Introduction to Electroencephalogram: Epilepsy - Essay Example

Introduction to Electroencephalogram (EEG) Introduction to Electroencephalogram (EEG) EEG technique has been significantly used in the study and analysis of electrical fields of brain activity. In this case, it records the amplified potential difference between electrodes inserted on the scalp, straight on the cortex (e.g., with subdural electrodes), or using the deep electrode that is inserted into the brain matter. The technique enables the technician to determine the location, nature, and configuration theEEG generator so as to determine their patterns and whether they are abnormal or normal. This is important in diagnosing th epileptiform or nonepileptiform. In the brain, there is a three-dimensional volumes of cortex from which the electroencephalographic (EEG) signal is generated. Each dimension of the cortex produces unique signal and hence three different potential signals are are produced within the brain. Two of the signals are recorded from the surface of the scalp where they are recorded as two-dimensional fields against the voltage. This technique is accomplished by determining the physical and functional components of the EEG cortical generators. After determining the nature and the location of the EEG fields, the signal of the pd is characterized and graded according to inhibitory postsynaptic potentials (IPSPs) and excitatory postsynaptic potentials (EPSPs) The principle generators of EEG fields are created by the large, vertically oriented pyramidal neurons located in cortical layers III, V, and VI. According to the various tests that have been conducted on EEG fields, Epileptic spikes are negatively charged in nature. This is mainly caused by the depolarization of the superficial laminae. After the depolarization cycle, the subsequent repolarization cycle brings about the recurrent excitation and inhibition among laminae. This causes a sequence of negative spikes that normally translate to a negative wave detected by the electrodes. The Committee of the International Federation (CIF) of the body governing Electroencephalography and Clinical Neurophysiology (IFSECN) have made the recommendations that the placement of a specific system of electrode under standard conditions for use in all medical laboratories. The system, branded as the international 10-20 system, gives specific measurement parameters from bony landmarks and hence used to determine the nature of electrodes. Anatomical landmarks are useful in this technique as they give specific measurements made, and then approximately10% to 20% of a specified distance is useful in the electrode interval. The specific measurement enables the consistently in replication over time and between laboratories and hence the system is very reliable. However, a lot of vigilance needs to be taken. According to the American Clinical Neurophysiology Society a minimum of 21 electrodes in the international 10-20 system should be used for correct and safe finding. In order to obtain desirable outcome in this diagnosis, it is important to place the odd-numbered electrodes on the left side of the head, and the even-numbered electrodes on the right. Further, specific letters are used to designate the anatomical area. For instant, “F” means frontal. Apart from EEG voltage, there exists EEG montage that tends to maintain spatial relationships between electrodes in one direction better and the others direction. In this case, a montage is categorized as longitudinal if it maintains spatial relations best between electrodes in the sagittal direction. Similarly, a montage is transverse if it better maintains spatial correlations in the coronal direction. According to the International Federation of Clinical Neurophysiology Societies, EEG activation includes all procedures designed to elicit or enhance abnormal or normal EEG activity, particularly epileptiform abnormalities Activation procedures normally used regularly in the EEG laboratory for clinical concerns are photic stimulation, hyperventilation, and sleep. However, hyperventilation and photic stimulation are mostly preferred in activating epileptiform abnormalities, whereas sleep and drowsiness are useful for the activation of all forms of EEG abnormalities as well as normal epileptiform patterns. The steps that have been mentioned above seem quite simple and straight forward. However, they are not as simple as they have been analyzed. In this case, EEG analysis is a systematic and rational process that requires a series of organized steps that characterizes the recorded electrical potential in terms of specific description, parameter quantification and measurements. Clinically, abnormal EEG is characterized by cerebral dysfunction. If the normal pattern of the cerebral is altered, then an abnormal EEG will result and hence the cerebral dysfunction will emanate. Very often, the two types of abnormality are exhibited in the same recording. According to research, there exists a clear relationship between epileptiform activity in resting EEGs and convulsion disorders in children. However, there are chances that a patient will have cases of EEG spikes without necessarily experiencing a seizure disorder. Conversely, demonstration of spikes is not necessary for diagnosis and subsequent results of a seizure disorder. In patients already diagnosed with epilepsies, Epileptiform activity appears in up to 50% of one awake recording. However, the proportion may rise to between 80% and 85% if the test is carried out during sleep. When the recording is done for a number of times, the yield is increased as follow: two EEGs, 80% to 85%; four EEGs, 90%. Whether an epileptiform discharge has the morphological appearance of a “spike” or “sharp wave” depends on many factors, including the synchrony of the epileptic neuronal aggregate, the proximity of the epileptogenic cortical area to the recording electrodes, and extent of spread of the interictal epileptiform discharges within complex polysynaptic pathways before it is detected at the scalp. Rolandic spikes are characteristically stereotyped, abundant, high-voltage discharges with three clearly defined phases and prominent after-coming slow waves appearing singly or in groups in the central (rolandic) region (C3 or C4) using the 10–20 system. That spikes characteristic of the benign partial epilepsy of childhood may appear in association with other neurological diseases or in fully asymptomatic subjects indicates that their significance depends upon clinical correlation. Generalized Spike–Wave Complex, also referred to as generalized spike-and-slow-wave complexes, works using the same principle with generalized spike–waves. When a multiple spike is present in each and every complex, the occurrence is known as polyspike-and-waves. The most predominant components of a generalized spike–wave complex are synchronous bilaterally by a single spike. This is trailed by a series of rhythmic slow wave and as such, both serve as a surface-negative. The presence of generalized spike–wave complexes on the resting record or with hyperventilation gives very strong support to a clinical impression that the patient has a primary generalized seizure disorder. The Idiopathic Generalized Epilepsies (IGEs) The IGE comprises nearly a third of all case of epilepsies. These case are genetically determined and affect otherwise healthy people of both gender and all ethnicity/races. IGEs exhibits itself with characteristic absences, generalized tonic–clonic seizures and myoclonic jerks (GTCSs), alone or in varying combinations and severity Seizure-precipitating factors and photo sensitivity are common. Syndromes of IGE normally begin in childhood and adolescence, though some cases start during adulthood. They are commonly life-long, even though a few are age-related. New terminology for fundamental causes (structural-metabolic, genetic, and unknown) was initiated to replace the old (symptomatic, idiopathic, and cryptogenic) in 2010. Childhood absence epilepsy (CAE) The hallmark of the absence is abrupt, brief and severe impairment of consciousness with unresponsiveness and interruption of the ongoing voluntary activity, which is not restored during the ictus. Etiology: Although CAE is genetically determined, the precise mode of inheritance and the genes involved remain largely unidentified EEG: Inter-ictal EEG in CAE has normal background, with frequent rhythmic posterior delta activity, which may be a good prognostic sign. Focal spikes are common. Ictal discharges consist of 3 Hz generalized spike and wave discharges. Spikes are single, double or occasionally triple in the spike and slow-wave complexes Prognosis: the prognosis of CAE is excellent. Remission occurs before the age of 12 years. Less than 10% of the patients may develop infrequent or solitary GTCSs in adolescence or adult life. It is exceptional for patients to continue having absence seizures in their adult life. Management: Monotherapy with either valproate or ethosuximide controls absences in 80% of patients. Another option is lamotrigine monotherapy, although this is less effective with around half of patients becoming seizure free. If monotherapy shows failure or unacceptable undesirable reactions appear, the used drug should be replaced by another. Adding little dosage of lamotrigine to valproate is be the best combination in resistant cases. Juvenile Myoclonic Epilepsy (JME) JME is characterized, myoclonic jerks on awakening GTCSs in nearly all patients and typical absences in more than a third of the patients. Seizure-precipitating factors include Sleep deprivation and fatigue, particularly after excessive alcohol intake, is the most powerful precipitants of jerks and GTCSs in JME. Photosensitivity is confirmed with EEG in more than 30% of patients but this may be of no clinical significance Etiology JME is a genetically determined syndrome. Around 50–60% of families of probands with JME report seizures in first- or second-degree relatives. Inheritance is probably complex. The proposed models of inheritance include polygenic with a lower manifestation threshold for females, autosomal dominant with variable penetrance, a two-locus model with a dominant gene on chromo some 6p and an as-yet-unknown recessive gene, or the possibility that different geno types with different modes of inheritance underlie the phenotype. EEG The EEG in patients that have not been treated is typically abnormal, with 3–6 Hz generalized polyspikes and waves discharges, and with intradischarge fragmentations and unstable intradischarge frequency. A third of the patients show photoparoxysmal responses. A third may also have focal EEG abnormalities of single spikes, spike–wave complexes or slow waves. Prognosis All seizures are probably life-long, although improving after the fourth decade of life. JME may vary in severity from mild myoclonic jerks to frequent and severe falls and GTCSs if not appropriately diagnosed and treated. Seizures are usually well controlled with suitable dosage in above 90% of patients. Individuals with all three types of seizure are more likely to be resistant to treatment Management All formal current recommendations discourage or practically prohibit the use of valproate in women of childbearing age but provide no documented alternatives for their treatment in JME, where valproate has been the first line AED for the last 30 years. Converging evidence from multiple and independent sources indicate that levetiracetam is the first choice AED in the treatment in at least women with JME. Lamotrigine is widely used in JME. Benign childhood epilepsy with centrotemporal spikes (BCECTS) It starts from age 1 to 14 years; 75% start between 7 and 10 years (peak 8 or 9 years). There is a 1.5 male prevalence. Commonness is around 15% in children of age between 1–15 years with seizures. Incidence is 10–20 per 100,000 children aged 0–15 years. The cardinal characteristics of rolandic seizures are infrequent, often single, focal seizures consisting of unilateral facial sensorimotor symptoms (30% of patients) , oropharyngolaryngeal manifestations (53% of patients) , speech arrest (40% of patients) and hypersalivation (30% of patients). EEG Showed centero-temporal spikes (CTSs), which are the hallmark of BCECTS. They are age dependent, appearing at the age of 7–10 years, often continuing despite clinical reduction and usually disappearing by the age of 16 years. Although called CTSs, these are mainly high-amplitude, sharp and slow-wave complexes localized in the C3–C4 or C5–C6 (midway between central and temporal) electrodes. CTSs may be unilateral, but are more often bilateral, independently right or left. They are abundant (4–20/min) and usually occur in clusters. CTSs amplify during stages I–IV of sleep by a factor of two to five times without disturbing sleep organization Prognosis The prediction for rolandic seizures is consistently outstanding, with a risk of developing infrequent comprehensive seizures in adult life of less than 2%; absence seizures may be more frequent than GTCSs. Management Kids with rolandic seizures may not require AEDs, predominantly if the seizures are mild, infrequent, or nocturnal, or the treatment onset is close to the natural age of reduction of this age-limited abnormality. Patients with either secondarily frequent and seizures GTCSs or comorbid disorders may necessitate medication. carbamazepine is the favorite AED. Recent research found levetiracetam to be highly successful. References Cohen.L, Manion.L, Morrison.K (2011) Research Methods in Epilepsy disorder: 7th Edition Oxon,Reutledge Grice.K (2002) Eligibility under IDEA for Other Health Impaired Children Berg AT, Millichap JJ. The 2010 revised classification of seizures and epilepsy. Continuum (Minneap Minn). 2013 Jun;19(3 Epilepsy):571-97 Read More