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C7 Periodic lateralized epileptiform discharges (PLEDs)
Abstracts of the 13th European Congress of Clinical Neurophysiology / Clinical Neurophysiology 119 (2008), S1–S131 Another goal of monitoring is to use mapping techniques to identify the neural structures which are not always easily recognized anatomically (motor cortex, sensory cortex, CST, cranial nerves and nucleusus, roots, peripheral nerves, language mapping). Direct nerve stimulation with triggered EMG, phase reversal SEP, direct cortical and subcortical stimulation are commonly used methods. Factors influencing neuromonitoring include; factors related to the operation itself (ischemic or mechanical trauma); systemic factors (changes in the blood pressure or temperature); the anesthethic drugs or technical factors (electrode misplacement, wrong stimulation settings). It is important to choose a different scenario for each case, depending on neural structures under risk and use more then one method to increase the sensitivity of neuromonitoring. A preoperative electrophysiological examination may detect a co-existent pathology such as polyneuropathy, and if there are no responses it may alert the neurophysiologist to choose a different method for monitoring.
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When GPEDs are seen in EEG, the patient should carefully be checked for metabolic abnormalities and/or infectious diseases and intracranial lesions. GPEDs may be helpful in the determination of prognosis, showing the poor prognosis especially in cases when suppression-burst pattern is seen. Relatively little is known regarding the mechanism of GPEDs. For the mechanism of periodicity, cortical isolation theory has been proposed first by Cobb and Hill. It was suggested that periodic complexes in different clinical states might result from damaged white matter causing an anatomical or functional separation of cerebral cortex from normal afferent input. This theory is considered to be historically interesting now. Some investigators suggested that synchrony and periodicity may be related to virus-induced fusion of neuronal processes leading to electrotonic coupling between cells as GPEDs are commonly detected in viral diseases such as SSPE and CJD. But we still don’t know the real mechanism.
C7 Periodic lateralized epileptiform discharges (PLEDs) C6 Generalised periodic epileptiform discharges S. Saygi Professor of Neurology, School of Medicine, Hacettepe University Hospitals, Ankara, Turkey The term “periodic” refers to activity that is regularly recurrent in EEG; applies to waves or complexes occuring in sequence at an approximately regular state or intermittently at approximately regular intervals. Periodic patterns usually occupy most of a standard EEG rather than appearing as a transient portion. These complexes can be classified according to their distribution. If periodic complexes are limited to a focal brain area (often one hemisphere) they are known as periodic lateralised epileptiform discharges (PLEDs). When periodic complexes that occupied at least 50% of a standard 20 min EEG, occur over both hemispheres in a symmetric, diffuse and synchronised manner, they are known as generalised periodic epileptiform discharges (GPEDs). In this presentation, GPEDs will be discussed. GPEDs are very rare patterns. To classify these GPEDs, the interval between the discharges are used. Periodic short-interval diffuse discharges (PSIDDs) are the discharges with the interval duration 0.5–4 seconds. They occur in hypoxic or hepatic encephalopathy, drug toxicity, degenerative disorders such as Creutzfeldt–Jakob disease (CJD). PSIDDs due to anoxia were reported to be associated with a fatal outcome or severe neurological sequeals especially if it is associated with repetitive myoclonic jerks. Periodic long-interval diffuse discharges (PLIDDs) are the discharges with the interval duration 4–30 seconds. The complexes are polyphasic, containing an admixture of frequencies, including sharp components, and delta activity. They were detected mostly in subacute sclerosing panencephalitis (SSPE), drug toxicity and less commonly in hypoxic encephalopathy. Suppression-burst pattern is considered as a third group. Suppression-burst pattern is defined as high-voltage bursts of slow waves with intermingled sharp transients or spikes occur against a depressed background or complete flatness. The bursts are quasi-periodically repeated and frequently,but not invariably, accompanied by diffuse myoclonic jerks. Many records of deeply comatose patients are characterised by a suppression-burst pattern. Suppression-burst pattern often occur in hypoxic encephalopathy or drug overdose, particularly barbiturates or administration of anaesthetics such as sodium pentothal. In literature, there is no study with large number of patients having GPEDs excluding drug related or iatrogenic reasons and whose both neuroimaging studies were examined and metabolic abnormalities were evaluated. For this reason, we analysed the demographics, history of the seizures during the current illness, mental status, diagnosis, metabolic abnormalities, neuroimaging studies and prognosis of 37 adult patients who had GPEDs in their EEGs in Hacettepe University Hospital. Ages ranged from 17 to 82 years (mean 45 years). There were 19 males and 18 females. The most common aetiology of GPEDs was metabolic and/or infectious disease which was established in 22 patients (59.5%). Other aetiologies included subacute sclerosing panencephalitis (SSPE) in 11 patients (29.7%) and Creutzfeld–Jakob disease (CJD) in 4 patients (10.8%). We showed that structural lesions were found in most of the patients with GPEDs, but concurrent metabolic abnormalities and/or infectious diseases were also detected. Consciousness was impaired and clinical conditions were poor in various degrees in all of the patients when GPEDs were seen.
P. Tinuper Department of Neurological Sciences, University of Bologna, Italy PLEDs are non specific paroxysmal electroencephalographic abnormalities characterized by repetitive, periodic, and stereotyped lateralized spike, spike-and-wave or sharp wave complexes recurring at regular or nearly regular intervals that appear, normally transiently, in the occasion of an acute structural brain insult, and are associated with increase mortality. PLEDs are normally lateralized but in some case they may appear independently and asynchronously on both hemispheres (BIPLEDs). PLEDs Plus are instead characterized by PLEDs intermingled with high frequency, low voltage polyspike rhythms. Major ethiologies include cerebro-vascular acute disease, mainly hemmorrhage, traumatic brain injuries, brain tumors (either primitive and metastatic), encephalitis, anoxic or ischemic encephalopathies, acute methabolic brain sufference, and some particular condition as malformative brain lesions, Creutzfeld-Jacob disease, Rasmussen enchephalitis, subacute sclerosis panenchephalitis, Hashimoto enchephalipathy, etc. Rarely PLEDs may persist for long periods (more than 3 months), expecially in patient with subacute brain lesion as cerebral absesses or permanent lesions as tuberous scerosis or mesial temporal sclerosis. Neurophysiopathological hypothesis have considered the disruption of normal functional connections of cortical and subcortical structures but it seems that different mechanism act according to the different ethiologies.
C8 TMS basic course S. Rossi 1 , A. E. Oge 2 1 Dipartimento di Neuroscienze, Sezione Neurologia, University of Siena, Italy; 2 Noroloji AD, Istanbul Universitesi Istanbul Tip Fakultesi, Turkey In the first half of the course will provide basic information and practical demonstration as how to search individual resting motor threshold (RMT) of stimulation, recording a motor evoked potential (MEP), build up a paired-pulse curve for testing intracortical inhibitory (ICI) and facilitatory (ICF) circuits, and recording the cortical silent period (CSP). Some basic information as to how use these variables in a clinical/research settings will be provided as well. In the second half of the course, we will deal with central and peripheral motor conduction investigations. The following issues will be addressed: a. The sites of excitation in magnetic cortical and nerve root (or cranial nerve) stimulation. b. Central conduction time calculation by using the latencies of motor responses elicited by radicular stimulation and those of the F waves. c. Motor evoked potentials in diseases affecting the central nervous system. d. Localizing value of magnetic stimulation in spinal cord and nerve root lesions. e. Magnetic stimulation in brachial plexus lesions and other disorders affecting proximal regions of the peripheral nervous system. f. Magnetic stimulation in facial and trigeminal nerve disorders. g. Safety issues in single pulse TMS studies. h. TMS demonstration (on a patient or normal volunteer).
S65
When GPEDs are seen in EEG, the patient should carefully be checked for metabolic abnormalities and/or infectious diseases and intracranial lesions. GPEDs may be helpful in the determination of prognosis, showing the poor prognosis especially in cases when suppression-burst pattern is seen. Relatively little is known regarding the mechanism of GPEDs. For the mechanism of periodicity, cortical isolation theory has been proposed first by Cobb and Hill. It was suggested that periodic complexes in different clinical states might result from damaged white matter causing an anatomical or functional separation of cerebral cortex from normal afferent input. This theory is considered to be historically interesting now. Some investigators suggested that synchrony and periodicity may be related to virus-induced fusion of neuronal processes leading to electrotonic coupling between cells as GPEDs are commonly detected in viral diseases such as SSPE and CJD. But we still don’t know the real mechanism.
C7 Periodic lateralized epileptiform discharges (PLEDs) C6 Generalised periodic epileptiform discharges S. Saygi Professor of Neurology, School of Medicine, Hacettepe University Hospitals, Ankara, Turkey The term “periodic” refers to activity that is regularly recurrent in EEG; applies to waves or complexes occuring in sequence at an approximately regular state or intermittently at approximately regular intervals. Periodic patterns usually occupy most of a standard EEG rather than appearing as a transient portion. These complexes can be classified according to their distribution. If periodic complexes are limited to a focal brain area (often one hemisphere) they are known as periodic lateralised epileptiform discharges (PLEDs). When periodic complexes that occupied at least 50% of a standard 20 min EEG, occur over both hemispheres in a symmetric, diffuse and synchronised manner, they are known as generalised periodic epileptiform discharges (GPEDs). In this presentation, GPEDs will be discussed. GPEDs are very rare patterns. To classify these GPEDs, the interval between the discharges are used. Periodic short-interval diffuse discharges (PSIDDs) are the discharges with the interval duration 0.5–4 seconds. They occur in hypoxic or hepatic encephalopathy, drug toxicity, degenerative disorders such as Creutzfeldt–Jakob disease (CJD). PSIDDs due to anoxia were reported to be associated with a fatal outcome or severe neurological sequeals especially if it is associated with repetitive myoclonic jerks. Periodic long-interval diffuse discharges (PLIDDs) are the discharges with the interval duration 4–30 seconds. The complexes are polyphasic, containing an admixture of frequencies, including sharp components, and delta activity. They were detected mostly in subacute sclerosing panencephalitis (SSPE), drug toxicity and less commonly in hypoxic encephalopathy. Suppression-burst pattern is considered as a third group. Suppression-burst pattern is defined as high-voltage bursts of slow waves with intermingled sharp transients or spikes occur against a depressed background or complete flatness. The bursts are quasi-periodically repeated and frequently,but not invariably, accompanied by diffuse myoclonic jerks. Many records of deeply comatose patients are characterised by a suppression-burst pattern. Suppression-burst pattern often occur in hypoxic encephalopathy or drug overdose, particularly barbiturates or administration of anaesthetics such as sodium pentothal. In literature, there is no study with large number of patients having GPEDs excluding drug related or iatrogenic reasons and whose both neuroimaging studies were examined and metabolic abnormalities were evaluated. For this reason, we analysed the demographics, history of the seizures during the current illness, mental status, diagnosis, metabolic abnormalities, neuroimaging studies and prognosis of 37 adult patients who had GPEDs in their EEGs in Hacettepe University Hospital. Ages ranged from 17 to 82 years (mean 45 years). There were 19 males and 18 females. The most common aetiology of GPEDs was metabolic and/or infectious disease which was established in 22 patients (59.5%). Other aetiologies included subacute sclerosing panencephalitis (SSPE) in 11 patients (29.7%) and Creutzfeld–Jakob disease (CJD) in 4 patients (10.8%). We showed that structural lesions were found in most of the patients with GPEDs, but concurrent metabolic abnormalities and/or infectious diseases were also detected. Consciousness was impaired and clinical conditions were poor in various degrees in all of the patients when GPEDs were seen.
P. Tinuper Department of Neurological Sciences, University of Bologna, Italy PLEDs are non specific paroxysmal electroencephalographic abnormalities characterized by repetitive, periodic, and stereotyped lateralized spike, spike-and-wave or sharp wave complexes recurring at regular or nearly regular intervals that appear, normally transiently, in the occasion of an acute structural brain insult, and are associated with increase mortality. PLEDs are normally lateralized but in some case they may appear independently and asynchronously on both hemispheres (BIPLEDs). PLEDs Plus are instead characterized by PLEDs intermingled with high frequency, low voltage polyspike rhythms. Major ethiologies include cerebro-vascular acute disease, mainly hemmorrhage, traumatic brain injuries, brain tumors (either primitive and metastatic), encephalitis, anoxic or ischemic encephalopathies, acute methabolic brain sufference, and some particular condition as malformative brain lesions, Creutzfeld-Jacob disease, Rasmussen enchephalitis, subacute sclerosis panenchephalitis, Hashimoto enchephalipathy, etc. Rarely PLEDs may persist for long periods (more than 3 months), expecially in patient with subacute brain lesion as cerebral absesses or permanent lesions as tuberous scerosis or mesial temporal sclerosis. Neurophysiopathological hypothesis have considered the disruption of normal functional connections of cortical and subcortical structures but it seems that different mechanism act according to the different ethiologies.
C8 TMS basic course S. Rossi 1 , A. E. Oge 2 1 Dipartimento di Neuroscienze, Sezione Neurologia, University of Siena, Italy; 2 Noroloji AD, Istanbul Universitesi Istanbul Tip Fakultesi, Turkey In the first half of the course will provide basic information and practical demonstration as how to search individual resting motor threshold (RMT) of stimulation, recording a motor evoked potential (MEP), build up a paired-pulse curve for testing intracortical inhibitory (ICI) and facilitatory (ICF) circuits, and recording the cortical silent period (CSP). Some basic information as to how use these variables in a clinical/research settings will be provided as well. In the second half of the course, we will deal with central and peripheral motor conduction investigations. The following issues will be addressed: a. The sites of excitation in magnetic cortical and nerve root (or cranial nerve) stimulation. b. Central conduction time calculation by using the latencies of motor responses elicited by radicular stimulation and those of the F waves. c. Motor evoked potentials in diseases affecting the central nervous system. d. Localizing value of magnetic stimulation in spinal cord and nerve root lesions. e. Magnetic stimulation in brachial plexus lesions and other disorders affecting proximal regions of the peripheral nervous system. f. Magnetic stimulation in facial and trigeminal nerve disorders. g. Safety issues in single pulse TMS studies. h. TMS demonstration (on a patient or normal volunteer).