable, particularly if related to status epilepticus. On the contrary, over-aggressive antiepileptic therapy entails risks. The management of seizures should therefore be guided individually, based on the underlying cause, the severity of illness and patient comorbidities.
We provide a pragmatic approach for the management of electrographic seizures in neuro-ICU patients. International consensus guidelines on continuous electroencephalography monitoring and seizure therapy are needed and would represent the rationale for a future multicenter randomized trial.
Hashimoto encephalopathy is characterized by severe neuropsychiatric findings, including psychosis, confusion, seizures, stupor, stroke-like episodes, tremor, and myoclonus. The combination of findings is variable. Hashimoto encephalopathy constitutes an important differential diagnosis in patients with encephalopathy. The triad of encephalopathy, corresponding electroencephalographic slowing, and increased protein content in cerebrospinal fluid should prompt testing of anti-thyroid antibodies in blood and cerebrospinal fluid. Elevated antibody levels support the diagnosis. We describe a 15-year-old girl with a fluctuating course of Hashimoto encephalopathy. Electroencephalograms revealed no specific alterations, but widespread slowing of the background activity occurred during two episodes of fluctuating encephalopathy. Cortical edema was indicated by cranial magnetic resonance imaging during the first episode of encephalopathy, in the context of cerebral seizures. Laboratory findings were in accordance with Hashimoto encephalopathy, which was steroid-responsive.
By studying neuronal activity through neuronal electrogenesis, neurophysiological investigations provide a functional assessment of the nervous system and, therefore, has been used for quantitative assessment and follow-up of hepatic encephalopathy (HE). The different clinical neurophysiological approaches can be classified depending on the function to explore and their sensitivity to HE. The reliable techniques are those that reflect cortical function, i.e., cognitive-evoked potentials (EPs) (P300 paradigm), electroencephalogram (EEG), visual EPs (latency>100 ms) and somatosensory EPs (SEPs) (latency between 25 and 100 ms). Short-latency EPs (brainstem acoustic EPs, SEPs of a latency<25 ms) are in principle insensitive to HE, but can disclose brainstem conduction deficits due to oedema. SEPs and motor EPs can disclose myelopathies. Because of its parallelism to the clinical examination, clinical neurophysiology can complement the neurological examination: (i) to provide evidence of HE in patients who have normal consciousness; (ii) to rule out, at least under some conditions, disturbances of consciousness due to other causes (e.g. drug-induced disturbances, non-convulsive status epilepticus) with the reservation that the mildest degrees of encephalopathy might be associated with an EEG pattern similar to that induced by drugs; and (iii) to demonstrate the worsening or, conversely improvement, of HE in the follow-up period.
Because of recent technical advances, it is now possible to record and monitor the continuous digital electroencephalogram (EEG) of many critically ill patients simultaneously. Continuous EEG monitoring (cEEG) provides dynamic information about brain function that permits early detection of changes in neurologic status, which is especially useful when the clinical examination is limited. Nonconvulsive seizures are common in comatose critically ill patients and can have multiple negative effects on the injured brain. The majority of seizures in these patients cannot be detected without cEEG. cEEG monitoring is most commonly used to detect and guide treatment of nonconvulsive seizures, including after convulsive status epilepticus. In addition, cEEG is used to guide management of pharmacological coma for treatment of increased intracranial pressure. An emerging application for cEEG is to detect new or worsening brain ischemia in patients at high risk, especially those with subarachnoid hemorrhage. Improving quantitative EEG software is helping to make it feasible for cEEG (using full scalp coverage) to provide continuous information about changes in brain function in real time at the bedside and to alert clinicians to any acute brain event, including seizures, ischemia, increasing intracranial pressure, hemorrhage, and even systemic abnormalities affecting the brain, such as hypoxia, hypotension, acidosis, and others. Monitoring using only a few electrodes or using full scalp coverage, but without expert review of the raw EEG, must be done with extreme caution as false positives and false negatives are common. Intracranial EEG recording is being performed in a few centers to better detect seizures, ischemia, and peri-injury depolarizations, all of which may contribute to secondary injury. When cEEG is combined with individualized, physiologically driven decision making via multimodality brain monitoring, intensivists can identify when the brain is at risk for injury or when neuronal injury is already occurring and intervene before there is permanent damage. The exact role and cost-effectiveness of cEEG at the current time remains unclear, but we believe it has significant potential to improve neurologic outcomes in a variety of settings.
Localized delta activity appears in cortex overlying a circumscribed white matter lesion. Less commonly, localized delta activity may result from a localized thalamic lesion. Unilateral diffuse delta activity appears on the side of thalamic or hypothalamic lesions. Bilateral delta activity results from bilateral lesions of the midbrain tegmentum. Localized lesions of the cerebral cortex, unilateral mesencephalic tegmental lesions, and vasogenic edema of the cerebral white matter do not produce delta activity. Marked edema of a cerebral hemisphere when no surgical decompression is provided may produce unilateral delta activity by pressure on or displacement of the brain stem or diencephalon.
To define the EEG and associated clinical features of septic encephalopathy, we studied 62 patients with positive blood cultures. Patients were divided into three clinical groups: nonencephalopathic (NE), mildly encephalopathic (ME), and severely encephalopathic (SE); the latter two groups had diffuse cerebral dysfunction. EEGs were classified into five groups: normal, excessive theta, predominant delta, triphasic waves, and suppression or burst suppression, in ascending order of severity. The EEG (1) was more sensitive than our clinical criteria for encephalopathy, (2) showed features that were, when considered with clinical and laboratory characteristics, compatible with a potentially reversible encephalopathy, and (3) had well-defined categories that correlated with percent mortality, even within a single clinical group. We conclude that the EEG is a sensitive index of brain function in septic encephalopathy and that it is especially useful in the intensive care monitoring of patients with sepsis.
A blind analysis of 56 EEGs with triphasic wave patterns was performed to determine the diagnostic specificity of individual electrographic features. EEG and clinical variables analyzed included longitudinal topography, phase lags, symmetry, background activity, reactivity, longitudinal bipolar phase reversal sites, responses to photic stimulation and mental status at the time of recording. The only statistically significant finding for any of the diagnostic groups tested was the presence of severe background slowing in cases of hepatic encephalopathy (P less than 0.001). We found no evidence to suggest that other features may contribute to a more highly characteristic pattern for hepatic encephalopathy. None of the features studied reliably distinguished hepatic encephalopathy from other forms of metabolic encephalopathy.
The catatonic syndrome has a wide differential diagnosis that includes both psychiatric and organic disorders. We present the cases of two patients with catatonia seen acutely in the emergency department. In these cases, the striking clinical picture proved to be secondary to psychiatric disturbances, and were accompanied by dementia in the second patient. The examining physicians were confused by the presentations, and the correct diagnosis and disposition were delayed. The clinical presentation of the catatonic complex, its differential diagnosis, and the pertinent physical signs are discussed.
Clinical data on 18 patients whose EEGs showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) were reviewed and compared with those of 45 patients with periodic lateralized epileptiform discharges (PLEDs). A recent stroke was the most frequent cause of PLEDs (33%), while anoxic encephalopathy (28%) and CNS infection (28%) accounted for the majority of BIPLEDs. Focal neurologic deficits, focal seizures, and focal computed tomographic scan abnormalities were frequent in those with PLEDs, while coma predominated in the group with BIPLEDs (72% vs 24%). Mortality was also higher in patients with BIPLEDs--61% vs 29%.
It is the purpose of this review to critically consider and organize the literature dealing with the ephemeral electroencephalographic (EEG) pattern periodic lateralized epileptiform discharges (PLEDs). Although the retrospective nature of these studies limits their ability to discuss accurately the clinical and pathophysiological aspects of this EEG entity, the available data strongly emphasize stroke as the dominant etiology and its high association with seizures. Recent evidence, particularly from functional neuroimaging studies, strongly suggests that PLEDs might reflect a key pattern for focal hyperexcitability in the penumbra zone of ischemic stroke. The authors prefer to consider PLEDs as an EEG signature of a dynamic pathophysiological state in which unstable neurobiological processes create an ictal-interictal continuum, with the nature of the underlying neuronal injury, the patient's preexisting propensity to have seizures, and the co-existence of any acute metabolic derangements all contributing to whether seizures occur or not. This review underlines the need for further sophisticated prospective controlled studies implementing early continuous EEG monitoring in order to contribute to an understanding of the incidence, dynamics, and relevance of this pattern.
Hepatic encephalopathy (HE) accompanied by an impairment of consciousness from orientation disorder (grade II) to coma (grade IV) is considered to be overt HE and is treated as an emergency. However, subclinical hepatic encephalopathy (SHE) can be detected by sensitive and quantitative neuropsychological examinations in cirrhotic patients without overt HE. The introduction of the SHE concept is clinically important for preventing the deterioration of SHE (grades 0 and I) to overt HE (grade II and more severe), prolonging the compensated state of cirrhosis without its deterioration to hepatic failure, and the continuation of patient treatment at home. We developed a new diagnostic method for SHE using a quantitative neuropsychological test, with the computerization of all operations. Evaluations of cerebral function and morphology are useful for the determination of the pathophysiology of HE, and assist the diagnosis of SHE. The latencies of the P3 wave in the visually evoked potential and the P300 wave in the event-related potential are prolonged in cirrhotic patients with SHE and are well expressed in three-dimensional coloured topograms (brain mapping). Automated polysomnographic analysis is useful for continuous-monitoring electroencephalograms (EEG) and for the detection of the sleep disturbance observed in cirrhotic patients with SHE. Brain atrophy in computed tomography (CT), magnetic resonance imaging (MRI) and high signals in the basal ganglia in the MR-T1-weighted images have frequently been observed in patients with SHE. The reduction of regional cerebral blood flow (rCBF) by 99mtechnetium-1, 1-ethylcysteinate dimer (99mTc-ECD)-single photon emission computed tomography (SPECT) and the choline/N-acetylaspartic acid ratio by proton-magnetic resonance spectroscopy (1H-MRS) were observed in the hippocampus in patients with SHE. These approaches (cerebral function tests and imaging diagnoses of the brain) can also be used to evaluate the effectiveness of treatments for HE; for example, branched-chain amino acid (BCAA) was shown by automated continuous polysomnographic analysis to be a psychotropic drug which acts directly on the central nervous system and the clinical significance of choline administration to HE patients is now being evaluated by 1H-MRS and neuropsychological tests.
Hashimoto encephalopathy has been described as a syndrome of encephalopathy and high serum antithyroid antibody concentrations that is responsive to glucocorticoid therapy, but these could be chance associations.
To study a patient with Hashimoto encephalopathy and to review the literature to determine whether Hashimoto encephalopathy is an identifiable syndrome.
We searched the MEDLINE database to June 2002 for "Hashimoto" or "autoimmune thyroiditis" and "encephalopathy" and examined all identified articles and articles referenced therein, including all languages. We included all patients with noninfectious encephalopathy (clouding of consciousness and impaired cognitive function) and high serum antithyroid antibody concentrations. We excluded patients if they did not meet these inclusion criteria or if their symptoms could be explained by another neurologic disorder. We recorded clinical features and the results of imaging, electroencephalographic, thyroid function, and cerebrospinal fluid studies.
We identified 85 patients (69 women and 16 men; mean age, 44 years) with encephalopathy and high serum antithyroid antibody concentrations. Among these patients, 23 (27%) had strokelike signs, 56 (66%) had seizures, 32 (38%) had psychosis, 66 (78%) had a high cerebrospinal fluid protein concentration, and 80 (98%) of 82 had abnormal electroencephalographic findings. Thyroid function varied from overt hypothyroidism to overt hyperthyroidism; the most common abnormality was subclinical hypothyroidism (30 patients [35%]). Among patients treated with glucocorticoids, 66 (96%) improved.
The combination of encephalopathy, high serum antithyroid antibody concentrations, and responsiveness to glucocorticoid therapy seems unlikely to be due to chance. However, there is no evidence of a pathogenic role for the antibodies, which are probably markers of some other autoimmune disorder affecting the brain.
Enter Queen, with a taper. GENTLEMAN: This is her very guise; and, upon my life, fast asleep. Observe her: stand close. DOCTOR: You see, her eyes are open. GENTLEMAN: Ay but their sense is shut. DOCTOR: What is it she does now? Look, how she rubs her hands. GENTLEMAN: It is an accustomed action with her, to seem thus washing her hands: I have known her to continue in this a quarter of an hour.... DOCTOR: Hark! She speaks: I will set down what comes from her, to satisfy my remembrance the more strongly.... [Later] DOCTOR: This disease is beyond my practice: Yet I have known those which have walked in their sleep who have died holily in their beds.... DOCTOR:... Look after her; remove from her the means of all annoyance, and still keep eyes upon her:-so, goodnight: My mind she has mated, and amazed my sight: I think, but dare not speak. GENTLEMAN: Goodnight, good doctor. [exit].
Electroecenphalography (EEG) is an integral part of the diagnostic process in patients with Creutzfeldt-Jakob disease (CJD). The EEG has therefore been included in the World Health Organisation diagnostic classification criteria of CJD. In sporadic CJD (sCJD), the EEG exhibits characteristic changes depending on the stage of the disease, ranging from nonspecific findings such as diffuse slowing and frontal rhythmic delta activity (FIRDA) in early stages to disease-typical periodic sharp wave complexes (PSWC) in middle and late stages to areactive coma traces or even alpha coma in preterminal EEG recordings. PSWC, either lateralized (in earlier stages) or generalized, occur in about two-thirds of patients with sCJD, with a positive predictive value of 95%. PSWC occur in patients with methionine homozygosity and methionine/valine heterozygosity but only rarely in patients with valine homozygosity at codon 129 of the prion protein gene. PSWC tend to disappear during sleep and may be attenuated by sedative medication and external stimulation. Seizures are an uncommon finding, occurring in less than 15% of patients with sCJD. In patients with iatrogenic CJD, PSWC usually present with more regional EEG findings corresponding to the site of inoculation of the transmissible agent. In genetic CJD, PSWC in its typical form are uncommon, occurring in about 10%. No PSWC occur in EEG recordings of patients with variant CJD.
A 56-year-old woman presented with an acute confusional state and moderate global aphasia. Thyroperoxidase antibody level was elevated (3,890 IU/mL) and SREAT was diagnosed. MRI findings were normal. Cerebrospinal fluid examination revealed only a mildly increased protein. The initial electroencephalogram EEG showed slowing and markedly decreased amplitude over the left hemisphere and left temporal sharp waves. An EEG performed after treatment with intravenous steroids showed a significant improvement of the background slowing, which correlated with clinical improvement. One week later, the patient had an episode of forced head-turning and fencing posture to the right. The EEG shortly afterward showed slowing and a decreased amplitude over the right hemisphere. Continuous EEG monitoring was performed at the time of steroid treatment. Again, there was a significant improvement of the EEG after this treatment that correlated with the clinical condition. SREAT is characterized by fluctuations in mental status and variable EEG findings. These patients often show an excellent clinical improvement to immunosuppressive therapy, including corticosteroids. This case report documents the dramatic clinical and EEG improvement with steroid therapy.
Lithium therapy can cause a confusional state by direct toxicity, precipitation of nonconvulsive status epilepticus, or by interplay with other neuroleptic medications to produce neuroleptic malignant syndrome or serotonin syndrome. These conditions resemble each other clinically, but EEG may help differentiate among them. We reviewed the EEG patterns with triphasic waves or rhythmic delta activity in lithium toxic patients and discuss clinical and EEG differentiation among syndromes. Lithium toxicity poses significant diagnostic challenges from EEG and clinical perspectives.
Patients frequently present to the emergency room (ER) with mental status changes without obvious cause. The EEG is underused in this population. The authors investigated whether an abbreviated EEG (AbEEG) can be incorporated in the early evaluation of these patients to provide useful information. A 5-minute AbEEG was performed using a preformed electrode placement system on 25 patients who presented to the ER with mental status changes of unknown cause. AbEEG findings were categorized as normal, showing diffuse abnormalities, focal abnormalities, electrographic seizures, or uninterpretable. Using retrospective chart review, the authors determined if the cause of mental status change was a diffuse encephalopathy or a nonneurologic event (DENNE), a focal brain abnormality, nonconvulsive status epilepticus (NCSE), psychogenic, or unknown, and if particular AbEEG findings were associated with specific causes of altered sensorium. The AbEEG identified NCSE in two patients who presented with new-onset seizures. The presence of diffuse slowing on the AbEEG was highly suggestive of mental status changes due to DENNE. AbEEGs can be successfully incorporated in the early evaluation of patients who present to the ER with mental status changes of unknown cause and provide useful information in this setting.
Evaluation of patients with recent onset of progressive cognitive and behavioral problems can be challenging. Psychiatric disorders, metabolic derangements, toxins and infections are generally considered in the differential diagnosis along with prion disorders (Creutzfeldt-Jakob disease) and rapidly progressive degenerative dementias. Some subacute encephalopathies are caused by autoimmune or inflammatory mechanisms, recognized by the association with autoantibody markers and/or clear response to immunomodulatory treatment. This review describes the clinical features of these potentially reversible autoimmune encephalopathies.
Morvan syndrome, paraneoplastic limbic encephalitis (PLE), and nonparaneoplastic autoimmune limbic encephalitis have characteristic clinical and serological features. Limbic encephalitis is characterized by short-term memory impairment, complex partial temporal lobe seizures and psychiatric symptoms. Signal abnormalities in the mesial temporal lobes without contrast enhancement are the typical MRI findings. Morvan syndrome presents with behavioral changes, hallucinations, severe insomnia, autonomic hyperactivity and neuromyotonia (spontaneous muscle activity). Corticosteroid-responsive encephalopathy associated with evidence of thyroid autoimmunity (sometimes called Hashimoto encephalopathy) has a broad range of clinical presentation. Cognitive impairment with tremor, seizures, stroke-like events (including transient aphasia) and normal thyroid hormone levels is a common scenario. In the absence of diagnostic serological findings, clinical improvement with corticosteroids may be the only evidence of autoimmune encephalopathy.
Autoimmune encephalopathies are an important cause of rapidly progressive cognitive and behavioral decline that probably remain under recognized. Electroencephalography, brain MRI, cerebrospinal fluid examination and serological tests are useful diagnostic tools. With increased clinical suspicion, these diseases may be diagnosed and treated successfully.
Nonconvulsive status epilepticus (NCSE) is a heterogeneous disorder with multiple subtypes. Although attempts have been made to define and classify this disorder, there is yet no universally accepted definition or classification that encompasses all subtypes or electroclinical scenarios. Developing such a classification scheme is becoming increasingly important, because NCSE is more common than previously thought, with a bimodal peak, in children and the elderly. Recent studies have also shown a high incidence of NCSE in the critically ill. Although strong epidemiological data are lacking, NCSE constitutes about 25-50% of all cases of status epilepticus. For the purposes of this review, we propose an etiological classification for NCSE including NCSE in metabolic disorders, NCSE in coma, NCSE in acute cerebral lesions, and NCSE in those with preexisting epilepsy with or without epileptic encephalopathy. NCSE is still underrecognized, yet potentially fatal if untreated. Diagnosis can be established using an electroencephalogram (EEG) in most cases, sometimes requiring continuous monitoring. However, in comatose patients, diagnosis can be difficult, and the EEG can show a variety of rhythmic or periodic patterns, some of which are of unclear significance. Although some subtypes of NCSE are easily treatable, such as absence status epilepticus, others do not respond well to treatment, and debate exists over how aggressively clinicians should treat NCSE. In particular, the appropriate treatment of NCSE in patients who are critically ill and/or comatose is not well established, and large-scale trials are needed. Overall, further work is needed to better define NCSE, to determine which EEG patterns represent NCSE, and to establish treatment paradigms for different subtypes of NCSE.
Major advances in the management of paraneoplastic neurologic disorders (PND) include the detection of new antineuronal antibodies, the improved characterisation of known syndromes, the discovery of new syndromes, and the use of CT and PET to reveal the associated tumours at an early stage. In addition, the definition of useful clinical criteria has facilitated the early recognition and treatment of these disorders. In this article, we review some classic concepts about PND and recent clinical and immunological developments, focusing on paraneoplastic cerebellar degeneration, opsoclonus-myoclonus, and encephalitides affecting the limbic system.
The purpose of this study was to investigate the frequency and clinical outcome of patients with encephalopathic electroencephalograms (EEGs) in a neurophysiology department based in a general hospital. We performed a retrospective review of all EEGs obtained during an 18-month period in a large tertiary referral hospital. The referral reasons for EEG, the diagnoses reached, and patient outcomes were reviewed according to EEG severity. One hundred and twenty-three patients with encephalopathic EEGs were reviewed. The most common referral reason found was for an assessment of a possible first-onset seizure. The most common diagnosis found was one of dementia or learning disability. Of patients who were followed-up for a median of 19 months, 20.7% had died. The mortality rate generally increased according to the severity of the encephalopathy on EEG. However, 21.4% of those patients with excessive theta activity only on EEG had died. This study highlights an increased mortality even in the apparently 'milder' degrees of EEG abnormalities.
Paraneoplastic syndromes of the CNS Bilateral independent periodic lateralized epileptiform discharges: clinical significance
- J Dalmau
- Mr Rosenfeld
- De
- D Paz
- Brenner
Dalmau J, Rosenfeld MR. Paraneoplastic syndromes of the CNS. Lancet Neurol 2008;7:327e340. de la Paz D, Brenner RP. Bilateral independent periodic lateralized epileptiform discharges: clinical significance. Arch Neurol 1981;38:713e722