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SPTLC1-related disorder is a late onset sensory-autonomic neuropathy associated with perturbed sphingolipid homeostasis which can be improved by supplementation with the serine palmitoyl-CoA transferase (SPT) substrate, l-serine. Recently, a juvenile form of motor neuron disease has been linked to SPTLC1 variants. Variants affecting the p.S331 residue of SPTLC1 cause a distinct phenotype, whose pathogenic basis has not been established. This study aims to define the neuropathological and biochemical consequences of the SPTLC1 p.S331 variant, and test response to l-serine in this specific genotype.We report clinical and neurophysiological characterisation of two unrelated children carrying distinct p.S331 SPTLC1 variants. The neuropathology was investigated by analysis of sural nerve and skin innervation. To clarify the biochemical consequences of the p.S331 variant, we performed sphingolipidomic profiling of serum and skin fibroblasts. We also tested the effect of l-serine supplementation in skin fibroblasts of patients with p.S331 mutations.In both patients, we recognised an early onset phenotype with prevalent progressive motor neuron disease. Neuropathology showed severe damage to the sensory and autonomic systems. Sphingolipidomic analysis showed the coexistence of neurotoxic deoxy-sphingolipids with an excess of canonical products of the SPT enzyme. l-serine supplementation in patient fibroblasts reduced production of toxic 1-deoxysphingolipids but further increased the overproduction of sphingolipids.Our findings suggest that p.S331 SPTLC1 variants lead to an overlap phenotype combining features of sensory and motor neuropathies, thus proposing a continuum in the spectrum of SPTLC1-related disorders. l-serine supplementation in these patients may be detrimental.

Highlights • Canakinumab is an IL-1β antibody that neutralizes the activity of IL-1β. • The effects of canakinumab in patients with COVID-19-related pneumonia were studied. • 33 patients received canakinumab and 15 received institutional standard of care. • Treatment with canakinumab rapidly restored normal oxygen status. • Canakinumab was also associated with favorable prognosis versus SoC., Objectives Canakinumab is an IL-1β antibody that neutralizes the activity of IL-1β. We studied the efficacy and safety of canakinumab in patients with moderate COVID-19-related pneumonia. Design The aim of our study was to evaluate the reduction in duration of hospitalization with adequate oxygen status. Forty-eight patients with moderate COVID-19-related pneumonia were asked to participate in the prospective case-control study; 33 patients (Cases) signed informed consent and received canakinumab (Cohort 1); 15 patients (Controls) refused to receive the experimental drug and received institutional standard of care (SoC), (Cohort 2). Results Hospital discharge within 21 days was seen in 63% of patients in Cohort 1 vs. 0% in Cohort 2 (median 14 vs 26 days, respectively; p

Many drugs that have been proposed for treatment of coronavirus disease 2019 (COVID-19) are reported to cause cardiac adverse events, including ventricular arrhythmias. In order to properly weigh risks against potential benefits, particularly when decisions must be made quickly, mathematical modeling of both drug disposition and drug action can be useful for predicting patient response and making informed decisions. Here, we explored the potential effects on cardiac electrophysiology of four drugs proposed to treat COVID-19: lopinavir, ritonavir, chloroquine, and azithromycin, as well as combination therapy involving these drugs. Our study combined simulations of pharmacokinetics (PKs) with quantitative systems pharmacology (QSP) modeling of ventricular myocytes to predict potential cardiac adverse events caused by these treatments. Simulation results predicted that drug combinations can lead to greater cellular action potential prolongation, analogous to QT prolongation, compared with drugs given in isolation. The combination effect can result from both PK and pharmacodynamic drug interactions. Importantly, simulations of different patient groups predicted that women with pre-existing heart disease are especially susceptible to drug-induced arrhythmias, compared with diseased men or healthy individuals of either sex. Statistical analysis of population simulations revealed the molecular factors that make certain women with heart failure especially susceptible to arrhythmias. Overall, the results illustrate how PK and QSP modeling may be combined to more precisely predict cardiac risks of COVID-19 therapies.

To evaluate serum markers of calcium metabolism in adult patients with epilepsy (PWE) treated with antiepileptic drugs (AEDs) and the effect of vitamin D supplementation on seizure frequency.Serum levels of calcium, phosphate, intact parathyroid hormone (iPTH) and 25-hydroxyvitamin D (25[OH]D) were compared in 160 PWE on chronic therapy with AEDs and 42 matched controls. Blood concentrations were analyzed taking into account the different features of epilepsy and treatment. Finally, the effect of vitamin D supplementation on seizure control was assessed in a subgroup of 48 drug resistant epileptic patients.PWE showed lower serum levels of 25[OH]D compared to control subjects (p .001). Only 25% PWE showed normal 25[OH]D levels, whereas 41,9% had a vitamin D failure and 33,1% a vitamin D deficiency (p .001). 25[OH]D serum levels depended on treatment duration, number of medications and enzyme-inducing AEDs (p .001, p .001, p = .013, respectively). Polytherapy and enzyme-inducing AEDs showed more detrimental effects on the 25[OH]D and calcium serum levels. The administration of vitamin D failed to significantly improve seizure control.PWE show deficiency of vitamin D. The serum levels of 25[OH]D depend on the features and duration of AEDs treatment. Vitamin D administration in drug resistant epilepsy patients does not result in a reduction of seizure frequency.

Backgrounds Mask-related side effects can negatively influence adherence to continuous positive airway pressure (CPAP). Nasal pillows (P) can be an alternative to the standard nasal masks (N), although there are no data about their long-term efficacy. This study aimed to assess long-term effectiveness and adherence to CPAP therapy delivered with nasal pillows in obstructive sleep apnea syndrome (OSAS) patients. Methods A retrospective observational design involving a series of consecutive CPAP-naive patients affected by OSAS. After an initial mask fitting session all patients were allowed to choose the type of nasal interface (N or P) they preferred. Outcomes were assessed 5 days after CPAP titration, and after 2 and 12 months. Patients were offered the option of switching to an alternative mask if needed. Results Data from 144 patients were analyzed. Subjects were predominantly male (76%), middle aged (58.14 ± 12.86), moderately obese (body mass index: 33.89 ± 7.56), and affected by severe OSAS (apnea-hypopnea index: 47.60 ± 21.31). A total of 102 patients (70.8%) chose P, and 42 (29.2%) chose N. Clinical and polygraphic features, and CPAP pressure levels were similar in P and N groups, both at baseline and at 12 months. A good adherence to treatment was observed in both groups (P, 5.5 ± 1.8 h; N, 5.3 ± 1.5 h). Seventy-six patients (53%) reported at least one side effect during the whole study period, without statistically significant between-group differences. Nostril pain was the most frequent side effect in P. Conclusions Nasal pillows showed equal long-term effectiveness and objective adherence as standard nasal masks.

Aims Atrial fibrillation (AF) prevalence increases with advanced stages of left ventricular (LV) dysfunction. Remote proarrhythmic effects of ventricular dysfunction on atrial electrophysiology remain incompletely understood. We hypothesized that repolarizing K(2P)3.1 K+ channels, previously implicated in AF pathophysiology, may contribute to shaping the atrial action potential (AP), forming a specific electrical substrate with LV dysfunction that might represent a target for personalized antiarrhythmic therapy.Methods and results A total of 175 patients exhibiting different stages of LV dysfunction were included. Ion channel expression was quantified by real-time polymerase chain reaction and Western blot. Membrane currents and APs were recorded from atrial cardiomyocytes using the patch-clamp technique. Severely reduced LV function was associated with decreased atrial K(2P)3.1 expression in sinus rhythm patients. In contrast, chronic (c) AF resulted in increased K(2P)3.1 levels, but paroxysmal (p) AF was not linked to significant K(2P)3.1 remodelling. LV dysfunction-related suppression of K(2P)3.1 currents prolonged atrial AP duration (APD) compared with patients with preserved LV function. In individuals with concomitant LV dysfunction and cAF, APD was determined by LV dysfunction-associated prolongation and by cAF-dependent shortening, respectively, consistent with changes in K(2P)3.1 abundance. K(2P)3.1 inhibition attenuated APD shortening in cAF patients irrespective of LV function, whereas in pAF subjects with severely reduced LV function, K(2P)3.1 blockade resulted in disproportionately high APD prolongation.Conclusion LV dysfunction is associated with reduction of atrial K(2P)3.1 channel expression, while cAF leads to increased K2P3.1 abundance. Differential remodelling of K(2P)3.1 and APD provides a basis for patient-tailored antiarrhythmic strategies.

Objective : A multiscale functional clustering approach is proposed to investigate the organization of the epileptic networks during different sleep stages and in relation with the occurrence of seizures. Method : Stereo-electroencephalographic signals from seven pharmaco-resistant epileptic patients (focal cortical dysplasia type II) were analyzed. The discrete wavelet transform provided a multiscale framework on which a data-driven functional clustering procedure was applied, based on multivariate measures of integration and mutual information. The most interacting functional clusters (FCs) within the sampled brain areas were extracted. Results : FCs characterized by strongly integrated activity were observed mostly in the beta and alpha frequency bands, immediately before seizure onset and in deep sleep stages. These FCs generally included the electrodes from the epileptogenic zone. Furthermore, repeatable patterns were found across ictal events in the same patient. Conclusion : In line with previous studies, our findings provide evidence of the important role of beta and alpha activity in seizures generation and support the relation between epileptic activity and sleep stages. Significance : Despite the small number of subjects included in the study, the present results suggest that the proposed multiscale functional clustering approach is a useful tool for the identification of the frequency-dependent mechanisms underlying seizure generation.

Unverricht-Lundborg disease or progressive myoclonic epilepsy type 1 (EPM1) is an autosomal recessive disease caused by mutation of the cystatin B gene (CSTB), located on chromosome 21q22.3. The most common mutation is an expansion of unstable dodecamer repetition (CCCCGCCCCGCG), whereas other types of mutations are rare. Among these, heterozygous compound mutations are described to induce a more severe phenotype than that of homozygous dodecameric repetition. We report two siblings affected by heterozygous compound mutations carrying a novel mutation of the deletion of three nucleotides in exon 2 of the gene in position 132-134 of the coding sequence (c.132-134del) in the allele not including the dodecamer repetition. This mutation results in the loss of two amino acid residues and insertion of an asparagine in position 44 (p.Lys44_Ser45delinsAsn). Our patients presented a very different clinical picture. The male patient had a severe myoclonus, drug-resistant epilepsy and psychiatric comorbidity, while his affected sister had only very rare seizures and sporadic myoclonic jerks at awakening. The revision of literature about heterozygous compound EPM1 patients confirms this gender phenotypic expressivity, with female patients carrying less severe symptoms than male patients. These data lead to the hypothesis of complex gender-specific factors interacting with CSTB expressivity in EPM1 patients.

Ischemia-reperfusion (I/R) injury causes dynamic changes in electrophysiological properties that promote the incidence of post-ischemic arrhythmias. High-resolution optical action potential mapping allows for a quantitative assessment of the electrophysiological substrate at a cellular resolution within the intact heart, which is critical for elucidation of arrhythmia mechanisms. We and others have found that pharmacological inhibition of the translocator protein (TSPO) is highly effective against postischemic arrhythmias. A major hurdle that has limited the translation of this approach to patients is the fact that available TSPO ligands have several confounding effects, including a potent negative ionotropic property. To circumvent such limitations we developed an in vivo cardiac specific TSPO gene silencing approach as an alternative. Here, we provide the methodological details of our optical action potential mapping studies that were designed to probe the effects of TSPO silencing in hearts from spontaneously hypertensive rats (SHR) that are prone to I/R injury.

Ischemia-reperfusion (I/R) injury causes dynamic changes in electrophysiological properties that promote the incidence of post-ischemic arrhythmias. High-resolution optical action potential mapping allows for a quantitative assessment of the electrophysiological substrate at a cellular resolution within the intact heart, which is critical for elucidation of arrhythmia mechanisms. We and others have found that pharmacological inhibition of the translocator protein (TSPO) is highly effective against postischemic arrhythmias. A major hurdle that has limited the translation of this approach to patients is the fact that available TSPO ligands have several confounding effects, including a potent negative ionotropic property. To circumvent such limitations we developed an in vivo cardiac specific TSPO gene silencing approach as an alternative. Here, we provide the methodological details of our optical action potential mapping studies that were designed to probe the effects of TSPO silencing in hearts from spontaneously hypertensive rats (SHR) that are prone to I/R injury.

In this study, a functional clustering approach is proposed and tested for the identification of brain functional networks emerging during sleep-related seizures. Stereo-EEG signals recorded in patients with Type II Focal Cortical Dysplasia (FCD type II), were analyzed. This novel approach is able to identify the network configuration changes in pre-ictal and early ictal periods, by grouping Stereo-EEG signals on the basis of the Cluster Index, after wavelet multiscale decomposition. Results showed that the proposed method is able to detect clusters of interacting leads, mainly overlapped on the Epileptogenic Zone (EZ) identified by a clinical expert, with distinctive configurations related to analyzed frequency ranges. This suggested the presence of coupling activities between the elements of the epileptic system at different frequency scales.

The research here presented aims to the investigation of the Autonomic Nervous System (ANS) and of the sympatho-vagal balance during sleep-related seizures in patients affected by Focal Cortical Dysplasia (FCD) type II. Heart Rate Variability (HRV) signal was recorded during sleep together with S-EEG (stereo EEG) acquisitions performed for pre-surgical evaluation. The sympatho-vagal balance was estimated in pre-ictal, ictal and post-ictal time, by means of parameters in the time and in the frequency domain. The results here presented are related to 10 epileptic seizures occurring during the same night in one patient. The obtained results testify a significant decrease (p < 0.005) in the RR mean value and standard deviation during the ictal and post-ictal periods in respect to the inter-ictal phase, and a significant decrease (p < 0.001) in the HF(%) power between inter-ictal and post-ictal periods. All these findings are associated to a sympathetic activation and to a vagal drive reduction. A deeper knowledge of the correlations between ANS and epilepsy can lead to better understand the causes of SUDEP (Sudden Unexpected Death in Epilepsy); can contribute to the development of methods for the detection and prediction of epileptic seizures and help to evaluate the effects of vagal nerve stimulation used in those cases in which the patient is not an ideal candidate for surgery.

Summary Objective Hyperventilation (HV) during electroencephalography (EEG) is a standard clinical procedure to trigger seizures in patients affected by mesial temporal lobe epilepsy (MTLE). Despite the pathophysiology of this susceptibility to HV is not definitively understood, it may be hypothesized to be related to ictal and interictal sympathetic nervous system abnormalities, the presence of which is well known in MTLE patients. In order to test this hypothesis we investigated the HV effect on heart rate variability (HRV) in a group of MTLE patients, compared to a matched group of healthy controls. Material and methods Forty patients affected by MTLE and 40 age- and sex-matched controls were enrolled in the study. In those subjects, a standard electroencephalographic recording has been acquired and the high and the low frequency components (HF, LF) of heart rate variability (HRV) and their ratio (LF/HF) have been analyzed at rest and during the HV. Indeed, LF/HF is a reliable index of sympathetic tone modulation. Results HRV did not differ between MTLE and healthy subjects at rest, whereas HV induced a significant LF/HF increase only in MTLE. Within the MTLE group, males showed higher LF/HF increase during HV respect to females, while no differences related to the side of the epileptic focus were found. Discussion MTLE patients showed an increased sympathetic response to HV compared to healthy subjects. HRV analysis points towards an autonomic overactivation as a pathophysiological pathway subtending seizure triggered by hyperventilation in MTLE. Autonomic susceptibility in MTLE may help to explain the increased prevalence of arrhythmic events in these patients, potentially predisposing to Sudden Unexpected Death in Epilepsy (SUDEP).

It has been proved that Transcranial DCS (tDCS) can modulate cortical excitability, enhancing or decreasing, respectively by anodal or cathodal polarity. The short-term and lasting alterations induced by tDCS are strictly related to the charge density, duration of stimulation and the depth of neuron below the skull. Epilepsy represents a pathophysiological model of unbalanced relation between cortical excitation and inhibition. In this line, tDCS can be exploited to counterbalance the neuronal hyper-excitation through electric neural modulation. This paper aims at providing the efficacy of cathodal tDCS in reducing seizures’ frequency in drug-resistant focal epilepsy. The study was single blind and sham-controlled and compared seizure rate in the 7 days before and after tDCS and after sham in a cross-over design. 9 patients affected by focal resistant epilepsy were enrolled. After tDCS 3 out 9 patients have not any change in seizure rate. 6 patients reduced their seizure frequency >50%. No significant modification were recorded after sham. This study represents the proof that cathodal tDCS may be efficient in reducing seizures’frequency in focal resistant epilepsy.

Palilalia is a kind of motor perseveration involving speech, consisting in the continuous repetition of words or phrases, or both. Rarely it occurs in seizure disorders as ictal or post-ictal manifestation. We report a case of epileptic palilalia in a 71-year-old patient with a previous history of intracerebral haemorrhage in the left frontal region, characterized by the continuous repetition of the same speech sequence for few minutes. EEG recordings during NREM sleep and wakefulness showed recurrent and prolonged focal subclinical epileptiform paroxysms in the left mesial frontal region. Our case confirms the role of the left frontal lobe, reliably of the supplementary motor area (SMA), as neuroanatomic origin of ictal palilalia.

It has been proved that Transcranial DCS (tDCS) can modulate cortical excitability, enhancing or decreasing, respectively by anodal or cathodal polarity. The short-term and lasting alterations induced by tDCS are strictly related to the charge density, duration of stimulation and the depth of neuron below the skull. Epilepsy represents a pathophysiological model of unbalanced relation between cortical excitation and inhibition. In this line, tDCS can be exploited to counterbalance the neuronal hyper-excitation through electric neural modulation. This paper aims at providing the efficacy of cathodal tDCS in reducing seizures' frequency in drug-resistant focal epilepsy. The study was single blind and sham-controlled with an observation period of one month during which the patients or the caregivers provided a detailed seizures' calendar (frequency as n°/week; basal, post sham and post tDCS). Patients received sham or real tDCS treatment on the 8th and 22th days. Two patients affected by focal resistant epilepsy were enrolled. They both underwent a consistent reduction of the seizures'frequency: about 70 % for Patient 1 and about 50% for Patient 2. This study represents the proof that cathodal tDCS may be efficient in reducing seizures'frequency in focal resistant epilepsy.

Summary Purpose Inflammation has been shown to play a key role in epilepsy, and may also affect both the iron status and metabolism. Consequently, a relationship between iron metabolism and neuronal excitability and seizures could be expected. Methods We aimed at characterizing in 37 adult patients affected by focal epilepsy during the interictal period serum inflammatory cytokines, such as interleukin 6 (IL-6), IL-6 soluble receptor (IL6-sR), interleukin 1 (IL-1), IL-1 receptor-antagonist (IL-1RA), tumor necrosis factor-α (TNF-α), and markers of iron status and metabolism: hemoglobin concentration (Hgb), mean corpuscular volume (MCV), hematocrit (Hct) red blood cell (RBC) count, serum iron and copper concentrations, ceruloplasmin ( i Cp), the ceruloplasmin enzymatic activity ( e Cp), the specific ceruloplasmin activity ( e Cp/ i Cp), total ferroxidase activity, transferrin (Tf), serum ferritin (SF), Tf saturation (Sat-Tf), and ratio of ceruloplasmin to transferrin (Cp/Tf). We investigated the correlations between these biological markers as well their relationship with patients' clinical features. A group of 43 healthy subjects had the same serologic measurements to serve as controls. Results Our findings showed in the group of patients with epilepsy an increase of IL-6 ( p =0.026) and a decrease of TNF-α ( p =0.002) with respect to healthy subjects. For the first time, we also detected significant changes in iron metabolism as an increase of Cp/Tf ( p =0.011) and a decrease of Tf ( p =0.031), possibly driven by cytokine modifications and consistent with inflammation as acute phase and antioxidant activity markers. Accordingly, TNF-α positively correlated with Tf ( p =0.005). Finally, a significant positive correlation between seizures frequency and e Cp ( p =0.046) and inversely with Hgb ( p =0.038) and Hct ( p =0.041), and an inverse correlation between TNF-α and the duration of epilepsy ( p =0.021) was detected. Conclusions Our findings demonstrate a relevant relationship between epilepsy and systemic inflammation, with a consistent link between seizures, inflammatory cytokines (IL-6 and TNF-α) and iron regulation and metabolism, as acute phase and antioxidant markers.

It has been proved that Transcranial DCS (tDCS) can modulate cortical excitability, enhancing or decreasing, respectively by anodal or cathodal polarity. The short-term and lasting alterations induced by tDCS are strictly related to the charge density, duration of stimulation and the depth of neuron below the skull. Epilepsy represents a pathophysiological model of unbalanced relation between cortical excitation and inhibition. In this line, tDCS can be exploited to counterbalance the neuronal hyper-excitation through electric neural modulation. This paper aims at providing the efficacy of cathodal tDCS in reducing seizures’ frequency in drug-resistant focal epilepsy. The study was single blind and sham-controlled and compared seizure rate in the 7 days before and after tDCS and after sham in a cross-over design. 9 patients affected by focal resistant epilepsy were enrolled. After tDCS 3 out 9 patients have not any change in seizure rate. 6 patients reduced their seizure frequency >50%. No significant modification were recorded after sham. This study represents the proof that cathodal tDCS may be efficient in reducing seizures’frequency in focal resistant epilepsy.

To examine the relationship between facial affect recognition (FAR) and subjective perceptual disturbances (SPDs), we assessed SPDs in 82 patients with DSM-IV schizophrenia (44 with first-episode psychosis [FEP] and 38 with multiple episodes [ME]) using two subscales of the Frankfurt Complaint Questionnaire (FCQ), WAS (simple perception) and WAK (complex perception). Emotional judgment ability was assessed using Ekman and Friesen's FAR task. Impaired recognition of emotion correlated with scores on the WAS but not on the WAK. The association was significant in the entire group and in the ME group. FAR was more impaired in the ME than in the FEP group. Our findings suggest that there is a relationship between SPDs and FAR impairment in schizophrenia, particularly in multiple-episode patients.

Nonconvulsive status epilepticus (NCSE) is a severe medical condition that shows increased incidence in the elderly and is frequently underdiagnosed because of its pleomorphic presentation. We report an NCSE in a 76-year-old woman affected by dementia with acute change of cognitive status and behavior. Intravenous diazepam solved clinical and electroencephalographic manifestations. Neuropsychological assessment after NCSE conclusion showed impairment of several fields that remained unchanged at 3-month followup. NCSE should be considered when sudden and transient cognitive fluctuations appear in the elderly. Epileptic events in dementia occur frequently and are often underrecognized; this could be a misleading factor when considering a quick progression of mnesic performances. Moreover, recent findings both in animal models and in humans demonstrated the deep link between epilepsy and dementia, also supporting the hypothesis that epileptiform activity could contribute to cognitive impairment.

The differential diagnosis of loss of consciousness (LOC) is sometimes difficult due to the possible coexistence of syncope and seizures in the same patient, so that also an expert neurologist can misdiagnose. Our aim was to evaluate the clinical usefulness of synchronous tilt testing and video-EEG monitoring in patients diagnosed with epilepsy. In epilepsy outpatient clinic, we selected 23 patients (47 ± 21 years) divided into: – Group A: 17 (74%) patients newly diagnosed with epilepsy due to LOC with neurological clinical features or EEG epileptiform discharges (N = 10). 8 (47%) patients were given antiepileptic drugs. – Group B: 6 (26%) epileptic patients followed in epilepsy outpatient clinic, suffering of new episodes of LOC with unusual clinical features. 17 tilt testing resulted in clinically relevant episodes (74%). – Group A: 12 patients (52%) had vasovagal syncope, 2 patients (9%) psycogenic episodes. 6 out of 8 patients (75%) discontinued antiepileptic drugs. – Group B: 3 patients (50%) had vasovagal syncope, avoiding the increase of therapy. Synchronous tilt testing and video-EEG monitoring has an unquestionable clinical value for the differential diagnosis of LOC both in epileptic patients and in non-epileptic patients presenting with a doubtful ictal semiology.

Introduction. We aimed to test differences between healthy subjects and patients with respect to slow wave activity during wakefulness and sleep. Methods. Fifteen patients affected by nonlesional focal epilepsy originating within temporal areas and fourteen matched controls underwent a 24-hour EEG recording. We studied the EEG power spectral density during wakefulness and sleep in delta (1-4 Hz), theta (5-7 Hz), alpha (8-11 Hz), sigma (12-15 Hz), and beta (16-20 Hz) bands. Results. During sleep, patients with focal epilepsy showed higher power from delta to beta frequency bands compared with controls. The effect was widespread for alpha band and above, while localized over the affected hemisphere for delta (sleep cycle 1, P = .006; sleep cycle 2, P = .008; sleep cycle 3, P = .017). The analysis of interhemispheric differences showed that the only frequency band stronger over the affected regions was the delta band during the first 2 sleep cycles (sleep cycle 1, P = .014; sleep cycle 2, P = .002). During wakefulness, patients showed higher delta/theta activity over the affected regions compared with controls. Conclusions. Patients with focal epilepsy showed a pattern of power increases characterized by a selective slow wave activity enhancement over the epileptic regions during daytime and sleep. This phenomenon was stronger and asymmetric during the first sleep cycles.