Diffuse Slow Waves Research Articles

Porous medium acoustics of wave-induced vorticity diffusion

A theory for attenuation and dispersion of elastic waves due to wave-induced generation of vorticity at pore-scale heterogeneities in a macroscopically homogeneous porous medium is developed. The diffusive part of the vorticity field associated with a viscous wave in the pore space—the so-called slow shear wave—is linked to the porous medium acoustics through incorporation of the fluid strain rate tensor of a Newtonian fluid in the poroelastic constitutive relations. The method of statistical smoothing is then used to derive dynamic-equivalent elastic wave velocities accounting for the conversion scattering process into the diffusive slow shear wave in the presence of randomly distributed pore-scale heterogeneities. The result is a simple model for wave attenuation and dispersion associated with the transition from viscosity- to inertia-dominated flow regime.

EEG and magnetic resonance imaging abnormalities in patients with acute limbic encephalitis

OBJECTIVE: To describe the characteristics of electroencephalography (EEG) and MRI in patients with acute limbic encephalitis (LE). PATIENTS AND METHODS: We retrospectively reviewed medical records of 57 patients with diagnosis of LE from May 1994 to April 2010 and selected those with available EEG and MRI records. We analyzed EEG characteristics (type of abnormality, location and periodicity), reviewed MRIs and compared both. RESULTS: We included 22 patients, age ranging from 3 months to 71 years. EEG was abnormal in 21 patients (95.5%): Periodic lateralized epileptiform discharges (PLEDs) in 9 patients (40.9%), epileptiform discharges and/or temporal slow waves in 7 (31.8%) and 5 (22.7 %) with only background slowing. MRI showed abnormalities in temporal lobes of 19 patients (86.4%). The presence of PLEDs was strongly associated with hyperintense MRI-FLAIR signal involving hippocampus and temporal lobe cortex. Bilateral periodic lateralized epileptiform discharges (Bi-PLEDs) seen in two patients were related to extensive symmetrical bitemporal hyperintense MRI-FLAIR signal. Three patients with PLEDs had only mild ipsilateral FLAIR-hyperintense abnormalities, while contralateral temporal areas were moderate to severely affected on MRI. In four patients with smaller asymmetric bilateral lesions we observed PLEDs in the most affected side. Diffuse slow waves were observed in three patients with discrete hyperintense signal on MRI. CONCLUSION: PLEDs are a typical EEG finding in LE, but not present in all cases. However EEG may predict the extension of MRI abnormalities: slow, mild and nonspecific EEG abnormalities may be related to discrete MRI lesions, while PLEDs to extensive lesions. Moreover, in bilateral, asymmetrical and widespread lesions PLEDS may be contralateral to the most affected ("burned-out") area on MRI.

Diffusion-weighted MRI for Differentiating Creutzfeldt-Jacob Disease Mimics

Sporadic Creutzfeldt-Jacob disease (CJD) is a rare neurodegenerative, prion disease characterized by rapidly progressive dementia, visual disturbances, myoclonus and extrapyramidal and pyramidal involvement. An 80-year-old woman presented with progressive dementia and visual and auditory hallucinations over a two-month period. Neurological examination revealed cognitive impairment and right hemiparkinsonism. Diffusion-weighted MR imaging (DWI) revealed high intensity lesions in the left putamen, caudate and cerebral cortex (Picture 1A). TC-ECD SPECT images showed hypoperfusion in the left fronto-temporal cortex and basal ganglia (Picture 1B). Cerebrospinal fluid (CSF) examination revealed no pleocytosis but showed increased neuronspecific enolase levels and positive 14-3-3 protein. Electroencephalography results showed diffuse slow waves with periodic discharges lateralized to the left hemisphere. The diagnosis of probable CJD was made based on clinical manifestations and CSF and imaging findings (1). Because CJD can present with various neurologic signs owing to differences in brain involvement and disease progression, nonconvulsive status epilepticus, encephalopathy, and other neurodegenerative diseases, especially in the early phase, can mimic CJD (2). The presence of hallucination with asymmetric parkinsonism initially suggested dementia with Lewy bodies or corticobasal degeneration. In the study using DWI, the value of apparent diffusion coefficient maps can be useful for the diagnosis of atypical parkinson syndrome (3); however, the findings that high signal intensity lesions observed in striatal and caudate in addition to diffuse cortical cortex on DWI strongly suggested CJD. Moreover,

Infantile spams without hypsarrhythmia: A study of 16 cases

In this study, we present the electroclinical features and evolution of patients with epileptic spasms (ES) in clusters without hypsarrhythmia and with or without focal or generalized paroxysmal discharges on the interictal EEG. We also discuss how to nosologically define these cases. Methods Between February 1, 1990, and December, 2009, sixteen patients met the electroclinical diagnostic criteria of ES in clusters without hypsarrhythmia. Results ES were cryptogenic in thirteen patients and symptomatic in three. Age at onset of ES was between 4 months and 30 months, with a mean age of 9 months and a median age of 7 months. Seven patients had seizures before the onset of ES. Focal spikes were observed in seven patients, bilateral spikes and spikes and waves in five, multifocal spikes in two, and two patients had a normal EEG. The ictal EEG recording showed diffuse high-amplitude slow waves in ten patients, diffuse slow waves followed by voltage attenuation in four patients, and diffuse fast rhythms in two. ES were cured in five patients. Mean follow-up was 6 years. Neuropsychological development has been normal in the five latter patients. Eleven patients continue with seizures refractory to antiepileptic drugs after a mean follow-up of 10 years. Of these eleven patients, five have severe mental retardation, three have moderate mental retardation, and two have mild mental retardation. All of them show behavioral disturbances. Conclusion The patients in this series may be considered to have a variant of West syndrome rather than an electroclinically distinct epileptic syndrome.

A confused patient with raised anti-thyroid antibodies – an unusual case

tumour or a paraneoplatic manifestation of an occult malignancy, hypoxic brain injury, non-convulsive status epilepticus as well as rare metabolic causes of encephalopathy. Further investigations were conducted in an attempt to exclude these pathologies and obtain a definitive diagnosis. An electroencephalogram (EEG) showed diffuse slow waves with no features to suggest an epileptic focus or encephalitis. CT chest, abdomen and pelvis were done to exclude an underlying malignancy and were normal. Magnetic resonance imaging (MRI) and magnetic resonance angiogram (MRA) of the brain revealed small vessel disease only with normal flow in cerebral vessels. Antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), auto-antibody screen, rheumatoid factor, antineuronal/purkinje cell antibodies and human immunodeficiency virus (HIV) test were all normal. Antithyroid peroxidase antibody (TPO) titres were grossly elevated at 1,300 (normal value 60 U/ml) with a marginally low complement 3 (C3) 0.69 (0.75‐1.65) and normal C4. The mildly raised CSF protein count could be consistent with viral meningitis; however this does not explain the full neurological findings in this patient. In the absence of any definitive results, a working diagnosis of presumed encephalitis was made on admission and intravenous (iv) ceftriaxone and acyclovir were started empirically. Case progression

Childhood refractory focal epilepsy following acute febrile encephalopathy

We describe a group of previously normal children who developed severe focal epilepsy after an acute/sub-acute illness resembling encephalitis. This is a retrospective study. An acute phase (encephalitis/encephalopathy period) and a chronic phase (chronic focal resistant epilepsy) were defined. Eight patients were enrolled. The median age at onset was 6.6 years (range 8 months-17.6 years). In the acute phase, fever was the first symptom in all cases and was associated with seizures and status epilepticus. All patients had focal seizures arising in both hemispheres. Seizure onset occurred in the frontal and temporal regions. EEGs showed slowing background activity associated with focal or diffuse slow waves with rare epileptiform abnormalities. Cerebrospinal fluid oligoclonal bands were observed in four out of six patients tested. MRI images showed bilateral peri-insular hyperintensity in four cases. Five patients received corticosteroids, and in four cases, they were given along with intravenous immunoglobulins. The median duration of the acute phase was 19 days (range 15-30 days). During the chronic phase, which followed the acute phase without interval, patients presented with drug-resistant focal seizures and neuropsychological deficits, which ranged from hyperactivity and attention deficits to short-term verbal memory deficit, pervasive developmental disorders, and language delay. Considering the clinical presentations, EEG findings, and the associated occurrence of non-specific immunological activations, a possible immune-mediated pathogenesis can be hypothesized, although firm conclusions cannot be drawn out.

A case of catatonia secondary to polysubstance abuse and acetaminophen overdose.

To the Editor: Emergency departments have a high turnover of patients with substance abuse and/or dependence problems.1 Compared to the general population, this group has increased risk of suicidal ideation and attempts.2 We present a case of catatonia in the context of polysubstance abuse and acetaminophen overdose. Case report. Mr A, a 41-year-old white man, was brought to the emergency department for medical evaluation in 2007. Earlier during the day, he was noticed “staring” outside a school. Police were called and they found him staring blankly, mute, and “very slow.” In the emergency department, he was lying on bed and staring at the ceiling. Vital signs were stable. He was mute and did not respond to questions or follow any commands. He had mildly dilated pupils, and sluggishly reacted to light. Resistance and rigidity on passive movements and hyperreflexia were noted. When the side rail dropped accidentally, he leaned over the side of bed in a slow motion and then returned back to lying position. Complete blood cell count, comprehensive metabolic panel, chest x-ray, and electrocardiogram revealed no abnormalities. Drug screen was positive for cannabis and cocaine. Computed tomography of the head revealed no abnormalities normal. Creatine kinase was 340 U/L. The patient's identity was established from his driver's license, and his family was contacted. His history was significant for polysubstance dependence (cocaine, intravenous methamphetamine, cannabis, and alcohol) and multiple suicide attempts. He was hepatitis C positive, but had stopped treatment a year ago. Given the history of overdose, testing for serum acetaminophen level was requested; the level was found to be 213 μmol/L. He was treated with N-acetylcysteine and supportive measures. He continued to be in a catatonic state for the next 24 hours. Electroencephalogram showed diffuse slow waves but no epileptiform activity. Catatonic signs started resolving after 36–48 hours, and he admitted to acetaminophen overdose following relapse of drug abuse. Liver enzymes peaked at an aspartate aminotransferase level of 7,170 U/L and an alanine aminotransferase level of 7,903 U/L. The transplant center was contacted, but he was considered a poor candidate given history of hepatitis C, polysubstance dependence, and multiple suicide attempts. Fortunately, liver function tests started to show improvement and the patient recovered without any complications. Catatonia is characterized by motor and behavioral signs. DSM-IV-TR lists motor immobility, excessive purposeless motor activity, extreme negativism or mutism, peculiarities of voluntary movements, echolalia, and/or echopraxia as the signs of catatonia.3 Catatonic features are classified at 3 places in DSM-IV-TR: (1) as secondary to general medical condition, (2) as a subtype of schizophrenia, and (3) as a specifier for mood disorder. Catatonic syndrome is seen in multiple conditions including infectious, metabolic, autoimmune, neurologic, psychiatric, and substance use disorders as well as with endocrinopathies. Neurotransmitters, especially dopamine, γ-aminobutyric acid and glutamate, are involved in the pathogenesis of catatonic signs. Substance intoxication/withdrawal is a well-known cause of catatonia, but the acetaminophen overdose, which was almost overlooked, could have been fatal. Incidence of catatonia is difficult to estimate as many cases are unrecognized and difficult to differentiate from delirium, encephalopathy, and postictal state. The above case illustrates the importance of recognizing catatonia, undertaking a comprehensive history and physical examination, and judicial use of investigations to complete assessment and formulate a management plan. Supportive care and precautions to prevent medical complications such as deep venous thrombosis and aspiration pneumonia are vital. Intravenous and/or intramuscular lorazepam, intravenous divalproate, carbamazepine, topiramate, and electroconvulsive therapy have been used in prolonged catatonia.4

妊娠中に発症し，抗ＮＭＤＡ受容体抗体が陽性であった非ヘルペス性辺縁系脳炎の１例

A 19-year-old female in her 2nd trimester (17 weeks) of pregnancy became irritable a few days before admission. She became unable to open her mouth and could not talk. She was admitted to the psychiatric hospital due to a rapid change in behavior and a consciousness disturbance. She was diagnosed as having schizophrenia by a psychiatrist. Her EEG showed diffuse high voltage and slow waves. Acute encephalitis was then suspected. Her past and family histories were not suggestive of viral infection. On physical examination, she had a low grade fever. She had hyperhidrosis, autophagia, and repeated oral dyskinesia. Her consciousness level fluctuated from somnolence to stupor. Although her blood CRP level was mildly elevated and she had mild pleocytosis, HSV-PCR was negative in the cerebrospinal fluid (CSF). Abdominal ultrasound examination and MRI showed no ovarian teratoma. Computed tomography (CT) and magnetic resonance imaging (MRI) showed no brain abnormalities. Before analysis for specific nervous system antibodies, the initial diagnosis was non-herpetic limbic encephalitis. She was twice treated with a 6-day course of methylprednisolone (500 mg/day) infusion. She was also given phenobarbital since she had a tonic-clonic seizure about 1 month after admission. Finally, she had a normal delivery at 37 weeks. The baby was healthy, and the patient was discharged without sequelae. We concluded that her diagnosis was anti-N-methyl-D-aspartate (NMDA) receptor (anti-NMDAR) encephalitis based on the presence of anti-NMDAR antibody in the CSF. This report is the first description of a patient with anti-NMDAR antibody encephalitis. The precise mechanism of this encephalitis is not clear, although there have been several reports of autoimmune encephalitis during pregnancy. The patient's CSF anti-NMDAR antibody titer during treatment was measured. Before treatment, the CSF anti-NMDAR antibody titer was strongly positive, but it decreased during treatment and then disappeared after delivery. We hypothesized that the presence of the embryo or placenta may have triggered an antigenic signal and/or antibody through inappropriate immunological modulation.

Convulsive syncope: a condition to be differentiated from epilepsy

The clinical presentation of epilepsy and syncope can be confusingly similar. We present a patient with reflex syncopal episodes that mimic seizures using video-EEG recordings. During the episodes, head/eye deviations, automatisms and dystonic movements, suggesting an epileptic seizure, were observed. The EEG revealed diffuse slow waves when the patient lost consciousness and complete cessation of the cerebral activity occurred when the dystonic movements started. On ECG recordings, bradycardia, followed by complete asystolia lasting for 40 seconds, was observed. We conclude that the differential diagnosis of epilepsy and syncope can be quite misleading and clinical features may not always be reliable. In cases where diagnosis is uncertain, circulatory and cardiac causes should always be kept in mind and video-EEG with simultaneous cardiac recordings are mandatory for accuracy of diagnosis.

Numerical modeling of 1D transient poroelastic waves in the low-frequency range

Propagation of transient mechanical waves in porous media is numerically investigated in 1D. The framework is the linear Biot model with frequency-independent coefficients. The coexistence of a propagating fast wave and a diffusive slow wave makes numerical modeling tricky. A method combining three numerical tools is proposed: a fourth-order ADER scheme with time-splitting to deal with the time-marching, a space–time mesh refinement to account for the small-scale evolution of the slow wave, and an interface method to enforce the jump conditions at interfaces. Comparisons with analytical solutions confirm the validity of this approach.

“Acquired” hepatocerebral degeneration in a patient heterozygote carrier for a novel mutation in ATP7B gene

Acquired hepatocerebral degeneration (AHD) is a rare type of hepatic encephalopathy characterized by neuropsychiatric symptomatology, and peculiar neuroradiologic findings, without the clinical evidence of Wilson’s disease (WD). We studied a patient with AHD responsive to penicillamine who was heterozygote carrier for a novel mutation in the ATP7B gene, and discussed the possible role of the mutation in facilitating the appearance of the syndrome. A 37-year-old man with liver cirrhosis related to chronic hepatitis C was admitted because of progressive consciousness impairment. Family history was negative for WD. Ammoniemia was 176 lmol/L (NR, 9–33 lmol/L); total bilirubin 1.71 mg/dL (NR, 0.2–1.3 mg/dL); serum albumin 2.6 g/dL (NR, 3.3–5 g/dL); AST 62 U/L (NR, 10–45 U/L). Electroencephalogram disclosed diffuse slow wave activity. After rifaximin, lactulose, and branched chain amino acid infusion, his arousal state went back normal in about 12 hours, and ammonia levels decreased to 94 lmol/L.

P‐wave dispersion and attenuation in fractured and porous reservoirs – poroelasticity approach

ABSTRACTNatural fractures in hydrocarbon reservoirs can cause significant seismic attenuation and dispersion due to wave induced fluid flow between pores and fractures. We present two theoretical models explicitly based on the solution of Biot's equations of poroelasticity. The first model considers fractures as planes of weakness (or highly compliant and very thin layers) of infinite extent. In the second model fractures are modelled as thin penny‐shaped voids of finite radius. In both models attenuation is a result of conversion of the incident compressional wave energy into the diffusive Biot slow wave at the fracture surface and exhibits a typical relaxation peak around a normalized frequency of about 1. This corresponds to a frequency where the fluid diffusion length is of the order of crack spacing for the first model and the crack diameter for the second. This is consistent with an intuitive understanding of the nature of attenuation: when fractures are closely and regularly spaced, the Biot's slow waves produced by cracks interfere with each other, with the interference pattern controlled by the fracture spacing. Conversely, if fractures are of finite length, which is smaller than spacing, then fractures act as independent scatterers and the attenuation resembles the pattern of scattering by isolated cracks. An approximate mathematical approach based on the use of a branching function gives a unified analytical framework for both models.

Rotavirus-Associated Encephalopathy With a Reversible Splenial Lesion

The case is reported of a 2-year-old boy with a rotavirus-induced mild encephalopathy that presented as transient intensified signal on the splenium of the corpus callosum. The boy also experienced persistent diarrhea, vomiting, fever, and sudden disturbance of consciousness. Although cerebrospinal fluid analysis did not manifest pleocytosis, electroencephalography demonstrated global diffuse slow waves and cranial magnetic resonance imaging demonstrated intensified signal on the splenium of the corpus callosum. Methylprednisolone was infused for 3 days. The disturbance of consciousness disappeared within 24 hours without any other complications, and the splenial signal and electroencephalogram returned to normal within 6 days.

Numerical modeling of transient poroelastic waves in the low frequency range

A numerical method is proposed to simulate the propagation of transient poroelastic waves across heterogeneous media, in the low frequency range. A velocity-stress formulation of Biot's equations is followed, leading to a first-order differential system. The latter is splitted in two parts: a propagative one discretized by a fourth-order ADER scheme, and a diffusive one solved analytically. Near sources and interfaces, a space-time mesh refinement is implemented to capture the small scales of evolution of the diffusive slow compressional wave. Lastly, an immersed interface method is implemented to accurately model the jump conditions at interfaces between the different media. Numerical experiments in one and two dimensions are shown, with porous/porous or fluid/porous interfaces. Comparisons with analytical solutions confirm the efficiency of the approach. [1] G. Chiavassa, B. Lombard, J. Piraux, Numerical modeling of 1-D transient poroelastic waves in the low-frequency range, soumis au J. Comput. Appl. Math., (2007), disponible sur http://hal.archives-ouvertes.fr/hal-00193103/fr/

The management of infantile spasms

Infantile spasms (IS) is the most frequent epilepsy syndrome in infancy. Although the consensus triad of spasms in clusters with hypsarrhythmia adversely affecting psychomotor development1 seems quite straightforward, the great...

Sjogren's syndrome-associated meningoencephalomyelitis: Cerebrospinal fluid cytokine levels and therapeutic utility of tacrolimus

Serial changes in the circulating and cerebrospinal fluid (CSF) cytokine levels were assessed in a patient with Sjogren's syndrome (SS)-associated meningoencephalomyelitis. A 16-yr-old girl diagnosed as having primary SS at 8 yr of age presented headache and vomiting. CSF studies revealed lymphocyte-dominant pleocytosis and high IgM index, but no evidence of infection. Disturbed consciousness and diffuse slow waves on electroencephalogram led to the diagnosis of SS-meningoencephalitis. The clinical condition subsided after a cycle of dexamethasone therapy, however, 2 months later urinary retention and paresthesia of the lower body developed. Craniospinal magnetic resonance imaging (MRI) showed extensive intraparenchymal lesions with high T2-weighted signal intensity adjacent to the posterior left horn of lateral ventricle of the brain and the longitudinal lesion from C5 to T10 of the spinal cord. High-dose methyl-prednisolone and subsequent tacrolimus therapy has effectively controlled the activity of SS-meningoencephalomyelitis. Monitoring of systemic and CSF cytokine levels during the course of illness revealed that CSF interleukin-6, but not interferon-gamma or tumor necrosis factor-alpha levels were the sensitive indicator of disease activity. The unique cytokine profile, differing from those of infectious meningitis may be useful for predicting the central nervous system involvement in autoimmune disease.

Adult epileptic spasms: a clinical and video‐polygraphic study

To analyse the video-polygraphic features of two patients with adult epileptic spasms (ES). Two patients with epileptic encephalopathy related to different cortical malformation; epileptic spasms had been present since the age of 18 and 25 years respectively. The patients underwent a clinical and neurophysiological examination (awake and sleep video-polygraphic monitoring). In patient 1, epileptic spasms were characterized by loss of contact and a drooping forward of the head and upper extremities. ES were in clusters, of brief duration, lasting for 20'''-1''; all events occurred during eating. Awake and sleep interictal EEG disclosed asynchronous paroxysmal abnormalities in the temporo-parieto-occipital regions. The ictal EEG showed a diffuse slow wave complex with intermingled fast activity, prevalent on both anterior regions; on polygraphic recordings, the prevalence of the muscle activation, in crescendo-decrescendo, was in the neck and the right side. In patient 2, ES were characterized by loss of awareness, head deviation to the left, jerks of the head and left limbs. ES occurred in cluster, and were of brief duration (< 1"), usually on awakening. Interictal EEG showed epileptiform abnormalities in the right fronto-centro-temporal regions; abnormalities present in the awake EEG were enhanced during NREM sleep. The ictal EEG showed a diffuse, slow wave complex with intermingled fast activity, prevalent in the right regions, with concomitant muscle activation, in crescendo-decrescendo, on the left deltoid and tibialis anterior. Our two cases of adult ES were characterized by distinct clinical and polygraphic features, which were of brief duration, mild intensity, rare frequency per minute, and with preservation of cluster organization. In one patient, ES were induced by eating (reflex periodic spasms triggered by eating). A firm diagnosis of adult ES can be reached using video-polygraphic monitoring.

Steroid-Responsive Encephalitis Lethargica Syndrome with Malignant Catatonia

We report a 47-year-old man who is considered to have sporadic encephalitis lethargica (EL). He presented with hyperpyrexia, lethargy, akinetic mutism, and posture of decorticate rigidity following coma and respiratory failure. Intravenous methylprednisolone pulse therapy improved his condition rapidly and remarkably. Electroencephalography (EEG) showed severe diffuse slow waves of bilateral frontal dominancy, and paralleled the clinical course. Our patient fulfilled the diagnostic criteria for malignant catatonia, so we diagnosed secondary malignant catatonia due to EL syndrome. The effect of corticosteroid treatment remains controversial in encephalitis; however, some EL syndrome patients exhibit an excellent response to corticosteroid treatment. Therefore, EL syndrome may be secondary to autoimmunity against deep grey matter. It is important to distinguish secondary catatonia due to general medical conditions from psychiatric catatonia and to choose a treatment suitable for the medical condition.

Naltrexone alteration of the nicotine-induced EEG and mood activation response in tobacco-deprived cigarette smokers.

The neural mechanisms contributing to the arousal-eliciting actions of smoking and nicotine involve multiple neurotransmitter systems. The current study examined the role of opioid neurotransmission in modulating the neuroelectric- and mood-activating response to acute nicotine administration in overnight tobacco-deprived smokers. In a randomized, double-blind, placebo-controlled design involving 18 (10 male, 8 female) overnight tobacco-abstinent smokers, spectrally analyzed electroencephalographic (EEG) activity and subjective reports of mood, euphoria, and smoking withdrawal were assessed in response to nicotine gum (4 mg) after pretreatment with placebo or with 50 mg of the opioid antagonist naltrexone. In addition to reducing withdrawal symptoms and increasing euphoria ratings, as well as subjective alertness in male participants, nicotine induced an EEG arousal response consisting of diffuse slow wave (delta, theta) amplitude reductions, frontal fast alpha wave amplitude increments, and elevations in beta wave amplitude, which were greater in female than in male smokers. Naltrexone attenuated the alerting and euphoric actions of nicotine but did not affect nicotine's ameliorating effects on withdrawal symptoms. Nicotine-induced frontal reductions in delta and global reductions in theta were prevented by naltrexone pretreatment, as were increases in anterior recordings of relative fast alpha. These findings suggest that the opioid system is involved in nicotine-induced subjective and neuroelectric arousal and implicate opioid-cholinergic interactions in the elicitation of these arousal responses to nicotine.

Thursday July 6, 2006 11:30-13:30 Hall 3A Discussion Group Session Further understanding of the pathophysiological mechanisms involved in Landau-Kleffener and related syndromes

Abstract 1 P. Van Bogaert ( 1 Université Libre de Bruxelles, Hôpital Erasme, Belgium ) The pathophysiological mechanisms underlying the EEG phenomenon of continuous spike-waves during sleep (CSWS) and related cognitive and behavioral deficits remain poorly understood. It is now admitted that diffusion of the epileptiform discharges during NREM sleep is related to a mechanism of secondary bilateral synchrony from a focal cortical onset. It is probable that thalamic nuclei play an important role in this phenomenon, presumably through a development of the physiological slow-sleep oscillation into diffuse slow waves because of the lack of inhibitory constraint. This hypothesis is supported by experimental CSWS-like pattern obtained in cats following unilateral thalamic ablation. The role of the thalamus in the generation of the CSWS phenomenon was recently emphasized by reports of patients showing thalamic clastic lesions on MRI. Studies performed using PET with 18F-fluorodeoxyglucose (FDG) by our group and by others in children with CSWS and normal MRI have failed to show consistent thalamic abnormalities, but data analysis is complicated by the fact that physiological metabolic changes occur in the thalamus during brain development. Indeed, the metabolic activity of the thalamus adjusted for global metabolism increases significantly during childhood. On the other hand, numerous studies have shown that cortical metabolic abnormalities are frequently found in epileptic children with CSWS. The latter consist in either focal hypermetabolism or focal hypometabolism. The analysis of our FDG-PET data led to the following conclusions: (1) The hypermetabolic zone is the ictal onset zone; (2) Hypermetabolic areas are usually associated with distinct cortical hypometabolic areas, probably as a result of either loss of functional connectivity or inhibition mechanism; (3) Both hypermetabolic and hypometabolic areas tend to decrease or even disappear at the recovery phase of CSWS; and (4) Similar types of metabolic patterns and evolution may be seen in children with CSWS associated with polymicrogyric-like lesions.